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At least 19 recordsLinked to original sources
PubMed1989

Is the adaptation of right ventricular refractoriness to an abrupt increase in heart rate impaired in chronic heart failure?

Chronic heart failure is associated with a high risk of ventricular arrhythmias and sudden death, although the mechanisms leading to these arrhythmias are not fully understood. To determine if the adaptation of ventricular refractoriness to an abrupt increase in heart rate is impaired in heart failure, electrophysiologic findings in 11 patients with structurally normal hearts (group I) were compared to findings in 28 patients with chronic heart failure (mean left ventricular ejection fraction 0.23 +/- 0.05). Heart failure was due to coronary artery disease in 14 patients (group II) and to idiopathic dilated cardiomyopathy in 14 patients (group III). The effective refractory period at the right ventricular apex was measured during unipolar cathodal pacing at twice diastolic threshold following a 12-beat ventricular drive at a cycle length of 600 msec. The pacing cycle length was then decreased to 400 msec for one, two, and three beats and the refractory period was determined for each beat at the faster rate. For each beat the mean refractory periods of group II and III patients were similar and were significantly longer than those of group I patients (p less than 0.01). The refractory period progressively shortened at the 400 msec cycle length and the percent decrease for each beat was similar among all three groups (p greater than 0.10). In the group II and III patients there was no correlation of the refractory period or change in refractory period with the pulmonary artery, right atrial, and pulmonary capillary wedge pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Drug therapy of chronic heart failure.

Chronic heart failure is an irremediable terminal syndrome. The inability of the heart to pump sufficient blood to meet the demands of metabolically active tissues is aggravated by reflex increases in peripheral vasoconstriction induced by the sympathoadrenal and renin-angiotensin-aldosterone systems. Vasoconstriction is partially attenuated by atrial natriuretic hormone, prostaglandin, and bradykinin. The aim of therapy is to improve the pumping performance of the heart and reduce arterial and venous constriction in the hope that this will reduce symptoms and improve the quality of life. Many drugs achieve such benefits, at least initially. Inotropic drugs increase cardiac pumping activity, and drugs acting directly on arteries and veins improve cardiac function by reducing afterload and preload. ACE inhibitors suppress angiotensin II formation, reducing its vasoconstrictive action, its ability to increase aldosterone secretion and the consequent salt retention and expansion of plasma volume. Since the proportionate role played by various hemodynamic factors in individual patients is unknown, it is likely that most benefit will be achieved by a combined therapeutic approach.

Chronic Disease↗
PubMed1978

Metabolism of procainamide in patients with chronic heart failure, chronic respiratory failure and chronic renal failure.

Fractional hydrolysis and acetylation of procainamide, acetylation of procainamide-derived p-aminobenzoic acid and plasma hydrolysis of procaine were studied in 20 patients with chronic heart failure (CHF), 20 patients with chronic respiratory insufficiency (CRI) and 20 patients with chronic renal failure (RF). The results were compared with those obtained in a group of 20 normal volunteers. Hydrolysis of procainamide and procaine were reduced in patients with CHF and CRI, but not in patients with RF. Moreover, more marked decreases in procainamide and procaine hydrolysis were seen in subgroups with secondary hepatic dysfunction. The diminution of hydrolysis of procainamide was not paralleled by changes in acetylation of procainamide or p-aminobenzoic acid. It is concluded that in patients with hepatic involvement secondary to advanced CHF or CRI, hepatic and plasmatic hydrolysis activity is decreased to a degree equivalent to primary liver failure.

Acetylation↗
PubMed1992

The ventilatory cost of exercise compared in chronic heart failure and chronic renal anaemia.

The cardiorespiratory responses to maximal treadmill exercise were compared in matched groups of patients with chronic renal anaemia or treated chronic heart failure, and in normal controls. Exercise capacity was similarly reduced in both patient groups compared to normal controls, the raised respiratory exchange ratio at peak exercise implying anaerobic metabolism due to limited oxygen delivery in heart failure and limited oxygen carrying capacity in anaemia. Minute ventilation (VE) was related linearly to minute CO2 production (VCO2) in all subjects (each r > 0.92) from all three groups. The slope of the VE/VCO2 relationship was normal in anaemia but steeper in heart failure, reflecting ventilation/perfusion mismatching in chronic heart failure.

