Search

Aim: This single blind cross-sectional study compared the vascular health of subjects suffering from severe chronic periodontitis, severe aggressive periodontitis and periodontal healthy controls by evaluating pulse wave velocity (PWV), augmentation index (AIx) and pulse pressure amplification (PPA)., Material and Methods: In a total of 158 subjects, 92 suffering from severe periodontitis and 66 matched periodontal healthy controls, PWV, AIx, central and peripheral blood pressure were recorded using an oscillometric device (Arteriograph)., Results: Subjects suffering from severe chronic or aggressive periodontitis exhibited significantly higher PWV (p = 0.00004), higher AIx (p = 0.0049) and lower PPA (p = 0.028) than matched periodontal healthy controls., Conclusions: The results of this study confirm the association between periodontal inflammation and increased cardiovascular risk shown by impaired vascular health in case of severe periodontitis. As impaired vascular health is a common finding in patients suffering from severe periodontal disease a concomitant routine cardiovascular evaluation may be advised.

Objective: Hypobaric hypoxia, physical and psychosocial stress may influence key cardiovascular parameters including blood pressure (BP) and pulse pressure (PP). We investigated the effects of mild hypobaric hypoxia exposure on BP and PP reactivity to mental and physical stress and to passive elevation by cable car., Methods: 36 healthy volunteers participated in a defined test procedure consisting of a period of rest 1, mental stress task (KLT-R), period of rest 2, combined mental (KLT-R) and physical task (bicycle ergometry) and a last period of rest both at Graz, Austria (353 m asl) and at the top station Dachstein (2700 m asl). Beat-to-beat heart rate and BP were analysed both during the test procedures at Graz and at Dachstein and during passive 1000 m elevation by cable car (from 1702 m to 2700 m)., Results: A significant interaction of kind of stress (mental vs. combined mental and physical) and study location (Graz vs. Dachstein) was found in the systolic BP (p = .007) and PP (p = .002) changes indicating that during the combined mental and physical stress task sBP was significantly higher under hypoxic conditions whereas sBP and PP were similar during mental stress both under normobaric normoxia (Graz) and under hypobaric hypoxia (Dachstein). During the passive ascent in cable car less trivialization (psychological coping strategy) was associated with an increase in PP (p = .004)., Conclusion: Our data show that combined mental and physical stress causes a significant higher raise in sBP and PP under hypoxic conditions whereas isolated mental stress did not affect sBP and PP under hypoxic conditions. PP-reaction to ascent in healthy subjects is not uniform. BP reactions to ascent that represents an accumulation of physical (mild hypobaric hypoxia) and psychological stressors depend on predetermined psychological traits (stress coping strategies). Thus divergent cardiovascular reactions can be explained by applying the multidimensional aspects of the biopsychosocial concept.

Background: The effects of smoking on central aortic pressures and the age-related increase in left ventricular mass (LVM) are largely unknown. We studied the relationship between smoking, arterial distensibility, central aortic pressures and left ventricular mass in two population-based studies., Methods: Data was obtained from two German population-based studies (KORA and SHIP, participants' ages 25-84 years). We identified 114 normotensive current smokers and 185 normotensive all-time non-smokers in KORA as well as 400 and 588 such individuals in SHIP. Echocardiographic LVM was obtained at baseline (T0) and follow-up after ten years (T1) in KORA and at follow-up (T1) in SHIP. Additionally, pulse-wave analysis-based central aortic pressure and augmentation index (AIx) were measured at T1 in KORA., Results: Cross-sectional analysis, using KORA T0 and SHIP T1, revealed in both studies a higher covariate-adjusted LVM and left ventricular mass index (LVMI) in smokers as compared with non-smokers. Moreover, in the KORA T1 examination, the smokers demonstrated a more pronounced increase, relative to baseline, of LVM (+13.5%) and LVMI (+13.4%) compared to non-smokers (+8.59% and +8.65%; p=0.036 and 0.042, respectively). Additionally, at KORA T1 smokers had a higher central systolic blood pressure and higher AIx than non-smokers (p=0.012 and p=0.001, respectively)., Conclusions: The difference in central aortic pressure due to enhanced and more prolonged wave reflection may explain our finding of a further pronounced increase in left ventricular wall thickness and mass over time in smokers., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

