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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The treatment of 34 patients with secondary aldosteronism with a new oral and parenteral preparation (Osyrol) is reported. On the strength of the clinical results with remissions of signs of heart failure and increase in the volume of urine, reduction of body weight and raising of serum potassium, the efficacy of the preparation with good general and local tolerance is described.
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PMID:[Clinical experience in the use of Osyrol 100 and Osyrol for injection (author's transl)]. 81 Jun 73

Angiotensin-converting enzyme (ACE) inhibitors act by lowering the level of angiotensin II. The therapeutic benefits of these drugs and their potential side-effects therefore result from suppression of the physiological effects of angiotensin II. It is rational to prescribe an ACE inhibitor when the renin-angiotensin system is activated, as in renin-dependent essential hypertension, malignant hypertension and hypertension associated with heart failure. The beneficial effects of ACE inhibitor must be weighed against the special risks of renovascular hypertension: risk of renal artery thrombosis in case of unilateral stenosis and risk of renal failure if the stenosis is bilateral or affects a solitary kidney. In some situations the renin-angiotensin system is not directly involved in hypertension but may play a local haemodynamic role, as in some cases of primary or diabetic nephropathy. In such case the ACE inhibitors are thought to exert a protective effect. ACE inhibitors were reputed to be less effective in the elderly than in younger patients, but we now know that they can be prescribed with equal success in both instances to reduce peripheral resistance and improve regional blood flow as well as arterial compliance. Finally, ACE inhibitors can be prescribed, albeit with limited effectiveness, when the renin-angiotensin system is not activated, as in low renin hypertension and idiopathic hyperaldosteronism due to adrenal hyperplasia. They are ineffective in case of Conn's adenoma and contra-indicated in pregnant women.
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PMID:[For which hypertensive patient should angiotensin-converting enzyme inhibitor be prescribed or forbidden?]. 129 38

Left ventricular hypertrophy is a major risk factor associated with the appearance of adverse cardiovascular events. A distortion in myocardial structure, mediated by an abnormal accumulation of fibrillar collagen within the adventitia of intramyocardial coronary arteries and neighbouring interstitial spaces, alters the electrical and mechanical behaviour of the myocardium. The mechanisms responsible for the regulation of cardiac myocyte growth and collagen accumulation are therefore of considerable interest. Herein we review results of in vivo studies conducted in the authors' laboratory that addressed these issues in various experimental models. The findings indicate that in arterial hypertension myocardial hypertrophy is related to ventricular systolic pressure work. Myocardial fibrosis, on the other hand, is not related to haemodynamic workload, but rather the presence of mineralocorticoid excess relative to sodium intake and excretion. Accordingly, fibrosis can appear in both the hypertensive left and non-hypertensive right ventricles. Pharmacological probes, administered in variable doses, were used to further test and support this hypothesis. In both primary and secondary hyperaldosteronism, it was possible to prevent the pathological structural remodelling of the myocardium with an aldosterone receptor antagonist, while in unilateral renal ischaemia ACE inhibition was similarly cardioprotective. Other studies demonstrated that it was feasible to regress the fibrous tissue response and normalise diastolic stiffness. This concept of cardioreparation suggests that heart failure due to this type of structural remodelling may be reversible.
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PMID:Regulatory mechanisms of myocardial hypertrophy and fibrosis: results of in vivo studies. 130 Dec 54

