Myocardial catecholamines in hypertrophic and dilated (congestive) cardiomyopathy: a biopsy study

A high performance liquid chromatographic method was used to determine myocardial norepinephrine and epinephrine concentrations in 66 biopsy specimens obtained from the right or left ventricle during routine diagnostic cardiac catheterization of 45 patients with dilated (congestive) or hypertrophic cardiomyopathy, or with heart disease other than cardiomyopathy, such as acute perimyocarditis, postmyocarditis and constrictive pericarditis. The validity of catecholamine determination in a 2 to 6 mg biopsy specimen to assess overall ventricular myocardial catecholamines was demonstrated. Norepinephrine concentrations in the myocardium were inversely correlated with the grade of hypertrophy in patients with congestive cardiomyopathy or heart disease other than cardiomyopathy, but not in patients with hypertrophic cardiomyopathy. The fact that the myocardial norepinephrine concentration was always lower in the left than in the right ventricle of the same patient may be explained by the simple dilution of sympathetic nerve endings in the left ventricle. There were some cases of hypertrophic cardiomyopathy in which the concentration of myocardial norepinephrine was exceptionally high, although its mean value was not significantly higher than that in patients with other types of heart disease who served as a control group without cardiomyopathy. Some patients with dilated cardiomyopathy had lower levels of myocardial norepinephrine than would be expected for the degree of interstitial fibrosis and the severity of heart failure. The mean plasma norepinephrine and epinephrine levels were significantly elevated in patients with dilated cardiomyopathy.     

螺内酯对扩张型心肌病心力衰竭患者某些体液因子的影响

目的 :探讨螺内酯对扩张型心肌病心力衰竭患者血浆儿茶酚胺、肾素活性、血管紧张素Ⅱ及醛固酮的影响。方法 :入选 2 0例扩张型心肌病心力衰竭患者 ,随机分入螺内酯组与对照组 ,各 10例 ,用螺内酯治疗前与治疗 1个月后 ,用高效液相色谱方法测定血浆去甲肾上腺素、肾上腺素 ,同时采用均相竞争放射免疫方法检测血浆肾素活性、血管紧张素 Ⅱ与醛固酮。结果 :治疗 1个月后螺内酯组血浆去甲肾上腺素、肾上腺素、肾素活性及醛固酮明显低于治疗前 ,也低于对照组。结论 :螺内酯可明显抑制扩张型心肌病心力衰竭患者的儿茶酚胺水平 ,降低肾素活性及醛固酮 ,这些改变有可能为螺内酯明显改善心力衰竭病人预后的重要机制     

Autoantibodies: new upstream targets of paroxysmal atrial fibrillation in patients with congestive heart failure

OBJECTIVES: The clinical implications of autoantibodies (Abs) were investigated as upstream indicators of paroxysmal atrial fibrillation in patients with congestive heart failure. METHODS: Circulating Abs against myosin (M-Abs) detected by immunofluorescence, Abs against beta 1-adrenergic receptors (Beta 1-Abs) detected by enzyme-linked immunosorbent assay (ELISA), and Abs against NA-K-ATPase (NKA-Abs) detected by ELISA were screened in 95 congestive heart failure patients with < or = 45% left ventricular ejection fraction (coronary artery disease, n = 48; dilated cardiomyopathy, n = 47) and 48 age-matched control patients with hypertension. No patient received antiarrhythmic therapy. All patients were enrolled with angiotensin converting enzyme inhibitors in the chronic stable state. Relationship of the presence of paroxysmal atrial fibrillation to other clinical variables were assessed by 48-hour Holter monitoring. RESULTS: No control patient had Abs. However, M-Abs, Beta 1-Abs, and NKA-Abs were detected in 22%, 26% and 16% of patients with congestive heart failure (coronary artery disease; 8%, 10%, and 4%, dilated cardiomyopathy; 36%, 43%, and 28%, respectively). Paroxysmal atrial fibrillation was more frequent in patients with dilated cardiomyopathy than in those with coronary artery disease (47% vs 15%, p < 0.01). Multivariate analysis suggested that NKA-Abs was an independent risk factor for the occurrence of paroxysmal atrial fibrillation (p < 0.01), although there were no differences in other clinical factors: age, sex, New York Heart Association functional class, concomitant medication, left ventricular ejection fraction, left atrial diameter, severity of mitral regurgitation, serum potassium, plasma norepinephrine, and atrial natriuretic peptide concentration. CONCLUSIONS: Autoantibodies against sarcolemmal Na-K-ATPase were closely related to the occurrence of paroxysmal atrial fibrillation in patients with congestive heart failure, so an autoimmune process may be an upstream factor in atrial fibrillation.     

