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)

In 15 patients with severe chronic left ventricular failure, plasma renin activity (PRA) ranged widely, from 0.2--39 ng/ml/hr. The level of PRA was unrelated to cardiac output (CO) or pulmonary artery wedge pressure (PWP), but was slightly negatively correlated with mean arterial pressure (MAP) (r = -0.45) and systemic vascular resistance (SVR) (r = -0.40). After infusion of the angiotensin converting enzyme inhibitor teprotide (SQ 20,881) PWP fell from 26.3 +/- 1.3 (SEM) to 20.3 +/- 1.4 mm Hg (P less than 0.001), CO rose from 3.94 +/- 0.23 to 4.75 +/- 0.31 l/min (P less than 0.001), MAP fell from 87.5 +/- 3.8 to 77.9 +/- 4.1 mm Hg (P less than 0.001) and SVR from 1619 +/- 148 to 1252 +/- 137 dyne-sec-cm-5 (P less than 0.001). The fall in MAP and in SVR was significantly correlated with control PRA (r = 0.68 and r = 0.58, respectively). When subjects were divided on the basis of control PRA the hemodynamic response to teprotide was greatest in the high renin group. PRA rose after teprotide (8.7 +/- 3.4 to 37.9 +/- 7.7 ng/ml/hr, P less than 0.05) but plasma norepinephrine fell (619.1 +/- 103.6 to 449.7 +/- 75.7, P less than 0.05). The renin-angiotensin system thus appears to have an important role in the elevated SVR in some patients with heart failure. Chronic inhibition of converting enzyme should be explored as a possible therapeutic approach.
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PMID:Role of the renin-angiotensin system in the systemic vasoconstriction of chronic congestive heart failure. 69 45

Clinical and autopsy study of 100 cases of patients dying during the first 3 weeks of hospitalisation for myocardial infarction revealed the following causes of death: cardiac failure in 59 cases (including 40 of cardiogenic shock), rupture of the heart in 29 cases (24 of rupture of the ventricular wall, 4 of the septum and 1 of a mitral papillary muscle). 4 ventricular arrhythmias and 6 haemorrhagic or embolic complications. In 2 cases, the cause of death could not be accurately determined. In cardiogenic shock, death usually occurred early. It was later in cases of refractory left ventricular failure. Conduction disturbances were much commoner in cases of myocardial infarction complicated by fatal cardiac failure (57.6%) than in the presence of any other complication (17.1%) (p less than 0.001). The responsible infarction was often extensive and recurrent. Rupture of the heart invariably occurred during the first three days of an infarction often initial (p less than 0.001), anterior (apart from septal rupture) and small in size (p less than 0.01). Other complications play only a secondary role in mortality at the present time, in particular arrhythmias, the gravity of which has greatly decreased since the reduction of delays before hospitalisation and improvements in anti-arrhythmic therapy.
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PMID:[Clinicopathological study of the causes of mortality during the acute phase of myocardial infarction (author's transl)]. 74 57

Infants with aortic arch interruption of juxtaductal coarctation of the aorta may depend on patency of the ductus arteriosus to provide adequate lower body perfusion. In many such infants the ductus arteriosus constricts after birth, resulting in severe heart failure, poor systemic perfusion and acidemia. We infused prostaglandin E1 (PGE1) at a rate of 0.05--0.1 microgram/kg/min into seven infants with aortic arch interruption and eight infants with coarctation. In one infant in each group the ductus arteriosus was already closed and did not reopen. In one infant with coarctation an adequate trial was not accomplished, and in another adequate pressure measurements were not obtained. Of the remaining 11, the ductus arteriosus was effectively dilated by PGE1 in 10 infants. This was evidenced by an increase in descending aortic blood pressures and a reduction in the pressure difference between the main pulmonary artery and descending aorta in six infants with aortic arch interruption and between ascending and descending aorta in four infants with coarctation. Lower body perfusion improved and left ventricular failure was improved. The infant who did not respond was 5 months old. There were no complications.
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PMID:Dilatation of the ductus arteriosus by prostaglandin E1 in aortic arch abnormalities. 75 9

1329 patients were discharged alive after acute myocardial infarction initially treated in a CCU. In a five-year follow-up, 537 (40%) of the patients died. Routine data registered uniformly during the CCU period showed that, apart from age, the most important factors regarding long-term prognosis in general were previous ischaemic heart disease and direct or indirect signs of heart failure registered in the CCU. The possibilities to predict sudden death (130 patients died within 2 hours of onset of final symptoms during the follow-up period) were small, although a definite dominance of this mode of death was noted in patients below 60 years of age. The clinical profile of the majority of the 134 patients who died during the first half-year was distinguished by a history of prior myocardial infarction and signs of left heart failure during the CCU stay. However, in a significant number of patients dying early after discharge, none of the ordinary unfavourable prognostic signs had been registered.
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PMID:Early and sudden deaths after myocardial infarction. A report from the Swedish CCU study. 76 Apr 5

