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PubMed2005

[Calpain involved in signal transduction of myocardial remodeling in patients with congestive heart failure].

OBJECTIVE: To investigate the regulation of calcium sensitive signal substance calpain in signal transduction of myocardial remodeling in patients with congestive heart failure. METHODS: All 39 congestive heart failure (CHF) patients with rheumatic mitral valve stenosis disease were selected and 38 cases of healthy persons were included as controls. Cardiac function parameters were measured by echocardiography. The concentration of angiotension II (AngII) in plasma and myocardial tissues was determined by radio immunoassay (RIA). Western blot was used to assay the protein expression of calpain, cain/cabin 1, cain/cabin 1Delta, and calcineurin (CaN) phosphorylation. RESULTS: The AngII concentrations in the plasma and myocardial tissues in patients with CHF were higher than those in the control group. Meanwhile the AngII concentrations positively correlated to the parameters of the cardiac dilation respectively but negatively correlated to the parameters of cardiac function. Pathological changes of myocardial tissues in CHF with valvular heart disease showed typical myocardial remodeling. The hypertrophy was dominant at early stage of CHF, while at the end stage the characteristics include disordered alignment of the myocytes, the discontinuity and dissolving of cardiomyofibrills, destroyed subcellular organs, and the hyperplasia of interstitial tissue. Compared to the control group, u-calpain, m-calpain, and cain/cabin 1Delta protein expression, CaN phosphorylation in myocardial tissues in CHF groups were highly expressed and their expressions were positively correlated to the severity of CHF. The expression of cain/cabin1 deceased and its expression was negatively correlated to the severity of CHF. CONCLUSION: The degradation of cain/cabin 1 by calpain may play an important role by causing the activation of CaN signal pathway in myocardial remodeling mediated by renin angiotension system in CHF.

Adaptor Proteins, Signal Transducing↗
PubMed1992

Left ventricular filling after long-term angiotensin converting enzyme inhibition in congestive heart failure.

As a rule, left ventricular relaxation is impaired in patients with coronary artery disease and congestive heart failure. In addition, the passive elastic properties in early and late diastole change when the ventricle dilates. Diastolic properties of the left ventricle were studied in 11 patients with congestive heart failure class II-IV (NYHA) before and 3 months after 10-20 mg enalapril was added to their regimen of salt restriction, a diuretic and occasionally digitalis. Haemodynamic studies were performed using radionuclide angiography and simultaneous pressure-volume measurements. Systemic vascular resistance decreased from 1479 to 1182 dynes.s.-1 cm-5 (P < 0.05) and left ventricular end-diastolic pressure from 19.2 to 15.9 mmHg (P < 0.05). Left ventricular end-diastolic volume index decreased from 130 +/- 22 to 81 +/- 22 ml (P < 0.01). Indices of early diastolic relaxation, such as peak filling rate (1.43 +/- 0.46 to 1.49 +/- 0.84 EDV/s), time to peak filling rate (460 +/- 70 to 490 +/- 70 ms), peak negative dP/dt (-903 +/- 190 to -891 +/- 190 mmHg/s) and tau, the time constant of isovolumic pressure decay (58.7 +/- 14.4 to 48.4 +/- 15.2 ms) did not change significantly. In nine patients pressure-volume loops shifted to the left in all patients but one due to reduction in end-systolic and end-diastolic volume. The steepness of the diastolic part of the pressure-volume relationship increased, indicating an increase in chamber stiffness. The stiffness constant increased about 25% towards a more normal value. The alteration in stiffness seemed to be mainly due to the change of the geometry of the ventricle and not to a major change in the visco-elastic properties of the ventricular wall. In conclusion, regression of remodelling induced by enalapril does not change diastolic function parameters in patients with chronic congestive heart failure beyond the changes caused by regression of ventricular dilation.

Blood Pressure↗
PubMed1990

Nitrendipine binding in congestive heart failure due to myocardial infarction.

Depressed cardiac pump function is the hallmark of congestive heart failure, and it is suspected that decreased influx of Ca2+ into the cardiac cell is responsible for depressed contractile function. Since Ca2+ channels in the sarcolemmal membrane are considered to be an important route for the entry of Ca2+, we examined the status of Ca2+ receptors/channels in failing rat hearts after myocardial infarction of the left ventricular free wall. For this purpose, the left coronary artery was ligated and hearts were examined 4, 8, and 16 weeks later; sham-operated animals served as controls. Hemodynamic assessment revealed decreased total mechanical energy (left ventricular systolic pressure x heart rate), increased left ventricular diastolic pressure, and decreased positive and negative dP/dt in experimental animals at 4, 8, and 16 weeks. Although accumulation of ascites in the abdominal cavity was evident at 4 weeks, other clinical signs of congestive heart failure in experimental rats were evident from the presence of lung congestion and cardiac dilatation at 8 and 16 weeks after induction of myocardial infarction. The density of Ca2+ receptors/channels in crude membranes, as assessed by [3H]nitrendipine binding assay, was found to be decreased in the uninfarcted experimental left ventricle at 8 and 16 weeks; however, no change in the affinity of nitrendipine was evident. A similar depression in the specific binding of another dihydropyridine compound, [3H]PN200-110, was also evident in failing hearts. Brain and skeletal muscle crude membrane preparations, unlike those of the right ventricle and liver, revealed a decrease in Ca2+ receptors/channels density in experimental animals at 16 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Diuretics in the treatment of patients who present congestive heart failure and hypertension.

