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At least 1,027 records · Page 57Linked to original sources
PubMed1999

A simple new model of physiologically working heterotopic rat heart transplantation provides hemodynamic performance equivalent to that of an orthotopic heart.

BACKGROUND: The widely used non-volume-loaded abdominal heterotopic heart transplant (NL) in rats undergoes atrophy after transplantation. Various techniques have been designed to load the transplanted heart because of its potential immunological impact. Our aim was to create a volume-loaded heterotopic heart transplantation model (VL) capable of ejection and practical for routine studies. Using this model, we tested the hypothesis that VL isografts would retain myocardial performance comparable to native hearts (NH). METHODS: Heterotopic hearts were transplanted using and end-to-side anastomosis between the donor's superior vena cava and the recipient's abdominal inferior vena cava. The right ventricle loads the left ventricle (LV) via a direct anastomosis of the pulmonary artery to the left atrium. The LV ejects volume through an end-to-side anastomosis of the donor's aorta to the recipient's abdominal aorta. Hemodynamic data (systolic and diastolic LV pressures, dP/dt max and min, tau) were studied in-situ (at baseline and after adding volume) and in a Langendorff perfusion system (at baseline and after stimulation with isoproterenol) 2 weeks after transplantation. RESULTS: In situ systolic pressure and diastolic function of VL was superior to NL, and beta-adrenergic stimulated performance in the Langendorff perfusion of VL showed hemodynamic performance equivalent to NH, unlike NL which had a diminished response. CONCLUSION: This technique results in a volume-loaded ejecting heart transplant model that preserves anatomical structures. The VL can be evaluated in situ and after explantation in Langendorff perfusion system and may offer advantages if workload of the graft is of significance to the study performed.

Abdomen↗
PubMed1999

Patient preferences for heart failure treatment: utilities are valid measures of health-related quality of life in heart failure.

BACKGROUND: Current standards hold that cost-effectiveness analyses should incorporate measures of both quantity and quality of life, and that quality of life in this context is best measured by a utility. We sought to measure utility scores for patients with heart failure and to assess their validity as measures of health-related quality of life (HRQL). METHODS AND RESULTS: We studied 50 patients with heart failure. We measured utilities with the time trade-off technique, exercise capacity with a 6-minute walk test, and HRQL with the Minnesota Living With Heart Failure questionnaire, the Medical Outcomes Study Short Form-36 (SF-36) questionnaire, and a visual analogue score. Validity was assessed by establishing correlation between utilities and these other measures. Mean utility score was 0.77 +/- 0.28. There were significant (P < .05) curvilinear relationships between utility score and visual analogue score, the physical function summary scale of the SF-36, 6-minute walk distance, and the Living With Heart Failure score. Utility scores on retest at 1 week were unchanged in a subset of 12 patients. Utilities did not vary systematically with age, sex, or ethnicity. CONCLUSION: Utilities are valid measures of HRQL in patients with heart failure, and cost-effectiveness analyses of heart failure treatments incorporating utilities in the outcome measure can be meaningful.

Adult↗
PubMed1997

Combination drug therapy in chronic heart failure: is treatment part of the problem in heart failure?

Despite advances in medical treatment, the annual mortality associated with severe heart failure remains over 40%, and even in mild heart failure the associated mortality is 40% over 4 years. Once it has been demonstrated that the morbidity and mortality to heart failure can be adequately addressed by combinations of drug therapy, then it is logical to attempt to strip out redundant components of these therapeutic regimes. In the meantime, however, combination therapy is required to counter many of the pathophysiological facets of the heart failure syndrome, including fluid retention, neuroendocrine activation, progressive ventricular dysfunction, and sudden cardiac death. Diuretics and ACE inhibitors are well-established drug treatments. Digoxin appears to lessen the rate of progression of heart failure without altering survival. New evidence suggests that beta-blockers may be useful additions to the heart failure therapeutic armamentarium, although whether all beta-blockers are equally effective remains to be established.

Adrenergic beta-Antagonists↗
PubMed1997

Tissue expression of components of the renin-angiotensin system in experimental post-infarction heart failure in rats: effects of heart failure and angiotensin-converting enzyme inhibitor treatment.

