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PubMed2004

Increased heart rate and reduced heart-rate variability are associated with subclinical inflammation in middle-aged and elderly subjects with no apparent heart disease.

AIM: Elevation of inflammation markers, high heart rate, and reduced heart-rate variability are all strong markers of mortality in a broad spectrum of patients. The association between these markers has not been clarified thoroughly. We investigated the associations between markers of inflammation, heart rate, and heart-rate variability. METHODS AND RESULTS: Six hundred and forty-three healthy men and women between 55 and 75 years of age and with no prior history of cardiovascular disease or stroke were included in the study. The baseline study included a physical examination, fasting laboratory tests, and 24-h ambulatory ECG monitoring. We selected the time-domain components of heart-rate variability for further analyses. C-reactive protein concentration and white blood cell count were selected as markers of inflammation. After identifying parameters related to measures of heart-rate variability, we used regression analyses to evaluate independent associations. Heart-rate variability, as measured by the standard deviation of the time between normal-to-normal complexes or the standard deviation of the average of normal-to-normal intervals for each 5-min period, was negatively associated with smoking, C-reactive protein, white blood cell count, blood sugar and triglyceride concentration, female gender, and diabetes. In contrast, physical activity was strongly associated with higher heart-rate variability. In multivariate regression analyses, increased heart-rate and reduced heart-rate variability were significantly and independently related to white blood cell count or C-reactive protein concentration. CONCLUSION: Increased heart rate and reduced heart-rate variability are associated with subclinical inflammation in healthy middle-aged and elderly subjects. The increased mortality that has been reported in these settings may thus have a common aetiology. An autonomic imbalance in favour of the sympathetic system may interact with inflammatory processes to play a more important role in the process of atherosclerosis than previously thought.

Aged↗
PubMed1987

Quantitative analysis of narrowings of intramyocardial small arteries in normal hearts, hypertensive hearts, and hearts with hypertrophic cardiomyopathy.

To clarify the pathophysiologic role of intramyocardial small artery (IMSA) diseases in hypertrophied hearts, narrowings of the IMSA were quantitatively evaluated in 39 autopsied hearts, 10 from patients with typical hypertrophic cardiomyopathy (HCM), four from patients with HCM showing features mimicking dilated cardiomyopathy (DCM-like HCM), 10 from patients with hypertension, and 15 from normal adults. The relations of narrowings of the IMSA to myocytic hypertrophy, myocardial fiber disarray, and fibrosis were also examined. The external caliber and the ratio of the luminal area to the total vascular area (percent luminal area, % lumen) were calculated by an image analyzer in 85 to 203 IMSAs from each patient. The external calibers of the IMSAs were similar among groups of hearts with HCM, hypertensive hearts, and normal hearts but were greater in those with DCM-like HCM. The mean % lumen of the IMSAs was similarly reduced in the hearts with HCM (29 +/- 5% in the ventricular septum and 31 +/- 5% in the left ventricular free wall) and in hypertensive hearts (30 +/- 8% and 31 +/- 7%) compared with that in normal hearts (40 +/- 5% and 38 +/- 5%) and was the lowest in the ventricular septum of hearts with DCM-like HCM (17 +/- 3%). The mean % lumen of the IMSA was inversely correlated with heart weight (r = -.59), the mean size of myocytes (r = -.66 in the ventricular septum, r = -.63 in the free wall), and percent fibrotic area in the septum (r = -.68). The mean % lumen values of the IMSAs in the tissues with and without disarray in the hearts with HCM were similar. Thus IMSA disease is of pathophysiologic importance in patients with HCM, DCM-like HCM in particular, or with hypertension.

Adult↗
PubMedDate not supplied

Special considerations for heart transplantation in congenital heart disease. The Paediatric Heart Transplant Group.

Congenital heart disease as an indication for heart transplantation accounts for a small number of the total heart transplant experience--less than 3% in most centers. We have performed heart transplantation in eight such patients, accounting for 4% of our total experience. All these patients had specific anatomic anomalies relevant to transplantation. None had morbidity directly related to their anatomic defect and subsequent transplant. Six of the eight had undergone no prior palliative or corrective repairs. One child had a left Blalock-Taussig shunt, and one had bilateral Glenn shunts and a Fontan repair. Technical considerations for orthotopic heart transplantation are described for transposition of the great arteries, left superior vena cava with and without bridging innominate vein, common atrium, presence of Blalock-Taussig shunt, bilateral Glenn shunts, and Fontan repair. Anatomic congenital heart disease is becoming a more frequent indication in heart transplantation. Heart transplantation in the presence of structural congenital heart disease may be technically challenging. Nevertheless, transplantation offers an effective therapeutic alternative for patients with end-stage congestive heart failure and congenital heart disease.

