Search

Background: Whether in volume-dependent primary hypertension, concentric left ventricular (LV) remodeling beyond hypertrophy (LVH) represents the impact of a pressure rather than a volume overload, is unclear., Methods: Using central arterial pressure, and aortic velocity and diameter measurements in the outflow tract (echocardiography), we determined the factors that associate with concentric LVH or remodeling in a community of African ancestry (n = 709) with prevalent volume-dependent primary hypertension., Results: Both left ventricular mass index (LVMI) and relative wall thickness (RWT) were positively and independently associated with end diastolic volume (EDV), stroke volume (SV), and peak aortic flow (Q) (P < 0.05 to <0.0001). However, neither LVMI nor RWT were positively and independently associated with systemic vascular resistance (SVR), or aortic characteristic impedance (Zc) or inversely associated with total arterial compliance (TAC). Consequently, both concentric (P < 0.0001) and eccentric (P < 0.0001) LVH were associated with similar increases in EDV, SV, and either office brachial, central arterial, or 24-hour blood pressures (BP), but neither increases in SVR or Zc nor decreases in TAC. LV RWT, but not LVMI was nevertheless independently and inversely associated with myocardial systolic function (midwall shortening and s') (P < 0.05 to <0.005) and decreases in LV systolic function were noted in concentric (P < 0.05), but not eccentric LVH., Conclusions: In volume-dependent primary hypertension, concentric LVH is determined as much by volume-dependent increases in systemic flow and an enhanced BP as eccentric LVH. Concentric remodeling nevertheless reflects decreases in systolic function beyond LVH., (© American Journal of Hypertension, Ltd 2021. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Background: Although, in-part through an impact on left ventricular mass (LVM), resistin (an adipokine) may contribute to heart failure, whether this is explained by the adverse effects of resistin on aortic stiffness and renal function is unknown., Methods: Relationships between circulating resistin concentrations and LVM index (LVMI), and LVM beyond that predicted by stroke work (inappropriate LVM [LVM inappr ]) (echocardiography) were determined in 647 randomly selected community participants, and in regression analysis, the extent to which these relations could be explained by aortic pulse wave velocity (PWV) or estimated glomerular filtration rate (eGFR) was evaluated., Results: Independent of confounders, resistin concentrations were independently associated with LVMI, LVM inappr , LV hypertrophy (LVH), PWV and eGFR. Furthermore, independent of confounders, LVMI, LVM inappr and LVH were independently associated with PWV and eGFR. However, adjustments for either PWV or eGFR failed to modify the relationships between resistin concentrations and LVMI, LVM inappr or LVH. Moreover, in multivariate regression analysis neither PWV nor eGFR significantly modified the contribution of resistin to LVM inappr or LVMI., Conclusions: Independent relationships between circulating concentrations of the adipocytokine resistin and LVM are not explained by the impact of resistin on ventricular-vascular coupling or renal dysfunction. Resistin's effects on LVM are therefore likely to be through direct actions on the myocardium.

Aims: Although the development of left ventricular (LV) dysfunction in hypertension has traditionally been viewed as a transition process from a phase of structural LV remodelling to dysfunction, the extent to which LV mass (LVM) and remodelling account for blood pressure (BP)-associated alterations in LV diastolic function is uncertain. In product of coefficient mediation analysis, we aimed to determine the extent to which LVM index (LVMI) or relative wall thickness (RWT) account for relations between BP and LV diastolic function., Methods: In 709 randomly selected participants from a community sample with a high prevalence of hypertension (49.6%), we determined BP and LVMI, RWT and several indices of diastolic function from transmitral blood flow and myocardial tissue Doppler (E/A, e'/a', e' and E/e') and left atrial volume using standard echocardiographic techniques., Results: With adjustments for confounders, LVMI (P < 0.001-0.0001) and RWT (P < 0.05-0.001) were independently associated with E/A, e'/a', e' and E/e'. However, in product of coefficient mediation analysis, LVM and RWT failed to account for most BP-associated changes in diastolic function. Indeed, whilst a one SD increase in DBP or SBP (13 and 22 mmHg, respectively) translated into a 0.07, 0.13 and 0.53 decrease in E/A, e'/a', e' and a 0.73 increase in E/e', respectively, in mediation analysis LVMI accounted for only 0.0005, 0.0017, 0.05 and 0.08 of the impact of a one SD effect of LVMI on E/A, e'/a', e' and E/e', respectively. Similar contributions of RWT as for LVMI to BP-associated LV diastolic functional changes were noted and the contribution of LVMI or RWT to BP-related alterations in diastolic function was similar in those participants not receiving antihypertensive therapy., Conclusion: Although structural LV remodelling is independently associated with changes in LV diastolic function, LVMI and RWT account for only a minor proportion of the impact of BP on diastolic function. Thus, most BP-associated decreases in LV diastolic function are likely to be a transition process independent of LV hypertrophy or concentric remodelling.