1. It has been suggested that local tissue renin-angiotensin systems may be activated in heart failure and that effects on such systems may, at least partially, explain the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in this syndrome. To investigate these hypotheses, we examined expression of renin-angiotensin system components in several tissues in a rodent model of post-myocardial infarction (MI) heart failure, and analysed whether such expression is modified by ACE inhibitor treatment. 2. Four groups of rats (n = 8 - 12 per group) were studied 30 days after surgery: (A) sham-operated rats with no treatment, (B) rats with post-MI heart failure induced by ligation of the left coronary artery, (C) sham-operated rats treated with the ACE inhibitor perindopril (1.5 mg day-1 kg-1), and (D) rats as per B, but treated with perindopril. Expression of renin, angiotensinogen, ACE and angiotensin subtype 1 receptor was assessed by quantification of their respective mRNAs by Northern blotting. 3. Renal renin mRNA increased 2-fold in animals with MI (group B) compared with controls (group A) (P < 0.05) and between 50 and 100-fold after ACE inhibitor treatment (P < 0.001). No change in renin gene expression was found in any extra-renal site either following MI or after ACE inhibitor treatment. Hepatic angiotensinogen mRNA level was similar in all groups, but kidney angiotensinogen mRNA level was increased 1.6-fold (P < 0.01) in the groups receiving perindopril. ACE mRNA level in the lung was not affected by ACE inhibitor treatment but decreased by 50% following MI (groups B and D, P < 0.01). This was associated with a similar (50%, P < 0.01) fall in lung ACE activity and was correlated with the severity of heart failure. Angiotensin subtype 1 receptor mRNA level was not affected in any tissue by either MI or ACE inhibitor treatment. 4. We did not find a systematic activation of tissue renin-angiotensin systems, as assessed by steady-state mRNA levels of key components of the system in experimental post-MI heart failure, or a major effect of ACE inhibitor treatment on expression of these components. However, we observed tissue-specific changes in expression of selected components of the renin-angiotensin system in the kidney and the lung in post-MI heart failure and after ACE inhibitor treatment, which may be of relevance to the pathophysiology of the syndrome and the effects of ACE inhibition.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

High and low pulmonary vascular resistance in heart transplant candidates. A 5-year follow-up after heart transplantation shows continuous reduction in resistance and no difference in complication rate.

BACKGROUND: In heart transplantation candidates, high pulmonary vascular resistance has been found to decrease promptly after heart transplantation without any further reduction during follow-up. Pulmonary hypertension has been described as associated with an increased peri- and postoperative complication rate and mortality. This study describes the evolution of pulmonary vascular resistance and the outcome for patients during 5 years following heart transplantation. METHODS AND RESULTS: Haemodynamic data, complication rate and mortality have been analysed during 5-year follow-up in all patients (n = 80) who were heart transplanted at Sahlgrenska University Hospital from 1988 through 1990. We found a significant and continuous reduction in pulmonary vascular resistance both in patients with a pre-operative high (> 3 Wood Units; n = 36), but reversible on nitroprusside, and pre-operative low (< or = 3 Wood Units; n = 44) pulmonary vascular resistance. A multivariate analysis showed that a pre-operative high mean pulmonary artery and low mean pulmonary capillary wedge pressure predicted the decline in pulmonary vascular resistance during 5 years after heart transplantation. The need for a postoperative assist device, complication rate, and early and late mortality were independent of the pre-operative level of pulmonary vascular resistance. CONCLUSIONS: A continuous reduction in pulmonary vascular resistance during 5 years following heart transplantation was found in patients with both high, but reversible, and low pre-operative resistance levels. The outcome and survival were independent of the pre-operative pulmonary vascular resistance level.

Adolescent↗
PubMed1996

The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. U.S. Carvedilol Heart Failure Study Group.