Adolescent↗
PubMed1990

Increased cardiac angiotensin-converting enzyme in rats with chronic heart failure.

1. Chronic heart failure was induced in rats by ligation of the left coronary artery to produce a left ventricular myocardial infarct. 2. Cardiac angiotensin-converting enzyme (ACE) was estimated by radioligand binding in myocardial homogenates and by autoradiography studies of radioligand binding to ACE in heart sections. 3. Radioligand binding studies demonstrated an increase in binding sites in animals with myocardial infarction, compared with sham operated animals. Mean increases were 457% in right atrium, 295% in left atrium, 326% in right ventricle, 187% in left ventricle and 530% in the region of the left ventricular infarct, compared with the sham left ventricle. 4. Autoradiography studies confirmed tissue homogenate binding studies, demonstrating (i) a marked increase in ligand binding in the infarct area and (ii) an increase in binding density in the hypertrophied myocardium of right and left atrium, and right and left ventricle. 5. The induction of cardiac ACE in the myocardium of rats with chronic heart failure may participate in the pathophysiology of cardiac hypertrophy.

Animals↗
PubMed1992

[Clinical aspects of differential drug therapy of chronic heart failure].

Treatment of chronic heart failure with ACE-inhibitors has greatly improved the prognosis. In addition to ACE-inhibitors, diuretics seem to be necessary to decrease mortality, whereas the importance of cardiac glycosides has not been demonstrated unequivocally. Nevertheless, modern treatment of chronic heart failure in all stages should be a combination of diuretics, digitalis, and ACE-inhibitors rather than a stepwise addition of drugs depending on the severity of the disease. An increased heart rate leads to increased myocardial O2-consumption, decreased O2-supply, ischemia, and reduced contractility. Betablocker-induced reduction of heart rate does, however, not necessarily improve symptoms or hemodynamic conditions. The optimal heart rate in large failing hearts is not known yet. Probably, it is dependent on the type and severity of myocardial disease or impairment. In this respect, the sarcoplasmatic release and uptake of Ca2+ plays the most important role in the disordered force-frequency-relation in chronic heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

[Abnormalities of the peripheral circulation and tolerance to exertion of patients with heart failure].

Chronic heart failure is attended by a number of abnormalities of peripheral circulation. To a great extent, these abnormalities determine the patients' functional symptoms, their tolerance to exercise and their response to treatment, at least in the short term. The response to exercise of heart failure patients depends on their maximal oxygen consumption which is determined by their maximal cardiac output and by various peripheral adjustments, such as distribution of regional blood flow and peripheral oxygen extraction. Abnormalities of peripheral arteriolar and capillary dilatation are determined by hyperstimulation of neurohormonal systems. An increase in maximal muscular blood flow, which determines the patients' capacity of exercise, can be obtained with drugs which increase the muscular perfusion pressure (inotropic drugs) or which decrease muscular resistances without lowering the perfusion pressure (venous or balanced vasodilators, diuretics). Physical rehabilitation may improve maximal oxygen consumption by improving the peripheral use of oxygen. Thus, a better understanding of the physiopathology of heart failure will in the future improve the functional symptoms of these patients and prolong their survival, which has not always been the case with conventional therapies.

Heart Failure↗
PubMed1992

Furosemide-induced natriuresis is augmented by ultra-low-dose captopril but not by standard doses of captopril in chronic heart failure.