Background: The contribution of steady-state pressures and the forward (Pf) and backward (reflected) (Pb) wave pressure components of pulse pressure to risk prediction have produced contrasting results. We hypothesized that the independent contribution of steady-state pressures (mean arterial pressure [MAP]), Pf and Pb, to cardiovascular damage is organ specific and age dependent., Methods: In 1,384 black South Africans from a community sample, we identified independent relations between MAP, Pf, or Pb (applanation tonometry and SphygmoCor software) and left ventricular mass index (LVMI) (n = 997) (echocardiography), carotid intima-media thickness (IMT) (n = 804) (B-mode ultrasound), or aortic pulse wave velocity (PWV) (n = 1,217)., Results: Independent of risk factors, relations between Pf and IMT were noted in those over 50 years (P < 0.02), whereas in those less than 50 years, MAP (P < 0.005) was independently associated with IMT. Pb failed to show independent relations with IMT at any age (P > 0.37) In contrast, independent relations between Pb and LVMI were noted in those less than (P < 0.0001), and greater than (P < 0.02) 50 years, whereas MAP was not independently associated with LVMI at any age (P > 0.07) and Pf tended to show significant relations only in the elderly (P = 0.05). Moreover, although MAP (P < 0.005) and Pb (P < 0.01) showed independent relations with PWV at any age, Pf failed to show independent relations (P > 0.10)., Conclusion: Independent of confounders, steady-state and aortic Pf and Pb show associations with end-organ measures that are organ specific and age dependent.

Background: A reason for concentric left ventricular (LV) remodelling predicting cardiovascular outcomes independent of conventional risk factors and LV mass (LVM) has not been provided. We hypothesized that independent of LVM, concentric LV remodelling is associated with inflammatory changes rather than a pressure load on the LV., Methods: In 764 randomly selected community participants, we assessed relations between several inflammatory markers (ELISA) and LV relative wall thickness (RWT) (echocardiography), LV mass index (LVMI), and indexes of diastolic function., Results: No independent relations were noted between circulating concentrations of inflammatory markers and LVM index (LVMI) (p > 0.13 for all). However, independent of confounders including LVMI and blood pressure (BP), circulating tumour necrosis factor-α (TNF-α) (partial r = 0.14, p < 0.0005) and to a lesser degree interleukin-6 (partial r = -0.09, p < 0.02) were associated with RWT. The impact (standardized β-coefficient) of TNF-α on RWT (0.12 ± 0.03, p < 0.0005) was at least as strong as age (0.13 ± 0.05, p < 0.005), and second only to LVMI (0.27 ± 0.04, p < 0.0001), whilst neither office, 24-hour, central aortic BP, nor aortic stiffness were associated with RWT independent of LVMI. With adjustments, as compared to participants with a normal LVMI and geometry (12.7 ± 0.8), circulating TNF-α concentrations (pg/ml) were increased as much in participants with concentric LV remodelling (16.8 ± 1.5, p < 0.05) as in those with concentric LV hypertrophy (LVH) (17.0 ± 1.3, p < 0.005), whilst eccentric LVH (13.7 ± 0.9) was not. No independent relations between inflammatory markers and LV diastolic function (trans-mitral and tissue Doppler) were noted., Conclusions: Independent of LVMI, a pro-inflammatory state rather than BP load is strongly associated with LV concentric remodelling., (Copyright © 2018 Elsevier B.V. All rights reserved.)