Hormonal profile in patients with congestive heart failure

BACKGROUND: Recent progress has been made in the understanding of the cellular and molecular mechanisms of growth hormone action and of its effects on cardiac tissue. The aim of this study was to measure growth hormone concentrations, along with various other hormones, in patients with stable chronic congestive heart failure due to idiopathic dilated cardiomyopathy. METHODS: The study included 23 ambulatory men, 51.2+/-9.3 years of age, on standard medical therapy for heart failure due to idiopathic dilated cardiomyopathy. All patients underwent clinical and laboratory evaluations, including echocardiogram, radionuclide ventriculography, right heart catheterization, coronary angiography, and right ventricular endomyocardial biopsy. Serum or plasma concentrations of growth, thyroid, sex and adrenal hormones were measured in all patients and compared with those found in 20 age-matched healthy men. RESULTS: Growth hormone, insulin-like growth factor I, and free testosterone values in patients with idiopathic dilated cardiomyopathy and heart failure were 0.37+/-0.2 ng/ml, 123.7+/-50 ng/ml and 48.6+/-23.8 pmol/l, respectively, versus 0.5+/-0.4 ng/ml (P<0.01), 236.3+/-66.4 ng/ml (P<0.001) and 105+/-17 pmol/l (P<0.01), respectively, in the healthy age-matched individuals. All other hormone concentrations were comparable in both groups. CONCLUSIONS: Chronic heart failure due to idiopathic dilated cardiomyopathy is associated with a significant decrease in growth hormone, insulin-like growth factor I, and testosterone concentrations, probably due to chronic disease.     

Sympathetic activity in patients with heart failure due to idiopathic dilated cardiomyopathy: effect of ACE inhibitors and other vasodilators

A decrease in cardiac output in patients with congestive heart failure due to dilated cardiomyopathy is compensated by stimulation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. The increase in plasma norepinephrine and depletion of norepinephrine in the myocardium as well as the disturbance of beta-adrenal and baroreceptor function reflect the limits of the sympathetic nervous stimulation. Together with augmented levels of angiotensin II and vasopressin, this stimulation leads to a significant increase in systemic vascular resistance. Sustained stimulation of at least one of these mechanisms can cause further impairment of the left ventricular function. The severity and prognosis of congestive heart failure due to dilated cardiomyopathy is expressed by the plasma norepinephrine concentration and by its myocardial depletion. Ultimately, activation of the compensatory mechanisms provides the basis for therapeutic approaches: 1. reduction of afterload and systemic vascular resistance and/or 2. diminution of the sympathetic nervous activity. For about the last ten years, ACE inhibitors have been used as pharmacological treatment in addition to positive inotropic and vasodilating substances. Captopril, one of the first orally applicable drugs, reduces left ventricular filling pressure, pulmonary capillary pressure, systemic vascular resistance and increases the cardiac output. Beside the hemodynamic improvement, a decrease in plasma norepinephrine and aldosterone can be observed. Vasodilators and alpha-blocking agents can also reduce afterload and systemic vascular resistance in patients with congestive heart failure due to dilated cardiomyopathy, and may lead to hemodynamic improvement. The main limitations of their long-term application are relatively short duration of action, reflex activation of the renin-angiotensin system due to vasodilation and induction of tolerance.     

Erythrocyte Na+, K+-ATPase activity in patients with congestive heart failure.

