76 results on '"Nightingale AK"'
Search Results
2. 8 Diagnostic performance of ECG detection of left atrial enlargement in patients with arterial hypertension relative to the cardiac magnetic resonance gold-standard: Impact of obesity: Abstract 8 Table 1
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Erdei, T, primary, Rodrigues, JC, additional, McIntyre, B, additional, Dastidar, A Ghosh, additional, Burchell, AE, additional, Ratcliffe, L, additional, Hart, EC, additional, Paton, JF, additional, Hamilton, M, additional, Nightingale, AK, additional, and Manghat, NE, additional
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- 2016
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3. 1043Role and cost-effectiveness of a stress imaging guided strategy in patients with non-culprit lesion at primary percutaneous coronary intervention
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Ghosh Dastidar, A, primary, Cengarle, M, additional, McAlindon, E, additional, Augustine, D, additional, Nightingale, AK, additional, and Bucciarelli-Ducci, C, additional
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- 2013
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4. Endothelial Dysfunction is Not the Limiting Factor in Skeletal Muscle Function of Patients with Chronic Heart Failure
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Nightingale, AK, primary, Crilley, JG, additional, Pegge, NC, additional, Schmitt, M, additional, Field, R, additional, Mumford, C, additional, and Frenneaux, MP, additional
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- 2001
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5. Effect of Vitamin C on Ventricular Vascular Coupling in Patients with CHF
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Nightingale, AK, primary, Schmitt, M, additional, Pegge, NC, additional, Field, R, additional, Mumford, C, additional, and Frenneaux, MP, additional
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- 2001
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6. Anp Regulates Venous Capacitance in Man
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Schmitt, M, primary, Nightingale, AK, additional, Broadley, A, additional, Taylor, J, additional, Campbell, R, additional, Cockcroft, J, additional, and Frenneaux, MP, additional
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- 2001
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7. Vitamin C Improves Ejection Duration in Chronic Heart Failure Patients by Delaying Wave Reflection
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Schmitt, M, primary, Nightingale, AK, additional, Cockcroft, JR, additional, Wilkinson, IB, additional, Broadley, AJ, additional, Morris-Thurgood, JA, additional, and Frenneaux, MP, additional
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- 2001
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8. Preoperative dehydration is unnecessary for pacemaker implantation
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Nash, A, primary, Nightingale, AK, additional, Turner, MS, additional, and Marshall, AJ, additional
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- 2001
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9. A case report of a normal aorta misdiagnosed as type A dissection by modern multidetector computed tomography.
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Hamilton MC, Nightingale AK, Masey S, Stuart AG, Angelini G, Hopkins R, McGann G, Hamilton, M C K, Nightingale, A K, Masey, S, Stuart, A G, Angelini, G, Hopkins, R, and McGann, G
- Abstract
Computed tomography (CT) is generally considered the investigation of choice to exclude acute aortic syndrome. We report an important potentially disastrous misdiagnosis using a modern 32 slice multidetector CT system. [ABSTRACT FROM AUTHOR]
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- 2010
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10. Whipple's disease.
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Williams OM, Nightingale AK, Hartley J, Bramkamp M, Ruggieri F, Schneemann M, Raoult D, Fenollar F, and Puéchal X
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- 2007
11. Preoperative dehydration is unnecessary for pacemaker implantation.
- Author
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Nash, A, Nightingale, AK, Turner, MS, and Marshall, AJ
- Published
- 2000
12. Abstracts
- Author
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Doulaptsis, C, Masci, PG, Goetschalckx, K, Janssens, S, Bogaert, J, Ferreira, VM, Piechnik, SK, DallArmellina, E, Karamitsos, TD, Francis, JM, Ntusi, N, Holloway, C, Choudhury, RP, Kardos, A, Robson, MD, Friedrich, MG, Neubauer, S, Miszalski-Jamka, T, Sokolowska, B, Szczeklik, W, Karwat, K, Miszalski-Jamka, K, Belzak, K, Malek, L, Mazur, W, Kereiakes, DJ, Jazwiec, P, Musial, J, Pedrotti, P, Masciocco, G, DAngelo, L, Milazzo, A, Quattrocchi, G, Zanotti, F, Frigerio, M, Roghi, A, Rimoldi, O, Kaasalainen, T, Kivistö, S, Holmström, M, Pakarinen, S, Hänninen, H, Sipilä, O, Lauerma, K, Banypersad, S.M, Fontana, M, Maestrini, V, Sado, D.M, Pinney, J, Wechalekar, A.D, Gillmore, J.D, Lachmann, H, Hawkins, P.N, Moon, J.C, Barone-Rochette, G, Pierard, S, Seldrum, S, de Ravensteen, CM, Melchior, J, Maes, F, Pouleur, A-C, Vancraeynest, D, Pasquet, A, Vanoverschelde, J-L, L Gerber, B, Captur, G, Muthurangu, V, Flett, AS, Wilson, R, Barison, A, Anderson, S, Cook, C, Sado, DM, McKenna, WJ, Mohun, TJ, Elliott, PM, Moon, JC, Pepe, A, Meloni, A, Gulino, L, Rossi, G, Paci, C, Spasisno, A, keilberg, P, Restaino, G, Resta, MC, Positano, V, lombardi, M, Reiter, U, Reiter, G, Kovacs, G, Schmidt, A, Olschewski, H, Fuchsjäger, M, Macmillan, A, Dabir, D, Rogers, T, Monaghan, M, Nagel, E, Puntmann, V, Semaan, E, Spottiswoode, B, Freed, B, Carr, M, Wasielewski, M, Fortney-Campione, K, Shah, S, Carr, J, Markl, M, Collins, J, Sung, YM, Hinojar, R, Ucar, EA, Dabir, D, Voigt, T, Gaddum, N, Schaeffter, T, Nagel, E, Puntmann, VO, Dabir, D, Rogers, T, Ucar, EA, Kidambi, A, Plein, S, Gebker, R, Schnackenburg, B, Voigt, T, Schaeffter, T, Nagel, E, Puntmann, VO, McAlindon, E, Bucciarelli-Ducci, C, Sado, D, Maestrini, V, Piechnik, S, Porter, J, Yamamura, J, Fischer, R, Moon, J, Symons, R, Doulaptsis, C, Masci, P.G, Goetschalckx, K, Dymarkowski, S, Janssens, S, Bogaert, J, Yalin, K, Golcuk, E, Ozer, CS, Buyukbayrak, H, Yilmaz, R, Dursun, M, Bilge, AK, Adalet, K, Reinstadler, SJ, Klug, G, Feistritzer, HJ, Mayr, A, Harrasser, B, Krauter, L, Mair, J, Schocke, MF, Pachinger, O, Metzler, B, Rigolli, M, To, A, Edwards, C, Ding, P, Christiansen, J, Rodríguez-Palomares, JF, Ortiz, JT, Bucciarelli, C, Lee, D, Wu, E, Bonow, RO, Karwat, K, Tomala, M, Miszalski-Jamka, K, Licholaj, S, Mazur, W, Kereiakes, DJ, Nessler, J, Zmudka, K, Jazwiec, P, Miszalski-Jamka, T, Peltonen, J, Kaasalainen, T, Kivistö, S, Holmström, M, Lauerma, K, Rutz, T, Meierhofer, C, Martinoff, S, Ewert, P, Hess, J, Stern, H, Fratz, S, Groarke, JD, Waller, AH, Blankstein, R, Kwong, RY, Steigner, M, Alizadeh, Z, Alizadeh, A, Khajali, Z, Mohammadzadeh, A, Kaykhavani, A, Heidarali, M, Singh, A, Bekele, S, Gunarathne, A, Khan, J, Nazir, SN, Steadman, CD, Kanagala, P, Horsfield, MA, McCann, GP, Duncan, RF, Dundon, BK, Nelson, AJ, Williams, K, Carbone, A, Worthley, MI, Zaman, A, Worthley, SG, Monney, P, Piccini, D, Rutz, T, Vincenti, G, Koestner, S, Stuber, M, Schwitter, J, Gripari, P, Maffessanti, F, Pontone, G, Andreini, D, Bertella, E, Mushtaq, S, Caiani, EG, Pepi, M, El ghannudi, S, Nghiem, A, Germain, P, Jeung, M-J, Roy, C, Gangi, A, Nucifora, G, Muser, D, Masci, PG, Barison, A, Piccoli, G, Rebellato, L, Puppato, M, Gasparini, D, Lombardi, M, Proclemer, A, Nucifora, G, Muser, D, Masci, PG, Barison, A, Piccoli, G, Rebellato, L, Puppato, M, Gasparini, D, Lombardi, M, Proclemer, A, Pöyhönen, P, Kivistö, S, Holmströn, M, Hänninen, H, Thorning, C, Bickelhaupt, S, Kampmann, C, Wentz, KU, Widmer, U, Juli, CF, Miszalski-Jamka, K, Klys, J, Glowacki, J, Kijas, M, Miszalski-Jamka, T, Adamczyk, T, Kwiecinski, R, Bogucka-Czapska, J, Ozaist, M, Mazur, W, Kluczewska, E, Kalarus, Z, Kukulski, T, Karakus, G, Marzluf, B, Bonderman, D, Tufaro, C, Pfaffenberger, S, Babyev, J, Maurer, G, Mascherbauer, J, Kockova, R, Tintera, J, Kautznerova, D, Cerna, D, Sedlacek, K, Kryze, L, El-Husseini, W, Sikula, V, Segetova, M, Kautzner, J, Vasconcelos, M, Lebreiro, A, Martins, E, Cardoso, JS, Madureira, AJ, Ramos, I, Maciel, MJ, Florian, A, Ludwig, A, Rösch, S, Sechtem, U, Yilmaz, A, Monmeneu, J.V, López-Lereu, M.P, Bonanad, C, Sanchis, J, Chaustre, F, Merlos, P, Valero, E, Bodí, V, Chorro, F.J, Yalin, K, Golcuk, E, Ozer, CS, Buyukbayrak, H, Yilmaz, R, Dursun, M, Bilge, AK, Adalet, K, Klug, G, Reinstadler, SJ, Feistritzer, HJ, Mayr, A, Riegler, N, Schocke, M, Esterhammer, R, Kremser, C, Pachinger, O, Metzler, B, Siddiqi, N, Cameron, D, Neil, C, Jagpal, B, Singh, S, Schwarz, K, Papadopoulou, S, Frenneaux, MP, Dawson, D, Robbers, LFHJ, Eerenberg, ES, Teunissen, PFA, Jansen, MF, Hollander, MR, Horrevoets, AJG, Knaapen, P, Nijveldt, R, Levi, MM, van Rossum, AC, Niessen, HWM, Marcu, CB, Beek, AM, van Royen, N, Everaars, H, Robbers, LFHJ, Nijveldt, R, Beek, AM, Teunissen, PFA, Hirsch, A, van Royen, N, Zijlstra, F, Piek, JJ, van Rossum, AC, Goitein, O, Grupper, A, Hamdan, A, Eshet, Y, Beigel, R, Medvedofsky, D, Herscovici, R, Konen, E, Hod, H, Matetzky, S, Cadenas, R, Iniesta, AM, Refoyo, E, Antorrena, I, Guzman, G, Cuesta, E, Salvador, O, López, T, Moreno, M, López-Sendon, JL, Alam, SR, Spath, N, Richards, J, Dweck, M, Shah, A, Lang, N, Semple, S, MacGillivray, T, Mckillop, G, Mirsadraee, S, Pessotto, R, Zamvar, V, Newby, DE, Henriksen, P, Reiter, G, Reiter, U, Kovacs, G, Olschewski, H, Fuchsjäger, M, Ahmad, S, Raza, U, Malik, A, Sun, JP, Eisner, R, Mazur, W, ODonnell, R, Positano, V, Meloni, A, Santarelli, MF, Landini, L, Tassi, C, Grimaldi, S, Gulino, L, De Marchi, D, Chiodi, E, Renne, S, Lombardi, M, Pepe, A, Wu, L, Germans, T, Güçlü, A, Allaart, CP, van Rossum, AC, Kalisz, K, Lehenbauer, K, Katz, D, Bi, X, Cordts, M, Guetter, C, Jolly, M-P, Freed, B, Shah, S, Markl, M, Flukiger, J, Carr, J, Collins, J, Osiak, A, Tyrankiewicz, U, Jablonska, M, Jasinski, K, Jochym, PT, Chlopicki), S, Skorka, T, Kalisz, K, Semaan, E, Katz, D, Bi, X, Cordts, M, Guetter, C, Jolly, MP, Freed, B, Flukiger, J, Lee, D, Kansal, P, Shah, S, Markl, M, Carr, J, Collins, J, Groarke, JD, Shah, RV, Waller, AH, Abbasi, SA, Kwong, RY, Blankstein, R, Steigner, M, Chin, CWL, Semple, S, Malley, T, White, A, Prasad, S, Newby, DE, Dweck, M, Pepe, A, Meloni, A, Lai, ME, Vaquer, S, Gulino, L, De Marchi, D, Cuccia, L, Midiri, M, Vallone, A, Positano, V, Lombardi, M, Pedrotti, P, Milazzo, A, Quattrocchi, G, Roghi, A, Rimoldi, O, Barison, A, De Marchi, D, Masci, P, Milanesi, M, Aquaro, GD, Keilberg, P, Positano, V, Lombardi, M, Positano, Vincenzo, Barison, Andrea, Pugliese, Nicola Riccardo, Masci, Piergiorgio, Del Franco, Annamaria, Aquaro, Giovanni Donato, Landini, Luigi, Lombardi, Massimo, Dieringer, MA, Deimling, M, Fuchs, K, Winter, L, Kraus, O, Knobelsdorff-Brenkenhoff, FV, Schulz-Menger, J, Niendorf, T, Hinojar, R, Ucar, EA, DCruz, D, Sangle, S, Dabir, D, Voigt, T, Gaddum, N, Schaeffter, T, Nagel, E, Puntmann, VO, Sung, YM, Pontone, G, Andreini, D, Bertella, E, Mushtaq, S, Gripari, P, Cortinovis, S, Loguercio, M, Baggiano, A, Conte, E, Pepi, M, El ghannudi, S, Hop, O, Germain, P, Jeung, M-J, De Cesare, A, Roy, C, Gangi, A, Barone-Rochette, G, Pierard, S, Seldrum, S, De Meester de Ravensteen, C, Melchior, J, Maes, F, Pouleur, A-C, Vancraeynest, D, Pasquet, A, Vanoverschelde, J-L, L Gerber, B, Bekele, S, Singh, A, Khan, JN, Nazir, SA, Kanagala, P, McCann, GP, Singh, A, Steadman, CD, Bekele, S, Khan, JN, Nazir, SA, Kanagala, P, McCann, GP, Paelinck, BP, Vandendriessche, T, De