BACKGROUND: Controlled clinical trials have shown that beta-blockers can produce hemodynamic and symptomatic improvement in chronic heart failure, but the effect of these drugs on survival has not been determined. METHODS: We enrolled 1094 patients with chronic heart failure in a double-blind, placebo-controlled, stratified program, in which patients were assigned to one of the four treatment protocols on the basis of their exercise capacity. Within each of the four protocols patients with mild, moderate, or severe heart failure with left ventricular ejection fractions < or = 0.35 were randomly assigned to receive either placebo (n = 398) or the beta-blocker carvedilol (n = 696); background therapy with digoxin, diuretics, and an angiotensin-converting-enzyme inhibitor remained constant. Patient were observed for the occurrence death or hospitalization for cardiovascular reasons during the following 6 months, after the beginning (12 months for the group with mild heart failure). RESULTS: The overall mortality rate was 7.8 percent in the placebo group and 3.2 percent in the carvedilol group; the reduction in risk attributable to carvedilol was 65 percent (95 percent confidence interval, 39 to 80 percent; P < 0.001). This finding led the Data and Safety Monitoring Board to recommend termination of the study before its scheduled completion. In addition, as compared with placebo, carvedilol therapy was accompanied by a 27 percent reduction in the risk of hospitalization for cardiovascular causes (19.6 percent vs. 14.1 percent, P = 0.036), as well as a 38 percent reduction in the combined risk of hospitalization or death (24.6 percent vs, 15.8 percent, P < 0.001). Worsening heart failure as an adverse reaction during treatment was less frequent in the carvedilol than in the placebo group. CONCLUSIONS: Carvedilol reduces the risk or death as well as the risk of hospitalization for cardiovascular causes in patients with heart failure who are receiving treatment with digoxin, diuretics, and an angiotensin-converting-enzyme inhibitor.

Adrenergic alpha-Antagonists↗
PubMed2002

Vasopeptidase inhibitor reduces inhospital costs for patients with congestive heart failure: results from the IMPRESS trial. Inhibition of Metallo Protease by BMS-186716 in a Randomized Exercise and Symptoms Study in Subjects With Heart Failure.

BACKGROUND: The Inhibition of Metallo Protease by BMS-186716 in a Randomized Exercise and Symptoms Study in Subjects With Heart Failure (IMPRESS) clinical trial randomized patients with congestive heart failure to a daily regimen of either omapatrilat or lisinopril. At 24 weeks, patients randomized to omapatrilat had a significant reduction in the combined end point of death, hospitalization, or discontinuation of study drug for worsening heart failure when compared with patients randomized to lisinopril. They also had significantly fewer serious cardiac adverse events. OBJECTIVE: This study sought to determine the economic consequences of the lower event rates of patients who were given omapatrilat. METHODS: Economic outcomes (major hospitalizations and their associated medical costs) were compared between treatment groups and assessed by use of the societal perspective. Hospitalization information was obtained from the IMPRESS trial's standardized case report and serious adverse event forms. Hospital costs were evaluated by means of assigning each hospital admission a diagnosis-related group and an average cost for physician and hospital services. Emergency department visits were included only when they were made for worsening heart failure and were assigned costs equivalent to the average hospital and physician Medicare reimbursement for these visits in Duke University Medical Center's heart failure program. Drug costs were not assessed. RESULTS: Although the typical patient in both treatment groups was event-free, there was a trend toward a greater number of hospitalizations in the patients given lisinopril than in the patients given omapatrilat (P =.07). Differences in the distribution of cardiac hospitalizations between patients given lisinopril and patients given omapatrilat were significant (P =.03). There was a trend toward lower medical costs at 24 weeks in patients given omapatrilat versus patients given lisinopril ($1930 vs $2002, P =.09). Considering only cardiac medical costs, this trend toward reduced medical costs was significant ($1240 vs $1442, P =.03). CONCLUSIONS: At 24 weeks, patients with heart failure treated with omapatrilat had fewer hospitalizations and lower medical costs than patients treated with lisinopril. However, drug treatment costs were not available for this analysis.

Cardiotonic Agents↗
PubMed2006

Prognostic value of a novel classification scheme for heart failure: the Minnesota Heart Failure Criteria.