The cannabinoid receptors, CB1 and CB2, are expressed in the heart, but their role under pathological conditions remains controversial. This study examined the effect of CB1 receptor blockade on cardiovascular functions after experimental MI and in experimental metabolic syndrome. MI was induced in Wistar rats by permanent ligation of the left coronary artery. Treatment with the CB1 receptor antagonist rimonabant (10 mg/kg i.p. daily) started 7 days before or 6 h after MI and continued for 6 weeks. Haemodynamic parameters were measured via echocardiography and intracardiac Samba catheter. CB1 blockade improved systolic and diastolic heart function, decreased cardiac collagen and hydroxyproline content and down-regulated TGF-β1. Additionally, rimonabant decreased arterial stiffness, normalised QRS complex duration and reduced brain natriuretic peptide levels in serum. In primary cardiac fibroblasts, rimonabant decreased MMP-9 activity and TGF-β1 expression. Furthermore, rimonabant improved depressed systolic function of spontaneously hypertensive obese rats and reduced weight gain. Blocking of CB1 receptor with rimonabant improves cardiac functions in the early and late stages after MI, decreases arterial stiffness and reduces cardiac remodelling. Rimonabant also has cardioprotective actions in rats characterised by the metabolic syndrome. Inhibition of proteolysis and TGF-β1 expression and reduced collagen content by rimonabant may attenuate destruction of the extracellular matrix and decrease fibrosis after MI.

Background: Emotional stress is considered a risk factor for cardiovascular events, the underlying pathophysiology remains unclear., Methods: To evaluate how emotional stress effects hemodynamics, thirteen healthy German soccer fans (mean 37.6 years, 24-56 years) were studied during live TV coverage of the finals with German national team participation (GP) and the respective finals without German participation (noGP). Peripheral blood pressure, heart rate, central blood pressure, augmentation pressure and index, cardiac output and peripheral resistance were measured., Results: In the 1st hour before the match all parameters were not significantly different between the groups. In the GP group peripheral systolic pressure (1st halftime noGP 118 ± 1(s.e.m) versus GP 126 ± 2 mmHg, p<0.05, 2nd 117 ± 1 vs. 125 ± 2 mmHg, p<0.05), mean blood pressure, diastolic blood pressure, heart rate (1st 73 ± 2 vs. 86 ± 3 bpm, p<0.05, 2nd 75 ± 2 vs. 87 ± 2 bpm, p<0.05), cardiac output (1st 4,4 ± 0,1 versus 4,8 ± 0,1L/min, p<0.05, 2nd 4,6 ± 0,1 versus 4,7 ± 0,11 L/min, p>0.05) and peripheral resistance were significantly increased compared to the noGP group during the matches. Systolic central aortic pressure (noGP: 101 ± 2 versus GP 107 ± 2 mmHg, p<0.05) and central pulse pressure (noGP: 31.3 ± 1.3 mmHg vs. GP: 38.5 ± 2.7 mmHg, p<0,05) remained elevated during the second hour after the match., Conclusions: We observed persistent changes in central hemodynamics 2h after emotional stress. Despite normalization of peripheral values after the end of the finals, we observed prolonged elevation of central systolic blood and pulse pressure. Our findings contribute to the understanding of the increased risk of cardiovascular events in emotional stress., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

The circadian pattern of numerous cardiovascular events (myocardial infarction, sudden cardiac death, stroke) reveals a peak in the early hours of the morning. A circadian rhythm peaking in the morning is also found for so-called silent myocardial ischaemia, which occurs in more than 20% of patients with arterial hypertension, and can be regularly detected in combined 24-h-ABPM/EKG examinations. Comparative studies have shown that hypertensives with SMI suffer more cardiac events than those with no SMI. It has further been demonstrated that an elevated blood pressure amplitude, with is considered an independent risk factor for cardiac events, is associated with an increased incidence of SMI in patients with micro- or macro-angiopathy. Accordingly, consideration should be given to SMI when deciding on treatment, also in hypertensives with no angina pectoris symptoms.