A decreased aortic-to-brachial pulse pressure (PP) amplification, which is independently associated with cardiovascular outcomes, may index several aortic functional changes. However, that aortic functional change most likely to account for this effect is uncertain. In 706 randomly selected community participants of African ancestry with a mean age of 44.4 ± 18.2 years, we assessed aortic function using radial applanation tonometry and SphygmoCor software (including forward [Pf] and backward [Pb] wave separation analysis assuming a triangular flow waveform) and left ventricular mass index (LVMI) (echocardiography). In multivariate models with the inclusion of brachial PP, 1/PP amplification (partial r = 0.12, P < .005), reflected wave pressures (partial r = 0.09, P < .05), and aortic pulse wave velocity (PWV; partial r = 0.09, P < .05) were independently associated with LVMI. Similarly, in multivariate models with the inclusion of brachial PP, 1/PP amplification (P < .005), the reflected wave pressure (P < .01), and aortic PWV (P < .01) were independently associated with LVH. With adjustments for reflected wave pressures, the brachial PP-independent relationships between 1/PP amplification and LVMI or LVH were abolished (P > .08 for both). However, adjustments for PWV failed to modify brachial PP-independent relations between 1/PP amplification and LVMI or LVH. Similar results were noted when brachial systolic blood pressure rather than PP was included in regression models and in sensitivity analysis conducted in participants not receiving antihypertensive therapy. In conclusion, the independent relations between the reciprocal of aortic-to-brachial PP amplification and LVMI or LVH in a largely young to middle-aged sample are accounted for by variations in backward wave pressures rather than aortic stiffness., (Copyright © 2017 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Aortic pulse wave velocity (PWV) and backward waves, as determined from wave separation analysis, predict cardiovascular events beyond brachial blood pressure. However, the extent to which these aortic hemodynamic variables contribute independent of each other is uncertain. In 749 randomly selected participants of African ancestry, we therefore assessed the extent to which relationships between aortic PWV or backward wave pressures (Pb) (and hence central aortic pulse pressure [PPc]) and left ventricular mass index (LVMI) occur independent of each other. Aortic PWV, PPc, forward wave pressure (Pf), and Pb were determined using radial applanation tonometry and SphygmoCor software and LVMI using echocardiography; 44.5% of participants had an increased left ventricular mass indexed to height 1.7 . With adjustments for age, brachial systolic blood pressure or PP, and additional confounders, PPc and Pb, but not Pf, were independently related to LVMI and left ventricular hypertrophy (LVH) in both men and women. However, PWV was independently associated with LVMI in women (partial r = 0.16, P < .001), but not in men (partial r = 0.03), and PWV was independently associated with LVH in women (P < .05), but not in men (P = .07). With PWV and Pb included in the same multivariate regression models, PWV (partial r = 0.14, P < .005) and Pb (partial r = 0.10, P < .05) contributed to a similar extent to variations in LVMI in women. In addition, with PWV and Pb included in the same multivariate regression models, PWV (P < .05) and Pb (P < .02) contributed to LVH in women. In conclusion, aortic PWV and Pb (and hence pulse pressure) although both associated with LVMI and LVH produce effects which are independent of each other., (Copyright © 2017 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Aim: To determine the degree to which an extended time to the peak of the aortic forward wave or early wave reflection time enhance associations between aortic backward wave pressure and hence central aortic pulse pressure (PPc) and left ventricular mass index (LVMI)., Methods: In 701 adult participants from a community sample either receiving no antihypertensive therapy or receiving low-dose thiazide diuretic monotherapy for at least a year (the major therapy employed), we assessed aortic haemodynamics (SphygmoCor software and wave separation analysis; AtCor Medical, West Ryder, New South Wales, Australia) and LVMI (echocardiography)., Results: An interaction between time to the peak of the aortic forward wave and aortic backward wave pressure was independently associated with aortic augmented pressure (P < 0.01), PPc (P < 0.005), LVMI (P < 0.01), and LV hypertrophy (LVH; P = 0.01). The time to the peak of the aortic forward wave-aortic backward wave pressure interaction translated into a stepwise increase in the independent association between aortic backward wave pressure and aortic augmented pressure or PPc across quartiles of time to the peak of the aortic forward wave (P < 0.05 to < 0.0001 for comparison of slopes of relations). Furthermore, the time to the peak of the aortic forward wave-aortic backward wave pressure interaction translated into an increase in the independent association between PPc or aortic backward wave pressure and LVMI (P < 0.05 to < 0.001 for comparison of slopes and strength of relations) or LVH (P < 0.05 for comparisons of odds ratios), but not between forward wave pressures and LVMI or LVH across quartiles of time to the peak of the aortic forward wave. A markedly better ability of aortic backward wave pressure and PPc, but not forward wave pressures to detect LVH was noted in the highest as compared with the first three quartiles of time to the peak of the aortic forward wave (P < 0.05). In contrast, reflection time failed to influence the impact of aortic backward wave pressure or PPc on LVMI., Conclusions: Time to the peak of the aortic forward wave, but not early wave reflection markedly influences the impact of aortic backward wave pressure and hence aortic pulse pressure on LVMI and LVH in adults.