Adult↗
PubMed2000

Awareness, perception, and knowledge of heart disease risk and prevention among women in the United States. American Heart Association Women's Heart Disease and Stroke Campaign Task Force.

CONTEXT: One of 2 women in the United States dies of heart disease or stroke, yet women are underdiagnosed and undertreated for these diseases and their risk factors. Informed decisions to prevent heart disease and stroke depend on awareness of risk factors and knowledge of behaviors to prevent or detect these diseases. OBJECTIVE: Assess (1) knowledge of risks of heart disease and stroke and (2) perceptions of heart disease and its prevention among women in the United States. DESIGN AND SETTING: Telephone survey conducted in 1997 of US households, including an oversample of African American and Hispanic women. PARTICIPANTS: One thousand respondents 25 years or older; 65.8% white, 13.0% African American, and 12.6% Hispanic. MAIN OUTCOME MEASURES: Knowledge of heart disease and stroke risks, perceptions of heart disease, and knowledge of symptoms and preventive measures. RESULTS: Only 8% of the respondents identified heart disease and stroke as their greatest health concerns; less than 33% identified heart disease as the leading cause of death. More women aged 25 to 44 years identified breast cancer as the leading cause of death than women 65 years or older. Women aged 25 to 44 years indicated they were not well informed about heart disease and stroke. Although 90% of the women reported that they would like to discuss heart disease or risk reduction with their physicians, more than 70% reported that they had not. CONCLUSIONS: Most women do not perceive that heart disease is a substantial health concern and report that they are not well informed about their risk. Age influenced knowledge to a greater extent than ethnicity. Programs directed at young women that address the effects of lifestyle behaviors on long-term health are needed. Better communication between physicians and patients is also warranted.

Adult↗
PubMed1998

Is heart rate variability a reliable method to assess autonomic modulation in left ventricular dysfunction and heart failure? Assessment of autonomic modulation with heart rate variability.

Autonomic dysfunction seems to be involved in the progression and prognosis of congestive heart failure. Measurement of heart rate variability (HRV) provides a noninvasive method to obtain reliable and reproducible information on autonomic modulation of heart rate, but there is a difficulty in using HRV as a quantitative estimate of autonomic dysfunction in heart failure. This study was aimed at testing the hypothesis that abnormal modulation of heart rate assessed by power spectrum analysis may be present also in asymptomatic patients with left ventricular dysfunction and progress in patients with overt symptoms of congestive heart failure. HRV was measured in three groups of subjects: Group 1: 30 patients with chronic heart failure; Group 2: 21 patients with asymptomatic left ventricular dysfunction; and Group 3: 25 healthy volunteers as control group. HRV was evaluated by autoregressive spectral analysis with 600-beat ECG samples, while subjects were quietly recumbent (BSI), in conditions of controlled breathing (15 acts/min) (RSC) and passive orthostatism after tilting (80 degrees) (TLT). Patients in group 1 showed a reduction in the standard deviation of the R-R intervals (SDRR) (p<0.0003) and in the low frequency component (LF) (p<0.0001) compared to normal subjects. Low frequency component was not detectable in 11 patients of group I (p<0.0008). On RSC and TLT, group 1 failed to show any modification in the low frequency and high frequency components (HF) under any stimulation. Group 2 showed no modification at baseline evaluation, no increase in the high frequency component on RSC and in LF during TLT compared to controls (p<0.01 and p<0.0001 respectively). At baseline, group 1 had a lower SDRR (p<0.03) and LF (p<0.0001) vs. group 2, whereas during stimulation the two groups exhibited the same behaviour. In conclusion, reduced heart rate variability is specific for both asymptomatic and symptomatic post-ischemic left ventricular dysfunction. Our results suggest that frequency domain analysis of heart rate variability during a stimulation test allows a more accurate definition of the degree of autonomic control of heart rate.

Autonomic Nervous System↗
PubMed1987

Pathogenetic role of myocardial fiber disarray in the progression of cardiac fibrosis in normal hearts, hypertensive hearts and hearts with hypertrophic cardiomyopathy.

