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)

The principal echocardiographic features of the main cardiovascular emergencies are discussed. After setting out a method of detailed analysis for echocardiography, the changes found in the main causes of severe chest pain, systemic embolisation and sudden heart failure are described. Special emphasis is laid on the signs of aortic root dissection, pericarditis and tamponade, ruptured valve, the mechanical complications of acute myocardial infarction and, in particular, on the assessment of residual myocardial function. Finally, the authors maintain that echocardiography should be a systematic complementary investigation for patients in the coronary care unit.
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PMID:[Echocardiographic aspects of left atrial thrombosis in 1 case of severe mitral stenosis]. 11 38

The principal echocardiographic features of the main cardiovascular emergencies are discussed. After setting out a method of detailed analysis for echocardiography, the changes found in the main causes of severe chest pain, systemic embolisation and sudden heart failure are described. Special emphasis is laid on the signs of aortic root dissection, pericarditis and tamponade, ruptured valve, the mechanical complications of acute myocardial infarction and, in particular, on the assessment of residual myocardial function. Finally, the authors maintain that echocardiography should be a systematic complementary investigation for patients in the coronary care unit.
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PMID:[Value of echocardiography in cardiovascular emergencies (not including congenital cardiopathies)]. 11 40

The prognostic value of a limited treadmill exercises test performed one day before hospital discharge after acute myocardial infarction was studied in 210 consecutive patients who had no over heart failure and had been free of chest pain for at least four days. No complications occurred. During a one-year follow-up period 28 of 43 patients (65 per cent) who had chest pain during the test reported angina, as compared with 60 of 167 (36 per cent) who had no chest pain during test (P less than 0.001). The one-year mortality rates were 2.1 per cent (three of 146) in patients without changes in the S-T segment during exercise and 27 per cent (17 of 64) in those with depression of the S-T segment (P less than 0.001). Sudden death occurred in one of 146 (0.7 per cent) patients who showed no change in the S-T segment and in 10 of 64 (16 per cent) with depression of the segment (P less than 0.001). Thus, a limited treadmill exercise test performed before hospital discharge after acute myocardial infarction is safe and can predict mortality in the subsequent year.
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PMID:Prognostic value of exercise testing soon after myocardial infarction. 46 Mar 22

The pooling of blood in the lower part of the human body when it is subjected to longitudinal +Gz acceleration is one of the major reasons for cardiac insufficiency and the consequent impairment of certain important physiological functions. Headache, abdominal pain, change in heart rate, chest pain, impairment of vision, and hemorrhage are some of the manifestations of acceleration trauma. To predict the effects of time-dependent accelerations on the circulation, a mathematical model independent of assumptions extrapolated from normal G conditions must be considered. The model in the present study consists of a closed-loop hydrodynamic system comprising a heart pump, elastic tubes to represent the large arteries and veins, and a baroreceptor feedback mechanism to help to overcome cardiac insufficiency. The governing equations consist of the Navier-Stokes equations for fluid motion in the blood vessels, and equations of motion for time-dependent blood vessel deformation and ventricular contraction derived from nonlinear elasticity theory. In a numerical example, an experimentally measured deceleration profile is used and the calculated aortic flow is compared with the experimental values.
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PMID:Mathematical model of the cardiovascular system under acceleration stress. 62 95

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

A prospective analysis of 155 patients with pulmonary embolism was undertaken to describe the radiographic characteristics of associated pleural effusions and related abnormalities. Approximately one half of these patients had pleural effusions. Patients with other potential causes of effusion, such as heart failure, pneumonia, or cancer, were eliminated from further analysis. In the remaining 62 patients, radiographic evidence of pulmonary infarction accompanied pleural effusions in one half of the cases. One third of patients with parenchymal consolidation had no evidence of effusion. Atelectasis and other nonspecific radiographic abnormalities occurred in less than one fifth of the cases. Typically, pleural effusions were small and unilateral, appeared soon after symptoms of thromboembolism began, and tended to reach their maximal size very early in the course of the disorder. Pulmonary infarction was associated with larger effusions that cleared more slowly and were more often bloody in appearance on thoracentesis. Chest pain occurred in all but one patient and was a valuable diagnostic clue. Pain and pleural effusions were always ipsilateral and almost always unilateral, but neither correlated well with the presence or time course of infarction. Effusions that were delayed in onset or that enlarged late in the course were associated with recurrent pulmonary embolism or superinfection. These radiographic features may be helpful in the diagnosis and management of pulmonary embolism.
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PMID:Radiographic features of pleural effusions in pulmonary embolism. 65 89