In order to determine if the Na+, K+-ATPase activity in erythrocyte membranes is altered in congestive heart failure, and to examine its clinical significance with respect to other clinical variables, erythrocyte Na+, K+-ATPase activity was measured in 51 patients with left ventricular ejection fractions <40% (coronary artery disease, n=26; dilated cardiomyopathy, n=25) and 24 control patients. Na+, K+-ATPase activity was lower in both coronary artery disease and dilated cardiomyopathy groups than control group even in the absence of digitalis use. There was a significant inverse correlation between Na+, K+-ATPase activity and plasma norepinephrine. The presence of non-sustained ventricular tachycardia was associated with a lower Na+, K+-ATPase activity in both groups with congestive heart failure without digitalis use than those without ventricular tachycardia. Plasma norepinephrine was higher in patients with non-sustained ventricular tachycardia than those without in the coronary artery disease group, but not in the dilated cardiomyopathy group. Na+, K+-ATPase activity may be helpful in predicting electrophysiologic instability in patients with heart failure.     

Increase in plasma norepinephrine during prazosin therapy for chronic congestive heart failure

To investigate the mechanism of pharmacodynamic tolerance reported to occur during prazosin therapy of chronic congestive heart failure, we measured plasma norepinephrine, plasma epinephrine, plasma renin activity (PRA) and plasma aldosterone, as well as hemodynamics in eight patients with chronic congestive heart failure, functional class III and IV (NYHA), before and during 10 weeks of prazosin therapy.Initially, prazosin therapy produced significant hemodynamic improvement, but no significant changes were noted in norepinephrine, epinephrine, plasma renin activity or aldosterone. During ambulatory therapy, fluid retention developed in four patients, and three of them had symptoms or clinical evidence of congestive heart failure for which they required an increase in diuretic or prazosin therapy. Plasma norepinephrine levels for the whole group were signficantly higher after four weeks of therapy (p < 0.01). Repeat inpatient studies after 10 weeks showed a persistent hemodynamic response to prazosin in seven patients. One patient demonstrated complete hemodynamic tolerance whereas three others showed partial tolerance. In these four patients the cardiac output increased only to 3.78 ± 1.17 liters/min compared to 5.04 ± 2.11 liters/min during initial prazosin therapy. Plasma norepinephrine increased further and levels were significantly higher for the whole group than before prazosin therapy (p < 0.05). No significant changes in epinephrine, plasma renin activity or aldosterone were demonstrated.This increase in plasma norepinephrine suggests that the sympathetic nervous system could be involved in the pharmacodynamic tolerance to prazosin therapy in congestive heart failure. Further studies are necessary to extend these results.     

Therapy of dilated cardiomyopathy with digitalis, diuretics and vasodilators

The treatment of dilated cardiomyopathy is primarily concerned with that of congestive heart failure. Digitalis is widely use in dilated cardiomyopathy but an improvement in the prognosis has not yet been demonstrated. Furthermore, the effects of digitalis in patients with sinus rhythm are debatable. If dilated cardiomyopathy induces atrial fibrillation and tachyarrhythmia, digitalis should be used. Diuretics are helpful in the treatment of congestive heart failure associated with dilated cardiomyopathy. By reducing hypervolemia and by venous dilatation, diuretics lower preload and afterload. This leads to relief of congestion and termination of the vicious cycle of congestive heart failure. Accordingly, the prognosis of dilated cardiomyopathy might be improved by diuretics. There are numerous diuretics acting differently on the renal tubules, the choice of which depends on the renal function and serum electrolyte concentrations. Reduction of preload and afterload improves congestive heart failure as has been demonstrated repeatedly. Many substances have therefore been used for arterial and venous dilation with differing results. At least for short-term periods, congestion is reduced and cardiac output increases. Especially inhibitors of angiotensin II converting enzyme are very effective since they act both in the arterial and venous systems. Additionally, inhibition of the action of angiotensin may be regarded as causal therapy since the renin-angiotensin system is the trigger for vasoconstriction and fluid retention in congestive heart failure. Unlike other substances, ACE inhibitors have been demonstrated to improve prognosis of patients with congestive heart failure. At present, combined diuretic therapy and angiotensin conversion enzyme inhibition would seem the most reasonable treatment for patients with dilated cardiomyopathy and sinus rhythm. If atrial fibrillation and tachyarrhythmia develop, additional digitalis therapy is effective.     

