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PubMed2002

Prognostic value of heart rate variability in chronic congestive heart failure (Veterans Affairs' Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure).

Although the value of heart rate variability (HRV) for risk stratification after acute myocardial infarction has been demonstrated, the value of low HRV as a predictor of sudden cardiac death in patients with ischemic cardiomyopathy has not been shown convincingly to date. We retrospectively analyzed electrocardiographic data from 179 patients in the Veterans Affairs' Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure to determine if HRV (expressed as the SD of the normal-to-normal RR intervals [SDNN]) would be useful as a predictor of overall mortality and sudden death. Because our goal was to identify high-risk patients, we compared patients in the lowest quartile of HRV with the remaining patients. Among the 127 patients meeting inclusion criteria, SDNN <65.3 ms (the lowest quartile) was the sole independent factor predictive of survival in a multivariate model (p = 0.0001). A Cox proportional-hazards model revealed that each increase of 10 ms in SDNN conferred a 20% decrease in risk of mortality (p = 0.0001). Furthermore, patients with SDNN <65.3 ms had a significantly increased risk of sudden death (p = 0.016). Thus, HRV was the sole independent predictor of overall mortality and was significantly associated with sudden death in this population.

Aged↗
PubMed1996

Pathophysiological targets for beta-blocker therapy in congestive heart failure.

The treatment of congestive heart failure has seen considerable changes: while treatment with diuretics, digitalis glycosides and vasodilators has remained the mainstay of therapy, recently neurohumeral inhibition has been developed as an important principle: ACE-inhibitors have been shown to significantly improve quality of life and exercise performance and to substantially reduce mortality. Beta-blockers have been employed with increasing success mainly in congestive heart failure due to dilated idiopathic cardiomyopathy, in which a significant improvement in symptoms and life expectancy has been demonstrated. However, the precise mechanisms by which beta-blockade improves congestive heart failure remain to be elucidated. In addition to direct sympathoadrenal inhibition, reduction of heart rate may also play a major role in the therapeutic efficacy of beta-blockade in congestive heart failure. In the normal human heart increase in heart rate is accompanied by an increase in myocardial contractile performance (Bowditch-Treppe phenomenon). In chronic heart failure the myocardium undergoes a phenotype change which includes alterations of the activity of enzymes regulating calcium homoeostasis. The sarcoplasmic reticulum calcium ATPase (SERCA) is depressed both in function, as well as in expression. At the same time the sarcolemmal sodium-calcium exchanger is increased both in function and in expression. The result is a characteristic change in calcium homoeostasis with decreased diastolic uptake of calcium into the sarcoplasmic reticulum with subsequently reduced calcium release during the next systole, resulting in reduced contractile performance. At the same time increased capacity of the sodium-calcium exchanger extrudes intracellular calcium ions to the extra-cellular space, thereby rendering these ions unavailable for the contractile cycle. A result of these, seemingly specific, phenotype changes is an alteration of the force/frequency relationship. Instead of increasing force of contraction with increasing heart rates, in the chronically failing myocardium the contractile performance declines with increasing heart rates and only improves with decreasing rates. Optimal performance can be seen at heart rates as low as 30 beats.min. Studies employing photoluminescence markers of free cytosolic calcium, such as aequorin, have shown that there is a direct correlation between free cytosolic calcium and contractile performance at different levels of heart rate. It is likely, therefore, that the heart rate reduction with beta-blockade may provide the major explanation for the therapeutic benefits of beta-blockade in chronic congestive heart failure.

Adrenergic beta-Antagonists↗
PubMed2002

Rationale and design of a study assessing treatment strategies of atrial fibrillation in patients with heart failure: the Atrial Fibrillation and Congestive Heart Failure (AF-CHF) trial.

BACKGROUND: Nonrandomized studies suggest that atrial fibrillation is independently associated with increased mortality in patients with heart failure. Whether restoring and maintaining sinus rhythm will have a beneficial impact on cardiovascular mortality in patients with heart failure has never been tested in an adequately powered randomized trial. OBJECTIVE: The primary objective of the Atrial Fibrillation and Congestive Heart Failure (AF-CHF) trial is to determine whether restoring and maintaining sinus rhythm significantly reduces cardiovascular mortality compared with a rate-control strategy in patients with atrial fibrillation and CHF. METHODS: AF-CHF is a prospective multicenter trial (109 centers in Canada, United States, South America, Europe, and Israel), that will randomize 1450 patients with CHF with left ventricular ejection fraction < or =35% and atrial fibrillation to 1 of 2 treatment strategies: (1) rhythm control with the use of electrical cardioversion combined with antiarrhythmic drugs (amiodarone or other class III agents), (2) rate control with the use of beta-blockers, digoxin, or pacemaker and AV nodal ablation. Cardiovascular mortality is the primary end point and the intention-to-treat approach the primary method of analysis. We anticipate an 18.75% 2-year cardiovascular mortality in the rate control arm with a 25% mortality reduction in the rhythm control group. RESULTS: As of August 13, 2002, 334 patients have been enrolled from 68 participating centers. Enrollment is expected to be concluded in May 2003 with a minimum follow-up of 2 years. CONCLUSION: The results of this trial should provide definitive information concerning 2 widely applicable treatment strategies of atrial fibrillation in a large cohort of patients with CHF.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