To define the pathogenetic role of myocardial fiber disarray in the progression of cardiac fibrosis, the percent area of fibrosis in tissue with disarray was compared with that in tissue without disarray. Thirty autopsied hearts, 10 from patients with hypertrophic cardiomyopathy, 10 from patients with hypertension and 10 from normal adults, were studied. The percent areas of fibrosis in tissues with and without disarray were significantly different (p less than 0.01) among hearts with hypertrophic cardiomyopathy (12.6 +/- 4.0 and 8.2 +/- 3.3%), hypertensive hearts (6.6 +/- 3.6 and 2.5 +/- 1.4%) and normal hearts (2.8 +/- 1.2 and 1.0 +/- 0.4%). The percent area of fibrosis in tissue with disarray was greater than in that without disarray in all 3 groups and the ratios of these percentages were similar in the 3 groups: 2.9 +/- 4.2 in hypertrophic cardiomyopathy 2.5 +/- 1.7 in hypertensive hearts and 2.5 +/- 1.8 in normal hearts. The conclusions are: 1) disarray promotes fibrosis to a similar degree, not only in hypertrophic cardiomyopathy, but also in hypertensive hearts and normal hearts; 2) the increased level of fibrosis in hearts with hypertrophic cardiomyopathy and in hypertensive hearts, together with widespread fibrosis in hearts with hypertrophic cardiomyopathy in particular cannot be explained by disarray alone.

Cardiomegaly↗
PubMed2005

High prevalence of cardiotropic viruses in myocardial tissue from explanted hearts of heart transplant recipients and heart donors: a 3-year retrospective study from a German patients' pool.

BACKGROUND: The prevalence of some cardiotropic viruses in virus-associated inflammatory cardiac disease remains controversial. The aim of this study was to examine myocardial tissue samples from explanted hearts of heart transplant recipients and heart donors for nucleic acids of myocardiotropic viruses and to observe the potential risk of viral-induced post-transplantation complications in recipients of cardiac allografts or heart valve homografts. METHODS: Myocardial tissue samples were analyzed by polymerase chain reaction (PCR) for enteroviruses, adenoviruses, human cytomegalovirus (HCMV), parvovirus B19 (PVB19), and influenza viruses. The results were compared with serologic and histopathologic findings. RESULTS: PCR analysis of 449 myocardial tissue samples from explanted hearts indicated infection in 34 (47%) of 73 heart transplant recipients and 48 (60%) of 80 donors. The prevalence of virus infection in donors aged over 65 years was significantly higher than in heart transplant recipients (p = 0.005) or donors aged under 65 years (p = 0.02). The most frequently detected viruses were enteroviruses (group B coxsackievirus) and adenoviruses. HCMV and PVB19 were found less frequently. All samples were negative for influenza viruses. Although the serologic findings and PCR results for different viruses were discordant in 4% to 27% of cases, PCR and histopathologic findings were highly correlated (88%). CONCLUSIONS: The frequent detection of viral genome sequences in myocardial tissue of both heart transplant recipients and heart donors suggests a significant risk for graft-transmitted viral infection in cardiac and heart valve transplant recipients.

Adenoviridae↗
PubMed1999

The relationship between QT intervals and mortality in ambulant patients with chronic heart failure. The united kingdom heart failure evaluation and assessment of risk trial (UK-HEART)

AIMS: Mortality in patients with heart failure remains high and is difficult to predict. QT interval parameters on a 12-lead ECG have been shown to predict arrhythmic events in patients with a variety of myocardial diseases. There is some, but not consistent, evidence that QT interval parameters may act as predictors of mortality, in particular sudden death, in patients with heart failure. In an adequately powered prospective study we have studied QT interval parameters in patients with stable chronic heart failure in order to determine whether they are predictive of all-cause mortality or mode of death. METHODS AND RESULTS: Five hundred and fifty-four ambulant outpatients with chronic heart failure were recruited. A 12-lead ECG, chest radiograph, echocardiogram, 24 h ambulatory electrocardiogram and serum for biochemical analysis were obtained at baseline. Patients were followed for 471+/-168 days. QT intervals were measured in all leads blinded to patient's characteristics and outcome, were corrected for heart rate, and the maximum QT intervals, and QT dispersion (range of QT intervals) were determined. The same parameters were determined for JT intervals. The primary end-point was all-cause mortality, secondary end-points were sudden cardiac death and death due to progressive heart failure. Multivariate analysis with the Cox's proportional hazards model was used to determine which variables were independently related to outcome. Four hundred and ninety-five patients had analysable ECGs at study entry and of these 71 died during follow-up. The heart rate corrected QT dispersion and maximum QT interval were significant univariate predictors of all-cause mortality (P=0.026 and <0.0001 respectively), and also of sudden death and progressive heart failure death, but were not related to outcome in the multivariate analysis. The independent predictors of all-cause mortality were cardiothoracic ratio (P=0.0003), creatinine (P=0.0009), heart rate (P=0.007), echocardiographically derived left ventricular end-diastolic dimension (P=0.007) and ventricular couplets on 24 h electrocardiographic monitoring (P=0.015). CONCLUSION: In an adequately powered prospective study none of the QT or JT parameters were shown to be independent predictors of outcome in patients with mild to moderate congestive heart failure. These variables do not therefore add to the prognostic information which can be gained from simple radiographic, biochemical, echocardiographic and Holter data in this group of patients.