The main operational objective of diuretic therapy in patients who present congestive heart failure and hypertension is to reduce or to suppress excess bodily fluid. Effective diuretic therapy decreases cardiac size when the heart is dilated, and it reduces lung congestion and excess water. Consequently, external respiratory work diminishes and cardiac output would be redistributed in favour of systemic vascular beds other than that of the respiratory muscles; dyspnoea decreases markedly and there is a slight reduction in fatigue. This clinical improvement and the fall in body weight caused by diuretics entail an increase in effort capacity. Subsequent exercise training ameliorates the abnormal ventilatory response to physical effort and the skeletal muscle myopathy that occur in heart failure, and thereby it attenuates dyspnoea and decreases fatigue further. Loop and/or thiazide-type diuretics may be used to augment natriuresis in patients with congestive heart failure and hypertension. The state of renal function, the existence of certain co-morbid conditions, potential untoward drug actions, and possible interactions of diuretics with nutrients and with other drugs are some of the factors that must be considered at the time of deciding on the diuretic drug(s) and dose(s) to be prescribed. Spironolactone has been found to increase life expectancy and to reduce hospitalisation frequency when added to the conventional therapeutic regimen of patients with advanced congestive heart failure and systolic dysfunction. Therefore, spironolactone should be the drug of choice to oppose the kaliuretic effect of a loop or of a thiazide-type diuretic.

Diuretics↗
PubMed1979

Effect of isosorbide dinitrate on response to submaximal and maximal exercise in patients with congestive heart failure.

Isosorbide dinitrate is an effective vasodilator that improves resting left ventricular performance in patients with congestive heart failure, but little is known of the effect of the drug on the response to exercise. Bicycle exercise to symptomatic maximum was performed by 18 patients with class II to IV congestive heart failure before and 90 minutes after administration of isosorbide dinitrate, 40 mg orally. Although resting pulmonary wedge pressure and systemic vascular resistance were significantly reduced after isosorbide dinitrate, exercise duration was not altered and maximal oxygen consumption was not significantly changed (13.6 +/- 1.3 [SEM] standard error of the mean versus 13.8 +/- 1.2 ml/kg per min). At peak exercise pulmonary wedge pressure of 37.1 +/- 1.7 mm Hg, cardiac index of 4.19 +/- 0.35 liters/min per m2, and systemic vascular resistance of 14.7 +/- 1.3 units were not significantly different after nitrate administration. However, at submaximal loads, pulmonary wedge pressure was reduced from 33.6 +/- 1.7 to 27.9 +/- 1.8 mm Hg (P less than 0.01), and systemic resistance from 16.5 +/- 1.5 to 13.7 +/- 1.0 units (P less than 0.01) after administration of isosorbide dinitrate. Thus, short-term administration of nitrates does not improve maximal exercise capacity or left ventricular performance at maximal exercise in patients with congestive heart failure, but it does appear to improve pump function at submaximal work loads and may therefore enable patients to perform limited exercise more comfortably.

Administration, Oral↗
PubMed1995

Chronic congestive heart failure is associated with a phenotypic shift of intramyocardial endothelial cells.

