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)

A prospective study of 208 consecutive survivors of acute myocardial infarction was undertaken to determine the differences between Q- and non-Q-wave infarction, concerning data from the history, clinical course, and 6-month follow-up. There were 177 patients with Q-wave infarction and 31 patients with non-Q-wave infarction. There were no significant differences for the following variables: age, sex, diabetes mellitus, smoking, positive family history, hypertension, obesity, previous infarction, history of unstable angina, heart failure or chronic obstructive pulmonary disease (COPD), Killip class in the Coronary Care Unit (CCU), arrhythmias and conduction defects in the CCU as well as drugs used. Patients with non-Q wave infarction had a higher incidence of stable angina before the myocardial infarction and a lower value of creatine kinase (CK) and serum glutamic oxalacetic transferase (SGOT). During the 6-month follow-up, 9 cardiac deaths and 17 reinfarctions occurred, while 74 patients presented angina. There were no differences between the two groups concerning the incidence of cardiac death or angina, but patients with non-Q-wave infarction had a higher incidence of reinfarction at 6 months (p less than 0.001). We conclude that although patients with non-Q-wave myocardial infarction have a lesser degree of myocardial damage, they have a high incidence of early reinfarction which puts them in a high-risk group.
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PMID:Q- versus non-Q-wave myocardial infarction: clinical characteristics and 6-month prognosis. 671 48

Both segmental and global left ventricular performance were assessed simultaneously in 29 patients with acute myocardial infarction using two-dimensional echocardiography. Comparisons were made between left ventricular wall motion versus peak CK-MB, site of infarction, and occurrence of heart failure. Two-dimensional echocardiography identified areas of dyssynergy which corresponded to electrocardiographic areas of infarction in 89% of all cases. Patients with heart failure had more dyssynergic segments, and these segments manifested more severe dyssynergy than patients without heart failure. Patients with severe global dysfunction manifested higher peak CK-MB values, and those with anterior infarction had more global dyssynergy than did those patients with inferior infarction. These observations suggest that two-dimensional echocardiography is a useful technique for localization and assessment of segmental and global dyssynergy in acute myocardial infarction. Information so derived correlates with the clinical status of patients with acute myocardial infarction, and may offer important insights into both prognosis and treatment.
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PMID:Simultaneous assessment of segmental and global left ventricular function by two-dimensional echocardiography in acute myocardial infarction. 687 68

MB isoenzyme of creatine kinase was measured every 3 hours during the first 24 hours of admission to C.C.U. and successively every 4-6 hours in the next 24-48 hours in 42 patients with acute transmural myocardial infarction. The pain-C.C.U. admission time interval was less than 6 hours in all cases. 22 patients were treated by propranolol (2 mg bolus followed by 0.1 mg/Kg/die for the next 48 hours in continuous i.v. infusion), 20 patients served as a control. Cumulated activity, peak plasma value, rate of release and total duration of release of MB-CK did not differ significantly between the two groups. In patients treated within 3 hours from pain onset (n = 12) cumulated activity, peak plasma value and rate of release of MB-CK were significantly inferior than control group. In patients treated between the 3rd and 6th hour from pain onset (n = 10) the total duration of release of isoenzyme was significantly prolonged. No treated patients developed clinical or radiologic signs of cardiac insufficiency. The incidence of ventricular arrhythmias was 17% in the treated group vs. 62% in the control group (P < 0.05). The data show that propranolol, if started early in the course of acute myocardial infarction, reduces significantly infarct size and slows down the evolution of necrotic process.
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PMID:[Changes on release of MB isoenzyme of creatine kinase by propranolol in acute myocardial infarction (author's transl)]. 700 91