Bock, D, De Maeyer, C, Parizel, PM, Christiaan, J, Trauzeddel, RF, Gelsinger, C, Butter, C, Barker, A, Markl, M, Schulz-Menger, J, von Knobelsdorff, F, Florian, A, Schäufele, T, Ludwig, A, Rösch, S, Wenzelburger, I, Yilmaz, A, Sechtem, U, López-Lereu, M.P, Bonanad, C, Monmeneu, J.V, Sanchís, J, Estornell, J, Igual, B, Maceira, A, Chorro, F.J, Focardi, M, Cameli, M, Bennati, E, Massoni, A, Solari, M, Carbone, F, Banchi, B, Mondillo, S, Miia, H, Kirsi, L, Helena, H, Tiina, H, Jyri, L, Pauli, P, Sari, K, Schumm, J, Greulich, S, Grün, S, Ong, P, Klingel, K, Kandolf, R, Sechtem, U, Mahrholdt, H, Raimondi, F, Ou, P, Boudjemline, Y, Bajolle, F, Iserin, F, Bonnet, D, Collins, J, Kalisz, K, Benefield, B, Sarnari, R, Katz, D, Bi, X, Cordts, M, Guetter, C, Jolly, M-P, Freed, B, Flukiger, J, Kansal, P, Lee, D, Shah, S, Markl, M, Carr, J, Sokolowska, B, Miszalski-Jamka, T, Szczeklik, W, Karwat, K, Miszalski-Jamka, K, Belzak, K, Mazur, W, Kereiakes, DJ, Jazwiec, P, Musial, J, Silva, G, Almeida, AG, Resende, C, Marques, JS, Silva, D, David, C, Amaro, C, Costa, P, Silva, JAP, Diogo, AN, Tsokolov, AV, Senchilo, VG, Vertelkin, AV, Hoffmann, P, Mykjåland, G, Wangberg, H, Tønnessen, T, Sjaastad, I, Nordsletten, L, Hjørnholm, U, Løset, A, Rostrup, M, Meloni, A, Gulino, L, Keilberg, P, Palazzi, G, Maddaloni, D, Ascioti, C, Missere, M, Salvatori, C, Positano, V, Lombardi, M, Pepe, A, Meloni, A, Filosa, A, Gulino, L, Pulini, S, Salvatori, C, Chiodi, E, Ascioti, C, Keilberg, P, Positano, V, Lombardi, M, Pepe, A, Meloni, A, Gulino, L, Pietrapertosa, A, Izzi, G, De Marchi, D, Valeri, G, Preziosi, P, Positano, V, Lombardi, M, Pepe, A, Meloni, A, Ruffo, GB, Keilberg, P, Gulino, L, Gerardi, C, Sallustio, G, Tudisca, C, Positano, V, Lombardi, M, Pepe, A, Greulich, S, Backes, M, Schumm, J, Grün, S, Sechtem, U, Mahrholdt, H, Dorniak, K, MSc, AS, Szurowska, E, Fijalkowski, M, Rawicz-Zegrzda, D, Dudziak, M, Raczak, G, Hamdan, A, Baker, FA, Klein, M, Di Segni, E, Goitein, O, Fibisch, G, Konen, E, Müller-Bierl, B, Tanaka, K, Buls, N, Fierens, Y, van Cauteren, T, Willekens, I, van Laere, S, Luypaert, R, de Mey, J, Muzzarelli, S, Faragasso, E, Pedrazzini, G, Sürder, D, Pasotti, E, Moccetti, T, Faletra, F, Qayyum, AA, Hasbak, P, Larsson, HB, Mathiasen, AB, Vejlstrup, NG, Kjaer, A, Kastrup, J, Moschetti, K, Favre, D, Pinget, C, Pilz, G, Petersen, S, Wagner, A, Wasserfallen, JB, Schwitter, J, Ghosh Dastidar, A, Cengarle, M, McAlindon, E, Augustine, D, Nightingale, AK, Bucciarelli-Ducci, C, Dandekar, VK, Ertel, AW, Dickens, C, Gonzalez, RC, Farzaneh-Far, A, Ripley, DP, Higgins, D, McDiarmid, AK, Bainbridge, GJ, Uddin, A, Kidambi, A, Herzog, B, Greenwood, JP, Plein, S, Khanji, M, Newton, T, Westwood, M, Sekhri, N, and Petersen, SE
- Abstract
Background-Aims: Early post-infarction pericardial injury is a common finding but its diagnosis remains elusive. Though C-reactive protein (CRP) is considered a marker of myocardial damage, reflecting myocardial inflammation at the infarcted area, we sought to assess the relationship between CRP and pericardial injury depicted by cardiovascular magnetic resonance (CMR) imaging in patients with ST elevation myocardial infarction (MI). Methods and results: 181 MI patients (84% male) were studied with CMR in the first week and at 4 months post-infarction to assess infarct characteristics, left ventricular volumes/function and pericardial injury. The latter was defined as pericardial fluid >4mm and/or enhancement on late gadolinium enhancement CMR. The CRP-value at day 2 (according to previous literature) was used for correlation with CMR and clinical parameters. Pericardial injury was noted in 87 patients, i.e. effusion (n = 30), inflammation (n = 46), both (n = 11). Patients with pericardial injury had significantly higher peak values of cardiac biomarkers (p<0.001) and higher peak CRP-values than patients with normal pericardium (median 13 vs 43 mg/dl, p<0.001). A strong correlation was found between peak CRP-values and a) left venticular ejection fraction and infarct size both at 1 week and 4 months, b) myocardial hemorrhage, microvascular obstruction (MVO) and pericardial injury at 1 week, c) cardiac biomarkers values and time to PCI. However in a multiple regression model only pericardial injury (p = 0.003) and less importantly time to PCI (p = 0.022) were the independent predictors of CRP values. Conclusion: Pericardial damage described by cardiac MRI occurs often after acute ST elevation MI. CRP-values at the acute phase of MI reflect not only inflammation at the infarcted area but even more the inflammation of the surrounding pericardial tissue.
Table 1 Comparison of baseline clinical and biochemical parameters of patients with or without evidence of early post-infarct pericardial damage on CMR Normal Group (n = 94) Pericardial injury group (n = 87) p-value Agem, years 59±11 60±12 0.48 Male, n(%) 83 (88) 69 (79) 0.10 Diabets, n(%) 12 (13) 9 (10) 0.61 Smoker, n(%) 52 (55) 44 (51) 0.52 Hyperlipidemia, n(%) 56 (60) 55 (63) 0.62 BSA m2 2.0 ± 0.2 2.0 ± 0.2 0.20 Time to PCI, min 195 (155 − 274) 223 (160 − 335) 0.20 Troponin I, μ/l 44 (19 − 92) 90 (44 − 149) >0.001 CK-MB, U/L 128 (77 − 216) 250 (143 − 443) >0.001 CRP, mg/dL 13 (7 − 28) 43 (16 − 96) >0.001 Day of peak CRP 2 (1 − 3) 2 (1 − 3) 0.39 Table 2 Significant correlations between CRP Values and corresponding CMR measurements, cardic biomarkers and clinical related parameters Varibles Spearmanscorrelations r p-value CMR parameters 1 week LV EF −0.28 >0,001 Infractsize(%ofLV) 0.40 >0,001 Microvasular obstruction 0.27 >0,001 Hemorrhage 0.33 >0,001 Size of area atrisk 0.31 >0,001 Transmurality 0.30 >0,001 Pericaldial damage 0.43 >0,001 CMR parameters 4 months LVEF −0.43 >0,001 Infarctsize(%ofLV) 0.46 >0,001 Cardiac Biomarkers Peak TnI 0.34 >0,001 Peak CK-MB 0.32 >0,001 Other Time to PCI 0,182 0,007 - Published
- 2013
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13. The endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) predicts LV mass independent of afterload
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Michael P. Frenneaux, Kumaril Mishra, Aaron L. Sverdlov, Thomas H. Marwick, John D. Horowitz, Doan T.M. Ngo, Sharmalar Rajendran, Tamila Heresztyn, Rebecca H. Ritchie, Angus K Nightingale, Sverdlov, Aaron, Ngo, Doan Thi Minh, Nightingale, AK, Rajendran, Sharmalar, Mishra, K, Heresztyn, Tamila, Ritchie, RH, Marwick, TH, Frenneaux, MP, and Horowitz, John
- Subjects
Male ,Cancer Research ,medicine.medical_specialty ,Physiology ,Clinical Biochemistry ,Population ,asymmetric dimethylarginine ,Diastole ,Blood Pressure ,Endogeny ,left ventricular mass ,Arginine ,Nitric Oxide ,Left ventricular hypertrophy ,Biochemistry ,Nitric oxide ,chemistry.chemical_compound ,Afterload ,nitric oxide ,Predictive Value of Tests ,Internal medicine ,medicine ,Humans ,cardiovascular diseases ,education ,Aged ,Aged, 80 and over ,education.field_of_study ,business.industry ,Myocardium ,diastolic function ,Middle Aged ,medicine.disease ,Magnetic Resonance Imaging ,Endocrinology ,chemistry ,Quartile ,Echocardiography ,Multivariate Analysis ,vascular funtion ,Cardiology ,Female ,Hypertrophy, Left Ventricular ,Nitric Oxide Synthase ,Asymmetric dimethylarginine ,business ,Software - Abstract
Background: Nitric oxide (NO) is a modulator of left ventricular hypertrophy (LVH) and myocardial relaxation. The impact of NO availability on development of LVH has never been demonstrated in humans. We tested the hypotheses that elevation of asymmetric dimethylarginine (ADMA) concentrations (biochemical marker of decreased NO generation), and impairment of vascular responsiveness to NO donor GTN, would each predict the presence of LVH and associated LV diastolic dysfunction in a normal aging population. Conclusions: These data imply that NO bioavailability within the myocardium modulates earliest stages of LVH development and facilitates development of diastolic dysfunction at a given LV mass. Methods and results: In 74 subjects aged 68 ± 6 years, LV volumes and mass indexed to height2.7 (LVMI) were calculated from cardiac MRI. Despite the absence of clinically-defined LVH, there was a relationship (r = 0.29; p = 0.01) between systolic BP and LVMI. Both elevation of ADMA levels to the highest quartile or impairment of GTN responsiveness (determined by applanation tonometry) to the lowest quartile were determinants of LVMI independent of systolic BP (p = 0.01 and p = 0.03, respectively). Filling pressure (E/E0 ratio from echocardiography) was increased in patients with impaired vascular NO responsiveness (p < 0.05) irrespective of LVMI. ADMA remained a significant determinant of LVMI on multivariate analysis. Refereed/Peer-reviewed
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- 2011
14. Lack of association between aortic sclerosis and left ventricular hypertrophy in elderly subjects
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John D. Horowitz, Tamila Heresztyn, Doan T.M. Ngo, Sharmalar Rajendran, Aaron L. Sverdlov, Angus K Nightingale, Kumaril Mishra, Nightingale, AK, Sverdlov, Aaron, Rajendran, Sharmalar, Mishra, K, Heresztyn, Tamila, Ngo, Doan Thi Minh, and Horowitz, John
- Subjects
Male ,Aortic valve ,medicine.medical_specialty ,Population ,Heart Valve Diseases ,Coronary Artery Disease ,Left ventricular hypertrophy ,cardiac magnetic resonance ,chemistry.chemical_compound ,Afterload ,endothelial function ,Internal medicine ,medicine ,Humans ,Endothelial dysfunction ,aortic valve sclerosis ,education ,Aged ,Ultrasonography ,Aged, 80 and over ,education.field_of_study ,business.industry ,aging ,Age Factors ,Middle Aged ,medicine.disease ,left ventricular hypertrophy ,Blood pressure ,medicine.anatomical_structure ,chemistry ,Aortic Valve ,Ventricular pressure ,Cardiology ,cardiovascular system ,Female ,Hypertrophy, Left Ventricular ,Cardiology and Cardiovascular Medicine ,Asymmetric dimethylarginine ,business - Abstract
Background: The presence of aortic sclerosis has been associated with increased LV mass, particularly in hypertensive subjects. However, aortic sclerosis has also been associated with endothelial dysfunction, which may provide stimuli for development of left ventricular hypertrophy independent of afterload. Thus, we have sought to determine whether aortic sclerosis is a determinant of increased left ventricular mass in a non-hypertensive cohort of aging subjects. Methods: 79 subjects, mean age 68±6 years, without existing cardiovascular disease or previous antihypertensive therapywere studied. LV volumeswere calculated from the short axis stack of cardiacMRI and LV mass was indexed to height2.7. The presence of aortic sclerosiswas assessedwith echocardiography using backscatter from the aortic valve (AVBS) and visual scoring. Plasma asymmetric dimethylarginine levels and vascular responses to salbutamol were used to assess endothelial function. ANCOVA was used to test the relationship between LVmass index and afterload. Univariate and multivariate analyses were performed to find determinants of increased LV mass. Results: 15 (19%) of subjects had aortic sclerosis on the basis of AVBS; none had aortic valve areas b1.5 cm2. There was no significant difference in LV mass between subjects with and without aortic sclerosis.While LV mass was directly related to systolic blood pressure, this relationship was independent of the presence/absence of aortic sclerosis. On multivariate analysis, significant correlates of increased LV mass were male gender, systolic blood pressure and increased BMI, but not presence of aortic sclerosis. Conclusions: In this aging normotensive population free of established cardiovascular disease, aortic sclerosis is not associated with left ventricular hypertrophy. Refereed/Peer-reviewed