Death, Sudden, Cardiac↗
PubMedDate not supplied

Does heart rate identify sudden death survivors? Assessment of heart rate, QT interval, and heart rate variability.

The objective was to test whether the circadian variability of several electrocardiographic variables distinguishes sudden cardiac death survivors from heart disease patients without a history of cardiac arrest and from normal subjects. Heart rate, heart rate variability, and QT interval have been reported to identify survivors of sudden cardiac death. Computer-assisted continuous QT measurement and heart rate variability analysis were performed on 24-hour Holter records for three groups: (1) 14 sudden death survivors; (2) 14 control patients with diagnosis and therapy matched to survivors; and (3) 14 healthy subjects. There were no significant differences in 24-hour mean RR and QT intervals between groups. However, heart rate was significantly different between the three groups at night but not during the day because the expected nighttime decline was markedly blunted in survivors and somewhat blunted in control patients. The QT interval and frequency domain heart rate variability measures followed a similar circadian pattern. The mean QTc was significantly longer in control patients. The QTc had a wide range in all groups, but less in sudden death survivors. Of ten common time and frequency domain heart rate variability indices, only SDANN and SDNN were significantly lower in sudden death survivors. Reduced circadian variation of heart rate, with marked blunting of the nighttime heart rate decline, identifies sudden cardiac death survivors as well as does SDANN and SDNN, and, in contrast to heart rate variability measures, can easily be obtained from a Holter report without complex calculations.

Case-Control Studies↗
PubMed2005

Association of metabolic syndrome with exercise capacity and heart rate recovery in patients with coronary heart disease in the heart and soul study.

It is not known whether the metabolic syndrome is associated with poor exercise capacity among patients who have established coronary heart disease. We evaluated the association of the metabolic syndrome with treadmill exercise capacity and heart rate recovery among patients who had coronary heart disease. We measured treadmill exercise capacity (METs) and heart rate recovery (beats per minute) in 943 subjects who had known coronary heart disease. Of these, 377 (40%) had the metabolic syndrome as defined by criteria of the National Cholesterol Education Program. Participants who had the metabolic syndrome were more likely to have poor exercise capacity (METs <5, 33% vs 18%, p <0.0001) and poor heart rate recovery (<or=16 beats/min, 34% vs 21%, p <0.0001) than those who did not have the metabolic syndrome. In ordinal logistic regression analyses, the metabolic syndrome was associated with decreased exercise capacity (odds ratio [OR] 2.2, 95% confidence interval [CI] 1.7 to 2.8, p <0.0001) and decreased heart rate recovery (OR 1.8, 95% CI 1.4 to 2.3, p <0.0001). These associations remained strong after adjusting for potential confounding variables (OR 1.6, 95% CI 1.2 to 2.1, p = 0.003 for decreased exercise capacity; OR 1.4, 95% CI 1.1 to 1.9, p = 0.02 for decreased heart rate recovery). The metabolic syndrome is independently associated with poor exercise capacity and poor heart rate recovery in patients who have established coronary heart disease. Decreased exercise capacity may contribute to the adverse outcomes associated with the metabolic syndrome.

Aged↗
PubMed2006

Heart retransplantation for heart allograft failure in Chinese heart transplant recipients: NTUH experience.

We investigated the short- and long-term results after heart retransplantation in terms of different causes of heart allograft failure. We sought to establish the data of heart retransplantation in Chinese compared with Western counterparts due to differences in heart allograft vasculopathy. From March 1995 to May 2005, eight heart transplantation recipients with allograft failure underwent retransplantation. Heart allograft failure was due to coronary vasculopathy (CAV) in six patients (75%) and acute rejection in two patients (25%). The mean interval to retransplantation was 32 to 84 months (mean 54.3 months). There were five patients who survived after heart retransplantation for CAV and no patient survived after an earlier diagnosis of acute rejection. Heart retransplantation is a feasible method with acceptable long-term survival rate for heart allograft failure. After careful pretransplant evaluation, retransplantation is acceptable. The survival after retransplantation for CAV is notably great than that after acute rejection. Heart retransplantation is the only way for patients who have cardiac allograft failure to achieve long-term survival.