The value of intraaortic balloon counterpulsation in limiting infarct size and improving survival was studied in patients with early transmural myocardial infarction complicated by acute heart failure. Thirty such patients, previously well, were randomly assigned to counterpulsation (14 patients) or standard therapy (16 patients). Counterpulsation was begun 4.8 to 13.7 hours (mean 7.1) after the onset of pain and continued for less than 1 to 11 days (mean 4.5). Peak creatine kinase was 1,794 +/- 846 IU/liter (mean +/- standard deviation) in patients receiving counterpulsation compared with 1,688 +/- 908 for those receiving standard therapy; cumulative creatine kinase was 3,590 +/- 1,936 IU/liter for patients receiving counterpulsation and 2,945 +/- 1,803 for those receiving standard therapy. Hospital mortality was similar (counterpulsation, 7 of 14; standard therapy, 7 of 16 [p = 0.05 for 25 percent mortality reduction]) as was mortality at follow-up (counterpulsation, 8 of 14; standard therapy, 10 of 16 [p = 0.09 for 25 percent mortality reduction]). Functional class at follow-up examination 1 to 36 months (mean 15) after infarction was also similar in the two groups. Counterpulsation did not appear to modify infarct size or to alter morbidity or mortality when initiated as primary therapy 4.8 to 13.7 hours after the onset of symptoms of myocardial infarction.
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PMID:Randomized controlled trial of intraaortic balloon counterpulsation in early myocardial infarction with acute heart failure. 701 Sep 76

We gave sodium nitroprusside by intravenous infusion to 163 randomly selected patients during the first 24 hours after hospitalization for typical acute myocardial infarction, and we studied its effects on mortality at one week, on the incidence of cardiogenic shock, on clinical signs of left ventricular failure, and on peak levels of creatine kinase isoenzyme MB. A control group of 165 patients received standard medical treatment and infusion of 5 per cent glucose. The end point of the study was a significant reduction in mortality in the nitroprusside group; this was reached when five deaths had occurred in this group, as compared with 18 among the controls (P less than 0.05). The incidence of cardiogenic shock, clinical signs of left-heart failure, and mean peak levels of creatine kinase isoenzyme MB were all reduced (P less than 0.05). The results indicate that infusion of nitroprusside in the early phase of acute infarction limits complications, possibly by reducing infarct size. The drug was particularly effective in anterior-wall infarction.
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PMID:Effect of sodium nitroprusside on mortality in acute myocardial infarction. 704 Sep 55

To define the role of portable two-dimensional echocardiography (2-D echo) in the immediate diagnosis of acute chest pain syndrome, 80 consecutive patients were studied. Adequate 2-D echo studies were obtained in 65 (81%). Thirty-three patients had clinical evidence of transmural or nontransmural acute myocardial infarction (AMI), 18 of whom had nondiagnostic initial ECGs. Thirty-two did not have a clinical AMI. Thirty-one of the 33 (94%) patients with clinical AMI had regional wall motion abnormalities on the initial 2-D echo; the other two had uncomplicated nontransmural AMIs, diagnosed only by ECG in one and by ECG and moderate elevation of CK-MB isoenzyme in the other. Twenty-seven of the 32 patients without clinical AMI had normal regional wall motion on the initial 2-D echo and none had a complication (severe arrhythmia, recurrent pain, heart failure or death) during the hospital course. Conversely, 10 of the 36 patients with initial 2-D echo regional wall motion abnormalities had a complication (p less than 0.05). Thus, in patients with acute chest pain syndrome, an initial 2-D echo that shows no regional wall motion abnormality suggests that such patients will not develop an AMI or clinical complication during the hospital course. An initial 2-D echo with regional wall motion abnormality identifies a high-risk group of patients who are likely to have AMI and important cardiac complications and may, therefore, benefit from admission to an intensive care unit.
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PMID:Immediate diagnosis of acute myocardial infarction by two-dimensional echocardiography. 705 90

The Syrian hamster polymyopathy is a hereditary disease, transmitted by an autosomal recessive gene, involving the heart and the entire musculature. The chronology of the pathologic events in the myocardium and skeletal muscle has been investigated in UM-X7.1 myopathic hamsters aged 0-250 days. A phasic pattern in the progression of the disease process was evident. Microscopic necrotic changes in the heart were visible prior to or at 50 days of age with increasing severity until 100 days of age and subsidence thereafter. More than 50% of the animals died before 250 days of age with signs of cardiac failure. The intensity and extent of myocardial calcific changes together with scar formation were determinant factors in curtailing the survival of animals. Changes in serum creatine kinase (CK) activity followed a phasic pattern similar to the progression of the myopathic disease. Because of the disparity of disease manifestations between the different myopathic hamster lines, it is essential to consider the time course of the heart and skeletal muscle microscopic changes when evaluating the severity of the hamster polymyopathy.
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PMID:Hereditary polymyopathy and cardiomyopathy in the Syrian hamster. I. Progression of heart and skeletal muscle lesions in the UM-X7.1 line. 705 1

