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

Hypertensive damage to the target organ "heart" comprises the sum and interactions of the cardiac organ manifestations of arterial hypertension such as myocardial hypertrophy and disease of large and small coronary arteries. Because the prognosis of arterial hypertension is determined to a considerable extent by these cardiac complications, the aim of treatment of hypertensive heart disease is reversal of the myocardial hypertrophy in order to prevent later progression to hypertensive heart failure. A further goal of therapy is reversal of the hypertensive small coronary disease in order to improve the coronary reserve. Once the stage of hypertensive heart failure is reached, the principles of medical management of heart failure with digitalis, diuretics and angiotensin-converting enzyme inhibitors apply. Whereas the evidence that regression of hypertrophy can be induced by suitable antihypertensive drugs (calcium channel blockers of the dihydropyridine type, angiotensin-converting enzyme inhibitors and sympathicolytic substances) is practically conclusive, clinical evidence of reversal of the hypertensive disease of small coronary arteries has yet to be provided. Moreover, to what extent the prognosis of hypertensive heart disease can be improved by reversal of hypertrophy is still unknown.
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PMID:Differential therapy of hypertensive heart disease. 213 59

Cardiac hypertrophy is characterized by marked abnormalities in the contraction/relaxation pattern of the heart. For example, delayed relaxation is a prominent feature, impairing ventricular filling and coronary flow. In intact heart preparations the relative contribution of fibrosis and of the myocardial cell itself to these abnormalities cannot be correctly assessed. Biochemical studies on the mechanisms of impaired contraction and relaxation and hypertensive heart failure are hampered by the fact that 75% of all heart cells are non-myocytes. We therefore established the model of the isolated calcium-tolerant, adult rat cardiomyocyte as a new approach to the investigation of these problems. Contractility was measured using a videomicroscope system with high time resolution (1 ms). Angiotensin II induced a marked relaxation delay in the cardiomyocyte from normotensive rats and showed a moderate positive inotropic effect, whereas isoproterenol had a strong positive inotropic effect but accelerated relaxation. Therefore, angiotensin II is capable of inducing a relaxation delay even in the absence of coronary ischaemia or hypertension. These first results show that the isolated cardiomyocyte model may be a useful approach to investigating the mechanisms of hypertensive heart disease.
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PMID:Isolated myocardial cells: a new tool for the investigation of hypertensive heart disease. 214 54

As previously reported, 1007 patients with chronic atrial fibrillation participated in the Copenhagen AFASAK study. Before inclusion to trial, they all had a physical examination, chest roentgenogram, and echocardiogram with determination of left atrial size. This study evaluated the importance of cardiovascular risk factors for development of thromboembolic complications. To exclude any treatment effects on occurrence of thromboembolic complications, we included only the 336 patients from the placebo group. Using Cox's regression model, previous myocardial infarction was a significant risk factor for development of thromboembolic complications. Age, gender, heart failure, chest pain, hypertensive heart disease, diabetes, systolic and diastolic blood pressure, smoking, relative heart volume, and left atrial size were all without statistical importance.
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PMID:Risk factors for thromboembolic complications in chronic atrial fibrillation. The Copenhagen AFASAK study. 218 33

The present multicenter open investigation was designed to provide information on the adverse reaction rate, drug interaction, and survival in a group of 544 cardiac patients treated for 1 year with ibopamine either alone or in association with digitalis, diuretics, and other drugs. Some efficacy parameters were also considered. Heart failure was due to idiopathic dilated cardiomyopathy (21%), ischemic heart disease (32%), hypertensive heart disease (31%), and others (16%). Ibopamine was given alone to 39 patients; the others were given the drug in association with digitalis, diuretics, and vasodilators. One hundred forty patients did not complete the trial (25.7%). The most common causes of discontinuation were death (12.5%), noncompliance with the protocol (5%), and adverse events (3.9%). The clinical conditions and NYHA functional class improved in most patients. The cardiothoracic ratio decreased on average. The 1-year mortality rates associated with NYHA class II, III, and IV were 4.4, 13.8, and 37.2%, respectively. Survival tended to be shorter in a small group of 22 patients with hyponatremia, thus confirming some previous reports. Adverse experiences were mainly related to cardiovascular and gastrointestinal systems; the symptoms were considered severe only in 1 of 544 patients enrolled. Ibopamine seems not to induce dangerous arrhythmias. Blood pressure and heart rate did not change over time during ibopamine treatment. Laboratory tests were not significantly affected; fluctuations observed in some tests were related to concomitant variations in the severity of the primary disease. No tolerance to ibopamine seems to be observed during this long-term therapeutic trial.
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PMID:Long-term therapy of chronic congestive heart failure with ibopamine: a multicenter trial. 248 46