Aim: To identify whether the more recently developed equation for estimated glomerular filtration rate (eGFR) [Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI)] is more closely associated with end-organ changes than previous equations in a group of black African descent., Methods: In 1221 randomly recruited participants of black African ancestry in South Africa, we evaluated serum creatinine concentrations, echocardiographic left ventricular mass index (n = 833), carotid-femoral (aortic) pulse wave velocity (PWV) (n = 1053) and carotid intima-media thickness (n = 633). We calculated eGFR from the Jelliffe, five Cockcroft-Gault, Salazar-Corcoran, Modification of Diet in Renal Disease (MDRD) and CKD-EPI equations., Results: After multivariate adjustments, eGFR calculated from all formulae was inversely associated with left ventricular mass index (P < 0.0001) and PWV (P < 0.05 to <0.001), but not with carotid intima-media thickness (P > 0.08). However, although eGFR determined from all equations except Cockcroft-Gault lean body weight or adjusted body weight was independently associated with left ventricular hypertrophy (n = 390 of 833), CKD-EPI-derived eGFR, but not eGFR determined from alternative equations, was independently associated with an increased PWV (n = 88 of 1053). eGFR derived from the CKD-EPI and MDRD equations showed a better performance (area under the receiver operator characteristic curve) for the detection of left ventricular hypertrophy (P < 0.0005) than eGFR determined from alternative equations., Conclusions: In black Africans, eGFR derived from the CKD-EPI equation is better at detecting end-organ measures than eGFR derived from either the MDRD or alternative equations. To enhance risk prediction in black African communities, eGFR calculated from the CKD-EPI equation may be preferred to other equations.

Background: Although the adipokine resistin may play a role in heart failure, the mechanisms of this effect are uncertain. Relations with left ventricular mass (LVM) and function are uncertain., Methods: In 739 randomly selected participants from a community sample (43.6% obese), we assessed relations between circulating resistin concentrations and LVM index (LVMI), LVM beyond that predicted by stroke work (inappropriate LVMI [LVMinappr]) and systolic and diastolic LV function (echocardiography)., Results: Resistin concentrations were not independently associated with blood pressure (BP). However, resistin concentrations were associated with LVMI (partial r=0.12, p<0.0005), LVMinappr (partial r=0.18, p<0.0001) and LV hypertrophy (partial r=0.13, p<0.001) independent of BP, BMI, the homeostasis model of insulin resistance and additional confounders. Independent relations between resistin concentrations and LVMI and LVMinappr persisted with further adjustments for C-reactive protein concentrations. Resistin concentration (partial r=-0.12, p<0.002 in all and partial r=-0.15, p<0.0005 in untreated) was the only factor independently associated with LV midwall fractional shortening and these relations were enhanced at incremental concentrations of CRP. Resistin was not independently associated with transmitral and myocardial tissue Doppler indices of LV diastolic function., Conclusions: Resistin in-part explains variations in LVM, hypertrophy and myocardial systolic dysfunction, and these effects are independent of insulin resistance and general inflammatory changes., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Aim: We determined whether left ventricular hypertrophy (LVH) which exceeds that predicted from workload [inappropriate LV mass (LVM(inappr))] is associated