With the increasing use of blood pressure self-measurement in pharmacological studies, the question arises as to whether this method can replace office blood pressure measurement or ambulatory 24-h blood pressure measurement for testing and comparing the efficacy of antihypertensives. Ambulatory 24-h blood pressure measurement or self-measurement available for analysis can be obtained in 70 to 90% of patients. Self-measurement shows a better correlation with the prognostically relevant ambulatory 24-h blood pressure measurement than office blood pressure measurement for appraising the antihypertensive effect. Although similar antihypertensive effects were found for ambulatory 24-h blood pressure measurement and self-measurement in the group comparison, substantial discrepancies can be observed in the individual patient owing to the different nature of these two methods of measurement. Both ambulatory 24-h blood pressure measurement and self-measurement are superior to office blood pressure measurement in terms of their reproducibility. This increases the sensitivity of clinical studies and reduces the number of cases required. Owing to the white-coat effect, variable compliance and drug holidays and their effects on the efficacy of antihypertensive medication are not detected by office blood pressure measurement and ambulatory 24-h blood pressure measurement. Self-measurement detects drug holidays, which are reflected in an increase of the blood pressure measurement values, and per se promotes compliance. Self-measurements and ambulatory 24-h measurements in pharmacological studies must be regarded as complementary, so that it is appropriate to use both methods whenever possible. Data management, data analysis and monitoring in pharmacological studies are facilitated by instruments with automatic data storage which allows telemonitoring.

Background: Various statements are made concerning peaks of heart rate (HR), blood pressure (BP) and double product (product of HR and systolic BP) as triggers for ST-segment depression. The aim of the present study was to identify determinants of ST-segment depression with a new ambulatory device for simultaneous 24-h electrocardiogram (ECG) and BP monitoring., Methods: A total of 63 treated patients (63 +/- 9 years, 33 women and 30 men) with arterial hypertension and ischemic heart disease were studied with a new ambulatory 24-h BP measurement (ABPM) device evaluated according to the BHS protocol (Cardiotens, Meditech, Hungary). This device allows simultaneous ST-segment analysis with extra BP recordings triggered by episodes of ST-segment depression., Results: ST-segment (Holter ECG) depression (> 1 mm and > 60 s) was demonstrated in 26 patients with a mean duration of 4.95 +/- 2.6 min and a peak in the early morning hours. All ST-segment depressions were silent and occurred during a significant increase of BP (15 +/- 11 mmHg systolic and 10 +/- 5 mmHg diastolic, compared with the mean ABPM values) and a significant increase of the double product from 10 921 +/- 2 395 (24-h mean) to 14 515 +/- 2329 (during ST-depression). The recorded systolic and diastolic BP (SBP, DBP) values from the pre ST-event were significant higher compared with 24-h values (153 +/- 19 versus 145 +/- 22 mmHg systolic, 83 +/- 12 versus 78 +/- 14 diastolic). The mean pulse pressure (PP) value in the group with ST-depression was significantly higher than in the group without ST changes (69 +/- 16 versus 58 +/- 10 mmHg; P < 0.005). A total of 73% of patients with ST-events compared with 35% without ST-events showed a PP >or= 60 mmHg (P = 0.025)., Conclusion: Simultaneous ABPM and ST-segment analysis identifies episodes of silent myocardial ischemia during increases of BP and HR. Hypertensive patients with ischemic heart disease and ST events show higher mean pulse pressure values than are observed in patients without events. A PP of >or= 60 mmHg is linked to an increased risk of silent myocardial ischemias.