Since left ventricular hypertrophy is considered to be a precursor of later hypertensive heart failure, a treatment that can prevent or even reverse myocardial hypertrophy is a highly desirable goal. In order to evaluate which type of antihypertensive treatment is able to induce regression of hypertensive hypertrophy, experimental and clinical studies were performed. Experimental studies were performed in spontaneously hypertensive rats (SHRs). Left ventricular hypertrophy and pumping function were studied after antihypertensive treatment with a beta-receptor blocker (metoprolol), an arteriolar vasodilator (hydralazine), and a calcium channel blocker (nifedipine) had been instituted for a period of 20-40 weeks. Patients with hemodynamically compensated hypertensive heart disease were treated with a calcium channel blocker (nifedipine), an angiotensin-converting enzyme (ACE) inhibitor (enalapril), an antisympathetic agent (clonidine), and prazosin. Comparing the amount of blood pressure reduction with the extent of hypertrophy reversal, nifedipine, prazosin, and enalapril were equipotent, whereas clonidine was most efficient in this respect. Muscle mass was overproportionally reduced in relation to blood pressure reduction following treatment with clonidine. It is likely that this was caused by lowered catecholamine levels secondary to clonidine therapy. Left ventricular pumping function was enhanced as a result of a reduction in left ventricular afterload, whereas myocardial contractility was found to be unchanged.
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PMID:Regression of cardiac hypertrophy: experimental and clinical results. 248 21

Hypertensive left ventricular hypertrophy is associated with a variety of complications including congestive heart failure, arrhythmias, and ischemic heart disease. Unloading the system in time by antihypertensive drug treatment should prevent or reverse left ventricular hypertrophy. Although most antihypertensive agents can control blood pressure in a majority of patients, only a select subset of these pharmacologic agents will reverse left ventricular mass. There is evidence to suggest that angiotensin-converting enzyme (ACE) inhibitors can play an important role in protecting the heart during the various phases of evolution of hypertensive heart disease both acutely and on a long-term basis. Several studies in hypertensive humans and experimental animals have documented the effectiveness of ACE inhibitors in reducing cardiac hypertrophy. In hypertensive patients with left ventricular hypertrophy, the ACE inhibitor captopril 3 and 9 months after starting treatment significantly reduced left ventricular mass as well as left ventricular posterior wall and septal wall thickness. The mechanism of regression of left ventricular mass by ACE inhibition is speculative. The absence of a reflex hyperadrenergic state in the face of blood pressure control may be of importance. In addition, interference with angiotensin II generation by these agents may also play a role either through the myocardial effects of angiotensin II on protein synthesis or because of its facilitation of cardiac sympathetic neurotransmitter release. ACE inhibition appears to be associated with the maintenance of normal coronary flow reserve and in high renin states ACE inhibition may increase coronary blood flow. ACE inhibitors are also indicated under conditions of hypertensive heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of hypertensive heart disease with ACE inhibitors. 248 24

The hypertensive damage to the target organ "heart" comprises the sum and interactions of the cardiac organ manifestations of arterial hypertension such as myocardial hypertrophy and disease of large and small coronary arteries. As the prognosis of arterial hypertension is determined, to a considerable extent, by these cardiac complications, the aim of treatment of hypertensive heart disease is reversal of the myocardial hypertrophy in order to prevent later progression to hypertensive failure. A further goal of therapy is reversal of hypertensive small coronary disease in order to improve the coronary reserve. While the evidence that regression of hypertrophy can be induced by suitable antihypertensive drugs (calcium channel blockers of the dihydropyridine type, ACE inhibitors, and sympathicolytic substances) is practically conclusive, clinical evidence of reversal of hypertensive small coronary disease has yet to be provided. Moreover, we do not know at present to what extent the prognosis of hypertensive heart disease can be improved by reversal of hypertrophy. Once the stage of hypertensive heart failure is reached, the principles of medical management of heart failure with digitalis, diuretics, and ACE inhibitors apply.
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PMID:[Treatment of myocardial and coronary effects of arterial hypertension]. 253 67