Dose-related effects of ACE inhibition in man: quinapril in patients with moderate congestive heart failure. The Study Group on Neurohormonal Regulation in Congestive Heart Failure: Lausanne, Switzerland; Berlin, Düsseldorf, Munich, Germany.

Early treatment with ACE inhibitors of even moderate heart failure is clinically beneficial, even though haemodynamic measurements cannot adequately quantitate such improvement. Neurohumoral assessment is, however, supposed to be more accurate. In 55 patients with moderate heart failure (ejection fraction < or = 35%), we investigated the dose-dependent effects of ACE inhibition with quinapril taken orally (2.5, 5 or 10 mg b.i.d.) following a placebo-controlled, parallel design protocol over 12 weeks. Plasma components of the renin angiotensin system, catecholamines and ANF were measured together with haemodynamics both at rest and during exercise. Before ACE inhibitor treatment, median PRA, Ang I and II and catecholamines were normal, while ANF was increased. All these parameters, including ACE activity, rose during exercise. Chronic inhibition of ACE activity was dose-dependent and the maximal fall in Ang II occurred with quinapril 20 mg.day-1. Humoral changes appeared more assessible than haemodynamic alterations even though many of these changes were reasonably correlated. The effects of chronic ACE inhibition on circulating neurohumoral components in patients with moderate heart failure are small and dose-dependent. Since humoral changes are related to haemodynamics they should account for the clinical benefit. Appropriately high doses of ACE inhibitors should be chosen for treatment of heart failure.

Administration, Oral↗
PubMed2005

Current treatments and novel pharmacologic treatments for hyponatremia in congestive heart failure.

Hyponatremia in congestive heart failure (CHF) is associated with increased morbidity and mortality, underlining the importance of adequate assessment and treatment of this electrolyte imbalance in patients with CHF. Current treatment options for hyponatremia in CHF include hypertonic saline solution, loop diuretics, fluid restriction, and other pharmacologic agents, such as demeclocycline, lithium carbonate, and urea. Hypertonic saline solution must be administered with extreme caution because excessively slow or rapid sodium correction can lead to severe neurologic adverse effects. Loop diuretics are useful for reducing the water retention caused by CHF. However, the potent diuresis induced by agents such as furosemide results in loss of sodium and other essential electrolytes, which may exacerbate hyponatremia. Fluid restriction is only moderately effective and often difficult to implement in the hospital setting. Agents such as demeclocycline and lithium have potentially serious renal and cardiovascular side effects. The arginine vasopressin (AVP) receptor antagonists are a promising new class of aquaretic agents that increase free-water excretion while maintaining levels of sodium and other essential electrolytes. Tolvaptan (OPC-41061), lixivaptan (VPA-985), and conivaptan (YM-087) are currently under development for the treatment of hyponatremia. Although tolvaptan and lixivaptan are selective for the vasopressin-2 (V(2)) receptor responsible for the antidiuretic actions of AVP, conivaptan demonstrates activity at both the V(2) receptor and the V(1a) receptor responsible for the vasoconstricting properties of AVP. This dual receptor activity may be particularly useful in patients with CHF. These patients may benefit from the increased cardiac output, reduced total peripheral resistance, and reduced mean arterial blood pressure that results from V(1a) receptor blockade as well as the reduced congestion, reduced cardiac preload, and increased sodium concentrations induced by V(2) receptor antagonism.

Acute Disease↗
PubMed1998

Effect of clonidine on heart rate variability in congestive heart failure.