BACKGROUND: There is evidence that patients with chronic congestive heart failure have endothelial cell-related abnormalities of the peripheral circulation and the coronary microvasculature. For that reason, we have studied the phenotypic expression of endothelial cells in hearts of patients with congestive heart failure. METHODS AND RESULTS: We studied cardiac explants (n = 19) and autopsy hearts (n = 5) of patients with chronic congestive heart failure caused by either a dilated cardiomyopathy (n = 12) or ischemic heart disease (n = 12) and compared them with normal hearts (n = 12). The antigenic expression obtained with several endothelial cell markers (factor VIII-related antigen, EN-4, Ulex europaeus agglutinin-1 (UEA-1), PAL-E, endoglin, and endothelin) and adhesion molecules (intercellular adhesion molecule [ICAM], vascular cell adhesion molecule [VCAM], or E-selectin) was compared by use of immunohistochemical techniques. On the basis of the initial findings, the number of PAL-E- and EN-4-positive vessels was counted. The incidence of PAL-E-positive vessels per area was quantified and related to the percentage of heart muscle cells and the total number of vessels per area. In control hearts, endothelial cells rarely were positive for PAL-E. In hearts of patients with ischemic cardiomyopathies, there was distinct staining with this marker. Hearts of patients with dilated cardiomyopathies showed a marked increase in the number of PAL-E-positive endothelial cells. Vessels with a muscular media were PAL-E-negative. Two-sample analysis revealed a statistically significant difference between hearts with dilated cardiomyopathies and ischemic cardiomyopathies (P < .01), between hearts with dilated cardiomyopathies and control hearts (P < .01), and between hearts with ischemic cardiomyopathies and control hearts (P < .01). Endoglin and ICAM were positive but nondiscriminating. Endothelin, VCAM, and E-selectin were negative. CONCLUSIONS: A phenotypic shift in endothelial antigen expression of the coronary microvasculature occurs in both ischemic hearts and hearts with dilated cardiomyopathies, as revealed by PAL-E, compared with control hearts. The change may relate to compensatory mechanisms in long-standing chronic heart failure.

Adult↗
PubMed1996

Prevention of disease progression, left ventricular hypertrophy and congestive heart failure in hypertension treatment trials.

OBJECTIVES: This work was done to determine the role of hypertension treatment in the prevention of disease progression, left ventricular hypertrophy and congestive heart failure. BACKGROUND: Lowering of blood pressure in hypertensive patients has been reported to reduce morbidity and mortality from strokes and myocardial infarction. Data on primary prevention of disease progression, left ventricular hypertrophy and congestive heart failure have not previously been carefully quantified. METHODS: All the major long-term hypertension treatment trials over the past 20 years were reviewed. RESULTS: One thousand four hundred ninety-three of 13,342 subjects in the control groups compared with only 95 of 13,389 in the treated groups progressed from less severe to severe hypertension. The incidence of left ventricular hypertrophy in treated compared with control or placebo subjects was 140 of 6,150 and 216 of 6,098 subjects, respectively; congestive heart failure occurred in 240 of 6,923 subjects in the control group compared with only 112 of 6,914 treated subjects. CONCLUSIONS: The lowering of blood pressure over a 3- to 5-year period of time is effective in preventing severe disease, left ventricular hypertrophy and congestive heart failure in addition to strokes and myocardial infarction. In an era when expensive and often complicated methods are being used to prevent recurrence of congestive heart failure or myocardial infarction, it is important to highlight the role of antihypertensive therapy in primary prevention.

Antihypertensive Agents↗
PubMed2006

[The cardio-renal anemia syndrome: what is it? With a focus on congestive heart failure].

The cardio-renal anemia syndrome describes how the three conditions congestive heart failure, chronic kidney insufficiency and anemia form a vicious circle in which each condition is capable of causing or being caused by another. As the prevalence of congestive heart failure is steadily rising, it must be expected that more patients will develop this syndrome. The optimal treatment for patients with the cardio-renal anemia syndrome is yet to be determined, but new trials, in which patients were treated with erythropoietin and intravenous iron, promise a better outcome for these patients in the future.

Anemia↗
PubMed1997

Hemodynamic and clinical effects of oral levodopa in children with congestive heart failure.

OBJECTIVES: This study was undertaken to evaluate the safety, efficacy and pharmacodynamic variables of oral levodopa in pediatric patients with congestive heart failure refractory to standard therapy. BACKGROUND: Therapeutic options for children with congestive cardiomyopathies are limited to digoxin, diuretic agents and angiotensin-converting enzyme inhibitors. Previous work in adults with congestive heart failure has shown a short-term effectiveness of levodopa and improvement of cardiac function. METHODS: Baseline two-dimensional and M-mode echocardiography, surface electrocardiography, Holter monitoring and exercise testing, when applicable, were performed. Levodopa was administered in a dose escalation scale from 8 mg/kg body weight per dose to 20 mg/kg per dose over 3 days with concomitant metoclopramide and pyridoxine. Catecholamine levels at initiation of the trial and throughout dose escalation were measured, with echocardiographic and electrocardiographic correlation. After 24-h drug washout, cardiac catheterization was performed both before and after administration of levodopa. RESULTS: Between February 1992 and December 1995, nine children (age 10 +/- 1.7 years, weight 27.8 +/- 4.3 kg) were enrolled in this study. At cardiac catheterization, serum dopamine levels rose from 108.5 +/- 59.2 pg/ml to 1,375.8 +/- 567.9 pg/ml (p = 0.03) at 100 +/- 14.8 min after levodopa administration without a significant change in serum norepinephrine or epinephrine levels. Paralleling these increases, there were significant changes in the cardiac index (1.7 +/- 0.3 to 3.2 +/- 0.7 liters/min per m2), stroke volume index (16.1 +/- 3.2 to 31.2 +/- 7.0 ml/m2 per min), oxygen consumption (138.6 +/- 24.4 to 188.3 +/- 30.8 ml/min per m2) and systemic vascular resistance (36.8 +/- 8 to 21.9 +/- 5.5 indexed Wood's units; all p < 0.01). There was a significant reversal of the daily fluid volume output/input ratio from 0.8 +/- 0.1 to 1.2 +/- 0.1 (p < 0.01). Levodopa administration was complicated by hypertension or tachycardia, or both, requiring a dose reduction in three patients, and by significant gastrointestinal distress in one. There was sustained symptomatic improvement a median of 19.5 months after drug initiation in seven of the patients. CONCLUSIONS: These preliminary data support the hemodynamic value of oral levodopa in the treatment of severe congestive heart failure in children.