with reduced left ventricle (LV) systolic chamber function independent of and more closely than absolute or indexed left ventricular mass (LVM)., Methods: In 626 randomly selected adult participants from a community sample of black Africans, using echocardiography we assessed absolute LVM, LVM indexed to height(2.7) (LVMI), LVM(inappr), LV wall stress, ejection fraction, and midwall fractional shortening (FSmid). LVM(inappr) was determined as percentage of observed/predicted LVM. Predicted LVM was calculated from a previously validated formula that incorporates stroke work. LVMI(inappr) more than 150% was considered to be inappropriate LVH. This threshold was identified from the upper 95% confidence interval for LVMI(inappr) determined in 140 healthy participants., Results: A total of 21.7% of participants had LVH (LVMI > 51 g/m(2.7)) and 18.5% had inappropriate LVH. With adjustments for LV stress and other confounders there was a strong inverse relationship between LVM(inappr) and ejection fraction (partial r = -0.41, P < 0.0001), whereas only modest inverse relations between LVM or LVMI and ejection fraction were noted (partial r = -0.07 to -0.09, P < 0.05-0.09) (P < 0.0001, comparison of partial r values). The independent relationship between LVM(inappr) and ejection fraction persisted with further adjustments for LVM or LVMI (partial r = -0.52, P < 0.0001). LVM(inappr) and FSmid were similarly inversely related (P < 0.0001) and these relations were also stronger and independent of LVM or LVMI., Conclusion: Inappropriate LVH is strongly and inversely related to variations in ejection fraction independent of and more closely than LVM or LVMI in a community sample of black African ancestry. These data suggest that LVH is a compensatory response to workload, but when exceeding that predicted by workload, is associated with LV systolic chamber decompensation.

Although in cross-sectional studies left ventricular mass (LVM), which exceeds that predicted by workload (inappropriate LVM [LVM(inappr)]) but not absolute LVM or LVM index (LVMI), is inversely related to LV ejection fraction (EF), whether on-treatment decreases in LVM(inappr) (%observed/predicted LVM) account for increases in EF beyond LVM or LVMI is unclear. Echocardiography was performed in 168 mild-to-moderate hypertensives treated for 4 months. Although in patients with an LVMI >51 g/m(2.7) (n=112; change in LVMI, -13.7±14.0 g/m(2.7); P<0.0001) but not in patients with an LVMI ≤51 g/m(2.7) (n=56; change in LVMI, 1.3±9.3 g/m(2.7)) LVMI decreased with treatment, treatment failed to increase EF in either group (1.2±10.8% and 2.7±10.7%, respectively). In contrast, in patients with inappropriate LV hypertrophy (LVM(inappr) >150%; n=33) LVM(inappr) decreased (-32±27%; P<0.0001) and EF increased (5.0±10.3%; P<0.05) after treatment, whereas in patients with an LVM(inappr) ≤150% (n=135), neither LVM(inappr) (-0.5±23%) nor EF (0.9±10.3%) changed with therapy. With adjustments for circumferential LV wall stress and other confounders, whereas on-treatment decreases in LVM or LVMI were weakly related to an attenuated EF (partial r=0.17; P<0.05), on-treatment decreases in LVM(inappr) were strongly related to increases in EF even after further adjustments for LVM or LVMI (partial r=-0.63 [CI, -0.71 to -0.52]; P<0.0001). In conclusion, decreases in LVM(inappr) are strongly related to on-treatment increases in EF beyond changes in LVM and LVMI. LV hypertrophy can, therefore, be viewed as a compensatory change that preserves EF, but when in excess of that predicted by stroke work, it can be viewed as a pathophysiological process accounting for a reduced EF.