BACKGROUND: Ten chronic heart failure patients were studied on three occasions in randomized double-blind fashion to compare the acute hemodynamic, neurohormonal, and renal sodium-handling responses to 1 mg captopril versus 25 mg captopril, both in the absence of loop diuretic therapy and during furosemide-stimulated natriuresis. METHODS AND RESULTS: Compared with placebo, 1 mg captopril caused nonsignificant decreases in mean arterial pressure and circulating angiotensin II level and had no effect on glomerular filtration rate as determined by 51Cr-EDTA elimination. Captopril (25 mg) produced marked suppression of serum angiotensin II with or without oral furosemide (both p less than 0.002), a marked decrease in mean arterial pressure (p less than 0.001) that was accentuated by furosemide (p less than 0.00001), and a decrease in glomerular filtration rate (p = 0.0007). No difference from placebo in renal sodium excretion was noted with either 1 or 25 mg captopril in the absence of furosemide. In contrast, while 25 mg captopril caused slight attenuation of the natriuretic response to furosemide, 1 mg captopril significantly enhanced furosemide-induced natriuresis (p less than 0.05). No correlation was found in our patients between the natriuretic effect of furosemide and either absolute mean arterial pressure or change in mean arterial pressure during the furosemide phase of each study session. This suggests that blood pressure is not the important factor mediating the divergent renal responses to furosemide of the two captopril dosage regimens. CONCLUSIONS: We propose that in the face of furosemide-induced postglomerular vasodilatation in chronic heart failure, captopril at a starting dose of 1 mg (but not 25 mg) preserves enough circulating angiotensin II to maintain efferent arteriolar tone and thus glomerular filtration, while offsetting the antinatriuretic renal tubular effects of angiotensin II.

Aged↗
PubMed1991

[Neuroendocrine adaptations in chronic congestive heart failure].

Chronic congestive heart failure is typically accompanied by an abnormal production of vasoconstrictor antinatriuretic hormones and vasodilator natriuretic hormones. Decompensation occurs when the former prevail over the latter. These neuroendocrine abnormalities are increasingly taken into account to determine the prognosis and to decide on the best therapeutic approach in individual patients with chronic heart failure.

Adaptation, Physiological↗
PubMed1977

The mechanism of adaptation of left atrial stretch receptors in dogs with chronic congestive heart failure.

Chronic congestive heart failure (CHF) was induced in dogs by the construction of an aorto-caval fistula below the level of the renal arteries. Aorto-caval fistula dogs showed signs of CHF which included ascites, hind limb edema, and pulmonary congestion. Ventricular catheterization indicated a significantly higher left ventricular end diastolic pressure and lower maximum velocity of left ventricular pressure development/left ventricular end diastolic pressure in CHF dogs when compared to sham-operated controls. Heart weight/body weight ratios were significantly higher in CHF dogs. Electrophysiological recordings from medullated left atrial type B receptors from the cervical vagus indicated a depressed sensitivity of these receptors in CHF dogs when compared to sham-operated control dogs. For any given change in left atrial pressure, the discharge of left atrial receptors was significantly reduced in CHF dogs compared with sham-operated controls. The mechanism for this depressed sensitivity was investigated. Sonomicrometry of the left atrial appendage indicated a decreased compliance of the left atrial appendage in the dogs with chronic CHF. In addition, microscope examination of the complex unencapsulated receptor endings taken from the left atrial endocardium indicated a marked alteration in receptor morphology. A loss of the end arborization was the most typical finding. It is concluded that chronic CHF brought about by an aorto-caval fistula results in a depressed left atrial stretch receptor response and that both decreased left atrial compliance and structural alterations in the receptor endings may account for this depressed sensitivity.

Animals↗
PubMed1990

[Beta adrenergic receptors in circulating lymphocytes of patients with chronic heart failure].

Severe decompensated chronic heart failure is associated to increased levels of circulating catecholamines and decreased density of myocardial beta-adrenergic receptors. In 14 patients with stable, class II-III heart failure we studied circulating lymphocytes to determine the number of beta adrenergic receptors, the dissociation constant of 3H dihydroalprenolol (kd) and the intracellular content of cyclic AMP (AMPc). Results (mean +/- SEM) were compared to those obtained in 10 healthy controls. The number of beta receptors was significantly decreased (105 +/- 16 vs 185 +/- 24, fmol/mg of membrane protein, p less than 0.01). No differences were found in Kd (1.65 +/- 0.2 vs. 1.36 +/- 0.28 nm) nor the level of AMPc (7.9 +/- 2.1 vs 7.1 +/- 2.9 pmol/mg protein), respectively. The decreased number of beta adrenergic receptors in the circulating lymphocytes may be related to the increased level of circulating catecholamines that have been shown to be present during exercise in these patients.