The authors present the Minnesota Heart Failure Criteria (MHFC), derived using latent class analysis from widely available items in the Framingham Criteria. The authors used 1995 and 2000 data on hospitalized Minnesota Heart Survey subjects discharged after myocardial infarction or heart failure (N = 7,379). Selected Framingham Criteria variables (dyspnea, pulmonary rales, cardiomegaly, interstitial or pulmonary edema on chest radiograph, S(3) heart sound, tachycardia) plus left ventricular ejection fraction were used. The discriminatory power of the MHFC was evaluated using age- and sex-adjusted 2-year mortality. A five-class latent class analysis model was collapsed into cases and noncases. Mortality estimates discriminated noncases (18%) from cases (43%) (p < 0.001). The MHFC performed better than previous truncated criteria (Framingham Criteria: 26% noncases, 43% cases; Duke Criteria: 29%, 40%; Killip Score: 31%, 44%; Boston Score: 28%, 45%). In a subset of patients admitted for heart failure (n = 5,128), the MHFC identified all but 2% (116/4,746) of cases found with a nearly full version of the Framingham Criteria. In terms of prognostic value, the MHFC are as precise as or more precise than several previous sets of truncated criteria. They closely approximate a nearly full version of the Framingham Criteria but require many fewer variables and can facilitate epidemiologic case-finding for heart failure.

Adult↗
PubMed1987

Morphometric quantification of myocyte dimensions validated in normal growing rat hearts and applied to hypertrophic human hearts.

To obtain quantitative information on changes in myocyte size in hearts with increased myocardial mass light microscopical morphometry was used in fixed and stained myocardial tissue sections. A modification of the azan staining procedure made longitudinal (sarcolemma) and transverse (intercalated discs) boundaries visible with a contrast that allowed morphometric analysis. The method was validated in left ventricular tissue of rats ranging in age from 4 to 17 weeks. Myocyte width, cut surface area, length, and volume were significantly correlated with left ventricular weight with residual errors of 5%, 5%, 6%, and 8% respectively. The method was applied to 21 human hearts, nine of which had left ventricular hypertrophy. Myocyte width, area, length, and volume both in subepicardial and subendocardial left ventricular tissue were significantly greater in hypertrophic than in normal hearts. Although the mean weight of the hypertrophic hearts exceeded that of normal hearts by 40%, myocyte volumes in subepicardial and subendocardial left ventricular tissue of hypertrophic hearts were higher by 78% and 43% respectively, indicating a transmural difference in the extent of myocyte hypertrophy. The method is accurate and reproducible and gives useful quantitative information on changes in myocyte dimensions during normal cardiac growth as well as in cardiac hypertrophy.

Animals↗
PubMed1994

Activation of the renin-angiotensin system in heart failure and hypertrophy--studies in human hearts and transgenic rats.

Numerous in vitro studies have demonstrated that angiotensin II has distinctive cellular effects in the cardiovascular system, independent from its effects on blood pressure. These have led to the hypothesis that activation of the angiotensin system in the heart could be of functional relevance for the adaptive processes in several cardiovascular disorders, such as cardiac hypertrophy and heart failure. This concept has been supported by clinical studies showing the beneficial effects of blockers of the system such as angiotensin converting enzyme (ACE) inhibitors in these circumstances. In order to study the regulation of gene expression of renin angiotensin system components in cardiac disorders we have performed two studies. First, we investigated the gene expression of ACE in human heart failure. Results showed that the enzyme is activated locally in this condition, supporting previous studies in animals. Second, in a different approach, we asked whether the selective activation of the renin angiotensin system in the hearts of transgenic rats expressing an additional renin gene leads to the development of pathological changes in the cardiovascular system. The results of this study demonstrated that the transgenic animals developed cardiac hypertrophy and heart failure independent of the increase in blood pressure seen in these rats. Taken together, these studies provide further evidence for the functional role of local angiotensin systems in the heart.

Animals↗
PubMed1998

Assessing public health capacity to support community-based heart health promotion: the Canadian Heart Health Initiative, Ontario Project (CHHIOP).