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- 2011
15. Carotid body dysregulation contributes to Long COVID symptoms.
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El-Medany A, Adams ZH, Blythe HC, Hope KA, Kendrick AH, Abdala Sheikh AP, Paton JFR, Nightingale AK, and Hart EC
- Abstract
Background: The symptoms of long COVID, which include fatigue, breathlessness, dysregulated breathing, and exercise intolerance, have unknown mechanisms. These symptoms are also observed in heart failure and are partially driven by increased sensitivity of the carotid chemoreflex. As the carotid body has an abundance of ACE2 (the cell entry mechanism for SARS-CoV-2), we investigated whether carotid chemoreflex sensitivity was elevated in participants with long COVID., Methods: Non-hositalised participants with long-COVID (n = 14) and controls (n = 14) completed hypoxic ventilatory response (HVR; the measure of carotid chemoreflex sensitivity) and cardiopulmonary exercise tests. Parametric and normally distributed data were compared using Student's unpaired t-tests or ANOVA. Nonparametric equivalents were used where relevant. Peason's correlation coefficient was used to examine relationships between variables., Results: During cardiopulmonary exercise testing the V
E /VCO2 slope (a measure of breathing efficiency) was higher in the long COVID group (37.8 ± 4.4) compared to controls (27.7 ± 4.8, P = 0.0003), indicating excessive hyperventilation. The HVR was increased in long COVID participants (-0.44 ± 0.23 l/min/ SpO2 %, R2 = 0.77 ± 0.20) compared to controls (-0.17 ± 0.13 l/min/SpO2 %, R2 = 0.54 ± 0.38, P = 0.0007). The HVR correlated with the VE /VCO2 slope (r = -0.53, P = 0.0036), suggesting that excessive hyperventilation may be related to carotid body hypersensitivity., Conclusions: The carotid chemoreflex is sensitised in long COVID and may explain dysregulated breathing and exercise intolerance in these participants. Tempering carotid body excitability may be a viable treatment option for long COVID patients., (© 2024. The Author(s).)- Published
- 2024
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16. Aging in females is associated with changes in respiratory modulation of sympathetic nerve activity and blood pressure.
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Adams ZH, Blythe HC, Charkoudian N, Curry TB, Joyner MJ, Kendrick AH, Nightingale AK, Abdala Sheikh AP, and Hart EC
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- Adult, Female, Male, Humans, Blood Pressure, Respiratory Rate, Respiration, Autonomic Nervous System, Aging, Hypertension, Hypotension
- Abstract
Sympathetic nerve activity (SNA) is tightly coupled with the respiratory cycle. In healthy human males, respiratory modulation of SNA does not change with age. However, it is unclear how this modulation is affected by age in females. We investigated whether respiratory sympathetic modulation is altered in healthy postmenopausal (PMF) versus premenopausal female (YF), and younger male (YM) adults, and determined its relationship to resting blood pressure. Muscle SNA (MSNA; microneurography), respiration (transducer belt), ECG, and continuous blood pressure were measured in 12 YF, 13 PMF, and 12 YM healthy volunteers. Respiratory modulation of MSNA was quantified during two phases of the respiratory cycle: mid-late expiration and inspiration/postinspiration. All groups showed respiratory modulation of MSNA ( P < 0.0005). There was an interaction between the respiratory phase and group for MSNA [bursts/100 heartbeats (HB) ( P = 0.004) and bursts/min ( P = 0.029)], with smaller reductions in MSNA during inspiration observed in PMF versus the other groups. Respiratory modulation of blood pressure was also reduced in PMF versus YF (6 [2] vs. 12 [9] mmHg, P = 0.008) and YM (13 [13] mmHg, P = 0.001, median [interquartile range]). The magnitude of respiratory sympathetic modulation was related to resting blood pressure in PMF only, such that individuals with less modulation had greater resting blood pressure. The data indicate that aging in postmenopausal females is associated with less inspiratory inhibition of MSNA. This correlated with a higher resting blood pressure in PMF only. Thus, the reduced modulation of MSNA could contribute to the age-related rise in blood pressure that occurs in females. NEW & NOTEWORTHY The current study demonstrates that respiratory modulation of sympathetic nerve activity (SNA) is reduced in healthy postmenopausal (PMF) versus premenopausal females (YF). Furthermore, respiratory sympathetic modulation was negatively related to resting blood pressure in postmenopausal females, such that blood pressure was greater in individual with less modulation. Reduced respiratory sympathetic modulation may have implications for the autonomic control of blood pressure in aging postmenopausal females, by contributing to age-related sympathetic activation and reducing acute, respiratory-linked blood pressure variation.
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- 2023
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17. Ventilatory Efficiency Is Reduced in People With Hypertension During Exercise.
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Hope K, Chant B, Hinton T, Kendrick AH, Nightingale AK, Paton JFR, and Hart EC
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- Humans, Middle Aged, Aged, Oxygen Consumption physiology, Lung, Prognosis, Exercise Test methods, Essential Hypertension, Exercise Tolerance, Heart Failure diagnosis, Hypertension diagnosis
- Abstract
Background An elevated ventilatory efficiency slope during exercise (minute ventilation/volume of expired CO
2 ; VE /VCO2 slope) is a strong prognostic indicator in heart failure. It is elevated in people with heart failure with preserved ejection, many of whom have hypertension. However, whether the VE /VCO2 slope is also elevated in people with primary hypertension versus normotensive individuals is unknown. We hypothesize that there is a spectrum of ventilatory inefficiency in cardiovascular disease, reflecting an increasingly abnormal physiological response to exercise. The aim of this study was to evaluate the VE /VCO2 slope in patients with hypertension compared with age-, peak oxygen consumption-, and sex-matched healthy subjects. Methods and Results Ramped cardiovascular pulmonary exercise tests to peak oxygen consumption were completed on a bike ergometer in 55 patients with primary hypertension and 24 normotensive controls. The VE /VCO2 slope was assessed from the onset of exercise to peak oxygen consumption. Data were compared using unpaired Student t test. Age (mean±SD, 66±6 versus 64±6 years; P =0.18), body mass index (25.4±3.5 versus 24±2.4 kg/m2 ; P =0.13), and peak oxygen consumption (23.2±6.6 versus 24±7.3 mL/min per kg; P =0.64) were similar between groups. The VE /VCO2 slope was elevated in the hypertensive group versus controls (31.8±4.5 versus 28.4±3.4; P =0.002). Only 27% of the hypertensive group were classified as having a normal VE /VCO2 slope (20-30) versus 71% in the control group. Conclusions Ventilatory efficiency is impaired people with hypertension without a diagnosis of heart failure versus normotensive individuals. Future research needs to establish whether those patients with hypertension with elevated VE /VCO2 slopes are at risk of developing future heart failure.- Published
- 2023
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18. Prospective multiparametric CMR characterization and MicroRNA profiling of anthracycline cardiotoxicity: A pilot translational study.
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Harries I, Biglino G, Ford K, Nelson M, Rego G, Srivastava P, Williams M, Berlot B, De Garate E, Baritussio A, Liang K, Baquedano M, Chavda N, Lawton C, Shearn A, Otton S, Lowry L, Nightingale AK, Carlos Plana J, Marks D, Emmanueli C, and Bucciarelli-Ducci C
- Abstract
Background: Anthracycline cardiotoxicity is a significant clinical challenge. Biomarkers to improve risk stratification and identify early cardiac injury are required., Objectives: The purpose of this pilot study was to prospectively characterize anthracycline cardiotoxicity using cardiovascular magnetic resonance (CMR), echocardiography and MicroRNAs (MiRNAs), and identify baseline predictors of LVEF recovery., Methods: Twenty-four patients (age 56 range 18-75 years; 42 % female) with haematological malignancy scheduled to receive anthracycline chemotherapy (median dose 272 mg/m
2 doxorubicin equivalent) were recruited and evaluated at three timepoints (baseline, completion of chemotherapy, and 6 months after completion of chemotherapy) with multiparametric 1.5 T CMR, echocardiography and circulating miRNAs sequencing., Results: Seventeen complete datasets were obtained. CMR left ventricular ejection fraction (LVEF) fell significantly between baseline and completion of chemotherapy (61 ± 3 vs 53 ± 3 %, p < 0.001), before recovering significantly at 6-month follow-up (55 ± 3 %, p = 0.018). Similar results were observed for 3D echocardiography-derived LVEF and CMR-derived longitudinal, circumferential and radial feature-tracking strain. Patients were divided into tertiles according to LVEF recovery (poor recovery, partial recovery, good recovery). CMR-derived mitral annular plane systolic excursion (MAPSE) was significantly different at baseline in patients exhibiting poor LVEF recovery (11.7 ± 1.5 mm) in comparison to partial recovery (13.7 ± 2.7 mm), and good recovery (15.7 ± 3.1 mm; p = 0.028). Furthermore, baseline miRNA-181-5p and miRNA-221-3p expression were significantly higher in this group. T2 mapping increased significantly on completion of chemotherapy compared to baseline (54.0 ± 4.6 to 57.8 ± 4.9 ms, p = 0.001), but was not predictive of LVEF recovery. No changes to LV mass, extracellular volume fraction, T1 mapping or late gadolinium enhancement were observed., Conclusions: Baseline CMR-derived MAPSE, circulating miRNA-181-5p, and miRNA-221-3p were associated with poor recovery of LVEF 6 months after completion of anthracycline chemotherapy, suggesting their potential predictive role in this context. T2 mapping increased significantly on completion of chemotherapy but was not predictive of LVEF recovery., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2022 Published by Elsevier B.V.)- Published
- 2022
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19. Cerebrovascular Variants and the Role of the Selfish Brain in Young-Onset Hypertension.
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Manghat NE, Robinson E, Mitrousi K, Rodrigues JCL, Hinton T, Paton JFR, Wise RG, Nightingale AK, and Hart EC
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- Adult, Brain, Cerebrovascular Circulation physiology, Humans, Middle Aged, Retrospective Studies, Young Adult, Circle of Willis abnormalities, Circle of Willis diagnostic imaging, Circle of Willis pathology, Hypertension
- Abstract
Background: Variants in the posterior anatomy of the cerebral circulation are associated with hypertension and lower cerebral blood flow in midlife (age ≈55 years); however, whether these variants are a result of aging or long-term exposure to high blood pressure is unclear. Additionally, the role these variants play in early onset of hypertension (<40 years) and poor cerebral perfusion in this population is unknown., Methods: We retrospectively examined whether specific cerebrovascular variants (vertebral artery hypoplasia and absent/hypoplastic posterior communicating arteries (an incomplete posterior circle of Willis) measured via magnetic resonance angiography) were associated with a diagnosis of hypertension in 220 young adults (<40 years; n=164 primary hypertensive [mean age±SD, 32±6 years] and n=56 [30±6 years] normotensive adults). Whether cerebrovascular variants were associated with lower cerebral blood flow (phase-contrast angiography) was measured in the hypertensive group only (n=146)., Results: Binary logistic regression (adjusted for age, sex, and body mass index) showed that vertebral artery hypoplasia with an incomplete posterior circle of Willis was associated with hypertension diagnosis ( P <0.001, odds ratio; 11.79 [95% CI, 3.34-41.58]). Vertebral artery hypoplasia plus an incomplete circle of Willis was associated with lower cerebral blood flow in young adults with hypertension ( P =0.0172)., Conclusions: Vertebral artery hypoplasia plus an incomplete posterior circle of Willis independently predicts hypertension in young adults suggesting that this variant is not acquired with aging into midlife. Importantly this variant combination was associated with lower cerebral perfusion, which may have long-term consequences on cerebrovascular health in young adults with hypertension.
- Published
- 2022
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20. The effect of left ventricular longitudinal strain on left atrial function and ventricular filling in hypertension.