Aim: As it is uncertain whether arterial stiffness is related to left ventricular mass and left ventricle mean wall thickness independent of blood pressure measured at the brachial artery, we aimed to ascertain this effect in never-treated participants with a high prevalence of risk factors for large artery dysfunction., Methods: The conventional and ambulatory blood pressure-independent relations between indices of large artery function and either left ventricular mass or mean wall thickness were determined in 309 never-treated randomly recruited South Africans of African ancestry with prevalent risk factors for large artery changes [24% were hypertensive, 63% were overweight/obese, and 17% had diabetes mellitus or abnormal blood glucose control (glycosylated hemoglobin A1c > 6.1%)]. Large artery function was assessed from applanation tonometry performed at the carotid, radial and femoral arteries and central augmentation index and aortic pulse wave velocity (carotid femoral pulse wave velocity) derived from these measures. Left ventricular mass indexed for height (left ventricular mass index) and mean wall thickness were determined using echocardiography., Results: Pulse wave velocity was associated with left ventricular mass index (r = 0.67, P < 0.0001) and mean wall thickness (r = 0.61, P < 0.0001) in women, but not in men (r = 0.04-0.08) (P < 0.0001 for the interaction between pulse wave velocity and gender). On multivariate analysis with appropriate adjustments including either conventional systolic blood pressure, pulse pressure or mean arterial pressure, pulse wave velocity was independently associated with left ventricular mass index (partial r = 0.25, P < 0.005 after adjustments for systolic blood pressure) and with mean wall thickness (partial r = 0.17, P < 0.05 after adjustments for systolic blood pressure) in women, but not in men. With the inclusion of 24-h ambulatory rather than conventional systolic blood pressure, pulse pressure or mean arterial pressure in the regression equation, pulse wave velocity was similarly independently associated with left ventricular mass index (partial r = 0.39, P < 0.001 after adjustments for 24-h systolic blood pressure) and mean wall thickness (partial r = 0.33, P < 0.003 after adjustments for 24-h systolic blood pressure) in women, but not in men. Central augmentation index was not independently associated with left ventricular mass index or mean wall thickness. In women, the contribution of pulse wave velocity to left ventricular mass index or mean wall thickness independent of systolic blood pressure (standardized beta-coefficient for left ventricular mass index=0.37 +/- 0.13, P < 0.005) was equivalent to the contribution of systolic blood pressure (standardized beta-coefficient for left ventricular mass index = 0.38 +/- 0.13, P < 0.005). Moreover, after adjusting for clinic or ambulatory systolic blood pressure and other confounders, in women every one standard deviation increase in pulse wave velocity (2.1 m/s) translated into a 4.3 or 6.2 g/m increase in left ventricular mass index, respectively., Conclusion: Arterial stiffness is associated with left ventricular mass index and left ventricle wall thickness independent of conventional or ambulatory blood pressure and additional confounders in a never-treated population sample of women, but not men, of African ancestry with prevalent risk factors for large artery dysfunction.

Background: In the treatment of hypertension in subjects of African origins, although hydrochlorothiazide (HCTZ) is not as effective as calcium channel blockers, indapamide is superior to HCTZ. In the present study we therefore compared the effects of slow release (SR) indapamide with the calcium channel blocker amlodipine, when used as initial therapy, on blood pressure (BP) and left ventricular mass (LVM) during 6 months of treatment in this group., Methods: Patients with a mean daytime ambulatory diastolic BP > or =90 mm Hg and < or =110 mm Hg (n = 125, aged 53 +/- 11 years, 68% women) were randomized to receive open-label 1.5 mg of indapamide SR or 5 mg of amlodipine. If daytime ambulatory diastolic BP at 1 month was >/=90 mm Hg, 4 mg of perindopril was added to indapamide SR or the dose of amlodipine was increased to 10 mg., Results: After 1 month of therapy, there was an equivalent decline in systolic and diastolic BP in both groups (P <.0001). In the indapamide-treated group (n = 62) the daytime BP decreased from 153 +/- 12/101 +/- 6 mm Hg to 138 +/- 15/92 +/- 10 mm Hg and for amlodipine (n = 58), it decreased from 152 +/- 13/99 +/- 5 mm Hg to 138 +/- 12/91 +/- 8 mm Hg. At 6 months daytime ambulatory BP decreased to 130 +/- 15/86 +/- 8 mm Hg and to 129 +/- 11/85 +/- 5 mm Hg for the indapamide SR (n = 42) and amlodipine (n = 44) treatment groups, respectively. Both groups showed equivalent regression of LVM index and relative wall thickness., Conclusions: These data suggest that in hypertensive patients of African ancestry initiating therapy with 1.5 mg of indapamide SR and then adding 4 mg of perindopril is equally as effective as amlodipine therapy at reducing BP, and modifying target organ damage.

