Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Fifty patients with symptoms due to chronic heart failure despite diuretic therapy were randomised to receive additional treatment with either hydralazine or captopril. The dose was titrated; 24 received hydralazine and 26 captopril up to a maximum daily dosage of 225 mg and 75 mg respectively. Forty-three patients had coronary heart disease and seven dilated cardiomyopathy. 2. Dyspnoea and tiredness were assessed using a visual analogue scale (0-100) before and during 12 weeks' treatment. Captopril produced a significantly greater reduction in breathlessness (F = 31.6, P less than 0.001) and tiredness (F = 65.8, P less than 0.001) compared with hydralazine. 3. There was an increase in treadmill exercise time during treatment with both hydralazine (from 5.5 (3.47-7.53) min to 6.9 (4.87-8.93) min), and captopril (from 5.0 (3.05-6.95) min to 7.8 (5.85-9.75) min), but the degree of improvement was significantly greater in the patients treated with captopril (F = 7.4, P less than 0.001). 4. There was no significant change in right ventricular ejection fraction (from 27.9 (19.3-36.5)% to 28.7 (20.1-37.3)%) or left ventricular ejection fraction (from 22.2 (14.2-30.2)% to 23.9 (15.9-31.9)%) during treatment with hydralazine. However, both right and left ventricular ejection fraction increased significantly during treatment with captopril (from 27.1 (18.9-35.3)% to 32.0 (23.8-40.2)%, P less than 0.05; and from 25.0 (17.2-32.8)% to 29.6 (21.8-37.4)%, P less than 0.05 respectively). 5. These results suggest that in patients with symptoms due to chronic heart failure despite diuretic therapy, treatment with captopril produces a greater symptomatic and haemodynamic improvement than treatment with hydralazine.
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PMID:Which vasodilator drug in patients with chronic heart failure? A randomised comparison of captopril and hydralazine. 201 67

Between 50 and 70% of patients with heart failure die suddenly and unexpectedly before they have deteriorated to New York Heart Association class IV symptoms. It has long been known that ventricular ectopy predicts sudden cardiac death in coronary heart disease, and this has also been shown in dilated cardiomyopathy. It is less certain whether antiarrhythmic drugs reduce this risk and improve prognosis. Supraventricular arrhythmias frequently develop in heart failure of all causes. They nearly always cause symptoms, and the establishment of atrial fibrillation may mark a permanent deterioration. Except for sustained ventricular tachycardia, ventricular arrhythmias are often occult. Hypokalemia and digitalis toxicity may have been precipitated by diuretics or interaction with antiarrhythmic drugs. In coronary heart failure, arrhythmias may be related to scar tissue or ischemia, which may also be responsible in dilated cardiomyopathy. Use of inotropes and inodilators may precipitate arrhythmias, whereas drugs that conserve energy or potassium, such as beta blockers and angiotensin-converting enzyme inhibitors, may prevent them. Since suppression of ventricular arrhythmias has not been shown to prevent sudden death or prolong life in patients with heart failure, it may be that such arrhythmias do not directly presage ventricular fibrillation except in so far as they are markers of a poor prognosis with a risk of sudden death. If so, such arrhythmias are most likely to be suppressed by agents that result in improvement of left ventricular function and, through that, prolongation of life.
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PMID:Genesis of arrhythmias in the failing heart and therapeutic implications. 202 Nov 15

The death diagnosis of myocardial infarction (including acute heart failure) was recorded and verified on the basis of standard criteria during a 5-year implementation of the Program on Multifactorial Prevention of Coronary Heart Disease among males aged 40-59 years. The analysis demonstrated that the hyperdiagnosis of acute heart failure as a death cause was observed in 29.0% of cases, death being due to acute alcohol intoxication in 43% of all the inconsistent diagnoses.
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PMID:[Diagnosis of myocardial infarct with fatal outcome within the framework of multifactorial prevention of ischemic heart disease in Moscow]. 204 Dec 95