History and Clinical Findings: A 71-year-old woman was admitted with arterial hypertension resistant to drug therapy (office readings 197/82 mmHg) under medication with beta-blocker, AT 1 -antagonist and a diuretic. The only physical pathologic finding was an adipositas., Diagnosis, Treatment and Course: The patient was suffering from isolated systolic hypertension, grade 3 corresponding to WHO-guidelines. Despite antihypertensive triple therapy office as well as self-measured blood pressure values (mean 170/82 mmHg) remained elevated. Thus, the patient fulfilled the criteria of a resistant hypertension. The degree of compliance was only 50 %, detected by using a Medication-Event-Monitoring-System (correct dosing interval 17.1 %). We discussed the results of compliance- and blood pressure self-measurement with the patient. In the following period of compliance- and blood pressure self-measurement (with unchanged antihypertensive therapy) the compliance increased dramatically with a degree of 90,9 % and self-measured blood pressure values almost normalized (mean 137/71 mmHg)., Conclusion: The control of compliance by using electronic compliance-monitoring may help to discover non-compliance as a frequent cause of resistant hypertension and to avoid unnecessary cost-extensive procedures.

Background: Gitelman's syndrome (GS) is characterized by hypokalemic metabolic alkalosis, hypomagnesemia and hypocalciuria and these phenotypic features have been shown to be attributable to mutations in the gene encoding the thiazide-sensitive Na/Cl cotransporter (NCCT). Until now, 55 different mutations have been reported and most of the families affected with GS exhibit autosomal recessive inheritance., Methods: All 26 exons of the human NCCT gene were investigated in 2 German NCCT-deficient patients and their families. Mutation detection was performed by either direct automated sequencing of polymerase chain reaction (PCR)-amplified DNA products or by sequence analysis of cloned PCR products., Results: In a 47-year-old German GS female a novel non-conservative missense mutation (S314F) and a complex deletion/insertion in the NCCT gene were found to be associated with the disorder. A further novel non-conservative substitution (S402F) together with a frequently observed R209W exchange were found in a 19-year-old German GS female., Conclusions: The observation of a compound heterozygote state in both females affected and the absence of a GS phenotype in their relatives carrying a single mutant allele is consistent with an autosomal recessive pattern of inheritance., (Copyright 2002 S. Karger AG, Basel)

Recent pharmacological evidence has implicated substance P and neurokinin A, natural ligands for neurokinin-1 and neurokinin-2 receptors, respectively, as neurotransmitters in brain neuronal circuits activated upon noxious stimulation. The expression of the inducible transcription factor, c-Fos, was used to identify areas in the brain activated by a noxious stimulus (the subcutaneous injection of formalin), and to investigate the effects of intracerebroventricular administration of selective, nonpeptide antagonists for neurokinin-1 and neurokinin-2 tachykinin receptors on the neural activity in these areas and on the behavioural response to formalin-induced pain. Formalin (5%, 50 microl), injected subcutaneously through a chronically implanted catheter in the region of the lower hindlimb, increased c-Fos expression in a number of brain areas related to nociceptive transmission or the integration of stress responses. Grooming behaviour, licking and biting directed to the injected site, was the most frequent behavioural response. Intracerebroventricular pretreatment of rats with either RP 67580 (500 pmol), the active enantiomer of a neurokinin-1 receptor antagonist, or with SR 48968 (500 pmol), the active enantiomer of a neurokinin-2 receptor antagonist, reduced the formalin-induced c-Fos staining in the prefrontal cortex, dorsomedial and ventromedial nuclei of the hypothalamus, the locus coeruleus and the periaqueductal gray. The neurokinin-1, but not the neurokinin-2, receptor antagonist attenuated the formalin-induced activation of c-Fos in the paraventricular nucleus of the hypothalamus. Simultaneous intracerebroventricular pretreatment with both neurokinin-1 and neurokinin-2 receptor antagonists did not produce any additional inhibitory effect on the post-formalin c-Fos expression. None of the tachykinin receptor antagonists had an effect on the formalin-induced c-Fos expression in the septohypothalamic nucleus, medial thalamus, parabrachial nucleus and central amygdaloid nucleus, indicating that neurotransmitters other than neurokinins are most probably responsible for the activation of these areas in response to noxious stimulation. While both tachykinin receptor antagonists reduced the grooming behaviour to formalin, the neurokinin-1 receptor antagonist was clearly more effective than the neurokinin-2 receptor antagonist. Intracerebroventricular pretreatment of rats with the inactive enantiomers of the tachykinin receptor antagonists, RP 68651 and SR 48965, was without effect. Our results show that (i) the modified formalin test elicited an intense grooming behaviour and expression of c-Fos in numerous forebrain and brainstem areas, (ii) both tachykinin receptor antagonists were able to attenuate the behavioural response to pain and to reduce the formalin-induced c-Fos expression in some, but not all, brain areas, and (iii) the neurokinin-1 antagonist, RP 67580, was more effective in inhibiting the behavioural response to formalin and the pain-induced activation of c-Fos than the antagonist for neurokinin-2 receptors, SR 48968, indicating that neurokinin-1 receptors are preferentially activated in neurokinin-containing pathways responding to noxious stimuli. Our results demonstrate that blockade of brain tachykinin receptors, especially of the neurokinin-1 receptor, reduces the behavioural response to pain and the pain-induced c-Fos activation in distinct brain areas which are intimately linked with nociceptive neurotransmission and the initiation and integration of central stress responses. Together with the previous findings of the inhibition of hypertensive and tachycardic responses to pain, the present data indicate that tachykinin receptor antagonists can effectively inhibit the generation of an integrated cardiovascular and behavioural response pattern to noxious stimuli.