The major risk factor associated with the appearance of adverse cardiovascular events and outcome attributable to cardiovascular disease is left ventricular hypertrophy (LVH). Why this should be so resides not in the increase in myocardial mass per se, but in the disruption of myocardial structure. An abnormal accumulation of fibrillar collagen within the adventitia of intramyocardial coronary arteries and neighboring interstitial spaces represents such a distortion in structure. Furthermore, this fibrosis disrupts the electrical and mechanical behavior of the hypertrophied myocardium. Mechanisms responsible for fibrillar collagen accumulation have been examined in intact animals and cultured cardiac fibroblasts. In vivo studies indicate that myocardial fibrosis is associated with the presence of chronic mineralocorticoid excess, relative to sodium intake and excretion, not hemodynamic workload. Accordingly, fibrosis can appear in both the hypertensive, hypertrophied and nonhypertensive, nonhypertrophied ventricles. In both primary and secondary hyperaldosteronism it was possible to prevent myocardial fibrosis with an aldosterone receptor antagonist, while in unilateral renal ischemia angiotensin converting enzyme (ACE) inhibition was similarly cardioprotective. A regression in fibrous tissue and normalization of diastolic stiffness has also been possible using ACE inhibition, bringing forward the concept of cardioreparation and the notion that heart failure due to fibrosis may be reversible. In vitro studies indicate that effector hormones of the renin-angiotensin-aldosterone system stimulate fibroblast collagen synthesis. Aldosterone, in pathophysiologic concentrations, and angiotensin II, in much larger concentrations, each enhance collagen synthesis without altering the mitogenic potential of these cells. Thus, elevations in circulating aldosterone and angiotensin II, relative to sodium intake, have the potential to not only alter sodium homeostasis and vascular tonicity, but also the structure of cardiovascular tissue. Thus, myocardial fibrosis represents a structural basis for pathologic hypertrophy and ultimately accounts for the appearance of adverse cardiovascular events and outcomes.
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PMID:Pathologic hypertrophy with fibrosis: the structural basis for myocardial failure. 136 63

In the present study: (a) physiopathology, (b) clinics, and (c) therapy of cardiothyreosis are discussed. (a) The hyperkinetic syndrome, the earliest clinical sign in thyrotoxicosis (vasodilatation, increase in inotropism, automatism, etc.), is mediated by a two-fold increase in the number of beta-receptors, and supported by an adequate synthesis of ATP and creatinphosphate (CP) in the young and, to a lesser extent, in the elderly. Genetical heart reserves are mobilized, thus significantly increasing the number and the size of mitochondria and also the enzymatic equipment (such as: the alpha-glycerophosphate-dehydrogenase, malic, pentosic cycles, etc.), a.s.o. Due to an excessive adrenergic action (glycogenolysis, an excessive oxygen consumption, up to necrosis, the ATP and CP syntheses dramatically drop; the phosphorus/oxygen ratio decreases to 2 (normal = 4). In this condition, the high functional cardiovascular performances are also impaired (the submaximal effort capacity is attained at a smaller and smaller oxygen consumption; Propranolol 2 mg i.v. decreased the cardiac output by above 30% (vs 10%--normal); electrocardiogram presents aspects of "coronary disease", tachycardia, etc.). An ultrastructural damage occurs: from "mitochondrial disease", partial lysis of myofibrils, to myofibrosis (revealed postmortem), in spite of a reduced degree of coronary atherosclerosis. Ultrastructural and biochemical experimental data support this point of view. (b) The incidence, precocity and severity of the thyrotoxic heart increase with age and the existence of a previous cardiovascular pathology. Cardiothyreosis is not present under 27 years; in 4,353 patients its incidence is of 25% (arrhythmia--21%, heart failure--12%, coronary insufficiency--1-3%). Of a major interest are tachyarrhythmias which may lead to a high mortality by hypodiastolic congestive heart failure, heart failure with secondary hyperaldosteronism, thromboembolic episodes and ventricular fibrillation. Thyrotoxicosis favours the disease of papillary muscles--mitral prolapse and insufficiency, reversible especially in children. (c) The treatment of thyrotoxic heart is an etiologic one (medical, surgical, radioactive--the last two being preferable after the adequate medical therapy). In particular, cardiothyreosis requires a reinforced irradiation (10,000 rads instead of 7,000 rads) in smaller 131I doses. The protection against the increased nocivity of catechols in thyrotoxicosis is very important (which explains the high mortality in the thyrotoxic "storm") and requires propranolol; doses above 2 mg/kilo body/day are recommended. In the elderly, the sensitivity to propranolol decreases: verapamil i.v. is more efficient in paroxysmal tachyarrhythmias (flutter, atrial fibrillation) and in those occurring intra-operatively during halothane narcosis. The anticoagulant therapy is administered in tachyarrhythmias with high ventricular rate, especially in the elderly, to avoid the embolic risk, higher in defibrillation condition.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiothyreosis. 182 Oct 70