Diabetic patients may have various abnormalities in left ventricular systolic and diastolic function not attributable to coronary heart disease, hypertension or other known cardiac disease. Although the exact causes of this diabetic heart muscle disease or "diabetic cardiomyopathy" are still incompletely understood, several mechanisms may contribute to it including disturbed myocardial energy metabolism, microvascular changes, structural changes in collagen, increased myocardial fibrosis, and cardiac autonomic neuropathy. Perhaps the most typical feature of diabetic heart muscle disease is an abnormal filling pattern of the left ventricle, suggesting reduced compliance or prolonged relaxation. Left ventricular systolic function is commonly normal at rest in asymptomatic diabetic patients, but it frequently becomes abnormal during exercise. The abnormalities in left ventricular systolic function may be partly reversible along with an improvement of metabolic control of diabetes. It is not known how frequently subclinical abnormalities in left ventricular function in diabetic patients result in clinically manifest heart failure.
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PMID:Diabetic heart muscle disease. 207 69

The authors have much experience in diagnosing and managing ventricular arrhythmias in patients with coronary heart disease. In most cases, the arrhythmogenic areas are present in the subendocardium and surgeries aimed at improving myocardial revascularization prove to be frequently ineffective in managing arrhythmias. Subendocardial resection proposed by the authors was used in 284 patients. Mortality rates were in 15%, the deaths were mainly due to phenomena of heart failure. Positive results were achieved in 160 (67%) patients. To evaluate the efficacy of the surgical management, the authors consider it advisable to apply programmed endocardial stimulation. The value of pre- and intraoperative mapping is the most important factor that determines the outcome of the surgical management. Subendocardial resection should be regarded as the method of choice just at early stages of the disease in patients with recurrent ventricular tachycardias occurring after acute myocardial infarction.
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PMID:[Subendocardial resection in the surgical treatment of ventricular arrhythmia in patients with ischemic heart disease]. 208 37

In the present study, the Ca2(+)-sensitivity and myosin light chain patterns of skinned fibers of right atrium and left papillary muscles of 27 patients suffering from mitral valve disease (MVD, moderate heart failure), ischemic cardiomyopathy (ICM, severe heart failure), dilated cardiomyopathy (DCM, severe heart failure), and coronary heart disease (CHD, no heart failure, no atrial hypertrophy) were investigated. Myosin light chains of both chemically skinned and intact samples were studied by two-dimensional gel electrophoresis (2D-PAGE). Ca2(+)-sensitivity of ventricular fibers was about 0.14 pCa-units higher than that of atrial fibers in all groups except dilated cardiomyopathy where this difference was markedly diminished (only 0.06 pCa-units). Generally, Ca2(+)-sensitivity of skinned ventricular fibers was the same among the different heart diseases. Skinned atrial fibers from patients with dilated cardiomyopathy, however, were significantly (about 0.08 pCa-units) more sensitive for Ca2+ than those of the other groups (coronary heart disease, mitral valve disease or ischemic cardiomyopathy) which showed similar Ca2(+)-tension relationships. Ventricle-specific P-light chain forms could be observed in atrial samples from patients of all groups, whereas no atrium-specific light chain forms were detectable in any ventricular sample. It is concluded that there is no difference in Ca2(+)-sensitivity of the ventricular contractile elements of the human heart in different heart diseases. In atrial myocardium, there is an increased Ca2(+)-sensitivity of skinned fibers from hearts with dilated cardiomyopathy which is probably related to an elevation of right atrial pressure.
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PMID:Calcium sensitivity and myosin light chain pattern of atrial and ventricular skinned cardiac fibers from patients with various kinds of cardiac disease. 208 58

In cardiovascular emergency medicine echocardiography allows in many patients a quick and gentle bedside examination. In particular in patients with acute arterial hypotension, suspected or known acute coronary heart disease and its complications and in patients with acute heart failure due to valvular heart disease a valuable narrowing down of the differential diagnosis can be achieved by the use of echocardiography. However, the use of echocardiography in acutely ill patients demands highly skilled investigators to avoid potentially dangerous errors. The echocardiographic examination in intensive or emergency care patients represents an invaluable diagnostic tool today and becomes a toy only in inexperienced hands.
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PMID:[Echocardiography in emergency medicine: tool or toy?]. 209 20

