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)

51 patients with coronary heart disease had exercise tests on a bicycle ergometer (86 +/- 32 watts). Compared to a normal control group, only 13 patients had normal contractile reserve (group 4.1). In 32 patients the increase in contractility during exercise was reduced (max dP/dt below 3200 mm Hg/s, group 4.2). Patients with reduced contractile reserve were graded according to the height of left ventricular enddiastolic pressure during exercise: In patients with grade 1, enddiastolic pressure was normal. In patients with grade 2, enddiastolic pressure increased between + 4 and + 15 mm Hg and in the patients with grade 3a a above + 15 mm Hg. Contractile and relaxation reserve decreased along with a rise in enddiastolic pressure and an increase in the complaints of the patients. Severe chest pain led to termination of exercise in patients of grade 3b. Enddiastolic pressure increased above + 15 mm Hg. During ischemia, peak-measured velocity of contractile elements (dP/dt/P) and the maximal rate of left ventricular pressure fall (min dP/dt) decreased. In conclusion, with increasing chest pain a decrease of contractile reserve was observed. Left ventricular enddiastolic pressure rose excessively. This has to be taken as a sign of myocardial failure due to ischemic dyskinesia and impeded relaxation.
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PMID:[Contractile and relaxation reserve of the left ventricle. IV. Patients with coronary heart disease (author's transl)]. 62 71

The operative results in 32 patients who underwent aortic valve replacement with aortic occlusion and normothermic myocardium (group 1) were compared with 54 similar patients in whom the myocardium was protected by hypothermic coronary perfusion through the aortic root (group 2). The operative mortality and the incidence of heart failure, subendocardial ischemia and myocardial infarction were the same in the two groups. The maximal concentrations of cardiac enzymes after operation in group 2 patients were significantly lower than those in group 1. The postoperative cardiac performance was significantly different in that only 5.6% of group 2 patients required inotropic agents after operation compared with 25% of group 1 patients. The patients in group 2 were easier to defibrillate after cardiopulmonary bypass.
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PMID:Myocardial protection during aortic valve replacement: normothermia versus hypothermia. 63 Apr 59

Starting from general assumptions on the clinical aspects of homeostasis and on the functional correlations lung-heart in physiological and pathological states, the difficulty to diagnose an individual pulmonary heart disease is stressed, as well as the necessity to differentiate it from the cases of coronary heart disease, when respiratory failure aggravates the latent cardiac ischemia and induces a global cardiac failure. The diagnosis criteria of the two distinct pathological pictures are established, emphasizing the importance of this differentiation for clinical practice and epidemiological research.
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PMID:Clinical aspects of cardio-respiratory homeostasis. 66 38

Both vasodilator and inotropic agents improve cardiac function in ischemic heart failure. However, since vasodilators may reduce coronary perfusion pressure and inotropic interventions may increase myocardial oxygen consumption (MVO2), both may increase myocardial ischemia. Accordingly, we determined myocardial blood flow and MVO2 in a canine model of failure induced by propranolol and volume load combined with acute coronary ligation. Both nitroprusside and digitalis reduced ventricular diastolic pressure (LVDP) and increased myocardial blood flow in the ischemic subendocardium. Decreased systolic wall tension also caused a significant reduction MVO2. The benefit of nitroprusside in failing hearts was obtained even with the addition of critical obstruction of the main left coronary artery (LCA). The role of preload reduction is emphasized by the contrasting results with nitroprusside in hearts with low LVDP: (1) decreased myocardial blood flow in ischemic subendocardium, and (2) left ventricular decompensation in animals with critical LCA obstruction. Thus, reduction of LVDP, which decreases subendocardial ischemia, is essential for the beneficial effects of vasodilators and inotropic interventions in ischemic heart failure. Decreased MVO2 caused by reduced heart size may also have a salutary role.
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PMID:Mechanisms of beneficial effects of vasodilators and inotropic stimulation in the experimental failing ischemic heart. 68 93

In 53 patients with mitral- or aortic-mitral valve disease, the content of ATP and lactate of the papillary muscles resected at the time of valve replacement was investigated at the beginning of ischemic arrest and at the time of reperfusion. Profound body hypothermia (25 degrees C) and injection cardioplegia using magnesium-aspartate-procaine were applied for myocardial protection. In hypertrophic papillary muscles the myocardial ATP content decreased at a slower rate (ATP decay 12% of the initial value after 60 minutes of ischemia) than in normal papillary muscles obtained from patients with isolated mitral stenosis (ATP decay 33% of the initial value after 40 minutes of ischemia). 20% of the patients required temporary inotropic circulatory support postoperatively for 12 to 88 hours. The ATP content of the papillary muscles of these patients differed only little from those, in who no myocardial failure occurred. However the myocardial lactate levels were higher in patients in whom a low cardiac output state evolved.
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PMID:[Behaviour of ATP and lactate in human papillary muscle during profound hypothermia and injection cardioplegia with magnesium-asparatate-procaine (author's transl)]. 75 Dec 88

Examples of toxic cardiomyopathies of various characteristics are presented. Daunomycin and doxorubicin, antineoplastic drugs, cause multifocal cardiomyopathies and intractable heart failure by cardiotoxic mechanisms; these effects are delayed and related to the cumulative dose. Cobalt caused diffuse vacuolar cardiomyopathy in chronic beer drinkers. The development of fulminant heart failure was the function of factors that increased the adsorption of cobalt or sensitized the myocardium to its cytotoxic effect. Beta-adrenergic receptor stimulant bronchodilators like isoproterenol or vasodilating antihypersensitive drugs like hydralazine are able to produce focal subendocardial necroses. This lesion is due to ischemia brought about by the acute exxagerated pharmacological effects of these compounds.
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PMID:Toxic cardiomyopathies. 79 2