This paper presents initial findings of the Canadian Heart Health Initiative, Ontario Project (CHHIOP). CHHIOP has two primary objectives. The programmatic objective is to coordinate and refine a system for supporting effective, sustained community-based heart health activities. This paper addresses the scientific objective: to develop knowledge of factors that influence the development of predisposition and capacity to undertake community-based heart health activities in public health departments. A systems theory framework for an ecological approach to health promotion informs the conceptualization of the key constructs, measured using a two-stage longitudinal design which combines quantitative and qualitative methods. This paper reports the results of the first round of quantitative survey data collected from all health departments in Ontario (N = 42) and individuals within each health department involved in heart health promotion (n = 262). Results indicate low levels of implementation of heart health activities, both overall and for particular risk factors and settings. Levels of capacity are also generally low, yet predisposition to undertake heart health promotion activities is reportedly high. Analyses show that implementation is positively related to capacity but not predisposition, while predisposition and capacity are positively related. Overall, results suggest predisposition is a necessary but not sufficient condition for implementation to occur; capacity-related factors appear to be the primary constraint. These findings are used to inform strategies to address CHHIOP's programmatic objective.

Causality↗
PubMed1989

Body fat distribution and self-reported prevalence of hypertension, heart attack, and other heart disease in older women.

The associations of self-reported body mass and fat distribution with self-reported prevalence rates of hypertension, heart attack, and other heart disease were examined in a sample of 40,000 women, aged 55-69 years. Fat distribution was measured by the waist-to-hip circumference ratio (WHR), which had a mean +/- SD of 0.838 +/- 0.085. Prevalence of hypertension was significantly and positively associated with both body mass index (BMI) and waist-to-hip ratio. The prevalence rate ratio for hypertension in the highest versus the lowest tertile of body mass index and waist-to-hip ratio (considered jointly) was 2.7. Prevalence rates of heart attack and other heart disease were significantly and positively associated with waist-to-hip ratio but not with body mass index. The prevalence rate ratios were 2.2 for heart attack and 1.4 for other heart disease in the highest versus the lowest tertile of body mass index and waist-to-hip ratio. Findings were substantiated using multiple logistic regression. These results support the hypothesis that a significant relationship exists between body fat distribution and the occurrence of cardiovascular disease in older women.

Adipose Tissue↗
PubMed1999

Resting heart rate is a risk factor for cardiovascular and noncardiovascular mortality: the Chicago Heart Association Detection Project in Industry.

In a prospective cohort study, associations of resting heart rate with risk of coronary, cardiovascular disease, cancer, and all-cause mortality in age-specific cohorts of black and white men and women were examined over 22 years of follow-up. Participants were employees from 84 companies and organizations in the Chicago, Illinois, area who volunteered for a screening examination. Participants included 9,706 men aged 18-39 years, 7,760 men aged 40-59 years, 1,321 men aged 60-74 years, 6,928 women aged 18-39 years, 6,915 women aged 40-59 years, and 1,151 women aged 60-74 years at the baseline examination in 1967-1973. Vital status was ascertained through 1992. For fatal coronary disease, multivariate-adjusted relative risks associated with a 12 beats per minute higher heart rate (one standard deviation) were as follows: for men aged 18-39 years, relative risk (RR) = 1.27 (95% confidence interval (CI) 1.08-1.48); for men aged 40-59 years, RR = 1.13 (95% CI 1.05-1.21); for men aged 60-74 years, RR = 1.00 (95% CI 0.89-1.12); for women aged 40-59 years, RR = 1.21 (95% CI 1.07-1.36); and for women aged 60-74 years, RR = 1.16 (95% CI 0.99-1.37). Corresponding risks for all fatal cardiovascular diseases were similar to those for coronary death alone. Deaths from cancer were significantly associated with heart rate in men and women aged 40-59 years. All-cause mortality was associated with higher heart rate in men aged 18-39 years (RR = 1.11, 95% CI 1.01-1.20), men aged 40-59 years (RR = 1.16, 95% CI 1.11-1.21), and women aged 40-59 years (RR = 1.20, 95% CI 1.13-1.27). Heart rate was not associated with mortality in women aged 18-39 years. In summary, heart rate was a risk factor for mortality from coronary disease, all cardiovascular diseases, and all causes in younger men and in middle-aged men and women, and for cancer mortality in middle-aged men and women.