The diagnosis of primary dilated cardiomyopathy depends on the recognition of a dilated poorly contracting left ventricle with increased end-diastolic and end-systolic volumes in the absence of a detectable cause. The diagnosis is made only after exclusion both of structural heart disease and of known causes of secondary heart muscle disorder. The natural history is still largely unknown and is probably as variable as the likely causes. The left ventricular disorder does not cause symptoms until heart failure supervenes except for occasional patients who develop an early atrial or ventricular dysrhythmia, conduction defect, chest pain or murmur of mitral regurgitation. This period of latency may be short, prolonged or even permanent since it is unlikely that all cases progess to the point of failure. A few patients recover normal or near-normal cardiac function. The interplay between high blood pressure, hypertensive heart failure and dilated cardiomyopathy is illustrated by patients who recover from heart failure to become hypertensive and vice versa and in current treatment with vasodilators and diuretics for patients at either end of the spectrum.
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PMID:Diagnosis and natural history of congested (dilated) cardiomyopathies. 70 14

Serial measurements on serum creatine phosphokinase (CPK) and alpha-hydroxybutyrate dehydrogenase (HBD) activity were made in 17 patients with acute myocardial infarction. Activities of both enzymes were measured 4-hourly from less than 12 h after the onset of chest pain until CPK activity had returned to near-normal levels. Blood was then sampled twice daily for a further 4--6 days in order to follow the decline in HBD activity. Degradation rates (KD) were calculated for both enzymes, and individual figures for KD were used in order to estimate the total cumulative release of each enzyme. We found a significant correlation between the duration (r = 0.66, P less than 0.01) and magnitude (r = 0.67, P less than 0.01) of release of the 2 enzymes, comparing different patients with one another. Duration od HBD release was 11 h greater than the duration of CPK release in 9 of the 17 patients who were suffering from cardiac failure (t = 0.01, P less than 0.02). Degradation rate (KD) for HBD was on average about one quarter of that for CPK, but there was no significant correlation between KD for the 2 enzymes. KD did not appear to be reduced in patients with cardiac failure. We conclude that the release patterns of CPK and HBD after myocardial infarction are similar, and this strengthens the case for acceptance of total enzyme release as a valid index of myocardial infarct size.
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PMID:Enzyme release after myocardial infarction: comparison of serial serum alpha-hydroxybutyrate dehydrogenase with creatine phosphokinase levels. 100 39

The aim of this prospective study was to assess the prognostic and most suitable management of AMI in elderly patients (age > or = 75 years). From September 1988 to August 1991, 129 such patients (pts) were evaluated: 35 (27%) were admitted to CCU because of arrhythmias or severe hemodynamic complications; 94 (73%) were addressed, according to bed availability, to CCU (55 pts) or Cardiology Ward (39 pts), where all patients underwent continuous ECG monitoring for at least 72 hours. Age, gender, history of previous angina or myocardial infarction, presence of chest pain or ECG ischemia on admission, site and extent of AMI, delay on admission, CPK-MB peak, recurrent angina, arrhythmias, heart failure, emotional disorders, hospital mortality and length of hospital stay were compared. Our results show that elderly patients who suffered from complicated AMI were at high risk for death and severe in-hospital complications. No significant prognostic differences were observed between the two groups with uncomplicated AMI. Thus hospitalization in the Cardiology Ward seems to be valuable, safe and well tolerated in our population of elderly patients with AMI, and without initial complications.
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PMID:[Management and prognosis of acute myocardial infarct in advanced age: comparison of the cardiac intensive care unit and the cardiology ward]. 129 24

A time course (48 hours) of plasma neuropeptide Y (NPY) levels has been carried out in a male, 66 years old, admitted to Coronary Care Unit with inferior acute myocardial infarction within 1 hour from the onset of chest pain. On admission an increase of plasma NPY levels (38 pg/ml) has been observed. The plasma NPY value decreased to normal range (15-25 pg/ml) within 12 hours and increased again (53 pg/ml) within 12 and 24 hours. A decrease in plasma NPY values to normal range has been observed within the second day in the Coronary Care Unit. A clearcut diuresis decrease, without pulmonary signs of heart failure, was present from 12 to 24 hours followed by marked polyuria within the second day. These data point out a relative importance of NPY in the diuresis adjustments. Thus, plasma NPY measurement might be a more reliable prognostic indicator of heart failure than plasma catecholamine levels. However, further investigations have to be performed.
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PMID:[Neuropeptide Y and heart failure]. 129 55


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