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Erdei T, Rodrigues JCL, Hartley-Davies R, Dastidar AG, Szantho GV, Hart EC, Nightingale AK, Manghat NE, and Hamilton MCK
- Subjects
- Atrial Function, Left, Echocardiography methods, Heart Atria diagnostic imaging, Heart Atria pathology, Heart Ventricles diagnostic imaging, Humans, Hypertension complications, Hypertension diagnostic imaging, Hypertension pathology, Ventricular Dysfunction, Left complications
- Abstract
Aim: To assess the relationship of global longitudinal strain during left atrial (LA) and left ventricular (LV) filling and emptying., Materials and Methods: Using magnetic resonance imaging in 47 hypertensive patients, biplane global LV longitudinal strain was evaluated and related to LA and LV filling and emptying (by volumetric analysis), and to pulmonary vein and trans-mitral flow (by phase-contrast imaging). The results were compared to normal subjects., Results: In hypertensive patients, reduced global longitudinal LV strain was associated with reduced LA reservoir (47 ± 10 versus 53 ± 9%, p<0.05), reduced LA conduit function (21 ± 9 versus 32 ± 11%, p<0.004), reduced LA early peak emptying rate (150 ± 77 versus 230 ± 88 ml/s, p=0.007), and slower early LV filling (373 ± 141 versus 478 ± 141 ml/s, p=0.03). LA peak filling rate showed a positive correlation to LV peak emptying rate (R=0.331, p=0.02)., Conclusion: In hypertensive heart disease, impaired LV longitudinal systolic function causes reduced LA filling and emptying, and this leads directly to impaired LV filling and diastolic dysfunction., (Crown Copyright © 2022. Published by Elsevier Ltd. All rights reserved.)
- Published
- 2022
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21. Sympathetic-transduction in untreated hypertension.
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Kobetic MD, Burchell AE, Ratcliffe LEK, Neumann S, Adams ZH, Nolan R, Nightingale AK, Paton JFR, and Hart EC
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- Adult, Aged, Blood Pressure physiology, Body Mass Index, Heart Rate physiology, Humans, Male, Middle Aged, Muscle, Skeletal blood supply, Muscle, Skeletal innervation, Hypertension diagnosis, Sympathetic Nervous System physiology
- Abstract
Transduction of muscle sympathetic nerve activity (MSNA) into vascular tone varies with age and sex. Older normotensive men have reduced sympathetic transduction so that a given level of MSNA causes less arteriole vasoconstriction. Whether sympathetic transduction is altered in hypertension (HTN) is not known. We investigated whether sympathetic transduction is impaired in untreated hypertensive men compared to normotensive controls. Eight untreated hypertensive men and 10 normotensive men (age 50 ± 15 years vs. 45 ± 12 years (mean ± SD); p = 0.19, body mass index (BMI) 24.7 ± 2.7 kg/m
2 vs. 26.0 ± 4.2 kg/m2 ; p = 0.21) were recruited. MSNA was recorded from the peroneal nerve using microneurography; beat-to-beat blood pressure (BP; Finapres) and heart rate (ECG) were recorded simultaneously at rest for 10 min. Sympathetic-transduction was quantified using a previously described method. The relationship between MSNA burst area and subsequent diastolic BP was measured for each participant with the slope of the regression indicating sympathetic transduction. MSNA was higher in the hypertensive group compared to normotensives (73 ± 17 bursts/100 heartbeats vs. 49 ± 19 bursts/100 heart bursts; p = 0.007). Sympathetic-transduction was lower in the hypertensive versus normotensive group (0.04%/mmHg/s vs. 0.11%/mmHg/s, respectively; R = 0.622; p = 0.006). In summary, hypertensive men had lower sympathetic transduction compared to normotensive individuals suggesting that higher levels of MSNA are needed to cause the same level of vasoconstrictor tone., (© 2021. The Author(s).)- Published
- 2022
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22. The corrected left ventricular ejection fraction: a potential new measure of ventricular function.
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Rodrigues JCL, Rooms B, Hyde K, Rohan S, Nightingale AK, Paton J, Manghat N, Bucciarelli-Ducci C, Hamilton M, Zhang H, and MacIver DH
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- Heart Ventricles diagnostic imaging, Humans, Predictive Value of Tests, Stroke Volume, Cardiomyopathy, Dilated diagnostic imaging, Ventricular Function, Left
- Abstract
Left ventricular ejection fraction (LVEF) has a limited role in predicting outlook in heart diseases including heart failure. We quantified the independent geometric factors that determine LVEF using cardiac MRI and sought to provide an improved measure of ventricular function by adjusting for such independent variables. A mathematical model was used to analyse the independent effects of structural variables and myocardial shortening on LVEF. These results informed analysis of cardiac MRI data from 183 patients (53 idiopathic dilated cardiomyopathy (DCM), 36 amyloidosis, 55 hypertensives and 39 healthy controls). Left ventricular volumes, LVEF, wall thickness, internal dimensions and longitudinal and midwall fractional shortening were measured. The modelling demonstrated LVEF increased in a curvilinear manner with increasing mFS and longitudinal shortening and wall thickness but decreased with increasing internal diameter. Controls in the clinical cohort had a mean LVEF 64 ± 7%, hypertensives 66 ± 8%, amyloid 49 ± 16% and DCM 30 ± 11%. The mean end-diastolic wall thickness in controls was 8 ± 1 mm, DCM 8 ± 1 mm, hypertensives 11 ± 3 mm and amyloid 14 ± 3 mm, P < 0.0001). LVEF correlated with absolute wall thickening relative to ventricular size (R
2 = 0.766). A regression equation was derived from raw MRI data (R2 = 0.856) and used to 'correct' LVEF (EFc ) by adjusting the wall thickness and ventricular size to the mean of the control group. Improved quantification of the effects of geometric changes and strain significantly enhances understanding the myocardial mechanics. The EFc resulted in reclassification of a 'ventricular function' in some individuals and may provide an improved measure of myocardial performance especially in thick-walled, low-volume ventricles.- Published
- 2021
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23. Retrograde blood flow in the internal jugular veins of humans with hypertension may have implications for cerebral arterial blood flow.
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Rodrigues JCL, Strelko G, Warnert EAH, Burchell AE, Neumann S, Ratcliffe LEK, Harris AD, Chant B, Bowles R, Nightingale AK, Wise RG, Paton JFR, and Hart EC
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- Cerebrovascular Circulation physiology, Female, Humans, Imaging, Three-Dimensional, Male, Middle Aged, Prospective Studies, Spin Labels, Cerebral Arteries physiopathology, Hypertension physiopathology, Jugular Veins diagnostic imaging, Jugular Veins physiopathology, Magnetic Resonance Imaging methods
- Abstract
Objectives: To use multi-parametric magnetic resonance imaging (MRI) to test the hypothesis that hypertensives would have higher retrograde venous blood flow (RVBF) in the internal jugular veins (IJV) vs. normotensives, and that this would inversely correlate with arterial inflow and gray matter, white matter, and cerebrospinal fluid volumes., Methods: Following local institutional review board approval and written consent, a prospective observational 3-T MRI study of 42 hypertensive patients (53 ± 2 years, BMI 28.2 ± 0.6 kg/m
2 , ambulatory daytime systolic BP 148 ± 2 mmHg, ambulatory daytime diastolic BP 101 ± 2 mmHg) and 35 normotensive patients (48 ± 2 years, BMI 25.2 ± 0.8 kg/m2 , ambulatory daytime systolic BP 119 ± 3 mmHg, ambulatory daytime diastolic BP 90 ± 2 mmHg) was performed. Phase contrast imaging calculated percentage retrograde venous blood flow (%RVBF), brain segmentation estimated regional brain volumes from 3D T1-weighted images, and pseudo-continuous arterial spin labeling measured regional cerebral blood perfusion. Statistical analysis included two-sample equal variance Student's T tests, two-way analysis of variance with Tukey's post hoc correction, and permutation-based two-group general linear modeling (p < 0.05)., Results: In the left IJV, %RVBF was higher in hypertensives (6.1 ± 1.5%) vs. normotensives (1.1 ± 0.3%, p = 0.003). In hypertensives, there was an inverse relationship of %RVBF (permutation-based general linear modeling) to cerebral blood flow in several brain regions, including the left occipital pole and the cerebellar vermis (p < 0.01). Percentage retrograde flow in the left IJV correlated inversely with the total matter volume (gray plus white matter volume) in hypertensives (r = - 0.49, p = 0.004)., Conclusion: RVBF in the left IJV is greater in hypertensives vs. normotensives and is linked to regional hypoperfusion and brain total matter volume., Key Points: • Hypertensive humans have higher retrograde cerebral venous blood flow, associated with regional brain hypoperfusion and lower tissue volume, compared with controls. • Cerebral retrograde venous blood flow may add further stress to already hypoperfused tissue in hypertensive patients. • The amount of retrograde venous blood flow in hypertensive patients may predict which patients might be at higher risk of developing cerebral pathologies.- Published
- 2020
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24. Investigation and Treatment of High Blood Pressure in Young People: Too Much Medicine or Appropriate Risk Reduction?
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Hinton TC, Adams ZH, Baker RP, Hope KA, Paton JFR, Hart EC, and Nightingale AK
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- Adult, Blood Pressure physiology, Blood Pressure Determination, Humans, Hypertension physiopathology, Life Style, Medical Overuse, Risk Reduction Behavior, Young Adult, Antihypertensive Agents therapeutic use, Hypertension drug therapy
- Abstract
Hypertension among young people is common, affecting 1 in 8 adults aged between 20 and 40 years. This number is likely to increase with lifestyle behaviors and lowering of hypertension diagnostic thresholds. Early-life factors influence blood pressure (BP) although the mechanisms are unclear; BP tracks strongly within individuals from adolescence through to later life. Higher BP at a young age is associated with abnormalities on heart and brain imaging and increases the likelihood of cardiovascular events by middle age. However, diagnosis rates are lower, and treatment is often delayed in young people. This reflects the lack of high-quality evidence that lowering BP in young adults improves cardiovascular outcomes later in life. In this review, we evaluate the current evidence regarding the association between BP in young adult life and adverse cardiovascular outcomes later in life. Following this, we discuss which young people with raised BP should be investigated for secondary causes of hypertension. Third, we assess the current models to assess cardiovascular risk and show a lack of validation in the younger age group. Fourth, we evaluate the evidence for lifestyle interventions in this age group and demonstrate a lack of persistence in BP lowering once the initial intervention has been delivered. Fifth, we address the pros and cons of drug treatment for raised BP in young people. Finally, there are unique life events in young people, such as pregnancy, that require specific advice on management and treatment of BP.
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- 2020
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25. Cerebral Blood Flow Response to Simulated Hypovolemia in Essential Hypertension: A Magnetic Resonance Imaging Study.
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Neumann S, Burchell AE, Rodrigues JCL, Lawton CB, Burden D, Underhill M, Kobetić MD, Adams ZH, Brooks JCW, Nightingale AK, Paton JFR, Hamilton MCK, and Hart EC
- Subjects
- Adult, Age Factors, Arterial Pressure physiology, Blood Flow Velocity physiology, Blood Pressure Determination methods, Case-Control Studies, Female, Humans, Hypovolemia physiopathology, Longitudinal Studies, Lower Body Negative Pressure methods, Male, Middle Aged, Reference Values, Risk Assessment, Sex Factors, Simulation Training, Cerebrovascular Circulation physiology, Essential Hypertension diagnostic imaging, Essential Hypertension physiopathology, Hypovolemia diagnostic imaging, Magnetic Resonance Imaging methods, Vascular Resistance physiology
- Abstract
Hypertension is associated with raised cerebral vascular resistance and cerebrovascular remodeling. It is currently unclear whether the cerebral circulation can maintain cerebral blood flow (CBF) during reductions in cardiac output (CO) in hypertensive patients thereby avoiding hypoperfusion of the brain. We hypothesized that hypertension would impair the ability to effectively regulate CBF during simulated hypovolemia. In the present study, 39 participants (13 normotensive, 13 controlled, and 13 uncontrolled hypertensives; mean age±SD, 55±10 years) underwent lower body negative pressure (LBNP) at -20, -40, and -50 mmHg to decrease central blood volume. Phase-contrast MR angiography was used to measure flow in the basilar and internal carotid arteries, as well as the ascending aorta. CBF and CO decreased during LBNP ( P <0.0001). Heart rate increased during LBNP, reaching significance at -50 mmHg ( P <0.0001). There was no change in mean arterial pressure during LBNP ( P =0.3). All participants showed similar reductions in CBF ( P =0.3, between groups) and CO ( P =0.7, between groups) during LBNP. There was no difference in resting CBF between the groups ( P =0.36). In summary, during reductions in CO induced by hypovolemic stress, mean arterial pressure is maintained but CBF declines indicating that CBF is dependent on CO in middle-aged normotensive and hypertensive volunteers. Hypertension is not associated with impairments in the CBF response to reduced CO.
- Published
- 2019
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26. Repaired coarctation of the aorta, persistent arterial hypertension and the selfish brain.