Adult↗
PubMed1996

Endothelium-dependent vasodilatation is not selectively impaired in patients with chronic heart failure secondary to valvular heart disease and congenital heart disease.

This study examined possible selective impairment of endothelial dysfunction in the peripheral vascular bed in patients with chronic heart failure in the absence of confounding factors influencing endothelial function (i.e. hypertension, hypercholesterolaemia and diabetes mellitus). Several recent studies have suggested that endothelium-dependent peripheral vasodilation is impaired but endothelium-independent vasodilation is preserved in patients with chronic heart failure. However, a classical paper has demonstrated that sodium nitrite-mediated calf blood flow is clearly depressed in patients with valvular heart disease and cardiomyopathy. We examined forearm blood flow changes mediated by acetylcholine and nitroprusside in patients with valvular heart disease (n = 55) or congenital heart disease (n = 13), and a comparison was made with healthy volunteers (n = 21). The blood flow changes mediated by acetylcholine and nitroprusside were significantly impaired in both patient groups (P < 0.01). When blood flow responses were collected from all patients, two types of vasodilatory capacity were found to have decreased significantly with increasing clinical severity of heart failure (New York Heart Association functional class; P < 0.01). This suggests that the peripheral vasodilatory responses mediated by endothelium-dependent and endothelium-independent vasodilators are significantly impaired in patients with symptomatic chronic heart failure due to non-ischaemic heart disease.

Acetylcholine↗
PubMed2001

Propranolol treatment of congestive heart failure in infants with congenital heart disease: The CHF-PRO-INFANT Trial. Congestive heart failure in infants treated with propanol.

AIM: Infants with congenital heart disease and left-to-right shunts may develop significant clinical symptoms of congestive heart failure in spite of therapy with digoxin and diuretics. We investigated the effects of beta-blockade in infants with severe heart failure. METHODS AND RESULTS: We performed a prospective, randomized, open monocenter trial in infants treated with digoxin and diuretics (n=10) in comparison to 10 infants receiving additional beta-blocker therapy. After 17 days on average beta-blocker treated infants (propranolol:1,6 mg/kg/day) improved significantly with respect to Ross heart failure score (3.3+/-2.3 vs. 8.3+/-1.9, P=0.002), lower renin levels (338+/-236 vs. 704+/-490 microU/l, P=0.008) and lower mean heart rates in Holter ECG (118+/-10 vs. 142+/-11 beats/min, P<0.001). While digoxin and diuretic treated infants had unchanged mean heart rate (149+/-8 vs. 148+/-10 beats/min), less decrease of symptoms (Ross Score: 8.5+/-1.7 vs. 6.8+/-2.3, P=0.02) but a significant increase of renin levels (139+/-102 vs. 938+/-607 microU/l, P=0.001). CONCLUSION: Additional propranolol treatment but not digoxin and diuretics alone can effectively reduce clinical symptoms of heart failure in infants with congenital heart disease, who suffer from increased neurohormonal activation.

Adrenergic beta-Antagonists↗
PubMed1989

[Myocardial catecholamine content in heart failure--I: Regional distribution in explanted hearts. Comparison between dilated cardiomyopathy and coronary heart disease].

To quantify the myocardial catecholamine content in heart failure patients and to assess the regional distribution of catecholamines, we investigated norepinephrine and dopamine concentrations in explanted hearts from 34 patients in end-stage heart failure. 28 patients with cardiomyopathy were compared with six patients with coronary artery disease. In comparison with the right atria of a control group without heart failure, reduced myocardial norepinephrine contents (in pg/micrograms non-collagen protein (NCP] were found in all areas of the explanted hearts: controls: right atrium 17.6 +/- 6.6; cardiomyopathy: right atrium 7.1 +/- 7.9, right ventricle 4.4 +/- 2.7, septum 3.8 +/- 1.5, left ventricle 3.5 +/- 1.4. Coronary artery disease: right atrium 7.0 +/- 6.9, right ventricle 4.2 +/- 2.6, septum 3.6 +/- 1.4, left ventricle 3.4 +/- 1.4. Highest norepinephrine levels were measured in the right atrium. Right ventricle, septum, base and midventricular portion of the left ventricle had lower concentrations and were not different from each other. In contrast to reduced norepinephrine (NE) levels in all patients, dopamine (Dop) was inhomogenously elevated (only in a subgroup of 44%). Catecholamine contents in any two arbitrarily selected areas correlated significantly (NA: r = 0.53-0.77; Dop: r = 0.81-0.93, p less than 0.05 in all cases). The patients with heart failure due to dilated cardiomyopathy and to coronary artery disease did not differ in myocardial catecholamine levels or distribution. In end-stage heart failure a significant loss of myocardial norepinephrine independent from the underlying disease is found. It affects all areas of the hearts but does not equalize catecholamine content in ventricles and atria.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