CT引导下胸交感神经阻滞治疗扩张型心肌病心力衰竭的临床价值

目的:探讨CT引导下胸交感神经阻滞治疗扩张型心肌病心力衰竭的临床价值。方法:选择2010年1月至2015年6月收治的扩张型心肌病心力衰竭患者80例,对照组(n=40)采用常规治疗,观察组(n=40)在对照组基础上联合使用CT引导下胸交感神经阻滞,比较两组治疗前后血浆肾上腺素(E)、去甲肾上腺素(NE)和脑钠肽(BNP)水平,治疗后24 h心率变异时域指标和治疗前后心功能相关指标。结果:治疗后两组BNP、E及NE水平均低于治疗前(P均0.05),且治疗后观察组BNP、E及NE水平均低于对照组(P均0.05);治疗后观察组全部正常窦性心搏间期标准差(SDNN)、24 h内每5 min节段平均正常窦性心动周期标准差(SDANN)和全程相邻心搏间期之差均方根值(RMSSD)均长于对照组(P均0.05),特定时间段相邻心搏间期50 ms心搏数所占百分比(PNN50)大于对照组(P0.05);治疗后两组左室内径、左室射血分数和心胸比较治疗前均明显改善(P均0.05),且治疗后观察组左室内径、左室射血分数和心胸比较对照组明显改善(P均0.05)。结论:对扩张型心肌病并发心力衰竭患者,CT引导下胸交感神经阻滞治疗能显著降低交感神经兴奋性,降低儿茶酚胺类激素水平,改善心脏功能。     

The role of endogenous dopamine in congestive heart failure

Although the effects of epinephrine and norepinephrine in congestive heart failure have been extensively studied, and exogenous dopamine, another of the catecholamines, has been widely used for the treatment of congestive heart failure, little attention has been paid to the physiological significance of endogenous dopamine in this condition. The present study was therefore designed to assess the physiological significance of endogenous dopamine in congestive heart failure. Nineteen patients with congestive heart failure caused by such conditions as acute myocardial infarction, valvular disease and dilated cardiomyopathy were examined before and after treatment with diuretics, digitalis and vasodilators. Electrolyte, creatinine and catecholamine concentrations in plasma and urine were analyzed. Urinary dopamine levels were increased in 13 out of 19 cases before treatment and returned to the normal range after treatment, falling from 2448 +/- 950.7 to 528.8 +/- 56.3 micrograms/day (normal level, less than 700 micrograms/day). Urinary dopamine excretion was markedly elevated within 24 hours after the onset of symptoms of heart failure, such as chest pain, palpitations and dyspnea. The relationship between urinary dopamine excretion and time after the onset of symptoms showed a strong statistical correlation (r = 0.55, p less than 0.001). Urinary dopamine excretion was also well correlated with plasma dopamine concentration, urinary norepinephrine excretion and venous pressure. From these results, it is concluded that endogenous dopamine seems to play an important role during the acute phase of congestive heart failure.     

Endogenous catecholamine levels in chronic heart failure. Relation to the severity of hemodynamic abnormalities

Plasma free epinephrine, norepinephrine, and dopamine concentrations were determined in 48, 63, and 45 patients, respectively, with overt congestive heart failure, and compared with those in 26 patients with stable angina but without heart failure. Systemic hemodynamic values were determined to assess the severity of heart failure. Arterial epinephrine levels were not different between patients with heart failure (73 +/- 92 pg/ml) and patients without heart failure (55 +/- 73 pg/ml). In patients with congestive heart failure, norepinephrine (665 +/- 510 pg/ml, mean +/- SD) and dopamine (407 +/- 405 pg/ml) levels were significantly higher than in patients with stable angina without heart failure (norepinephrine 184 +/- 136 pg/ml, p less than 0.001, and dopamine 197 +/- 259 pg/ml, p less than 0.02). However, in patients with congestive heart failure, the plasma norepinephrine levels did not correlate with cardiac index (r = 0.21, p = NS), pulmonary capillary wedge pressure (r = 0.11, p = NS), mean arterial pressure (r = 0.11, p = NS), or systemic vascular resistance (r = 0.18, p = NS). Similarly, there was no correlation between dopamine levels and the hemodynamic abnormalities in patients with congestive heart failure. These findings suggest that although endogenous norepinephrine and dopamine levels are frequently elevated in patients with heart failure, reflecting enhanced sympathetic activity, catecholamine levels do not reflect the severity of heart failure.     

