Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A reduction of the infarct-related mortality needs measures to diminish the extension of the infarction. A valuable approach is the thrombolysis, which proved useful in the past years. The aim of this study was to investigate the doctor's and the patient's behaviour related to the delay in hospital admission. During one year, the admission of 148 patients with suspected myocardial infarction was prospectively analysed. The median delay was 7.5 hours. 48% of the patients suffered from an acute myocardial infarction, 17% from an unstable angina, and 35% had no underlying heart disease. 38% reached the hospital within 4 hours (39% of the patients with confirmed myocardial infarction). The total delay was mainly due to the patients behaviour (median delay 3 hours) and in a lesser extent to the doctor's behaviour (median delay 1.5 hours). An immediate admission was only in 14% the first medical measure. In 40% an ECG was performed, in 6% a chest X-Ray, and in 11% laboratory investigations were undertaken. These results confirm the fact that people, especially the patients with known coronary artery disease should be better informed about the nature and the course of the illness and the efficient behaviour in case of onset of complications. The doctor's delay can be shortened by omission of useless diagnostic investigations.
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PMID:[Can the delay in hospitalization be shortened in acute myocardial infarct?]. 279 72

In a prospective study the complications of Heparin-Dihydroergotamine (HDHE) [2,500 units Heparin + 0.5 mg DHE] s c. twice daily as thromboembolic prophylaxis have been studied in patients undergoing a lumbar disc operation. During a two year period 616 patients were operated, 47 patients had to be excluded, 107 patients did not receive HDHE desired by the surgeon; 462 patients received HDHE as described in the protocol. Because the distribution of age, sex, duration of hospitalisation of the 107 patients without HDHE is the same as in the HDHE group, this group can be used as control group. Increased intraoperative bleeding--written down in the operation report--66 patients (14.3%) in HDHE group and 6 patients (5.6%) in the control group. There is no statistic significance between the both groups in superficial and deep wound hematomas, deep vein thromboses or pulmonary embolism. In the HDHE group two death appears. Both patients [a 37 year old, asymptomatic woman and a 65 year old man with mild ischemic symptoms 11 months prior to operation] died because of an acute myocardial infarction. The clinical course and the missing of stenosis or occlusion at autopsy let us think at the possibility of coronary arterial spasm, presumably caused by DHE, as the cause of myocardial infarction. We suggest not to apply HDHE to patients with coronary artery heart disease or with atypical thoracic pain.
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PMID:[Complications of thromboembolic prophylaxis with heparin-dihydroergotamine]. 280 59

Overall, echocardiography was well represented at the American College of Cardiology Annual Scientific Sessions and accounted for input into almost 25% of all abstracts presented. This included not only specialized sessions, predominantly attended by echocardiographers, but the clinical and surgical sessions dealing with virtually any and all forms of heart disease. This is a versatility of which we can be justifiably proud. The newer technique of catheter-mounted ultrasound transducers for intravascular imaging is exciting, and we all await further developments in this field. Finally, it would appear the ground is still fertile for investigation into left ventricular function as it relates to acute myocardial infarction in an era of evermore frequent intervention.
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PMID:Viewpoint on the echocardiographic presentations at the American College of Cardiology Annual Scientific Sessions. 290 88

Left ventricular dysfunction and complex VPCs are independent risk factors for subsequent cardiac death in patients with ischemic or nonischemic heart disease. The use of antiarrhythmic drugs during acute myocardial infarction is discussed. Patients with complex VPCs associated with heart disease should be treated with antiarrhythmic drugs. Drug efficacy should be evaluated by a 24-hour ambulatory ECG recording and by a treadmill exercise stress test. Blood drug levels should be measured at appropriate times. Maintenance doses of the various antiarrhythmic drugs are listed. Electrophysiologic testing with induction of ventricular tachycardia by extrastimulation may predict the clinical efficacy of the antiarrhythmic drug or combination of drugs needed for the long-term treatment of ventricular tachyarrhythmias. Electrophysiologic testing must be used for selecting antiarrhythmic drugs in patients who have experienced sustained ventricular tachycardia or ventricular fibrillation but who are free of VPCs during ambulatory ECG monitoring and exercise stress testing. If patients have life-threatening ventricular tachycardia or fibrillation resistant to antiarrhythmic drugs, surgical intervention is indicated. Complex VPCs in asymptomatic patients without heart disease should not be treated with antiarrhythmic drugs.
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PMID:Management of ventricular arrhythmias. 304 63