The prognostic use of right heart catheterization data in patients with advanced heart failure: how relevant are invasive procedures in the risk stratification of advanced heart failure in the era of neurohormones?

BACKGROUND: Right heart catheterization long has been a routine investigation in advanced heart failure, and its measurements have been linked variably to prognosis. However, in the modern era, newer potential markers of prognosis are coming to light. This study reconsiders the use of right heart catheterization data and compares their use to that of N-terminal pro-brain natriuretic peptide (NT-proBNP), a neurohormone linked with prognosis in chronic heart failure. METHODS: We assessed prospectively the prognostic potential of baseline right heart catheterization data in 97 consecutive patients with advanced heart failure referred to the Scottish Cardiopulmonary Transplant Unit for consideration of cardiac transplantation. Patients underwent baseline routine investigation, including right heart catheterization and blood draws for NT-proBNP analysis. Patients were observed for a median of 370 days. RESULTS: The primary end-point of all-cause mortality was reached in 17 patients (17.5%), and the secondary end-point of all-cause mortality or urgent cardiac transplantation was reached in 21 (21.6%) patients. Univariate predictors of all-cause mortality included pulmonary artery systolic pressure (PASP), pulmonary artery wedge pressure (PAWP), and NT-proBNP concentration greater than their median values. Univariate predictors of the secondary end-point included right atrial pressure, PASP, PAWP, and NT-proBNP concentration greater than their median values, and left ventricular ejection fraction, cardiac output, and cardiac index less than their median values. In multivariate analyses, however, only NT-proBNP concentration remained an independent predictor of all-cause mortality. Both NT-proBNP concentration and PAWP were independent predictors of all-cause mortality and of the need for urgent cardiac transplantation. CONCLUSION: Baseline data from routine right heart catheterization are of limited prognostic use in advanced heart failure. A baseline NT-proBNP concentration is a superior, non-invasive method of risk stratification in this era of measuring neurohormones.

Cardiac Catheterization↗
PubMed2003

Relation between heart rate, heart rhythm, and reverse left ventricular remodelling in response to carvedilol in patients with chronic heart failure: a single centre, observational study.

OBJECTIVE: To determine whether the process of reverse left ventricular remodelling in response to carvedilol is dependent on baseline heart rate (BHR), heart rhythm, or heart rate reduction (HRR) in response to carvedilol. DESIGN: Retrospective analysis of serial echocardiograms in 257 patients with chronic systolic heart failure at baseline and at 12-18 months after starting carvedilol. Reverse left ventricular remodelling was determined by changes in left ventricular end diastolic dimension (LVEDD), end systolic dimension (LVESD), and fractional shortening (LVFS). SETTING: Heart failure clinic within a university teaching hospital. MAIN OUTCOME MEASURES: Changes in LVEDD, LVESD, and LVFS. RESULTS: LVEDD and LVESD decreased by 2.6 (0.4) mm and 4.9 (0.5) mm, respectively (mean (SEM)), and LVFS increased by 4.3 (0.5)% (all p < 0.0001 v baseline). Simple regression revealed no significant relation between BHR or HRR and the changes in LVEDD, LVESD, or LVFS. Stratification of patients into high and low BHR groups (above and below the mean) or according to the baseline heart rhythm (sinus rhythm v atrial fibrillation) showed no differences between groups in the extent of reverse left ventricular remodelling. Improvements in left ventricular function and dimensions were associated with significant improvements in New York Heart Association functional class. CONCLUSIONS: The benefits of carvedilol in terms of reverse left ventricular remodelling and symptomatic improvement in patients with chronic heart failure are independent of BHR, heart rhythm, and the HRR that occurs in response to carvedilol.

Adrenergic beta-Antagonists↗