In patients with congestive heart failure, abnormal heart rate variability is a predictor of total mortality and sudden cardiac death. Drugs that improve heart rate variability may have a potential role for improving the survival among these patients. The effects of clonidine were studied in 24 patients with congestive heart failure, sinus rhythm, a left ventricular ejection fraction <0.40, and systolic blood pressure > 115 mm Hg. A 6-minute corridor walk test and 24-hour Holter monitoring were performed before and 42+/-24 days after initiation of clonidine therapy (Catapres-TTS patch, mean dose: 0.33+/-0.21 mg). Changes in other medications used at baseline were not allowed. One patient died suddenly. Two patients did not complete the protocol due to worsening congestive heart failure, which required changes in medications, 1 patient discontinued due to hypotension, and 2 for personal reasons. Among the 18 patients who completed the protocol, the mean RR interval of sinus beats increased from 760+/-106 to 822+/-125 ms (p=0.001) and the distance covered during the 6-minute walk test increased from 1,148+/-277 to 1,255+/-359 feet (p=0.042). Systolic blood pressure decreased from 139+/-15 to 119+/-10 mm Hg (p <0.0001). The following increases were noted in the heart rate variability measurements: high-frequency power in 0.15 to 0.40 Hz: 4.58+/-1.07 to 4.94+/-1.17 In (ms), p=0.002; SD: 47.0+/-16.9 to 52.5+/-18.4 ms, p=0.034; SD of the mean of all RR intervals in 24 hours: 116+/-94 to 130+/-19 ms, p=0.033; SD of all 5-minute mean RR intervals: 106+/-44 to 124+/-66 ms, p=0.042; root-mean square of difference of successive RR intervals: 28.8+/-10.7 to 34.1+/-14.2 ms, p=0.017. Clonidine improves heart rate variability in the patients with congestive heart failure by increasing the parasympathetic tone. It is well tolerated by most patients with heart failure and may have a beneficial effect on exercise capacity.

Adrenergic alpha-Agonists↗
PubMed1988

Prenalterol in severe congestive heart failure. II. Long-term oral treatment. Results with comments on the methods for evaluation of drugs in congestive heart failure.

Nine patients with severe congestive heart failure were treated with a partial beta-1-agonist prenalterol for 9.6 months on average. Five of the nine patients improved with an increase in NYHA-functional capacity of one class. In four of these patients, the improvement was maintained for 12 months. Upon discontinuation, deterioration occurred only in one case; in the latter, improvement reoccurred on reinstitution of prenalterol treatment. Significant improvement on exercise testing, however, occurred only in two patients. Prediction as to which patients would benefit from oral prenalterol was not possible from the pretreatment haemodynamic variables; similarly, the effect of oral prenalterol treatment could not be predicted from the response to prenalterol given intravenously. A critical review of the methods for evaluation of therapeutic intervention in congestive heart failure concludes the article.

Administration, Oral↗
PubMed1995

Relationship of changes in felodipine pharmacokinetics to haemodynamics during chronic oral treatment of congestive heart failure patients.

In congestive heart failure patients the kinetics of felodipine, a dihydropyridine calcium antagonist, show interpatient differences after acute i.v. administration that disappear after 8 weeks oral treatment with a change in kinetics in the patients with the largest clearances (CL) and the smallest volumes of distribution (Vss). Pharmacokinetic and haemodynamic data were combined to construct a haemodynamic-pharmacokinetic model. This model shows that the differences between the patients in i.v. pharmacokinetics are consistent with a difference in plasma flow distribution between liver and poorly perfused tissues. In patients in whom kinetics changed, felodipine treatment is supposed to cause a redistribution of flow from liver to peripheral tissues, accompanied by a decreased work load of the heart and a larger increase in VO2max during therapy than in the other patients, whose workload increased. This suggests a better therapeutic response in the patients whose kinetics changed. As change in kinetics is related to felodipine CL and CL to liver plasma flow, felodipine CL or even indocyanine CL might be predictive for the therapeutic effect of felodipine.

Administration, Oral↗
PubMed1993

Effects of cardiac transplantation on endothelium-dependent dilation of the peripheral vasculature in congestive heart failure.

Patients with congestive heart failure demonstrate attenuated endothelium-dependent vasodilation of the peripheral vasculature, but there are no data regarding the effect of therapies on this abnormality or whether this abnormality is reversible. This study was performed to address the hypothesis that abnormalities in endothelium-dependent vasodilation in heart failure are improved by heart transplantation. Forearm blood flow responses to the intraarterial administration of a dose range of methacholine, an endothelium-dependent vasodilator, and nitroprusside, an endothelium-independent vasodilator, were examined in 2 separate protocols. In protocol 1, forearm blood flow responses to methacholine in 14 heart transplant recipients were 5.02 +/- 3.11, 11.55 +/- 7.20 and 11.61 +/- 10.24 ml/min/100 ml forearm volume. These responses were significantly greater than those in 10 patients with heart failure (2.23 +/- 1.22, 4.60 +/- 3.43 and 6.70 +/- 4.91 ml/min/100 ml forearm volume; p < 0.05). In contrast, the responses to nitroprusside were nearly identical in the 2 groups. In protocol 2, six patients were studied before and 4 months (range 1 to 11) after transplantation. Methacholine responses before transplantation were 2.5 +/- 1.3, 5.2 +/- 1.5 and 7.3 +/- 1.5 ml/min/100 ml forearm volume and were significantly improved after transplantation to 5.7 +/- 1.2, 12.1 +/- 3.0 and 14.2 +/- 2.2 ml/min/100 ml forearm volume (p < 0.05). Peak reactive hyperemia responses increased significantly from 19.0 +/- 3.7 to 44.8 +/- 6.4 ml/min/100 ml forearm volume (p < 0.01) after transplantation. These data demonstrate that heart transplantation was associated with a significant improvement in the forearm blood flow responses to methacholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Racial differences in outcome and treatment effect in congestive heart failure.