Adult↗
PubMed1992

Myocardial beta adrenoceptor and voltage sensitive calcium channel changes in a canine model of chronic heart failure.

Effects of chronic heart failure upon receptor binding and cardiac function were studied in mongrel dogs. Heart failure was induced by three to seven, graded, sequential, intracoronary microembolizations performed 1 to 3 weeks apart. Depressed systolic and diastolic left ventricular function, reduced cardiac output, increased systemic vascular resistance, increased plasma norepinephrine concentration, left ventricular hypertrophy, and dilation were associated with the development of heart failure in this model. Three months after the last embolization, the density and affinity of myocardial beta adrenoceptors and voltage sensitive calcium channels were quantified by analyzing saturation isotherms of specific radioligand binding. [3H]Dihydroalprenolol and [3H]nitrendipine bound specifically and with high affinity to cardiac beta adrenoceptors and calcium channels, respectively. Scatchard transformation of the specific binding of these radioligands in membranes prepared following intracoronary embolization demonstrated a 47% decrease in the density of [3H]dihydroalprenolol binding sites (605 +/- 20 fmol/mg, normal, vs. 323 +/- 18 fmol/mg, failed; P < 0.05) and a 20% decrease in [3H]nitredipine binding sites (371 +/- 11 fmol/mg, normal, vs. 298 +/- 17 fmol/mg, failed; P < 0.05). The binding equilibrium dissociation constants for [3H]dihydroalprenolol and [3H]nitrendipine were not significantly different between normal and failed myocardium. There was no difference in the sialic acid content in the sarcolemmal membranes prepared from normal and failed dog hearts (31.07 +/- 0.76 nmol/mg, normal, vs. 30.58 +/- 5.25 nmol/mg, failed). This is inconsistent with the selective purification of membranes utilized in these radioligand binding studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Effects of physical training in chronic heart failure.

Eleven patients with chronic heart failure secondary to ischaemic heart disease (mean [SEM] age 63.0 [2.3] years; left ventricular ejection fraction 19 [8]% undertook 8 weeks of home-based bicycle exercise training and 8 weeks of activity restriction (rest) in a physician-blind, random-order, crossover trial. Training increased exercise duration from 14.2 (1.1) min to 16.8 (1.3) min and peak oxygen consumption from 14.3 (1.1) ml.min-1.kg-1 to 16.7 (1.3) ml.min-1.kg-1. Heart rates at submaximum workloads and rate-pressure products were significantly reduced by training, and there was also a significant improvement in patient-rated symptom scores. No adverse events occurred during the training phase. Thus home-based physical training programmes are feasible even in severe chronic heart failure and have a beneficial effect on exercise tolerance, peak oxygen consumption, and symptoms. The commonly held belief that rest is the mainstay of treatment of chronic heart failure should no longer be accepted.

Aged↗
PubMed1979

Paradox of improved exercise but not resting hemodynamics with short-term prazosin in chronic heart failure.

In patients with chronic heart failure exercise allows the simultaneous observation of the cardiovascular pathophysiology and the symptoms of these patients. We administered short-term, oral prazosin to 10 patients with severe chronic heart failure. Prazosin increased cardiac output and stroke volume significantly during exercise (both P less than 0.05) but not at rest (both P greater than 0.10). Prazosin decreased the arteriovenous oxygen difference and left ventricular filling pressure significantly during exercise (both P less than 0.05) but not at rest (both P greater than 0.10). There was no significant correlation between prazosin-induced changes at rest and during exercise in cardiac output (r = 0.12), stroke volume (r = 0.02), arteriovenous oxygen difference (r = 0.33) or left ventricular filling pressure (r = 0.43). Prazosin predominantly affects hemodynamics during exercise because its pharmacologic activity as an alpha-adrenergic blocking agent is most prominent during exercise. The full evaluation of prazosin-induced changes in the hemodynamics of patients of patients with chronic heart failure requires evaluation during exercise.

Aged↗