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Rodrigues JCL, Jaring MFR, Werndle MC, Mitrousi K, Lyen SM, Nightingale AK, Hamilton MCK, Curtis SL, Manghat NE, Paton JFR, and Hart EC
- Subjects
- Adult, Aortic Coarctation complications, Aortic Coarctation physiopathology, Central Nervous System Vascular Malformations diagnostic imaging, Central Nervous System Vascular Malformations physiopathology, Circle of Willis abnormalities, Circle of Willis diagnostic imaging, Databases, Factual, Female, Humans, Hypertension diagnosis, Hypertension physiopathology, Magnetic Resonance Angiography, Male, Middle Aged, Retrospective Studies, Risk Assessment, Risk Factors, Treatment Outcome, Vertebral Artery abnormalities, Vertebral Artery diagnostic imaging, Young Adult, Aortic Coarctation surgery, Arterial Pressure, Cardiac Surgical Procedures adverse effects, Central Nervous System Vascular Malformations complications, Cerebrovascular Circulation, Circle of Willis physiopathology, Hypertension etiology, Vertebral Artery physiopathology
- Abstract
Background: It has been estimated that 20-30% of repaired aortic coarctation (CoA) patients develop hypertension, with significant cardiovascular morbidity and mortality. Vertebral artery hypoplasia (VAH) with an incomplete posterior circle of Willis (ipCoW; VAH + ipCoW) is associated with increased cerebrovascular resistance before the onset of increased sympathetic nerve activity in borderline hypertensive humans, suggesting brainstem hypoperfusion may evoke hypertension to maintain cerebral blood flow: the "selfish brain" hypothesis. We now assess the "selfish brain" in hypertension post-CoA repair., Methods: Time-of-flight cardiovascular magnetic resonance angiography from 127 repaired CoA patients (34 ± 14 years, 61% male, systolic blood pressure (SBP) 138 ± 19 mmHg, diastolic blood pressure (DBP) 76 ± 11 mmHg) was compared with 33 normotensive controls (42 ± 14 years, 48% male, SBP 124 ± 10 mmHg, DBP 76 ± 8 mmHg). VAH was defined as < 2 mm and ipCoW as hypoplasia of one or both posterior communicating arteries., Results: VAH + ipCoW was more prevalent in repaired CoA than controls (odds ratio: 5.8 [1.6-20.8], p = 0.007), after controlling for age, sex and body mass index (BMI). VAH + ipCoW was an independent predictor of hypertension (odds ratio: 2.5 [1.2-5.2], p = 0.017), after controlling for age, gender and BMI. Repaired CoA subjects with VAH + ipCoW were more likely to have difficult to treat hypertension (odds ratio: 3.3 [1.01-10.7], p = 0.049). Neither age at time of CoA repair nor any specific repair type were significant predictors of VAH + ipCoW in univariate regression analysis., Conclusions: VAH + ipCoW predicts arterial hypertension and difficult to treat hypertension in repaired CoA. It is unrelated to age at time of repair or repair type. CoA appears to be a marker of wider congenital cerebrovascular problems. Understanding the "selfish brain" in post-CoA repair may help guide management., Journal Subject Codes: High Blood Pressure; Hypertension; Magnetic Resonance Imaging (MRI); Cardiovascular Surgery; Cerebrovascular Malformations.
- Published
- 2019
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27. Left ventricular extracellular volume fraction and atrioventricular interaction in hypertension.
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Rodrigues JCL, Erdei T, Dastidar AG, Szantho G, Burchell AE, Ratcliffe LEK, Hart EC, Nightingale AK, Paton JFR, Manghat NE, and Hamilton MCK
- Subjects
- Adult, Aged, Female, Fibrosis pathology, Heart Atria diagnostic imaging, Heart Atria pathology, Heart Ventricles diagnostic imaging, Heart Ventricles pathology, Humans, Hypertension diagnostic imaging, Hypertension pathology, Magnetic Resonance Imaging, Male, Middle Aged, Prospective Studies, Cardiac Volume physiology, Heart Atria physiopathology, Heart Ventricles physiopathology, Hypertension physiopathology
- Abstract
Objectives: Left atrial enlargement (LAE) predicts cardiovascular morbidity and mortality. Impaired LA function also confers poor prognosis. This study aimed to determine whether left ventricular (LV) interstitial fibrosis is associated with LAE and LA impairment in systemic hypertension., Methods: Following informed written consent, a prospective observational study of 86 hypertensive patients (49 ± 15 years, 53% male, office SBP 168 ± 30 mmHg, office DBP 97 ± 4 mmHg) and 20 normotensive controls (48 ± 13 years, 55% male, office SBP 130 ± 13 mmHg, office DBP 80 ± 11 mmHg) at 1.5-T cardiovascular magnetic resonance was conducted. Extracellular volume fraction (ECV) was calculated by T1-mapping. LA volume (LAV) was measured with biplane area-length method. LA reservoir, conduit and pump function were calculated with the phasic volumetric method., Results: Indexed LAV correlated with indexed LV mass (R = 0.376, p < 0.0001) and ECV (R = 0.359, p = 0.001). However, ECV was the strongest significant predictor of LAE in multivariate regression analysis (odds ratio [95th confidence interval] 1.24 [1.04-1.48], p = 0.017). Indexed myocardial interstitial volume was associated with significant reductions in LA reservoir (R = -0.437, p < 0.0001) and conduit (R = -0.316, p = 0.003) but not pump (R = -0.167, p = 0.125) function. Multiple linear regression, correcting for age, gender, BMI, BP and diabetes, showed an independent decrease of 3.5% LA total emptying fraction for each 10 ml/m
2 increase in myocardial interstitial volume (standard β coefficient -3.54, p = 0.002)., Conclusions: LV extracellular expansion is associated with LAE and impaired LA reservoir and conduit function. Future studies should identify if targeting diffuse LV fibrosis is beneficial in reverse remodelling of LA structural and functional pathological abnormalities in hypertension., Key Points: • Left atrial enlargement (LAE) and impairment are markers of adverse prognosis in systemic hypertension but their pathophysiology is poorly understood. • Left ventricular extracellular volume fraction was the strongest independent multivariate predictor of LAE and was associated with impaired left atrial reservoir and conduit function. • LV interstitial expansion may play a central role in the pathophysiology of adverse atrioventricular interaction in systemic hypertension.- Published
- 2019
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28. Wave intensity analysis in the internal carotid artery of hypertensive subjects using phase-contrast MR angiography and preliminary assessment of the effect of vessel morphology on wave dynamics.
- Author
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Neumann S, Sophocleous F, Kobetic MD, Hart EC, Nightingale AK, Parker KH, Hamilton MK, and Biglino G
- Subjects
- Aorta diagnostic imaging, Aorta pathology, Aorta physiopathology, Blood Pressure Determination, Carotid Artery, Internal pathology, Feasibility Studies, Female, Humans, Hypertension pathology, Image Interpretation, Computer-Assisted methods, Male, Middle Aged, Carotid Artery, Internal diagnostic imaging, Carotid Artery, Internal physiopathology, Hypertension diagnostic imaging, Hypertension physiopathology, Magnetic Resonance Angiography methods
- Abstract
Objective: Hypertension is associated with reduced cerebral blood flow, but it is not known how this impacts on wave dynamics or potentially relates to arterial morphology. Given the location of the internal carotid artery (ICA) and risks associated with invasive measurements, wave dynamics in this artery have not been extensively assessed in vivo. This study explores the feasibility of studying wave dynamics in the internal carotid artery non-invasively., Approach: Normotensive, uncontrolled and controlled hypertensive participants were recruited (daytime ambulatory blood pressure <135/85 mmHg and >135/85 mmHg, respectively; n = 38). Wave intensity, reservoir pressure and statistical shape analyses were performed on the right ICA and ascending aorta high-resolution phase-contrast magnetic resonance angiography data., Main Results: Wave speed in the aorta was significantly lower in normotensive compared to hypertensive participants (6.7 ± 1.8 versus 11.2 ± 6.2 m s
-1 for uncontrolled and 11.8 ± 4.6 m s-1 for controlled hypertensives, p = 0.02), whilst there were no differences in wave speed in the ICA. There were no significant differences between the groups for the wave intensity or reservoir pressure. Interestingly, a significant association between the anatomy of the ICA and wave energy (FCW and size, r2 = 0.12, p = 0.04) was found., Significance: This study shows it is feasible to study wave dynamics in the ICA non-invasively. Whilst changes in aortic wave speed confirmed an expected increase in arterial stiffness, this was not observed in the ICA. This might suggest a protective mechanism in the cerebral circulation, in conjunction with the effect of vessel tortuosity. Furthermore, it was observed that ICA shape correlated with wave energy but not wave speed.- Published
- 2018
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29. B-type natriuretic peptide-guided therapy for heart failure (HF): a systematic review and meta-analysis of individual participant data (IPD) and aggregate data.
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Pufulete M, Maishman R, Dabner L, Higgins JPT, Rogers CA, Dayer M, MacLeod J, Purdy S, Hollingworth W, Schou M, Anguita-Sanchez M, Karlström P, Shochat MK, McDonagh T, Nightingale AK, and Reeves BC
- Subjects
- Cause of Death, Heart Failure mortality, Humans, Mortality, Natriuretic Peptide, Brain blood, Randomized Controlled Trials as Topic, Heart Failure drug therapy, Hospitalization, Natriuretic Peptide, Brain drug effects, Quality of Life
- Abstract
Background: We estimated the effectiveness of serial B-type natriuretic peptide (BNP) blood testing to guide up-titration of medication compared with symptom-guided up-titration of medication in patients with heart failure (HF)., Methods: Systematic review and meta-analysis of randomised controlled trials (RCTs). We searched: MEDLINE (Ovid) 1950 to 9/06/2016; Embase (Ovid), 1980 to 2016 week 23; the Cochrane Library; ISI Web of Science (Citations Index and Conference Proceedings). The primary outcome was all-cause mortality; secondary outcomes were death related to HF, cardiovascular death, all-cause hospital admission, hospital admission for HF, adverse events, and quality of life. IPD were sought from all RCTs identified. Random-effects meta-analyses (two-stage) were used to estimate hazard ratios (HR) and confidence intervals (CIs) across RCTs, including HR estimates from published reports of studies that did not provide IPD. We estimated treatment-by-covariate interactions for age, gender, New York Heart Association (NYHA) class, HF type; diabetes status and baseline BNP subgroups. Dichotomous outcomes were analysed using random-effects odds ratio (OR) with 95% CI., Results: We identified 14 eligible RCTs, five providing IPD. BNP-guided therapy reduced the hazard of hospital admission for HF by 19% (13 RCTs, HR 0.81, 95% CI 0.68 to 0.98) but not all-cause mortality (13 RCTs; HR 0.87, 95% CI 0.75 to 1.01) or cardiovascular mortality (5 RCTs; OR 0.88, 95% CI 0.67 to 1.16). For all-cause mortality, there was a significant interaction between treatment strategy and age (p = 0.034, 11 RCTs; HR 0.70, 95% CI 0.53-0.92, patients < 75 years old and HR 1.07, 95% CI 0.84-1.37, patients ≥ 75 years old); ejection fraction (p = 0.026, 11 RCTs; HR 0.84, 95% CI 0.71-0.99, patients with heart failure with reduced ejection fraction (HFrEF); and HR 1.33, 95% CI 0.83-2.11, patients with heart failure with preserved ejection fraction (HFpEF)). Adverse events were significantly more frequent with BNP-guided therapy vs. symptom-guided therapy (5 RCTs; OR 1.29, 95% CI 1.04 to 1.60)., Conclusion: BNP-guided therapy did not reduce mortality but reduced HF hospitalisation. The overall quality of the evidence varied from low to very low. The relevance of these findings to unselected patients, particularly those managed by community generalists, are unclear., Systematic Review Registration: PROSPERO CRD42013005335.
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- 2018
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30. Antihypertensive Treatment Fails to Control Blood Pressure During Exercise.
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Chant B, Bakali M, Hinton T, Burchell AE, Nightingale AK, Paton JFR, and Hart EC
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- Aged, Baroreflex physiology, Body Mass Index, Exercise Test, Female, Follow-Up Studies, Humans, Hypertension physiopathology, Male, Oxygen Consumption, Prognosis, Retrospective Studies, Treatment Failure, Antihypertensive Agents therapeutic use, Blood Pressure physiology, Blood Pressure Determination methods, Exercise physiology, Hypertension drug therapy
- Abstract
An exaggerated blood pressure (BP) response to maximal exercise is an independent risk factor for cardiovascular events and mortality. It is unclear whether treating BP to guideline recommended levels could normalize the rise in BP during exercise, which is mediated by the metaboreflex. We aimed to assess the BP response to incremental exercise testing and metaboreflex activation in treated-controlled hypertension (n=16), treated-uncontrolled hypertension (n=16), and untreated hypertension (n=11) and 16 control participants with normal BP (n=16). All groups were matched for age and body mass index. BP was measured during an incremental Vo
2 peak test on a cycle ergometer and during metaboreflex isolation using postexercise ischemia. Data were analyzed using 2-way ANOVA with Tukey test for multiple comparisons. Aerobic fitness was similar among groups ( P =0.97). The rise in absolute systolic BP from baseline at peak exercise was similar in controlled, uncontrolled, and untreated hypertension but greater compared with normotensive controls (Δ71±3, 81±7, 79±8.5 versus 47±5 mm Hg; P =0.0001). Metaboreflex sensitivity was also similar in controlled, uncontrolled, and untreated hypertension but augmented compared with normotensive controls (Δsystolic BP: 21±2, 28±2, 25±3 versus 12±2 mm Hg; P <0.0001). An amplified pressor response to exercise occurred in patients taking antihypertensive medication, despite having controlled BP at rest and was potentially caused (in part) by enhanced metaboreflex sensitivity. Poor BP control during exercise, partially mediated by the metaboreflex, may contribute to the heightened risk of an adverse cardiovascular event even in treated-controlled patients., (© 2018 American Heart Association, Inc.)- Published
- 2018
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31. Noctural dipping status and left ventricular hypertrophy: A cardiac magnetic resonance imaging study.