BACKGROUND: In congestive heart failure (CHF), it is unknown whether race affects mortality and whether the effect of treatments differs by race. METHODS: This study was a post hoc analysis of data from the DIG study that evaluated the effect of digoxin on morbidity and mortality in CHF. RESULTS: Investigators followed 897 black and 6660 white participants for a mean of 37 months. Compared with whites, blacks were younger (60 +/- 13 vs 65 +/- 11 years). Total mortality was 34.2% in blacks and 33.6% in whites; hospitalization for worsening CHF occurred in 39% of blacks and 28% of whites. Cox regressions with race as the only covariate showed no effect of race on risk for death (relative risk = 1.04, 95% CI 0.93-1.18, P = .49) but an increase in CHF hospitalization in blacks (relative risk = 1.52, 95% CI 1.35-1.70, P = .0001). Multivariate Cox regression showed no difference by race in risk for death or death/hospitalization for CHF and no difference in the effect of digoxin on either end point. CONCLUSION: Race is not an independent predictor of mortality in CHF. The effect of digoxin on morbidity and mortality in CHF does not differ in blacks and whites.

Black People↗
PubMed2006

Proteomic analysis reveals significant alternations of cardiac small heat shock protein expression in congestive heart failure.

BACKGROUND: Because congestive heart failure (CHF) is a complex syndrome with many different underlying mechanisms of worsening of heart function, it is important to recognize the global alternations in protein expression associated with the processes of CHF. METHODS AND RESULTS: The purpose of our study was to use a proteomic approach to investigate global alternations in protein expression in tachycardia induced CHF dogs. We compared the 2-dimensional electrophoresis protein patterns of left ventricular samples from the normal with those from failing myocardium. Differentially expressed cardiac proteins showed approximately 500 cardiac protein spots. A total of 20 spots (14 increased, 6 decreased) was altered in CHF, whereas the more distinguishably increased spots in CHF were identified by using mass spectrometry as alpha B crystallin, heat shock protein (HSP) 27, and HSP20, which maintain both the morphologic and functional integrity of the cardiomyocytes and increase tolerance against various types of stress. Because phosphorylation is one of the most important posttranslational modifications, we evaluated whether or not the overexpressed small HSPs were phosphorylated in CHF. Phosphoprotein staining and Western blotting demonstrated that the phosphorylation of alpha B crystallin at serine (Ser)-59 site and of HSP27 at both Ser-78 and Ser-82 sites increased in CHF. CONCLUSION: Proteomics studies can provide new insights into molecular mechanisms in CHF and phosphorylated small HSPs may be involved in preventing cardiac dysfunction.

Animals↗
PubMed2002

Effect of non-insulin-dependent diabetes mellitus on pulmonary function and exercise tolerance in chronic congestive heart failure.

In chronic congestive heart failure (CHF), backward effects of left ventricular dysfunction alter pulmonary volumes and gas diffusion. Some of these disorders are detected in some patients with diabetes mellitus, possibly due to a microangiopathic process and nonenzymatic glycosylation of lung tissue proteins. We explored the possibility that coexistence of non-insulin-dependent diabetes mellitus (NIDDM) may potentiate the deterioration of lung function in CHF. In 20 normoglycemic patients (group 1) and in 20 patients with NIDDM (group 2), with New York Heart Association class II to III CHF due to idiopathic or ischemic cardiac disease, and in 20 controls (groups were age- and gender-matched), we investigated cardiac function, pulmonary volumes, carbon monoxide diffusion (DL(CO)) and its alveolar-capillary membrane (D(M)) subcomponent, oxygen uptake and dead space-to-tidal volume ratio (pVD/VT) at peak exercise (individualized ramp test), and slope of ventilation-to-carbon dioxide production ratio (VE/VCO(2)) during exercise. Although, compared with reference subjects, both patient groups had similar variations in left ventricular diastolic volume, ejection fraction, and pulmonary wedge pressure; in group 2 lung volumes, DL(CO), D(M), and oxygen uptake were significantly more reduced; in this group there was no overlap of individual results of DL(CO) and D(M) with those in controls; VE/VCO(2) slope and pVD/VT also were significantly increased, and inversely correlated with D(M). Thus, coexistence of NIDDM makes pulmonary dysfunction worse in CHF, and significantly enhances exercise intolerance.