Myocardial activities of several enzymes were measured in infarcted and non-infarcted areas of heart sections obtained from eight patients who died after acute myocardial infarction. Similar data were obtained from four patients with cardiovascular disorders who died from causes other than myocardial infarction and from six patients without previously known heart disease. It was found that both non-infarcted and infarcted tissue samples contained considerably altered enzyme activities. This finding explains the low correlations between enzymatic and histological estimates of infarct size previously reported. However, when the residual myocardial activities of different enzymes were compared with each other, a close correlation was found between creatine kinase, alpha-hydroxybutyrate dehydrogenase, and aspartate aminotransferase. It appears that the pathological changes in the myocardial activities of these enzymes may be explained by the phenomenon of diluted myocardium. This indicates that myocardial injury, as estimated from plasma enzyme activities, may still be expressed meaningfully in gram equivalents of healthy myocardium.
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PMID:Myocardial enzyme depletion in infarcted human hearts: infarct size and equivalent tissue mass. 324 32

In recent years calcium channel blockers have emerged as a new class of antiarrhythmic agents for the control of certain supraventricular and ventricular arrhythmias. Electrophysiologically, they are heterogeneous but their main action is mediated through a depressant effect on the slow calcium channel in cardiac muscle. In isolated muscle, their actions are modulated by their reflex actions and by their interaction with the autonomic nervous system due to the nonocompetitive adrenergic blocking actions that some of the compounds exhibit. The major agents exerting antiarrhythmic actions are verapamil, diltiazem, gallopamil, tiapamil, and bepridil; the dihydropyridines are devoid of significant electrophysiologic actions in vivo. Calcium antagonists prolong intranodal conduction time, lengthen the effective and functional refractory periods in the AV node, but exert little or no effect on atrial, ventricular, His-Purkinje, or bypass tract conduction or refractoriness (except in the case of bepridil, which has additional electrophysiologic properties). These effects form the basis of the clinical antiarrhythmic effects of this class of agents. The most striking action is the predictable and prompt termination of reentrant supraventricular tachycardia by intravenous verapamil and diltiazem and the slowing of the ventricular response in atrial flutter and fibrillation. These agents may also be of value in the chronic control of ventricular response in atrial flutter and fibrillation; their role in multifocal atrial tachycardia and other ectopic tachycardias is less well defined. Calcium antagonists reverse ischemic ventricular arrhythmias due to coronary artery spasm but exert little or no action in the usual forms of sustained ventricular tachyarrhythmias associated with severe structural heart disease. They are poor suppressants of premature ventricular contractions. Recent data have established their role in exercise-induced tachycardia occurring in the context of ischemic heart disease; they are also of value in ventricular tachycardia occurring in young subjects developing tachycardia with a right bundle branch block with left axis deviation morphology, an arrhythmia thought to be due to triggered automaticity. The role of calcium antagonists in reducing the incidence of sudden death in the survivors of acute myocardial infarction remains uncertain.
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PMID:Control of cardiac arrhythmias by calcium antagonism. 328 60

ACBGS is indicated in patients with stable angina who have left main coronary artery disease; three-vessel disease; three or four of the clinical variables set forth in the Veterans Administration Cooperative Study; obstruction in proximal third of left anterior descending coronary artery as part of two- or three-vessel disease; and two- or three-vessel disease and exercise-induced ischemic ST-segment depression greater than or equal to 1.5 mm. ACBGS may increase survival in patients with limited exercise capacity. Finally, ACBGS may be indicated to increase the quality of life in patients with disabling angina that is refractory to medical treatment. Patients with unstable angina who have an inadequate response to intensive medical therapy should have emergency ACBGS. Indications for elective ACBGS in patients with unstable angina who respond adequately to medical therapy are the same as those for stable angina. Patients with rupture of the ventricular septum, acute severe mitral regurgitation, and cardiogenic shock with vessels suitable for ACBGS should have urgent ACBGS after acute myocardial infarction. Patients with postinfarction angina after the first few days following acute myocardial infarction, especially non-Q-wave infarction, should be considered for ACBGS. Indications for elective ACBGS in postinfarction patients are the same as those in stable angina. Patients with coronary artery disease, especially those with a significant amount of ischemic myocardium, who must undergo cardiac surgery for valvular heart disease or for congenital heart disease should probably have ACBGS performed at the time of surgery.
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PMID:Indications for coronary artery bypass graft surgery. 331 16