Total creatine kinase (CK) and the myocardial isoenzyme CK MB activity were prospectively determined in 282 children hospitalized for cardiac catheterization and evaluation for suspected congenital cardiac abnormalities and compared with a hospitalized control group of children without such abnormalities. The percent CK MB and CK MB activity were abnormally elevated in symptomatic children with a large left to right shunt due either to a large ventricular septal defect (n = 22; p less than 0.001) or to complete atrioventricular canal (n = 10; p less than 0.001). Serum CK MB activity and percent CK MB were significantly related to the size of the shunt and the age of presentation with clinical symptoms of congestive heart failure in infants with a ventricular septal defect. CK MB activity was abnormally elevated in infants with symptomatic coarctation of the aorta, either with or without a ventricular septal defect (n = 15; p less than 0.001), and in infants with symptomatic aortic stenosis (n = 4; p less than 0.02). In contrast, CK MB activity was normal in asymptomatic children with coarctation of the aorta (n = 14) or aortic stenosis (n = 8) despite comparable systolic pressure gradients. CK MB activity and percent CK MB were abnormally elevated in those children with the cyanotic congenital cardiac abnormalities of either transposition of the great arteries (n = 32; p less than 0.001) or right ventricular outflow tract obstruction (n = 31; p less than 0.001). These results suggest that children with congenital cardiac abnormalities may have significant myocardial cell injury and release of CK MB that may be detected by the determination of serum CK MB activity. Cell injury may be secondary to arterial desaturation or acute pressure-volume overload, or both, as manifested by clinical symptoms of heart failure and measured hemodynamic variables.
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PMID:Myocardial injury in infants with congenital heart disease: evaluation by creatine kinase MB isoenzyme analysis. 709 Sep 95

28 patients with acute myocardial infarct (AMI), 10 of whom presenting left ventricular failure, have been studied. By serial determinations of alpha-hydroxybutyrate dehydrogenase (HBDH) and creatine kinase (CK), the releasing times (RT) and the total releases (TR) of the two enzymes have been calculated, according to the Shell's method modified by Norris. The RT of HBDH have resulted more prolonged in the decompensated patients (48.1 +/- 16.0 vs 37.3 +/- 9.1 h; t = 2.297; p less 0.05). Highly significant correlations have been demonstrated between the total releases of the two enzymes; r = 0.816, p less than 0.01 (with failure); r = 0.766, p less than 0.001 (without failure). For neither enzyme, instead, significant differences have been shown between the TR of the two patient groups. The following conclusions can be drawn. 1) infarct size probably is not the only factor able to induce heart failure during AMI; 2) infarct size can be equally calculated from both HBDH or CK values, though some considerations may make preferable the choice of CK; 3) the more prolonged release of HBDH during heart failure suggests the hypothesis that lactate accumulation is an important factor influencing the appearance of this compliance.
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PMID:[Markers of necrosis and anoxia in the post-infarct heart failure: determination of infarct size (author's transl)]. 728 31

Typical symptoms of acute myocardial infarction led to admission of a 66-year-old female. Creatine kinase (CK) was 720 U/l on admission and together with CK-MB of 108 U/l fitted the clinical picture. The ECG showed complete left bundle branch block. The patient died a few hours later in cardiac failure. Massive hypercalcaemia of 6.2 mmol/l and hyperphosphataemia of 1.6 mmol/l suggested acute primary hyperparathyroidism already clinically which later could be verified by a parathormone level of more than 100 000 ng/l ("C-terminal assay"). At necropsy chief cell adenoma of the epithelial bodies was found, typical changes of primary hyperparathyroidism in the skeleton and kidneys, and disseminated calcifications and fresh necroses of cardiac muscle. The coronaries were normal. This is the first clinical report of fatal acute primary hyperparathyroidism due to hypercalcaemia-induced myocardial necroses.
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PMID:[Calcium induced necroses of cardiac muscle causing death in acute hyperparathyroidism (author's transl)]. 735 14


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