Analysis of Variance↗
PubMed1996

Cheyne-Stokes respiration and prognosis in congestive heart failure.

Patients with congestive heart failure (CHF) frequently demonstrate Cheyne-Stokes respiration (CSR) with repetitive arousals and oxygen desaturations during sleep. Although it was evident from early publications that CSR during the daytime is a poor prognostic indicator in patients with CHF, it was speculated recently that CSR occurring during sleep could impede left ventricular function and even survival. We therefore followed up 36 patients with CHF and a left ventricular ejection fraction < or = 40% who underwent a sleep study at our institution. The patients showed a reduced ejection fraction (20 +/- 8%) and CSR with a median of 19% of total sleep time (lower and upper quartiles 9% and 56%). In 12 +/- 9% of their time in bed, the arterial oxygen saturation was <90%. No patient was lost to follow-up, which lasted for 32 +/- 15 months (range 11 to 53). One-year survival was 86 +/- 6%, and 2-year survival was 66 +/- 8%. Univariate comparisons for survival between groups stratified by the amount of CSR revealed no significant difference (log rank test, p = 0.84). However, the 20 patients with a left ventricular ejection fraction <20% had a shorter mean survival time than patients with an ejection fraction >20% (9.5 vs 28.3 months; log rank test, p = 0.013). Two patients with CSR during the daytime died within 1 month. No other patient had CSR during the daytime, and only 1 patient without daytime CSR died within 1 month (chi-square test, p <0.001). Higher age, reduced carbon dioxide end-tidal partial pressure, and increased transit time were found to be significantly related to the amount of nocturnal CSR. In conclusion, CSR occurring during sleep has no important prognostic impact in patients with CHF, but CSR present during the daytime suggests a high likelihood of dying within a few months.

Aged↗
PubMed1998

Ventilatory response to exercise correlates with impaired heart rate variability in patients with chronic congestive heart failure.

In chronic congestive heart failure (CHF) an overactivity of muscle ergoreceptors and peripheral chemoreceptors may lead to an increased ventilatory response to exercise and contribute to the autonomic imbalance. The analysis of heart rate variability (HRV), which is a reliable method of studying autonomic regulations within the cardiovascular system, showed depressed HRV indexes in CHF, but predictors of abnormal HRV pattern in CHF remain controversial. Considering a common mechanism involved in generation of both abnormal ventilation and autonomic dysfunction in CHF, we hypothesized that impaired ventilation may be better than other variables of CHF severity in determining HRV parameters. Seventy-two patients with CHF (57+/-9 years, ejection fraction: 28+/-11%) underwent cardiopulmonary exercise testing; the relation between ventilation and carbon dioxide production (VE/VCO2) was used as an index of the ventilatory response to exercise. Time and frequency-domain measurements of HRV were derived from 24-hour electrocardiographic monitoring. Patients had reduced exercise tolerance with abnormal ventilatory response (peak oxygen consumption [VO2max]: 17.8+/-5.5 ml/kg/min, VE/VCO2: 36.0+/-9.8). Correlations were found between HRV measures and etiology, New York Heart Association (NYHA) functional class, and VO2max, but the strongest relation was observed for VE/VCO2 slope (r values from -0.33 to -0.65, p <0.01). In the multiple regression analysis only VE/VCO2 was found to correlate independently with all HRV measurements. To investigate the role of peripheral chemoreceptor overactivity as the mechanism of autonomic imbalance and the increased ventilatory response to exercise, we assessed peripheral chemosensitivity in 22 patients (mean value of peripheral chemosensitivity: 0.62+/-0.34 L/min/%SaO2, significantly higher than in normal controls, mean value: 0.29+/-0.20 L/min/%SaO2 in our laboratory). The activity of the peripheral chemoreflex inversely correlated with all parameters of HRV. Increased ventilatory response to exercise correlated with depressed HRV measures in patients with CHF better than other clinical variables. An important role of the increased peripheral chemosensitivity in this relation may be relevant, being also a potential link between functional severity and sympathovagal imbalance in CHF.

Administration, Inhalation↗