In Australia, mortality rates from ischemic heart disease have declined by more than 40 per cent in the last 20 years. To investigate the reasons for this trend, detailed studies are being conducted in the Hunter Region of New South Wales, an area with high heart disease rates. Data on death rates and attack rates from 1979 to 1984-1985 were obtained from three sources: national mortality records, local hospital statistics, and heart disease registers conducted in 1979 and 1984-1985 using World Health Organization protocols. Age-standardized death rates from ischemic heart disease, hospitalization rates for acute myocardial infarction, and attack rates from myocardial infarction determined from the disease registers all showed declines of approximately 3-4 per cent per year from 1979 to 1985. The results differ from findings in New Zealand, where the decrease in ischemic heart disease mortality has been attributed to fewer sudden deaths. These discrepancies demonstrate the need for carefully standardized studies to gain insight into evolving patterns of heart disease in different populations.
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PMID:Ischemic heart disease in the Hunter Region of New South Wales, Australia, 1979-1985. 338 19

Plasma viscosity and erythrocyte aggregation, as the most important rheological factors in the microcirculation, and fibrinogen were measured in the blood of groups of patients in various stages of coronary-heart disease. Patients with unstable angina had viscosity and fibrinogen levels, even before any manifest infarction, that were higher than those of patients with stable angina. Plasma viscosity and hyperfibrinogenaemia (1.39 +/- 0.08 mPa.s in 48 patients and 394.4 +/- 82.7 mg/dl, respectively, in 33) were comparable to the values in patients with acute myocardial infarction (1.37 +/- 0.09 mPa.s [n = 45] and 390.2 +/- 126.9 mg/dl [n = 27], but significantly higher (P less than 0.02) than in those with stable angina (1.33 +/- 0.08 mPa.s [n = 78] and 295.3 +/- 68.6 mg/dl [n = 44], respectively). This abnormal viscosity in unstable angina plays a part in increasing myocardial ischaemia because oxygen delivery is already diminished and capillary flow slowed down. It thus contributes to progression of the angina and must be taken into account as an additional pathogenetic factor in the clinical instability.
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PMID:[Hyperfibrinogenemia and pathological plasma viscosity. Pathogenetic factors in unstable angina pectoris?]. 339 64

We report semi-quantitative histological data on coronary arteries, collected at autopsy from Japanese of both sexes (Group I) who had had unstable anginal attacks and transient ST elevation or depression in ECG within 1 month before death. The cause of death in all cases was acute myocardial infarction or coronary sudden death. A control group consisted of 28 autopsied patients (Group II) who had died of causes other than heart disease and who had been free from anginal attacks. The frequency of 51-75% and 76-100% luminal narrowing in the coronary arteries in Group I was statistically higher than that in Group II (P less than 0.01). Subendothelial infiltration of monocytes/macrophages with edematous change was most evident in Group I in all segments of the coronary artery, particularly in the proximal portions of the three main branches, regardless of mural or occlusive thrombotic sites of the coronary artery. The subendothelial infiltration of monocytes/macrophages, in terms of luminal narrowing, was the most frequent in the portions with 0-50% luminal narrowing, followed by portions with 51-75% narrowing. The subendothelial infiltration of mononuclear cells with edematous change, observed mostly in the proximal portions of three main branches of the coronary artery in Group I, was attributed to increased subendothelial permeability and endothelial damage caused by coronary vasospasm of recent occurrence. We propose that repeated vasospasm may lead to further progression of coronary atherosclerosis.
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PMID:Increased subendothelial infiltration of the coronary arteries with monocytes/macrophages in patients with unstable angina. Histological data on 14 autopsied patients. 342 53


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