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Rodrigues JCL, Amadu AM, Ghosh Dastidar A, Harries I, Burchell AE, Ratcliffe LEK, Hart EC, Hamilton MCK, Paton JFR, Nightingale AK, and Manghat NE
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- Adult, Aged, Antihypertensive Agents therapeutic use, Blood Pressure Monitoring, Ambulatory, Circadian Rhythm, Female, Humans, Hypertension drug therapy, Magnetic Resonance Imaging, Cine, Male, Middle Aged, Prospective Studies, Hypertension physiopathology, Hypertrophy, Left Ventricular diagnostic imaging
- Abstract
We investigate the impact of dipper status on cardiac structure with cardiovascular magnetic resonance (CMR). Ambulatory blood pressure monitoring and 1.5T CMR were performed in 99 tertiary hypertension clinic patients. Subgroup analysis by extreme dipper (n = 9), dipper (n = 39), non-dipper (n = 35) and reverse dipper (n = 16) status was performed, matched in age, gender and BMI. Left ventricular (LV) mass was significantly higher for extreme dippers than dippers after correction for covariates (100 ± 6 g/m
2 vs 79 ± 3 g/m2 , P = .004). Amongst extreme dippers and dippers (n = 48), indexed LV mass correlated positively with the extent of nocturnal blood pressure dipping (R = .403, P = .005). On post-hoc ANCOVA, the percentage of nocturnal dip had significant effect on indexed LV mass (P = .008), but overall SBP did not (P = .348). In the tertiary setting, we found a larger nocturnal BP drop was associated with more LV hypertrophy. If confirmed in larger studies, this may have implications on nocturnal dosing of anti-hypertensive medications., (©2018 Wiley Periodicals, Inc.)- Published
- 2018
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32. Myocardial Infarction With Nonobstructed Coronary Arteries: Impact of CMR Early After Presentation.
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Dastidar AG, Rodrigues JCL, Johnson TW, De Garate E, Singhal P, Baritussio A, Scatteia A, Strange J, Nightingale AK, Angelini GD, Baumbach A, Delgado V, and Bucciarelli-Ducci C
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- Acute Coronary Syndrome therapy, Adult, Aged, Clinical Decision-Making, Diagnosis, Differential, Female, Humans, Male, Middle Aged, Non-ST Elevated Myocardial Infarction therapy, Predictive Value of Tests, Prognosis, ST Elevation Myocardial Infarction therapy, Time Factors, Acute Coronary Syndrome diagnostic imaging, Coronary Vessels diagnostic imaging, Magnetic Resonance Imaging, Cine, Non-ST Elevated Myocardial Infarction diagnostic imaging, ST Elevation Myocardial Infarction diagnostic imaging
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- 2017
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33. Chronic Deep Brain Stimulation Decreases Blood Pressure and Sympathetic Nerve Activity in a Drug- and Device-Resistant Hypertensive Patient.
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O'Callaghan EL, Hart EC, Sims-Williams H, Javed S, Burchell AE, Papouchado M, Tank J, Heusser K, Jordan J, Menne J, Haller H, Nightingale AK, Paton JF, and Patel NK
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- Female, Humans, Hypertension physiopathology, Middle Aged, Treatment Outcome, Blood Pressure physiology, Deep Brain Stimulation methods, Hypertension therapy, Sympathetic Nervous System physiopathology
- Published
- 2017
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34. ECG strain pattern in hypertension is associated with myocardial cellular expansion and diffuse interstitial fibrosis: a multi-parametric cardiac magnetic resonance study.
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Rodrigues JC, Amadu AM, Ghosh Dastidar A, McIntyre B, Szantho GV, Lyen S, Godsave C, Ratcliffe LE, Burchell AE, Hart EC, Hamilton MC, Nightingale AK, Paton JF, Manghat NE, and Bucciarelli-Ducci C
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- Adult, Case-Control Studies, Comorbidity, Contrast Media, Female, Fibrosis diagnostic imaging, Fibrosis pathology, Gadolinium, Humans, Hypertension diagnosis, Male, Middle Aged, Myocardium pathology, Prognosis, Retrospective Studies, Severity of Illness Index, Electrocardiography methods, Hypertension epidemiology, Hypertrophy, Left Ventricular diagnostic imaging, Hypertrophy, Left Ventricular epidemiology, Magnetic Resonance Imaging, Cine methods
- Abstract
Aims: In hypertension, the presence of left ventricular (LV) strain pattern on 12-lead electrocardiogram (ECG) carries adverse cardiovascular prognosis. The underlying mechanisms are poorly understood. We investigated whether hypertensive ECG strain is associated with myocardial interstitial fibrosis and impaired myocardial strain, assessed by multi-parametric cardiac magnetic resonance (CMR)., Methods and Results: A total of 100 hypertensive patients [50 ± 14 years, male: 58%, office systolic blood pressure (SBP): 170 ± 30 mmHg, office diastolic blood pressure (DBP): 97 ± 14 mmHg) underwent ECG and 1.5T CMR and were compared with 25 normotensive controls (46 ± 14 years, 60% male, SBP: 124 ± 8 mmHg, DBP: 76 ± 7 mmHg). Native T1 and extracellular volume fraction (ECV) were calculated with the modified look-locker inversion-recovery sequence. Myocardial strain values were estimated with voxel-tracking software. ECG strain (n = 20) was associated with significantly higher indexed LV mass (LVM) (119 ± 32 vs. 80 ± 17 g/m2, P < 0.05) and ECV (30 ± 4 vs. 27 ± 3%, P < 0.05) compared with hypertensive subjects without ECG strain (n = 80). ECG strain subjects had significantly impaired circumferential strain compared with hypertensive subjects without ECG strain and controls (-15.2 ± 4.7 vs. -17.0 ± 3.3 vs. -17.3 ± 2.4%, P < 0.05, respectively). In subgroup analysis, comparing ECG strain subjects to hypertensive subjects with elevated LVM but no ECG strain, a significantly higher ECV (30 ± 4 vs. 28 ± 3%, P < 0.05) was still observed. Indexed LVM was the only variable independently associated with ECG strain in multivariate logistic regression analysis [odds ratio (95th confidence interval): 1.07 (1.02-1.12), P < 0.05)., Conclusion: In hypertension, ECG strain is a marker of advanced LVH associated with increased interstitial fibrosis and associated with significant myocardial circumferential strain impairment., (© The Author 2016. Published by Oxford University Press on behalf of the European Society of Cardiology.)
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- 2017
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35. Electrocardiographic detection of hypertensive left atrial enlargement in the presence of obesity: re-calibration against cardiac magnetic resonance.
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Rodrigues JC, Erdei T, Dastidar AG, McIntyre B, Burchell AE, Ratcliffe LE, Hart EC, Hamilton MC, Paton JF, Nightingale AK, and Manghat NE
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- Adult, Aged, Cardiac Imaging Techniques, Female, Heart Atria diagnostic imaging, Humans, Hypertension complications, Hypertension diagnostic imaging, Magnetic Resonance Imaging, Male, Middle Aged, Obesity diagnostic imaging, Electrocardiography, Heart Atria pathology, Hypertension pathology, Obesity complications
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Left atrial enlargement (LAE) has adverse prognostic implications in hypertension. We sought to determine the accuracy of five electrocardiogram (ECG) criteria for LAE in hypertension relative to cardiac magnetic resonance (CMR) gold standard and investigate the effect of concomitant obesity. One hundred and thirty consecutive patients (age: 51.4±15.1 years, 47% male, 51% obese, systolic blood pressure (BP): 171±29 mm Hg, diastolic BP: 97±15 mm Hg) referred for CMR (1.5 T) from a tertiary hypertension clinic were included. Patients with concomitant cardiac pathology were excluded. ECGs were assessed blindly for the following: (1) P-wave >110 ms, (2) P-mitrale, (3) P-wave axis <30°, (4) area of negative P-terminal force in V1 >40 ms.mm and (5) positive P-terminal force in augmented vector left (aVL) >0.5 mm. Left atrial volume ≥55 ml m
-2 , measured blindly by CMR, was defined as LAE. Sensitivity, specificity, positive predictive value, negative predictive value, accuracy and area under the receiver operator curve were calculated. The prevalence of LAE by CMR was 26%. All the individual ECG LAE criteria were more specific than sensitive, with specificities ranging from 70% (P-axis <30o ) to 99% (P-mitrale). Obesity attenuated the specificity of most of the individual ECG LAE criteria. Obesity correlated with significant lower specificity (48% vs 65%, P<0.05) and a trend towards lower sensitivity (59 vs 43%, P=0.119) when ≥1 ECG LAE criteria were present. Individual ECG criteria of LAE in hypertension are specific, but not sensitive, at identifying LAE. The ECG should not be used to excluded LAE in hypertension, particularly in obese subjects.- Published
- 2017
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36. Hypertensive heart disease versus hypertrophic cardiomyopathy: multi-parametric cardiovascular magnetic resonance discriminators when end-diastolic wall thickness ≥ 15 mm.
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Rodrigues JC, Rohan S, Ghosh Dastidar A, Harries I, Lawton CB, Ratcliffe LE, Burchell AE, Hart EC, Hamilton MC, Paton JF, Nightingale AK, and Manghat NE
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- Adult, Aged, Cardiomyopathy, Hypertrophic complications, Case-Control Studies, Contrast Media, Diagnosis, Differential, Female, Fibrosis, Gadolinium, Heart Diseases diagnostic imaging, Heart Diseases etiology, Heart Ventricles pathology, Humans, Hypertension complications, Hypertrophy, Left Ventricular etiology, Logistic Models, Magnetic Resonance Spectroscopy, Male, Middle Aged, Multivariate Analysis, Myocardium pathology, Organ Size, Retrospective Studies, Cardiomyopathy, Hypertrophic diagnostic imaging, Heart Ventricles diagnostic imaging, Hypertension diagnostic imaging, Hypertrophy, Left Ventricular diagnostic imaging
- Abstract
Objectives: European guidelines state left ventricular (LV) end-diastolic wall thickness (EDWT) ≥15mm suggests hypertrophic cardiomyopathy (HCM), but distinguishing from hypertensive heart disease (HHD) is challenging. We identify cardiovascular magnetic resonance (CMR) predictors of HHD over HCM when EDWT ≥15mm., Methods: 2481 consecutive clinical CMRs between 2014 and 2015 were reviewed. 464 segments from 29 HCM subjects with EDWT ≥15mm but without other cardiac abnormality, hypertension or renal impairment were analyzed. 432 segments from 27 HHD subjects with EDWT ≥15mm but without concomitant cardiac pathology were analyzed. Magnitude and location of maximal EDWT, presence of late gadolinium enhancement (LGE), LV asymmetry (>1.5-fold opposing segment) and systolic anterior motion of the mitral valve (SAM) were measured. Multivariate logistic regression was performed. Significance was defined as p<0.05., Results: HHD and HCM cohorts were age-/gender-matched. HHD had significantly increased indexed LV mass (110±27g/m
2 vs. 91±31g/m2 , p=0.016) but no difference in site or magnitude of maximal EDWT. Mid-wall LGE was significantly more prevalent in HCM. Elevated indexed LVM, mid-wall LGE and absence of SAM were significant multivariate predictors of HHD, but LV asymmetry was not., Conclusions: Increased indexed LV mass, absence of mid-wall LGE and absence of SAM are better CMR discriminators of HHD from HCM than EDWT ≥15mm., Key Points: • Hypertrophic cardiomyopathy (HCM) is often diagnosed with end-diastolic wall thickness ≥15mm. • Hypertensive heart disease (HHD) can be difficult to distinguish from HCM. • Retrospective case-control study showed that location and magnitude of EDWT are poor discriminators. • Increased left ventricular mass and midwall fibrosis are independent predictors of HHD. • Cardiovascular magnetic resonance parameters facilitate a better discrimination between HHD and HCM.- Published
- 2017
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37. Cardiac magnetic resonance imaging provides new insight into hypertensive heart disease-a reply.
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Rodrigues JC, Rohan S, Dastidar AG, Trickey A, Szantho G, Ratcliffe LE, Burchell AE, Hart EC, Bucciarelli-Ducci C, Hamilton MC, Nightingale AK, Paton JF, Manghat NE, and MacIver DH
- Subjects
- Heart Diseases, Humans, Magnetic Resonance Imaging, Heart, Hypertension
- Published
- 2017
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38. Comprehensive First-Line Magnetic Resonance Imaging in Hypertension: Experience From a Single-Center Tertiary Referral Clinic.
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Burchell AE, Rodrigues JC, Charalambos M, Ratcliffe LE, Hart EC, Paton JF, Baumbach A, Manghat NE, and Nightingale AK
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- Aged, Aortic Coarctation diagnostic imaging, Aortic Coarctation epidemiology, Coloboma diagnostic imaging, Coloboma epidemiology, Female, Humans, Hypertrophy, Left Ventricular diagnostic imaging, Hypertrophy, Left Ventricular epidemiology, Male, Middle Aged, Myocardial Infarction diagnostic imaging, Myocardial Infarction epidemiology, Pituitary Gland diagnostic imaging, Pituitary Gland pathology, Polycystic Kidney Diseases diagnostic imaging, Polycystic Kidney Diseases epidemiology, Renal Artery Obstruction diagnostic imaging, Renal Artery Obstruction epidemiology, Renal Insufficiency diagnostic imaging, Renal Insufficiency epidemiology, Retrospective Studies, Sensitivity and Specificity, Stroke Volume, Vesico-Ureteral Reflux diagnostic imaging, Vesico-Ureteral Reflux epidemiology, Hypertension complications, Hypertension diagnostic imaging, Magnetic Resonance Imaging methods
- Abstract
European guidelines recommend that patients with hypertension be assessed for asymptomatic organ damage and secondary causes. The authors propose that a single magnetic resonance imaging (MRI) scan can provide comprehensive first-line imaging of patients assessed via a specialist hypertension clinic. A total of 200 patients (56% male, aged 51±15 years, office BP 168±30/96±16 mm Hg) underwent MRI of the heart, kidneys, renal arteries, adrenals and aorta. Comparisons were made with other imaging modalities where available. A total of 61% had left ventricular hypertrophy (LVH), 14% had reduced ejection fraction, and 15 patients had myocardial infarcts. Echocardiography overdiagnosed LVH in 15% of patients and missed LVH in 14%. Secondary causes were identified in 14.5% of patients: 12 adrenal masses, 10 renal artery stenoses, seven thyroid abnormalities, one aortic coarctation, one enlarged pituitary gland, one polycystic kidney disease, and one renal coloboma syndrome. This comprehensive MRI protocol is an effective method of screening for asymptomatic organ damage and secondary causes of hypertension., (©2016 Wiley Periodicals, Inc.)