Plasma norepinephrine in congestive heart failure.

Resting plasma concentrations of norepinephrine, dopamine-beta-hydroxylase enzyme activity and peripheral blood lymphocyte beta adrenergic receptor sensitivity to isoproterenol as reflected in cyclic 3′,5′-adenosine monophosphate (cAMP) generation were studied in patients with congestive heart failure due to atherosclerotic heart disease or to congestive cardiomyopathy or hypertensive cardiovascular disease. Systolic time Intervals were also measured in nonhypertensive patients and correlated with the plasma norepinephrine concentration. Control patients were hospital employees without a previous history of heart disease or hypertension, and were matched for age to eliminate the effect of increasing age on the plasma norepinephrine concentration.The results of this study clearly demonstrate that the plasma norepinephrine concentration is directly related to the degree of left ventricular dysfunction in patients with congestive heart failure. When the systolic time intervals were correlated with the plasma norepinephrine levels, a significant prolongation of the preejection period was observed with progressively increasing plasma concentrations of norepinephrine. The reverse was true for the left ventricular ejection time, which demonstrated a significant Inverse relation with the plasma norepinephrine concentration. The ratio of the preejection period to the left ventricular ejection time, which is a reflection of left ventricular function, significantly increased with increasing levels of plasma norepinephrine. In addition, plasma lymphocytes from patients with the greatest degree of left ventricular dysfunction failed to generate normal amounts of cAMP after beta adrenergic receptor stimulation with isoproterenol. It Is suggested that beta adrenergic receptors are desensitized in these patients and that this desensitization contributes to the observed alterations in myocardial contractility.     

Dehydroepiandrosterone levels vary according as heart failure condition in patients with idiopathic dilated cardiomyopathy

The secretion of dehydroepiandrosterone sulfate (DHEAS) decreases with age, and the incidence of heart failure rises in the elderly population. We measured plasma DHEAS levels in 50 male patients (mean 66.7+/-9.1 years old) with congestive heart failure due to idiopathic dilated cardiomyopathy before and after treatment. The study included 50 age-matched control subjects with coronary spastic angina (mean 65.5+/-8.8 years old). DHEAS levels were significantly lower in patients with congestive heart failure than in controls (82.2+/-9.9 vs. 122.7+/-18.6 microg/dL, respectively, p<0.01), whereas there was no difference in cortisol levels between the 2 groups. After 3 months of treatment, NYHA functional class improved in all patients, and DHEAS levels increased (from 82.2+/-9.9 to 106.2+/-21.1 microg/dL, p<0.01). DHEAS levels vary according as heart failure condition in patients with idiopathic dilated cardiomyopathy.     

Beta-adrenergic contractile reserve as a predictor of clinical outcome in patients with idiopathic dilated cardiomyopathy.

To examine the ability of beta-adrenergic contractile reserve assessment to predict the outcome of patients with heart failure, a prospective study was undertaken in 35 patients with idiopathic dilated cardiomyopathy and radionuclide ejection fraction below 40%. During right- and left-sided catheterization, right atrial and left ventricular (LV) pressures, peak positive LV dp/dt, cardiac index, and plasma norepinephrine and epinephrine concentrations were measured at baseline. After a left main intracoronary infusion of dobutamine (25 to 200 micrograms.min-1), beta-adrenergic contractile responsiveness was assessed as the net increase in peak positive LV dp/dt (delta LV dp/dt). After the initial examination, patients were treated with diuretics, digitalis, and angiotensin converting enzyme inhibitors and then followed-up. After a mean follow-up period of 13 +/- 7 months, two groups of patients were distinguished: those who responded to medical therapy (group A, n = 26) and those with clinical deterioration (group B, n = 9) leading to death (n = 4) or heart transplantation (n = 5). Initial peak positive LV dp/dt, LV end-diastolic pressure, cardiac index, and LV ejection fraction were better in group A than in group B (p less than 0.001). Initial plasma norepinephrine and epinephrine concentrations were significantly higher and delta LV dp/dt was lower in group B than in group A (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