The product of minimal transit time (MTT) and heart frequency (HF) defines the number of heart beats which are necessary to transport the blood in a determined region of the circulatory system. According to own studies in physiological (stress) and pharmacological conditions this product is constant, independent from body size, length, age etc. In proportion to the degree of heart failure the MTT X HF increases. Measuring appropriate regions of the circulatory system, right and left heart failure can easily be determined. The method has the advantage of a noninvasive procedure and gives exact quantitive accessment of the pump performance of the heart. In view of the increasing use of radio-nuclides this procedure can be recommended because of its good reliability causing little or no discomfort to the patient, and making it applicable, even under extreme conditions, for instance in a CCU.
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PMID:[The definition of heart failure with the product of minimal transit time and heart frequency (author's transl)]. 79 64

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

Left ventricular failure was produced in dogs by inducing mitral insufficiency and the cardiac muscle was examined for ultrastructural changes in thsese failing hearts after 5-10 months of mitral insufficiency. The left ventricular failure was established by haemodynamic measurements, chest X-ray and examination of the heart. In the failing heart, the increased number of mitochondria showed close approximation with the sarcolemmal membrane in the T-tubules as well as in the intercalated discs (ID); this is in contrast to what is seen in normal hearts, where T-tubules were mostly coupled with sarcoplasmic reticulum. It is possible that in the heart failing on account of mitral insufficiency mitochondria may be taking over the function of the sarcoplasmic reticulum. Although ID were jumbled up in the failing heart, the intercellular gap and specialized membrane junctions (gap and tight junctions, desmosomes) were quite comparable to normal, indicating that intercellular communication at ID in this type of heart failure is probably maintained. Nuclear chromatin in the failing heart was condensed and lined the inner nuclear membrane. Microbodies with a single limiting membrane were frequent and so were lipofuscin granules. The latter could be an end product of degenerative mitochondria. Golgi bodies in the failing heart were also present in locations away from the nucleus.
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PMID:Ultrastructure of failing myocardium due to induced chronic mitral insufficiency in dogs. 87 78

Serial measurements of vital capacity (VC) were performed on nine patients on chronic haemodialysis. In six patients the VC remained stable, they were all adequately dialysed and working full-time. Reduction of dialysis time in one of these patients brought about a gradual onset of left heart failure which was preceeded by a decline of VC. In the three remaining patients a decrease of VC preceeded the onset of heart failure, and a rise of VC values signified improvement of cardiac performance. Serial recordings of VC are recommended as a useful objective guide to evaluation and treatment of patients on haemodialysis.
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PMID:Serial measurement of vital capacity in patients on chronic haemodialysis. 89 62

In 17 patients with coronary heart disease, hemodynamic measurements were performed before and after sublingual application of 10 mg isosorbide dinitrate (ISDN). 10 patients showed signs of heart failure with pulmonary congestion and a left ventricular filling pressure above 15 mmHg, resting hemodynamics were normal in 7 patients. Eight of the patients with left ventricular failure had sustained acute myocardial infarctions the size of which was assessed by serial determinations of serum creatine phosphokinase. Application of ISDN resulted in a significant decrease of systemic and pulmonary artery pressures and pulmonary capillary wedge and right atrial pressures of patients both with and without left ventricular failure. Cardiac index and stroke index as well as systemic and pulmonary resistances did not change significantly. ISDN did not affect left ventricular stroke work in patients with elevated filling pressures; however, a decrease of normal filling pressures was associated with a decrease of stroke work. Thus, in coronary patients with chronic congestive heart failure, sublingual application of nitrates results in a beneficial hemodynamic unloading. However, if the acute infarct size is taken into account, it can be demonstrated that hemodynamic improvement after ISDN--judged by the relation stroke work/filling pressure--becomes less pronounced with increasing infarct size.
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PMID:[Effect of sublingual isosorbide dinitrate on hemodynamics in coronary patients with and without congestive heart failure (author's transl)]. 89 50

On 55 patients with acute myocardial infarction blood gas changes and A-aDO2 while breathing room air were observed for a period of 5 weeks. PaO2 during the 35% O2 inhalation was measured on admission and 5 weeks later for comparisons with the PaO2 while breathing room air. Pulmonary circulatory hemodynamics was measured in 29 cases on admission using Swan-Ganz's right heart flow directed catheter 7F, and the catheter was kept in the pulmonary artery in 13 cases for a maximum of 9 days. The mean PaO2 while breathing room air on admission was 66.7 mmHg in the 55 cases. It was 52.3 mmHg in the heart failure group and 74.9 mmHg in the non-heart failure group, showing prominent hypoxemia in the heart failure group. The mean PaO2 recovered to normal (84.1 mmHg and 87.0 mmHg) 5 weeks later. Inhalation of 35% O2 was performed for 20 minutes on admission and 5 weeks later. The elevation of PaO2 during the oxygen inhalation on admission was smaller than that 5 weeks later, significantly smaller in the heart failure group (P less than 0.001). The mean A-aDO2 on admission was higher in the heart failure group (58.1 mmHg) than in the non-heart failure group (34.8 mmHg). PaO2 showed significant correlations with cardiac index and SvO2. Although it was significantly correlated with PA diast. and TPR, no correlation with CVP was observed. Hypoxemia in acute myocardial infarction is caused by the following process: the onset of myocardial infarction causes low output, leading to left ventricular failure. As the result of elevated left atrial pressure and pulmonary venous pressure, intestinal pulmonary edema develops provoking ventilation-perfusion inequality, intra-pulmonary shunting, and diffusing defect.
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PMID:Studies of hypoxemia and pulmonary hemodynamics in acute myocardial infarction. 93 22


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