Adult↗
PubMed1982

Resting heart rate and pressure-rate product of children in a total biracial community: the Bogalusa Heart Study.

Resting heart rates were ascertained during the 1978-1979 school year in 3590 children aged 5-17 years in the biracial geographic population of Bogalusa, Louisiana. These rates were found to be relatively independent of the method of measurement, whether supine by physician's stethoscope or dressed sitting radial pulse taken by a nurse, and in either case adhering to a strict measurement protocol. Apart from the known influences of age and sex, the authors found a small but consistent racial influence, with whites having 3-4 beats/min higher rates than blacks. Controlling for age, the authors found heart rate to be positively correlated with blood pressure in whites and with subcapsular skinfold thickness in boys. No consistent relation between heart rate and amount of cigarettes smoked was observed. Boys in the upper five percentiles of blood pressure-heart rate ("double") product values were found to have about twice the subscapular skinfold thickness compared to the lower five percentiles. Likewise, boys in the upper five percentiles of subscapular skinfold thickness had significantly increased double products. Since the double product is an index of cardiac oxygen consumption, this finding could point to a possible etiologic link between obesity and chronic cardiac stress in males beyond the mediation of lipoproteins, cholesterol, and diabetes mellitus in contributing to atherosclerotic heart disease, but this issue needs further study. Ascertainment of resting heart rate provides an additional parameter in the study of cardiovascular risk factor variables, in youth as in adulthood, to supplement the natural history of the atherosclerosis-hypertension syndrome with its sequelae.

Adolescent↗
PubMed1990

Different results in cardiopulmonary exercise tests after long-term treatment with felodipine and enalapril in patients with congestive heart failure due to ischaemic heart disease.

We evaluated the cardiopulmonary exercise test results before and after long-term (16 weeks) treatment with the dihydropyridine calcium antagonist, felodipine (10 mg b.i.d., n = 9), and the ACE inhibitor, enalapril (10 mg b.i.d., n = 11), in 20 patients with New York Heart Association class III congestive heart failure. There were no significant differences at baseline. After 16 weeks patients in the enalapril group showed a significant increase in exercise duration and VO2max, without changes in arterial pressures and heart rate. In the felodipine group, exercise duration and VO2max did not change significantly, but arterial pressures and heart rate were significantly reduced at all exercise levels. Between group analysis showed a significant reduction in arterial pressures and heart rate in the felodipine group compared with enalapril, but no differences in aerobic capacity and exercise duration. These results demonstrate that felodipine and enalapril have essentially different effects on cardiopulmonary exercise results in patients with congestive heart failure.

Aged↗
PubMed1996

Interaction of heart rate and hypothermia on global myocardial contraction of the isolated rabbit heart.

We studied the effects of mild hypothermia on cardiac contractility in isolated rabbit hearts perfused with Krebs-Henseleit solution according to the technique of Langendorff. Isovolumetric left ventricular pressure (LVP) was measured with a fluid-filled balloon. Hearts were paced after induction of atrioventricular block. At low heart rates ( < 30 bpm) mild hypothermia (cooling to 30 degrees C) induced a 32% increase in LVp (146.5 +/- 10 mm Hg at 30 degrees C vs 110.7 +/- 13 mm Hg at 37 degrees C) but this positive inotropic response was progressively lost by increasing heart rate. At pacing rates > or = 90 bpm, lower systolic LVP, higher diastolic LVP, and lower positive and negative LV dP/dt were obtained in hypothermic (93 +/- 12 mm Hg, 55 +/- 18 mm Hg, 584 +/- 137 mm Hg/s, and 323 +/- 57 mm Hg/s at 210 bpm, respectively) compared to normothermic hearts (123 +/- 4 mm Hg, 10 +/- 4 mm Hg, 1705 +/- 145.5 mm Hg/s, and 1155 +/- 78 mm Hg/s at 210 bpm, respectively.) The duration of mechanical diastole was reduced or suppressed in these hearts. Exposure to the beta-adrenoreceptor agonist, isoproterenol, improved this diastolic dysfunction during hypothermia and pacing at high rates, suggesting that the sarcoplasmic reticulum Ca2+ uptake might be involved. Our data are also consistent with an increase in myofilament Ca2+ sensitivity that is opposed by isoproterenol during hypothermia.