A prospective, randomized efficacy study of low-dose enalapril was undertaken in 38 outpatients (24 men, 14 women; mean age 58 [41-69] years) with chronic heart failure (NYHA functional class III-IV). All patients were pretreated with digitalis and diuretics, some also with conventional vasodilators. 19 patients (group E) received in addition to their previous medication, 5 mg enalapril daily, while the other 19 (group K) continued with their previous therapy. Three months later, 15 patients in group E improved by at least one NYHA functional class and none died (P less than 0.02). Four patients in group K died and only one patient improved by one class. After three months, left ventricular ejection fraction was significantly higher (P less than 0.0001) in group E (39 +/- 19%) compared to group K (30 +/- 14%). In group E, plasma aldosterone concentration decreased significantly (P less than 0.0001) by 33.4 +/- 6.5 ng/dl, while in group K no significant change occurred (delta 1.1 +/- 1.2 ng/dl). Thus, low-dose enalapril in addition to conventional therapy may improve the clinical status of patients in severe chronic heart failure. This improvement is associated with an increase in left ventricular ejection fraction and reduction in secondary hyperaldosteronism.
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PMID:[Low-dose enalapril as additional medication in severe chronic heart failure]. 240 84

In a 3-month prospective, single-blind, controlled trial, 38 patients in New York Heart Association functional class III-IV were assigned to group E (n = 19): enalapril 5 mg/day in addition to the previous therapy with digitalis and diuretics, or group C (n = 19): continuation of the previous therapy. In group E, 79% of the patients improved by at least one NYHA functional class after 3 months. In group C, the functional class did not change and four patients died. The echocardiographically determined end-diastolic diameter of the left ventricle decreased in group E from 72 +/- 8 mm to 63 +/- 6 mm (p less than 0.001), and the scintigraphically determined ejection fraction of the left ventricle increased from 33 +/- 18% to 40 +/- 19% (p less than 0.002). In contrast, no significant change was found in group C. Plasma-renin activity increased in group E from 8.2 +/- 1.8 ng/ml h to 29.7 +/- 14 ng/ml h (p less than 0.001), and plasma aldosterone decreased from 47.7 +/- 7.6 ng/dl to 19.9 +/- 4.8 ng/dl (p less than 0.01). In group C no significant change occurred. Comparing the actual changes (deltas) of the NYHA functional class (p less than 0.02), end-diastolic diameter and ejection fraction of the left ventricle, plasma-renin activity, and plasma aldosterone (p less than 0.0001), a significant difference between the two groups was found. Thus, low-dose enalapril resulted in a significant improvement of the NYHA functional class in patients with severe chronic heart failure, accompanied by an improvement in left ventricular function and a decrease in secondary aldosteronism.
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PMID:Low-dose enalapril in severe chronic heart failure. 256 37

Isolated ultrafiltration was performed in 107 patients with refractory heart failure (HF) which developed in the presence of different cardiovascular diseases. The beneficial action of isolated ultrafiltration in 71 patients (68%) with refractory HF was determined by complex interaction of the effects provoked by ultrafiltrate removal. Among those effects of paramount importance was correction of secondary hyperaldosteronism and reduction of the concentration of antidiuretic hormone accompanied by the improvement of liver and heart functions.
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PMID:[Isolated ultrafiltration of the blood in patients with refractory heart failure: the status of the renin-angiotensin-aldosterone system and the secretion of antidiuretic hormone]. 258 72

The positive action exerted by isolated ultrafiltration on 69 patients with refractory heart failure was shown to be due to the complex interaction of effects produced by ultrafiltrate removal. Among the effects, a leading role is played by therapy for hyperaldosteronism and reduction of antidiuretic hormone levels along with improvement of the functional status of the liver and heart.
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PMID:[Effect of isolated ultrafiltration on plasma hormone levels in patients with heart failure resistant to drug therapy]. 268 56

Application of isolated ultrafiltration (IUF) of blood in 70 out of 100 patients with refractory heart failure (HF) made it possible, acting on some mechanisms of water excretion disorders, to attain the compensation for the HF signs. At the same time the correction of the manifestations of secondary hyperaldosteronism, hypoproteinemia, hyperbilirubinemia, and azotemia was attained only thanks to the presence of the functional reserves of the liver and kidneys. In 35 patients with cachectic HF, IUF failure was determined by marked cardial liver cirrhosis together with depletion of the functional reserves of the cardiovascular system. The lack of sufficient diuresis, hyponatremia, hypoproteinemia, and hyperbilirubinemia may be unfavourable prognostic signs despite the reduction of HF intensity consequent on IUF.
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PMID:[The efficacy of isolated ultrafiltration of the blood in patients with refractory heart failure]. 276 1


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