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- 2017
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39. Is High Blood Pressure Self-Protection for the Brain?
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Warnert EA, Rodrigues JC, Burchell AE, Neumann S, Ratcliffe LE, Manghat NE, Harris AD, Adams Z, Nightingale AK, Wise RG, Paton JF, and Hart EC
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- Adult, Brain blood supply, Case-Control Studies, Cross-Sectional Studies, Essential Hypertension, Female, Humans, Magnetic Resonance Imaging methods, Male, Middle Aged, Retrospective Studies, Vascular Resistance physiology, Brain diagnostic imaging, Brain physiology, Cerebrovascular Circulation physiology, Hypertension diagnostic imaging, Hypertension physiopathology
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Rationale: Data from animal models of hypertension indicate that high blood pressure may develop as a vital mechanism to maintain adequate blood flow to the brain. We propose that congenital vascular variants of the posterior cerebral circulation and cerebral hypoperfusion could partially explain the pathogenesis of essential hypertension, which remains enigmatic in 95% of patients., Objective: To evaluate the role of the cerebral circulation in the pathophysiology of hypertension., Methods and Results: We completed a series of retrospective and mechanistic case-control magnetic resonance imaging and physiological studies in normotensive and hypertensive humans (n=259). Interestingly, in humans with hypertension, we report a higher prevalence of congenital cerebrovascular variants; vertebral artery hypoplasia, and an incomplete posterior circle of Willis, which were coupled with increased cerebral vascular resistance, reduced cerebral blood flow, and a higher incidence of lacunar type infarcts. Causally, cerebral vascular resistance was elevated before the onset of hypertension and elevated sympathetic nerve activity (n=126). Interestingly, untreated hypertensive patients (n=20) had a cerebral blood flow similar to age-matched controls (n=28). However, participants receiving antihypertensive therapy (with blood pressure controlled below target levels) had reduced cerebral perfusion (n=19). Finally, elevated cerebral vascular resistance was a predictor of hypertension, suggesting that it may be a novel prognostic or diagnostic marker (n=126)., Conclusions: Our data indicate that congenital cerebrovascular variants in the posterior circulation and the associated cerebral hypoperfusion may be a factor in triggering hypertension. Therefore, lowering blood pressure may worsen cerebral perfusion in susceptible individuals., (© 2016 American Heart Association, Inc.)
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- 2016
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40. Prevalence and predictors of asymmetric hypertensive heart disease: insights from cardiac and aortic function with cardiovascular magnetic resonance.
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Rodrigues JC, Amadu AM, Dastidar AG, Hassan N, Lyen SM, Lawton CB, Ratcliffe LE, Burchell AE, Hart EC, Hamilton MC, Paton JF, Nightingale AK, and Manghat NE
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- Adult, Age Distribution, Aged, Analysis of Variance, Aorta, Thoracic diagnostic imaging, Aorta, Thoracic pathology, Cardiomyopathy, Hypertrophic etiology, Cardiomyopathy, Hypertrophic pathology, Cohort Studies, Electrocardiography methods, Female, Humans, Hypertension diagnosis, Hypertrophy, Left Ventricular etiology, Hypertrophy, Left Ventricular pathology, Logistic Models, Male, Middle Aged, Multivariate Analysis, Predictive Value of Tests, Prevalence, Prognosis, Radiographic Image Enhancement methods, Retrospective Studies, Risk Assessment, Severity of Illness Index, Sex Distribution, Cardiomyopathy, Hypertrophic diagnostic imaging, Cardiomyopathy, Hypertrophic epidemiology, Hypertension complications, Hypertrophy, Left Ventricular diagnostic imaging, Hypertrophy, Left Ventricular epidemiology, Magnetic Resonance Imaging, Cine
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Aims: We sought to determine the prevalence of asymmetric hypertensive heart disease (HHD) overlapping morphologically with hypertrophic cardiomyopathy (HCM) and to determine predictors of this pattern of hypertensive remodelling., Methods and Results: One hundred and fifty hypertensive patients underwent 1.5 T cardiovascular magnetic resonance imaging. Twenty-one patients were excluded due to concomitant cardiac pathology that may confound the hypertrophic response, e.g. myocardial infarction, moderate-severe valvular disease, or other cardiomyopathy. Asymmetric HHD was defined as a segmental wall thickness of ≥15 mm and >1.5-fold the opposing wall in ≥1 myocardial segments, measured from short-axis cine stack at end-diastole. Ambulatory blood pressure, myocardial replacement fibrosis, aortic distensibility and aortoseptal angle were investigated as predictors of asymmetric HHD by multivariate logistic regression. Out of 129 hypertensive subjects (age: 51 ± 15 years, 50% male, systolic blood pressure: 170 ± 30 mmHg, diastolic blood pressure: 97 ± 16 mmHg), asymmetric HHD occurred in 21%. Where present, maximal end-diastolic wall thickness (EDWT) was 17.8 ± 1.9 mm and located exclusively in the basal or mid septum. In asymmetric HHD, aortoseptal angle (114 ± 10° vs. 125 ± 9° vs. 123 ± 12°, P < 0.05, respectively) was significantly reduced compared to concentric left ventricular hypertrophy (LVH) and compared to no LVH, respectively. Aortic distensibility in asymmetric HHD (1.01 ± 0.60 vs. 1.83 ± 1.65 mm
2 /mmHg × 103 , P < 0.05, respectively) was significantly reduced compared to subjects with no LVH. Age (odds ratio [95th confidence interval]: 1.10 [1.02-1.18], P < 0.05) and indexed LV mass (1.09 [0.98-1.28], P < 0.0001) were significant, independent predictors of asymmetric HDD., Conclusions: Asymmetric HHD morphologically overlapping with HCM, according to the current ESC guidelines, is common. Postulating a diagnosis of HCM on the basis of EDWT of ≥15 mm should be made with caution in the presence of arterial hypertension particular in male subjects with elevated LV mass., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.)- Published
- 2016
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41. The Relationship Between Left Ventricular Wall Thickness, Myocardial Shortening, and Ejection Fraction in Hypertensive Heart Disease: Insights From Cardiac Magnetic Resonance Imaging.
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Rodrigues JC, Rohan S, Dastidar AG, Trickey A, Szantho G, Ratcliffe LE, Burchell AE, Hart EC, Bucciarelli-Ducci C, Hamilton MC, Nightingale AK, Paton JF, Manghat NE, and MacIver DH
- Subjects
- Adult, Aged, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Stroke Volume, Ventricular Function, Left, Heart Diseases physiopathology, Heart Ventricles physiopathology, Hypertension physiopathology
- Abstract
Hypertensive heart disease is often associated with a preserved left ventricular ejection fraction despite impaired myocardial shortening. The authors investigated this paradox in 55 hypertensive patients (52±13 years, 58% male) and 32 age- and sex-matched normotensive control patients (49±11 years, 56% male) who underwent cardiac magnetic resonance imaging at 1.5T. Long-axis shortening (R=0.62), midwall fractional shortening (R=0.68), and radial strain (R=0.48) all decreased (P<.001) as end-diastolic wall thickness increased. However, absolute wall thickening (defined as end-systolic minus end-diastolic wall thickness) was maintained, despite the reduced myocardial shortening. Absolute wall thickening correlated with ejection fraction (R=0.70, P<.0001). In multiple linear regression analysis, increasing wall thickness by 1 mm independently increased ejection fraction by 3.43 percentage points (adjusted β-coefficient: 3.43 [2.60-4.26], P<.0001). Increasing end-diastolic wall thickness augments ejection fraction through preservation of absolute wall thickening. Left ventricular ejection fraction should not be used in patients with hypertensive heart disease without correction for degree of hypertrophy., (© 2016 Wiley Periodicals, Inc.)
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- 2016
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42. Comprehensive characterisation of hypertensive heart disease left ventricular phenotypes.
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Rodrigues JC, Amadu AM, Dastidar AG, Szantho GV, Lyen SM, Godsave C, Ratcliffe LE, Burchell AE, Hart EC, Hamilton MC, Nightingale AK, Paton JF, Manghat NE, and Bucciarelli-Ducci C
- Subjects
- Adult, Aged, Case-Control Studies, England, Female, Fibrosis, Humans, Hypertension diagnosis, Hypertrophy, Left Ventricular etiology, Hypertrophy, Left Ventricular pathology, Hypertrophy, Left Ventricular physiopathology, Male, Middle Aged, Myocardial Contraction, Outpatient Clinics, Hospital, Phenotype, Predictive Value of Tests, Tertiary Care Centers, Ventricular Dysfunction, Left etiology, Ventricular Dysfunction, Left pathology, Ventricular Dysfunction, Left physiopathology, Ventricular Remodeling, Hypertension complications, Hypertrophy, Left Ventricular diagnostic imaging, Magnetic Resonance Imaging, Cine, Myocardium pathology, Ventricular Dysfunction, Left diagnostic imaging, Ventricular Function, Left
- Abstract
Objective: Myocardial intracellular/extracellular structure and aortic function were assessed among hypertensive left ventricular (LV) phenotypes using cardiovascular magnetic resonance (CMR)., Methods: An observational study from consecutive tertiary hypertension clinic patients referred for CMR (1.5 T) was performed. Four LV phenotypes were defined: (1) normal with normal indexed LV mass (LVM) and LVM to volume ratio (M/V), (2) concentric remodelling with normal LVM but elevated M/V, (3) concentric LV hypertrophy (LVH) with elevated LVM but normal indexed end-diastolic volume (EDV) or (4) eccentric LVH with elevated LVM and EDV. Extracellular volume fraction was measured using T1-mapping. Circumferential strain was calculated by voxel-tracking. Aortic distensibility was derived from high-resolution aortic cines and contemporaneous blood pressure measurements., Results: 88 hypertensive patients (49±14 years, 57% men, systolic blood pressure (SBP): 167±30 mm Hg, diastolic blood pressure (DBP): 96±14 mm Hg) were compared with 29 age-matched/sex-matched controls (47±14 years, 59% men, SBP: 128±12 mm Hg, DBP: 79±10 mm Hg). LVH resulted from increased myocardial cell volume (eccentric LVH: 78±19 mL/m(2) vs concentric LVH: 73±15 mL/m(2) vs concentric remodelling: 55±9 mL/m(2), p<0.05, respectively) and interstitial fibrosis (eccentric LVH: 33±10 mL/m(2) vs concentric LVH: 30±10 mL/m(2) vs concentricremodelling: 19±2 mL/m(2), p<0.05, respectively). LVH had worst circumferential impairment (eccentric LVH: -12.8±4.6% vs concentric LVH: -15.5±3.1% vs concentric remodelling: -17.1±3.2%, p<0.05, respectively). Concentric remodelling was associated with reduced aortic distensibility, but not with large intracellular/interstitial expansion or myocardial dysfunction versus controls., Conclusions: Myocardial interstitial fibrosis varies across hypertensive LV phenotypes with functional consequences. Eccentric LVH has the most fibrosis and systolic impairment. Concentric remodelling is only associated with abnormal aortic function. Understanding these differences may help tailor future antihypertensive treatments., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/)
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- 2016
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43. Purinergic receptors in the carotid body as a new drug target for controlling hypertension.
- Author
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Pijacka W, Moraes DJ, Ratcliffe LE, Nightingale AK, Hart EC, da Silva MP, Machado BH, McBryde FD, Abdala AP, Ford AP, and Paton JF
- Subjects
- Animals, Blood Pressure drug effects, Carotid Body cytology, Hypertension drug therapy, Hypertension genetics, Male, Patch-Clamp Techniques, Purinergic P2X Receptor Antagonists pharmacology, Rats, Rats, Inbred SHR, Rats, Wistar, Reflex, Abnormal genetics, Sensory Receptor Cells drug effects, Sensory Receptor Cells metabolism, Blood Pressure genetics, Carotid Body metabolism, Chemoreceptor Cells metabolism, RNA, Messenger metabolism, Receptors, Purinergic P2X3 genetics
- Abstract
In view of the high proportion of individuals with resistance to antihypertensive medication and/or poor compliance or tolerance of this medication, new drugs to treat hypertension are urgently needed. Here we show that peripheral chemoreceptors generate aberrant signaling that contributes to high blood pressure in hypertension. We discovered that purinergic receptor P2X3 (P2rx3, also known as P2x3) mRNA expression is upregulated substantially in chemoreceptive petrosal sensory neurons in rats with hypertension. These neurons generate both tonic drive and hyperreflexia in hypertensive (but not normotensive) rats, and both phenomena are normalized by the blockade of P2X3 receptors. Antagonism of P2X3 receptors also reduces arterial pressure and basal sympathetic activity and normalizes carotid body hyperreflexia in conscious rats with hypertension; no effect was observed in rats without hypertension. We verified P2X3 receptor expression in human carotid bodies and observed hyperactivity of carotid bodies in individuals with hypertension. These data support the identification of the P2X3 receptor as a potential new target for the control of human hypertension.
- Published
- 2016
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44. Quantifying sympathetic neuro-haemodynamic transduction at rest in humans: insights into sex, ageing and blood pressure control.