Actin Cytoskeleton↗
PubMed2001

Relationships of heart rate and heart rate variability with conventional and ambulatory blood pressure in the population.

BACKGROUND: Most studies on relationships between blood pressure and autonomic nervous function, assessed by power spectral analysis of heart rate variability, have used conventional or clinic blood pressure measurements in selected subjects, which may have influenced the results. OBJECTIVE: We aimed to investigate, in a population-based approach, associations of heart rate and heart rate variability, assessed in basal resting conditions and in response to standing, with conventional blood pressure measured by an investigator, and with ambulatory blood pressure monitored outside the laboratory. METHODS: RR interval and respiration were registered in 614 men and women, ages 25-89 years. After exclusion of subjects with myocardial infarction or diabetes and elimination of unsatisfactory recordings, 549 subjects remained for analyses at supine rest and 515 of these to assess the orthostatic responses. Hypertension was present in 39% of the subjects. The low-frequency (LF) and high-frequency (HF) components of heart rate variability were quantified by use of autoregressive modelling and expressed in absolute and normalized units. RESULTS: At supine rest, indices of heart rate variability were not independently related to 24 h systolic blood pressure, whereas some indices showed weak associations with diastolic 24 h pressure; the relationships were in general stronger for conventional blood pressure. For example, partial correlation coefficients of the relationships of the LF: HF ratio with systolic pressure were 0.12 (P < or = 0.01) for conventional pressure and 0.02 (NS) for 24 h pressure; these coefficients amounted to 0.20 (P < or = 0.001) and 0.11 (P < or = 0.01) for the diastolic pressures. The decrease of HF power and the increase of the LF:HF ratio on standing were significantly blunted at higher blood pressure, both when measured conventionally and by ambulatory monitoring (P < or = 0.001 for the LF: HF ratio). CONCLUSIONS: Relationships between autonomic nervous function at rest, assessed by use of power spectral analysis of heart rate variability, and conventional blood pressure, can at least partly be ascribed to the influence of the measurement conditions, whereas the orthostatic autonomic responses appear to be influenced by blood pressure per se.

Adult↗
PubMed2002

Prevention of diastolic heart failure by endothelin type A receptor antagonist through inhibition of ventricular structural remodeling in hypertensive heart.

OBJECTIVES: Despite the clinical frequency of diastolic heart failure, its therapeutic strategy has not been established. Our recent study demonstrated activation of the endothelin (ET) system in a diastolic heart failure model with hypertension. Several studies have reported that ET type A (ETA) receptor antagonist improves systolic function and prevents systolic heart failure; however, its effects on diastolic heart failure are unknown. We investigated the effects of chronic administration of ET(A) receptor antagonist in diastolic heart failure. DESIGN AND METHODS: Dahl-Iwai salt-sensitive rats fed on a high-salt diet from 7 weeks of age, in which congestive heart failure develops following hypertension without cardiac chamber dilatation or systolic dysfunction, were divided into groups with and without administration of a subdepressor dose of ET(A) receptor antagonist. RESULTS: Hypertension induced compensatory left ventricular (LV) hypertrophy at 13 weeks in six untreated rats. Persistent pressure overload developed progressive LV hypertrophy and fibrosis from 13 to 19 weeks, resulting in elevated LV filling pressure and increased lung weight. Chronic ET(A) receptor blockade did not restrain compensatory LV hypertrophy at 13 weeks; however, it attenuated LV hypertrophy and fibrosis thereafter (n = 6). These beneficial effects resulted in the maintenance of normal LV filling pressure without changes in LV end-diastolic diameter, indicating prevention of LV stiffening. CONCLUSIONS: Chronic ET(A) receptor blockade is likely to exert beneficial effects in diastolic failure through attenuation of the progression of LV hypertrophy and fibrosis.

Animals↗