Adolescent↗
PubMed1977

The diurnal rhythm of plasma aldosterone and plasma renin activity in patients with congestive heart failure.

Study on a diurnal rhythm of plasma aldosterone (PA) and plasma renin activity (PRA) was performed in 8 patients with congestive heart failure. All patients had been digitalized and received diuretics under mild sodium restriction. An obvious diurnal rhythm of PA similar to the normal subjects, with the lowest value in the evening and the highest value in the morning, was observed in 7 of 8 cases, while a diurnal rhythm of PRA was obscure except in one case. The PA generally did not run parallel with PRA. Although the reason of the absence of PRA diurnal rhythm in congestive heart failure was not clear, it was considered that reninangiotensin system did not play a significant role for the development of PA diurnal rhythm in congestive heart failure. The determined PA values were entirely within normal range except in 2 cases, although they were administered the potent diuretics chronically. A high PA value was observed only in early morning in one case, while all determined PA values were extremely high in another case with severe congestive heart failure involved in cardiac liver cirrhosis. The PRA values were relatively low in 2 cases, normal in 5 and high in one.

Adult↗
PubMed1983

Combined vasodilator therapy for chronic congestive heart failure.

There are few data to support the potential efficacy of combined vasodilator therapy for severe congestive heart failure. For documentation of the feasibility of such an approach, a short-term hemodynamic study utilizing captopril, an oral converting enzyme inhibitor, followed by the addition of nitroprusside infusion, was made of 11 patients with severe chronic congestive heart failure. Captopril alone resulted in reduction of mean arterial pressure (84 +/- 7 to 70 +/- 3 mm Hg), associated with increase of cardiac index and stroke index. There was also a significant reduction of systemic resistance and pulmonary wedge pressure. The initial hemodynamic response to captopril was correlated with initial plasma renin activity (all values at least p less than 0.05). The addition of nitroprusside to captopril resulted in further hemodynamic improvement. Reduction of mean arterial pressure, systemic vascular resistance, and pulmonary wedge pressure were all significant, as were increases of cardiac index and stroke index. The degree of hemodynamic improvement with this sequence of vasodilator therapy was linearly related to the reduction of mean arterial pressure. Therefore vasodilators with dissimilar mechanisms of action may have an additive effect. These data support the potential feasibility of combined, long-term oral vasodilator therapy in selected subgroups of patients with congestive heart failure.

Adult↗
PubMed2005

Distribution of pleural effusion in congestive heart failure: what is atypical?

OBJECTIVES: This study was performed to determine the distribution of pleural effusion between the right and left hemithorax in patients with uncomplicated congestive heart failure, and to determine whether left-sided pleural effusion actually constitutes an atypical distribution in congestive heart failure. METHODS: The study group consisted of 120 consecutive patients with both clinical and radiographic evidence of uncomplicated congestive heart failure, and whose chest radiographs at the time of presentation also showed evidence of pleural effusion. The presence or absence of pleural effusion in the right and left hemithorax was recorded for each case, as was the size of each pleural effusion, and the distribution of pleural effusion in these 120 patients was entered into a 2 x 2 table and analyzed by chi2 analysis. RESULTS: There were 207 total pleural effusions, with 105 on the right and 102 on the left. Isolated right-sided pleural effusions occurred in 18 patients, there were bilateral pleural effusions larger on the right than the left in 25, there were bilateral pleural effusions of roughly equal size on each side in 36, there were bilateral pleural effusions larger on the left side than the right in 26, and there were isolated left-sided pleural effusions in 15. The difference was not statistically significant (chi2 = 0.316; P < or = 1.0). CONCLUSIONS: Left-sided pleural effusion is not an atypical finding in congestive heart failure and is not, in and of itself, an indication for further clinical or imaging evaluation.

Adult↗