The Rational for the Use of à -Blockers in the Treatment of Congestive Heart Failure

Limited clinical data suggest that in particular types of congestive heart failure, the cautious use of low-dose ? -blockers may be beneficial, despite the well-known cardiodepressant effect of these drugs. Downregulation of cardiac ? -adrenoceptors has been demonstrated repeatedly in various forms of congestive heart failure. This phenomenon is caused by the long-term exposure of these receptors to endogenous noradrenaline (a ? -adrenoceptor agonist), which is known to reach markedly elevated plasma concentrations in severe congestive heart failure. As but one example, the downregulation of ? -adrenoceptors explains the well-known tachyphylaxis in the inotropic response to ? -adrenoceptor agonists such as dobutamine. A beneficial effect of low-dose ? -blockers has been shown for metoprolol and bucindolol given for several months. Most studies with such agents have been done in patients with severe congestive heart failure resulting from dilated cardiomyopathy. The beneficial effect of such therapy may be explained by ? -adrenoceptor upregulation, thus allowing a better response to endogenous noradrenaline. Alternatively, the therapy may exert its effect by inhibiting tachycardia, which is known to accompany congestive heart failure.     

Activity of the sympathetic nervous system and renin-angiotensin system assessed by plasma hormone levels and their relation to hemodynamic abnormalities in congestive heart failure

Resting hemodynamic measurements and plasma levels of catecholamines and renin activity were studied in 55 hospitalized treated patients with congestive heart failure in clinically stable condition. Plasma norepinephrine (mean ± standard error of the mean 594 ± 51 pg/ml, range 153 to 1,868) and plasma renin activity (mean 12.9 ± 2.4 ng/ml per hr, range 0.6 to 85.2) values were significantly (probability [p] < 0.01) higher than in normal subjects. In 26 of these patients plasma norepinephrine and plasma renin activity measured on 3 successive days including the day of hemodynamic study did not change significantly. In contrast, plasma epinephrine (mean 138 ± 26 pg ml, range 24 to 1,099) increased significantly at the time of invasive studies, probably because of stress-induced adrenal discharge. When baseline plasma norepinephrine was compared with resting hemodynamic values, significant correlations were found with right atrial pressure (correlation coefficient [r] = +0.44), pulmonary arterial pressure (r = +0.45), pulmonary capillary wedge pressure (r = +0.42), pulmonary vascular resistance (r = +0.55), pulmonary arteriolar resistance (r = +0.41), cardiac index (r = ?0.42), systemic vascular resistance (r = +0.30) and heart rate (r = +0.52). Plasma renin activity was only weakly correlated with plasma norepinephrine (r = +0.38) and did not correlate significantly with any hemodynamic measurement.It is concluded that patients with congestive heart failure can be categorized on the basis of neurohumoral activity. The statistically significant correlations between plasma norepinephrine and hemodynamic evidence of cardiac dysfunction suggest that the sympathetic response is either a marker of or a contributor to the hemodynamic derangement. Because hemodynamic abnormalities did not correlate with plasma renin activity despite a statistically significant correlation between plasma norepinephrine and plasma renin activity, it appears that the two systems are independently activated in congestive heart failure but that sympathetic stimulation may be one factor contributing to renin release. Further studies are needed to assess the usefulness of plasma hormone levels in evaluating and treating patients with congestive heart failure.     