Parameter of catecholamine metabolism were examined in patients (Groups II to V) in chronic, stable stages of coronary heart disease (n = 45), dilated cardiomyopathy (n = 17) and healthy control subjects (Group I). Plasma and urinary catecholamine patterns, catecholamine plasma half-life and catecholamine metabolism following administration of levodopa were determined. In cases of slight (Group II, ejection fraction (EF) 54 +/- 7%) to marked left-heart damage (Group III, EF 44 +/- 5%), the findings indicate elevated catecholamine excretion and a beginning reduction of plasma clearance as the cause of excessive, circulating and renally excreted catecholamines (applies to noradrenaline, less to adrenaline). The renal 24-h dopamine elimination is already slightly reduced in these patients. In cases of severe left-heart damage, the findings are not uniform. In some cases, noradrenaline at rest and at comparable exercise levels are elevated (Group IV, EF 20 +/- 11%), in some cases they are normal (Group V, EF 16 +/- 4%). The 24-h dopamine elimination is reduced in both groups to 34-41% of normal. Noradrenaline and adrenaline elimination is normal, or reduced (Group V, adrenaline). The exercise-induced, maximum plasma noradrenaline concentrations in Group IV and V are much lower (33-40% of normal) than in the healthy control individuals and patients in Groups II and III. Oral administration of 2-4 g levodopa per day result in a 20- to 40-fold dopamine increase in patients with heart failure (Group IV) and healthy control persons (Group I) (free and conjugated plasma dopamine, as well as free urinary dopamine).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Catecholamine metabolism in heart failure patients and healthy control subjects. 209 27

One approach in the therapy of cardiac insufficiency is the administration of vasodilator substances for afterload reduction. Ketanserin selectively blocks the serotonin-2 receptors and thus inhibits the vasoconstrictor effect of serotonin. A hypotensive action of ketanserin has been documented in several studies. In 10 patients with coronary heart disease and cardiac insufficiency we investigated the haemodynamic effects of ketanserin after 24 h of intravenous administration (4 mg/h) and after 4 weeks of oral therapy (80 mg/day). Five patients received ketanserin for 12 months and were then re-examined. The resting mean arterial pressure dropped from 97.1 to 89.3 mm Hg after intravenous administration (p less than 0.05) and to 89.3 mm Hg after 4 weeks of oral intake (p less than 0.05). The resting mean pulmonary arterial pressure dropped from 15.2 to 12.0 mm Hg after intravenous administration (p less than 0.05) and to 11.7 mm Hg after 4 weeks of oral ingestion (p less than 0.01). Under exercise the pressure dropped from 35.3 to 28.1 mm Hg after intravenous administration (p less than 0.0025) and to 29.9 mm Hg after 4 weeks of oral intake (p less than 0.0025). Heart rate and cardiac output did not show any significant differences. The measured values after 12 months (in 5 patients) did not differ significantly from those measured after 4 weeks. In view of its low side effect liability ketanserin could be used as an afterload-lowering agent in patients with cardiac insufficiency.
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PMID:Serotonin antagonism in the treatment of cardiac insufficiency. 213 78

We studied the expression and distribution of atrial natriuretic polypeptide in the ventricles of 27 autopsied children with Kawasaki disease. Fourteen of the children had died in the acute stage of the disease. Three without any coronary artery aneurysms died due to myocarditis, while 11 with coronary artery aneurysms also had myocarditis but died of coronary heart disease. Histologic evidence of acute myocardial infarction was noted in three children who died of coronary heart disease. In the 14 children with acute-stage deaths, no abnormal expression of atrial natriuretic polypeptide was noted in the ventricles, despite the presence of heart failure in seven of them for 2 to 22 days before death. The other 13 patients had coronary artery aneurysms and died in the healed stage. In three patients with granulation tissue and congestive heart failure, myocytes in foci around the granulations were moderate to markedly positive for atrial natriuretic polypeptide. These three patients died over 8 days after the onset of their first myocardial infarct. Of 10 patients with old myocardial infarction, four had a history of congestive heart failure. They demonstrated moderate or marked atrial natriuretic polypeptide expression in extensive regions around sites of massive fibrosis, and foci of slight expression in the inner third of the noninfarcted region of the ventricle. In the other six patients without congestive heart failure, there was slight or moderate expression in foci around sites of massive fibrosis. We concluded that the expression of atrial natriuretic polypeptide appeared more than 1 week after the onset of acute myocardial infarction in the ventricles of children with Kawasaki disease who died in the healed stage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Expression and distribution of atrial natriuretic polypeptide in the ventricles of children with myocarditis and/or myocardial infarction secondary to Kawasaki disease: immunohistochemical study. 214 84


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