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Briant LJ, Burchell AE, Ratcliffe LE, Charkoudian N, Nightingale AK, Paton JF, Joyner MJ, and Hart EC
- Subjects
- Adolescent, Adrenergic beta-Antagonists pharmacology, Adult, Aged, Blood Pressure, Female, Humans, Male, Middle Aged, Propranolol pharmacology, Supine Position, Sympathetic Nervous System drug effects, Young Adult, Aging physiology, Sympathetic Nervous System physiology
- Abstract
Key Points: We have developed a simple analytical method for quantifying the transduction of sympathetic activity into vascular tone. This method demonstrates that as women age, the transfer of sympathetic nerve activity into vascular tone is increased, so that for a given level of sympathetic activity there is more vasoconstriction. In men, this measure decreases with age. Test-re-test analysis demonstrated that the new method is a reliable estimate of sympathetic transduction. We conclude that increased sympathetic vascular coupling contributes to the age-related increase in blood pressure that occurs in women only. This measure is a reliable estimate of sympathetic transduction in populations with high sympathetic nerve activity. Thus, it will provide information regarding whether treatment targeting the sympathetic nervous system, which interrupts the transfer of sympathetic nerve activity into vascular tone, will be effective in reducing blood pressure in hypertensive patients. This may provide insight into which populations will respond to certain types of anti-hypertensive medication., Abstract: Sex and age differences in the sympathetic control of resting blood pressure (BP) may be due to differences in the transduction of sympathetic nerve activity (SNA) into vascular tone. Current methods for dynamically quantifying transduction focus on the relationship between SNA and vasoconstriction during a pressor stimulus, which increases BP and may be contra-indicated in patients. We describe a simple analytical method for quantifying transduction under resting conditions. We performed linear regression analysis of binned muscle SNA burst areas against diastolic BP (DBP). We assessed whether the slope of this relationship reflects the transduction of SNA into DBP. To evaluate this, we investigated whether this measure captures differences in transduction in different populations. Specifically, we (1) quantified transduction in young men (YM), young women (YW), older men (OM) and postmenopausal women (PMW); and (2) measured changes in transduction during β-blockade using propranolol in YW, YM and PMW. YM had a greater transduction vs. OM (0.10 ± 0.01 mmHg (% s)(-1) , n = 23 vs. 0.06 ± 0.01 mmHg (% s)(-1) , n = 18; P = 0.003). Transduction was lowest in YW (0.02 ± 0.01 mmHg (% s)(-1) , n = 23) and increased during β-blockade (0.11 ± 0.01 mmHg (% s)(-1) ; P < 0.001). Transduction in PMW (0.07 ± 0.01 mmHg (% s)(-1) , n = 23) was greater compared to YW (P = 0.001), and was not altered during β-blockade (0.06 ± 0.01 mmHg (% s)(-1) ; P = 0.98). Importantly, transduction increased in women with age, but decreased in men. Transduction in women intersected that in men at 55 ± 1.5 years. This measure of transduction captures age- and sex-differences in the sympathetic regulation of DBP and may be valuable in quantifying transduction in disease. In particular, this measure may help target treatment strategies in specific hypertensive subpopulations., (© 2016 The Authors. The Journal of Physiology © 2016 The Physiological Society.)
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- 2016
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45. Unilateral Carotid Body Resection in Resistant Hypertension: A Safety and Feasibility Trial.
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Narkiewicz K, Ratcliffe LE, Hart EC, Briant LJ, Chrostowska M, Wolf J, Szyndler A, Hering D, Abdala AP, Manghat N, Burchell AE, Durant C, Lobo MD, Sobotka PA, Patel NK, Leiter JC, Engelman ZJ, Nightingale AK, and Paton JF
- Abstract
Animal and human data indicate pathological afferent signaling emanating from the carotid body that drives sympathetically mediated elevations in blood pressure in conditions of hypertension. This first-in-man, proof-of-principle study tested the safety and feasibility of unilateral carotid body resection in 15 patients with drug-resistant hypertension. The procedure proved to be safe and feasible. Overall, no change in blood pressure was found. However, 8 patients showed significant reductions in ambulatory blood pressure coinciding with decreases in sympathetic activity. The carotid body may be a novel target for treating an identifiable subpopulation of humans with hypertension.
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- 2016
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46. Renal artery sympathetic denervation: observations from the UK experience.
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Sharp AS, Davies JE, Lobo MD, Bent CL, Mark PB, Burchell AE, Thackray SD, Martin U, McKane WS, Gerber RT, Wilkinson JR, Antonios TF, Doulton TW, Patterson T, Clifford PC, Lindsay A, Houston GJ, Freedman J, Das N, Belli AM, Faris M, Cleveland TJ, Nightingale AK, Hameed A, Mahadevan K, Finegold JA, Mather AN, Levy T, D'Souza R, Riley P, Moss JG, Di Mario C, Redwood SR, Baumbach A, Caulfield MJ, and Dasgupta I
- Subjects
- Aged, Antihypertensive Agents therapeutic use, Blood Pressure Monitoring, Ambulatory, Drug Resistance, Drug Therapy, Combination, Female, Humans, Hypertension diagnosis, Hypertension physiopathology, Male, Middle Aged, Mineralocorticoid Receptor Antagonists, Office Visits, Registries, Retrospective Studies, Sympathectomy adverse effects, Sympathetic Nervous System physiopathology, Time Factors, Treatment Outcome, United Kingdom, Blood Pressure drug effects, Hypertension surgery, Kidney blood supply, Renal Artery innervation, Sympathectomy methods, Sympathetic Nervous System surgery
- Abstract
Background: Renal denervation (RDN) may lower blood pressure (BP); however, it is unclear whether medication changes may be confounding results. Furthermore, limited data exist on pattern of ambulatory blood pressure (ABP) response-particularly in those prescribed aldosterone antagonists at the time of RDN., Methods: We examined all patients treated with RDN for treatment-resistant hypertension in 18 UK centres., Results: Results from 253 patients treated with five technologies are shown. Pre-procedural mean office BP (OBP) was 185/102 mmHg (SD 26/19; n = 253) and mean daytime ABP was 170/98 mmHg (SD 22/16; n = 186). Median number of antihypertensive drugs was 5.0: 96 % ACEi/ARB; 86 % thiazide/loop diuretic and 55 % aldosterone antagonist. OBP, available in 90 % at 11 months follow-up, was 163/93 mmHg (reduction of 22/9 mmHg). ABP, available in 70 % at 8.5 months follow-up, was 158/91 mmHg (fall of 12/7 mmHg). Mean drug changes post RDN were: 0.36 drugs added, 0.91 withdrawn. Dose changes appeared neutral. Quartile analysis by starting ABP showed mean reductions in systolic ABP after RDN of: 0.4; 6.5; 14.5 and 22.1 mmHg, respectively (p < 0.001 for trend). Use of aldosterone antagonist did not predict response (p > 0.2)., Conclusion: In 253 patients treated with RDN, office BP fell by 22/9 mmHg. Ambulatory BP fell by 12/7 mmHg, though little response was seen in the lowermost quartile of starting blood pressure. Fall in BP was not explained by medication changes and aldosterone antagonist use did not affect response.
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- 2016
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47. Controversies Surrounding Renal Denervation: Lessons Learned From Real-World Experience in Two United Kingdom Centers.
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Burchell AE, Chan K, Ratcliffe LE, Hart EC, Saxena M, Collier DJ, Jain AK, Mathur A, Knight CJ, Caulfield MJ, Paton JF, Nightingale AK, Lobo MD, and Baumbach A
- Subjects
- Adult, Aged, Antihypertensive Agents therapeutic use, Blood Pressure Determination, Clinical Trials as Topic, Female, Humans, Hypertension drug therapy, Hypertension physiopathology, Kidney surgery, Male, Medication Adherence, Middle Aged, Treatment Outcome, United Kingdom, Hypertension therapy, Kidney innervation, Sympathectomy methods
- Abstract
Renal denervation (RDN) is a therapy that targets treatment-resistant hypertension (TRH). The Renal Denervation in Patients With Uncontrolled Hypertension (Symplicity) HTN-1 and Symplicity HTN-2 trials reported response rates of >80%; however, sham-controlled Symplicity HTN-3 failed to reach its primary blood pressure (BP) outcome. The authors address the current controversies surrounding RDN, illustrated with real-world data from two centers in the United Kingdom. In this cohort, 52% of patients responded to RDN, with a 13±32 mm Hg reduction in office systolic BP (SBP) at 6 months (n=29, P=.03). Baseline office SBP and number of ablations correlated with office SBP reduction (R=-0.47, P=.01; R=-0.56, P=.002). RDN appears to be an effective treatment for some patients with TRH; however, individual responses are highly variable. Selecting patients for RDN is challenging, with only 10% (33 of 321) of the screened patients eligible for the study. Medication alterations and nonadherence confound outcomes. Adequate ablation is critical and should impact future catheter design/training. Markers of procedural success and improved patient selection parameters remain key research aims., (©2016 Wiley Periodicals, Inc.)
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- 2016
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48. The effect of obesity on electrocardiographic detection of hypertensive left ventricular hypertrophy: recalibration against cardiac magnetic resonance.
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Rodrigues JC, McIntyre B, Dastidar AG, Lyen SM, Ratcliffe LE, Burchell AE, Hart EC, Bucciarelli-Ducci C, Hamilton MC, Paton JF, Nightingale AK, and Manghat NE
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- Adult, Aged, Female, Humans, Hypertrophy, Left Ventricular etiology, Magnetic Resonance Imaging, Male, Middle Aged, Prospective Studies, Electrocardiography standards, Hypertension complications, Hypertrophy, Left Ventricular diagnostic imaging, Obesity complications
- Abstract
Electrocardiograph (ECG) criteria for left ventricular hypertrophy (LVH) are a widely used clinical tool. We recalibrated six ECG criteria for LVH against gold-standard cardiac magnetic resonance (CMR) and assessed the impact of obesity. One hundred and fifty consecutive tertiary hypertension clinic referrals for CMR (1.5 T) were reviewed. Patients with cardiac pathology potentially confounding hypertensive LVH were excluded (n=22). The final sample size was 128 (age: 51.0±15.2 years, 48% male). LVH was defined by CMR. From a 12-lead ECG, Sokolow-Lyon voltage and product, Cornell voltage and product, Gubner-Ungerleidger voltage and Romhilt-Estes score were evaluated, blinded to the CMR. ECG diagnostic performance was calculated. LVH by CMR was present in 37% and obesity in 51%. Obesity significantly reduced ECG sensitivity, because of significant attenuation in mean ECG values for Cornell voltage (22.2±5.7 vs 26.4±9.4 mm, P<0.05), Cornell product (2540±942 vs 3023±1185 mm • ms, P<0.05) and for Gubner-Ungerleider voltage (18.2±7.1 vs 23.3±1.2 mm, P<0.05). Obesity also significantly reduced ECG specificity, because of significantly higher prevalence of LV remodeling (no LVH but increased mass-to-volume ratio) in obese subjects without LVH (36% vs 16%, P<0.05), which correlated with higher mean ECG LVH criteria values. Obesity-specific partition values were generated at fixed 95% specificity; Cornell voltage had highest sensitivity in non-obese (56%) and Sokolow-Lyon product in obese patients (24%). Obesity significantly lowers ECG sensitivity at detecting LVH, by attenuating ECG LVH values, and lowers ECG specificity through changes associated with LV remodeling. Our obesity-specific ECG partition values could improve the diagnostic performance in obese patients with hypertension.
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- 2016
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49. Deep brain stimulation for the treatment of resistant hypertension.
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O'Callaghan EL, McBryde FD, Burchell AE, Ratcliffe LE, Nicolae L, Gillbe I, Carr D, Hart EC, Nightingale AK, Patel NK, and Paton JF
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- Animals, Blood Pressure, Humans, Hypertension physiopathology, Autonomic Nervous System physiopathology, Deep Brain Stimulation, Hypertension therapy, Sympathetic Nervous System physiopathology
- Abstract
Hypertension is a leading risk factor for the development of several cardiovascular diseases. As the global prevalence of hypertension increases, so too has the recognition of resistant hypertension. Whilst figures vary, the proportion of hypertensive patients that are resistant to multiple drug therapies have been reported to be as high as 16.4 %. Resistant hypertension is typically associated with elevated sympathetic activity and abnormal homeostatic reflex control and is termed neurogenic hypertension because of its presumed central autonomic nervous system origin. This resistance to conventional pharmacological treatment has stimulated a plethora of medical devices to be investigated for use in hypertension, with varying degrees of success. In this review, we discuss a new therapy for drug-resistant hypertension, deep brain stimulation. The utility of deep brain stimulation in resistant hypertension was first discovered in patients with concurrent neuropathic pain, where it lowered blood pressure and improved baroreflex sensitivity. The most promising central target for stimulation is the ventrolateral periaqueductal gray, which has been well characterised in animal studies as a control centre for autonomic outflow. In this review, we will discuss the promise and potential mechanisms of deep brain stimulation in the treatment of severe, resistant hypertension.
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- 2014
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50. Rebuttal from L. E. K. Ratcliffe, W. Pijacka, F. D. McBryde, A. P. Abdala, D. J. Moraes, P. A. Sobotka, E. C. Hart, K. Narkiewicz, A. K. Nightingale and J. F. R. Paton.
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Ratcliffe LE, Pijacka W, McBryde FD, Abdala AP, Moraes DJ, Sobotka PA, Hart EC, Narkiewicz K, Nightingale AK, and Paton JF
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- Animals, Humans, Ablation Techniques methods, Autonomic Nervous System surgery, Carotid Sinus physiology, Denervation methods, Electric Stimulation Therapy, Hypertension surgery, Hypertension therapy, Kidney innervation
- Published
- 2014
- Full Text
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