Cardiovascular effects of natriuretic peptides and their interrelation with endothelin-1

The natriuretic peptides are a group of structurally related but genetically distinct peptides. Four types of natriuretic peptides have been found thus far: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP) and Dendroaspis natriuretic peptide (DNP). ANP and BNP are secreted mainly from the heart and function as hormones with vasodilatory and natriuretic effects. CNP originates mainly from endothelial cells with a paracrine effect to induce vasodilation. Other effects of natriuretic peptides including negative inotropy, antimitogenic and anticoagulation have been described. Three types of natriuretic peptide receptors mediate their functions, and among them two are cGMP-coupled. Clearance of natriuretic peptides is via its clearance receptor through the action of neutral endopeptidases. Natriuretic peptides interact with other vasoactive peptides including endothelin. The putative role of natriuretic peptides in the pathophysiology of various cardiovascular diseases including congestive heart failure, hypertension, ischemic heart disease, and cardiomyopathy are discussed. Natriuretic peptide plasma levels are used for the diagnosis and therapeutic follow-up of congestive heart failure patients. Increasing the levels of natriuretic peptides by natriuretic peptide mimetics and neutral endopeptidase inhibitors may provide a new therapeutic strategy for the treatment of cardiovascular diseases such as congestive heart failure and hypertension.     

Congestive heart failure in dialysis patients

To determine the prevalence of congestive heart failure in dialysis patients and the disorders with which it is associated, 85% of 153 nondiabetic patients who were undergoing maintenance dialysis had echocardiography and gated cardiac scan. Ten percent (n = 15) had congestive heart failure, 53% (n = 8) of whom had dilated cardiomyopathy, and 47% (n = 7) had hypertrophic hyperkinetic cardiomyopathy. Ischemic heart disease was an additional independent risk factor for congestive heart failure. Significantly more of those patients with dilated cardiomyopathy were smokers and none were hypertensive, whereas all those patients with hypertrophic cardiomyopathy were hypertensive. The prevalence of hypertrophic hyperkinetic disease was 11%, of dilated cardiomyopathy 18%, and of symptomatic ischemic heart disease 18%. We concluded that congestive heart failure in dialysis patients is associated not only with dilated cardiomyopathy but also with hypertrophic cardiomyopathy, a disease that requires echocardiography for diagnosis and that has different risk factors and management.     

Peripartum cardiomyopathy.

Peripartum cardiomyopathy is a relatively rare complication of pregnancy, characterized by heart failure of obscure etiology during the antepartal or postpartal period. During a 10-year period in our hospital, of 36,882 women who delivered, 6 were diagnosed as having peripartum cardiomyopathy. The incidence in our hospital was estimated as 1:6,147 deliveries. Among these 6 patients, 2 cases with fulminating courses died 1 month after treatment. Two other cases had cardiomyopathy and multiple congestive heart failure and died after 3 years and 6 years. Only one case, whose cardiac size returned to normal within 4 months, completely recovered from this disease. Another survivor with persistent cardiomegaly was followed for 5 years and remained clinically stable. In addition to congestive heart failure, the occurrence of complications such as sepsis, hepatorenal failure, and arrhythmia were the major causes of death. According to the results of our study, return of cardiac chamber size to the normal range indicated a good prognosis. We concluded that the prognosis of peripartum cardiomyopathy depends upon the degree of cardiac dysfunction and the response to therapy.     

Effects of bucindolol in heart failure

Bucindolol hydrochloride is a phenoxypropanolamine with potent nonselective β antagonist and mild vasodilatory properties. In humans with congestive heart failure, it is extremely well tolerated and produces improvements in left ventricular systolic (ejection fraction, systolic elastance, cardiac index, and stroke work) and diastolic (isovolumic relaxation) performance while reducin pulmonary artery pressures and heart rate. These improvements occur without an increase in myocardial oxygen extraction or oxygen consumption. In addition, functional class improves with this agent although exercise tolerance and maximal oxygen consumption (VO_2max) does not change, an effect that is not unexpected with a β-adrenergic antagonist. Bucindolol produces a decrease in plasma renin activity and plasma norepinephrine, effects that may be beneficial for the long-term treatment of congestive heart failure. However, these effects are most marked in patients with idiopathic dilated cardiomyopathy compared with patients with ischemic heart disease. This agent holds great promise for the treatment of heart failure patients.