Nitroglycerin reduces ischemic injury during acute myocardial infarction (AMI) in dogs--an effect that is potentiated when drug-induced hypotension and tachycardia are prevented with phenylephrine. To determine the effectiveness of nitroglycerin, alone or with phenylephrine, during AMI in man, 12 patients (five or whom had left heart failure) were evaluated by summing ST-segment abnormalities (sigmaST) from 35 precordial electrodes. The seven patients without heart failure did not benefit consistently from nitroglycerin alone; however, addition of phenylephrine to abolish nitroglycerin-induced arterial pressure reduction uniformly diminished sigmaST (4.9 to 3.2 mv; P less than 0.05). In patients with heart failure, nitroglycerin alone consistently reduced ischemia (5.8 to 4.4 mv, P less than 0.05); addition of phenylephrine often partially reversed this effect. Thus, administration of nitroglycerin, alone or with phenylephrine, can reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends on the presence or absence of left ventricular failure before treatment.
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PMID:Reduction in myocardial ischemia with nitroglycerin or nitroglycerin plus phenylephrine administered during acute myocardial infarction. 80 12

Recent epidemiologic studies have suggested that cardiac disease in common in diabetics and may often have a noncoronary basis. To examine the status of the left ventricle, 17 adult-onset diabetics of familial type without hypertension or obesity underwent hemodynamic study and were compared to 9 controls of similar age. Of the 17, 12 subjects had no significant occlusive lesions by coronary angiography. From this group eight without heart failure had a modest, but significant, elevation of left ventricular end-diastolic pressure. End-diastolic and stroke volumes were reduced, but ejection fraction and mean rate of fiber shortening were within normal limits. The left ventricular end-diastolic pressure/volume ratio was significantly higher than controls. Afterload increments effected a significant increase of filling pressure compared to normals without a stroke volume response, consistent with a preclinical cardiomyopathy. Four patients with prior heart failure had similar but more extensive abnormalities. None had local dyskinesia by angiography, and lactate production was not observed during pacing-induced tachycardia. Left ventricular biopsy in two patients without ventricular decompensation showed interstitial collagen deposition with relatively normal muscle cells. These findings suggest a myopathic process without ischemia. Postmortem studies were performed in 11 uncomplicated diabetics. Nine were without significant obstructive disease of the proximal coronary arteries, and the majority succumbed with cardiac failure. On left ventricular sections, none had evident luminal narrowing of the intramural vessels. All nine exhibited periodic acid-Schiff-positive material in the interstitium. Collagen accumulation was present in perivascular loci, between myofibers, or as replacement fibrosis. Multiple samples of left ventricle and septum revealed enhanced triglyceride and cholesterol concentrations, as compared to controls. Thus, a diffuse extravascular abnormality may be a basis for cardiomyopathic features in diabetes.
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PMID:Evidence for cardiomyopathy in familial diabetes mellitus. 89 79

The possible relationship between the cardiac volume, as determined radiologically in the supine position in 119 patients with angiographically proven coronary artery disease, and the results of ergometry and balloon catheterization was investigated. There was no relationship between the heart size on the one side and the maximum exercise tolerance and the maximum cardiac output on the other, except for the fact, that these parameters tended to decrease with increasing heart size. This was especially true in patients with angina. The maximum cardiac output of patients with angina was always below the value of patients without angina but comparable heart size. Reduced cardiac output under exercise (exertional cardiac insufficiency) was present in 50% of patients with enlarged hearts but already in 22% of patients with heart volumes in the lower range of normal. The diastolic pulmonary artery pressure, determined under exercise, was the only parameter with a significant relationship to the heart size: The larger the heart size, the higher the diastolic pulmonary artery pressure. On the other hand: the diastolic pulmonary artery pressure at rest was abnormal with significant frequency only, when the heart was enlarged. Our data suggest, that the hemodynamics are determined by 2 factors: Myocardial scarring secondary to infarction and coronary insufficiency (ischemia). Of these two factors only the former influences cardiac size. Therefore, determination of the heart volume helps evaluating the respective role of these two factors in individual cases.
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PMID:[Heart size and left ventricular function in coronary artery disease: I. Heart size, exercise tolerance, cardiac output and filling pressures (author's transl)]. 92 89

Plasma polyps can be found at the end of a normal pregnancy. Following NaF and MJA-intoxication, there is an extreme increase of plasma polyps. This accelerated formation can be prevented by the injection of Na-pyruvate and often the number of polyps can be reduced below the norm. 2,4-Dinitrophenol intoxication and breathing of hypoxic gas mixture (2,5% O2, 5% CO2, 92,5% N2) do not lead to increased plasma polyp formation. This proves, that it is not hypoxia, not an energy deficit secondary to separation of oxydative phosphorylation and not cardiac insufficiency leading to secondary ischemia which are responsible for the extreme increase in the number of plasma polyps following the injection of MJA and NaF.
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PMID:[The effect of 2,4-dinitrophenol, monoiodine acetate, sodium fluoride and hypoxia on the formation of plasma polyps in the placenta of guinea pigs (author's transl)]. 99 63


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