Background: The progression of central blood pressure (CBP) values and central hemodynamic parameters and its relationship with cardiovascular risk factors is quite unknown. We sought to investigate this association in a Spanish adult population without cardiovascular diseases., Methods: Prospective observational research with a 5-year follow-up. Randomly sampled 501 individuals (mean age 56 ± 14 years, 50.3% women). After 5 years, 480 individuals had a follow-up. Measurements taken using the SphygmoCor (AtCor Medical Pty Ltd., Head Office, West Ryde, Australia), following all the recommendations established in the "International task force" (Sharman JE, Avolio AP, Baulmann J, Benetos A, Blacher J, Blizzard CL, Boutouyrie P, Chen CH, Chowienczyk P, Cockcroft JR, Cruickshank JK, Ferreira I, Ghiadoni L, Hughes A, Jankowski P, Laurent S, McDonnell BJ, McEniery C, Millasseau SC, Papaioannou TG, Vlachopoulos C. Validation of non-invasive central blood pressure devices: ARTERY Society task force consensus statement on protocol standardization. Eur Heart J 2017; 38:2805-2812), giving an estimate of CBP relative to measured brachial blood pressure (type 1 device)., Results: Progressions during follow-up: central systolic blood pressure (cSBP): 4.16 ± 13.71 mm Hg; central diastolic blood pressure: 2.45 ± 11.37 mm Hg; central pulse pressure: 1.72 ± 12.43 mm Hg; pulse pressure amplification (PPA): 2.85 ± 12.20 mm Hg; ejection duration: 7.00 ± 47.87 ms; subendocardial viability ratio (SEVR): -8.04 ± 36.24%. In multiple regression analysis: cSBP positively associated with: body mass index (BMI) (β = 0.476); waist size (β = 0.159); number of cigarettes per day (β = 0.192). Inversely associated with peripheral systolic blood pressure (β = -0.282). Central diastolic blood pressure increase positively associated with number of cigarettes per day (β = 0.174). Inversely associated with peripheral diastolic blood pressure (β = -0.292). Central pulse pressure increase positively associated with BMI (β = 0.330). Inversely associated with peripheral pulse pressure (β = -0.262). Pulse pressure amplification increase positively associated with: BMI (β = 0.276); number of cigarettes per day (β = 0.281). Ejection duration progress inversely associated with basal plasma glucose (β = -0.286)., Conclusions: All measures increased except for SEVR. Progressions in CBP and PPA were positively associated with anthropometric parameters and number of cigarettes and CBP inversely associated with peripheral blood pressure, although this association was different according to sex., (© The Author(s) 2024. Published by Oxford University Press on behalf of American Journal of Hypertension, Ltd. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)