Background: In a single-center study, we compared to what extent changes in conventional and ambulatory blood pressure (BP) predicted regression of left ventricular mass (LVM) index in response to antihypertensive treatment in previously untreated and treated patients with sustained hypertension., Methods and Results: We enrolled 173 black African patients who, off treatment, had a daytime diastolic BP ranging from 90 to 114 mm Hg. Antihypertensive drugs were titrated and combined to reduce the daytime diastolic BP below 90 mm Hg. Echocardiograms were obtained at baseline and follow-up. Mean systolic/diastolic clinic BP, 24-hour BP, and LVM index were similar in previously untreated (n=64) and previously treated (n=109) patients and averaged 171/102 mm Hg, 151/97 mm Hg, and 118 g/m2, respectively. At 4 months, these values had decreased (P<0.001) by 26/12 mm Hg, 23/14 mm Hg, and 14 g/m2 in previously untreated patients and by 22/9 mm Hg, 21/13 mm Hg, and 19 g/m2 in previously treated patients. In the previously untreated patients, the regression in LVM index correlated to a similar degree (P=0.09) with the decreases in the conventional (r=0.34; P=0.005) and the 24-hour (r=0.26; P=0.04) systolic BP. In the previously treated patients, the corresponding correlations were 0.02 (P=0.82) and -0.10 (P=0.32), respectively. Compared with the 24-hour systolic BP, automated oscillometric measurements of systolic BP obtained at the clinic yielded similar results., Conclusions: In previously untreated patients with sustained hypertension followed at a single center, reductions in clinic and ambulatory systolic pressure in response to antihypertensive treatment equally predicted the regression in LVM index.

Objectives: The aim of this study was to determine whether left ventricular dilation and congestive heart failure in patients with acute rheumatic fever with carditis are accompanied by left ventricular contractile dysfunction., Background: Acute rheumatic fever with carditis involves both the myocardium and endocardium, with consequent valvular regurgitation. The relative contribution of volume overload induced by valvular regurgitation and myocardial dysfunction due to rheumatic myocarditis to the overall degree of left ventricular dilation and congestive heart failure in these patients is unknown., Methods: To investigate this, we evaluated 32 patients (15 male, 17 female, mean age 14 +/- 3 years) with documented active carditis and congestive heart failure. All 32 patients were found to have significant isolated mitral regurgitation or combined mitral and aortic regurgitation. Echocardiographic analysis of left ventricular dimensions and systolic performance was performed before and after isolated mitral or combined mitral and aortic valve replacement and the results were compared with those in 19 control subjects matched for age, gender and body surface area., Results: Both preoperative left ventricular end-diastolic diameter and percent fractional shortening were significantly increased in patients compared with control subjects (57 +/- 7 vs. 43 +/- 3 mm, p < 0.001, and 38 +/- 6% vs. 33 +/- 1%, p < 0.001, respectively). After valve replacement, left ventricular end-diastolic diameter decreased significantly (57 +/- 7 to 47 +/- 6 mm, p < 0.001). Although percent fractional shortening decreased significantly postoperatively (38 +/- 6% to 32 +/- 6%, p < 0.001), the postoperative percent fractional shortening did not differ from that in control subjects (32 +/- 6% vs. 33 +/- 1%, p = NS)., Conclusions: The results of this study indicate that left ventricular dilation and heart failure in patients with acute rheumatic carditis rarely occur in the absence of hemodynamically significant regurgitant valve lesions. Furthermore, rapid reduction in left ventricular dimensions and preservation of fractional shortening after isolated mitral or combined mitral and aortic valve replacement suggest that rheumatic carditis is not accompanied by any significant degree of myocardial contractile dysfunction.