Relaxation delay is an important feature of hypertensive heart disease which impairs diastolic coronary flow and ventricular filling and therefore contributes to heart failure. We investigated the hypothesis that impaired relaxation is a property of the myocardium, rather than the consequence of ischaemia or interstitial fibrosis. A new videomicroscope system was used to define the contraction-relaxation cycle of isolated cardiac myocytes from spontaneously hypertensive rats (SHR) and normotensive control (Wistar-Kyoto, WKY) rats. The SHR cells showed a marked relaxation delay. Angiotensin II (Ang II) increased the contraction maximum by about 35% in WKY rats and induced a relaxation delay. In SHR Ang II greatly potentiated this relaxation delay. Our results demonstrate that impairment of relaxation is a property of the single cardiomyocyte. Angiotensin II induces a relaxation delay that is independent of blood pressure. The combination of hypertrophy and high levels of Ang II potentiates relaxation impairment and may therefore contribute to hypertensive left ventricular failure.
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PMID:Impaired relaxation of the hypertrophied myocardium is potentiated by angiotensin II. 253

Clinical and hemodynamic studies were carried out for the purpose of evaluating the effects of enalapril in the treatment of chronic heart failure. Enalapril 10-20 mg was given once to 10 patients with moderate to severe congestive heart failure (coronary 6, hypertensive heart disease 2 and idiopathic congestive cardiomyopathy). Hemodynamic studies were done on the first day after drug administration and the same dose was maintained for 2 weeks. The results showed a decrease of mean BP of 18.29% (P less than 0.01), CVP 40.4% mPAP 23.9%, PCWP 41.2%, SVR 39.9% and PVR 41.3% respectively (P less than 0.001). Cardiac index increased 44.16% (P less than 0.001). The therapeutic action lasted more than 24 hours after a single dose. No further drop of BP was found weeks later, 6 patients in NYHA class III and 2 in class IV improved to class II. No severe side effects were found. The results showed that enalapril is well tolerated after a single dose and its therapeutic action lasts 2 weeks with improvement both in hemodynamics and subjective symptoms.
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PMID:[Hemodynamic study of a single oral dose of enalapril in patients with heart failure]. 256 Jul 2

Seventy-seven patients with drug-refractory sustained ventricular tachycardia (VT) (28 patients) or ventricular fibrillation (VF) (49 patients) underwent implantation of an automatic cardioverter defibrillator (AICD). The 67 men and 10 women, with a mean age of 60 +/- 12 years (range 18 to 79), had coronary artery disease (60 patients), idiopathic cardiomyopathy (eight patients), mitral valve prolapse (four patients), hypertensive heart disease (one patient), Ebstein's anomaly (one patient), long QT syndrome (one patient), and primary electrical disease (two patients). The mean left ventricular ejection fraction was 35 +/- 16% (range 10% to 75%). Sustained VT/VF was induced in 64 patients (83%) at baseline electrophysiologic testing. A mean of 4.1 +/- 1.3 antiarrhythmic drugs failed to control the arrhythmia. Associated surgery at AICD implantation included coronary artery bypass in 19 patients, coronary bypass with aneurysmectomy in six patients, and aneurysmectomy alone in one patient. Five patients had only prophylactic patches implanted during aneurysmectomy or coronary bypass and the AICD device was subsequently implanted under local anesthesia to prevent arrhythmia recurrence or to control persistently inducible VT. Operative mortality was 2.6% with two deaths from intractable VF. Fifty-two patients (69%) continued receiving antiarrhythmic drugs to suppress spontaneous VT. During a mean follow-up of 15 +/- 13 months (range 1 to 63), six patients died: two suddenly due to probable pulse generator failure (greater than 2 years old), one of acute myocardial infarction, two of heart failure, and one of respiratory failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical experience in seventy-seven patients with the automatic implantable cardioverter defibrillator. 277 68


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