Degree Of Myocardial Damage Research Articles

Enhanced thrombolytic efficacy and reduction of infarct size by simultaneous infusion of streptokinase and heparin.

Because paradoxical increase in thrombin activity was reported after the administration of streptokinase in patients with acute myocardial infarction the velocity of reperfusion and degree of myocardial damage were studied when heparin was infused during rather than after streptokinase infusion. Thirty seven consecutive patients with acute myocardial infarction were randomised to receive intravenous heparin during (group 1, n = 18) or after (group 2, n = 19) streptokinase (1.5 megaunits over 60 minutes). Markers of reperfusion were monitored every 15 minutes for 3 hours. The serum concentration of creatine kinase was measured every 2 hours. The two groups were similar in terms of age and sex distribution, infarct site, time to treatment, and baseline myocardial ischaemia. Patients in group 1 had a significantly shorter mean (SD) reperfusion time (57 (35) minutes v 101 (47)). From 60 to 120 minutes after randomisation there were significant differences in ST segment elevation between the groups. Serum creatine kinase MB peaked earlier (8 (2) hours) in group 1 than in group 2 (10 (4) hours). The peak concentration was significantly lower in group 1 (87 (47) mU/ml) than in group 2 (134 (96) mU/ml) and infarcts were smaller (25.2 (9.8) gram equivalents/m2) in group 1 than in group 2 (35.1 (10.2) gram equivalents/m2). Simultaneous infusion of heparin and streptokinase speeds up the appearance of signs of reperfusion and reduces infarct size.

Myocardial Protection: Role of Anesthetic Drugs

Summary and Conclusion Most anesthetic techniques can conceivably have favorable effects on myocardial ischemia in certain circumstances by reducing the hemodynamic and neurohumoral stress response to pain, anxiety, and surgical trauma.12,14 There is no one ideal anesthetic drug or technique for all situations and there are many complicating factors that may influence whether or not a specific drug has the potential to protect against ischemia. These include interactions with other drugs,88 the magnitude of the stress response to surgery, the degree of myocardial damage, the presence of coronary spasm, and the degree of collateral coronary circulation. Of the inhalation anesthetics, halothane and enflurane demonstrate protective effects on the nonfailing ischemic heart in animals when excessive hypotension is avoided. In patients with coronary artery disease they are associated with a low incidence of myocardial ischemia when sensitive methods of detection are used. Isoflurane may not be the drug of choice for patients with ischemic heart disease because of its potential for causing the adverse redistribution of coronary flow. Because they either decrease or have minimal effects on myocardial oxygen consumption, fentanyl, sufentanil, diazepam, midazolam, and etomidate are the intravenous agents most likely to favorably influence myocardial ischemia. None are complete anesthetics by themselves and thus have the potential to inadequately blunt the stress response to surgery or laryngoscopy. They are probably more effectively used in combinations with each other or with an inhalation anesthetic during periods of stimulation. We currently have a great deal of knowledge about how the anesthetic agents affect hemodynamic determinants of myocardial oxygen consumption and supply. It is well recognized that the use of anesthetic drugs to limit myocardial oxygen consumption while avoiding excessive decrements in supply has the potential to reduce the incidence of and improve tolerance to myocardial ischemia. Further work needs to be done to determine how anesthetic agents affect the occurrence of coronary vasospasm, how they influence intracellular metabolism during myocardial ischemia, and whether they have any effect on coronary thrombosis.

Inhibitory effect of anoxia on reperfusion- and digitalis-induced ventricular tachyarrhythmias.

In the isolated rat heart, anoxia or ischemia do not induce important ventricular tachyarrhythmias (VTAs). During the 1st min of reperfusion, VTAs are frequent. The frequency and severity of VTAs during reperfusion depend on the duration and the extent of the myocardial damage. Anoxia abolishes reperfusion-induced VTAs as did verapamil (2.5 X 10(-6) M). In isolated guinea pig hearts, beta-methyldigoxin (1.27 X 10(-6) M) provokes VTAs that are progressively increasing in severity. After 26 min of perfusion with an oxygenated beta-methyldigoxin-containing medium, all isolated guinea pig hearts develop ventricular fibrillation. By changing the abnormal rapid ventricular rhythms into progressively slower irregular idioventricular rhythm, anoxia counteracts all types of VTAs exhibited by the intoxicated guinea pig hearts. In conclusion, two conditions seem to be necessary for the development of VTAs during the reperfusion: 1) a sufficient degree of myocardial damage provoked by the preceding ischemic perfusion, and 2) the presence of oxygen during the reperfusion.

Clinical Estimation of Infarct Size by201 Thallium Perfusion Scintigraphy and by Creatine Kinase‐MB in Early Myocardial Infarction

201Thallium (201Tl) perfusion scintigraphy was performed in 22 patients with first acute transmural myocardial infarction within the initial 12 h after onset of symptoms. The size of the abnormally perfused area on 201Tl images was estimated by visual analysis and by a computer-assisted technique. 201Tl values for infarct size were compared to a biochemical estimate of infarct size using the cardiac specific esoenzyme creatine kinase-MB (CK-MB) and total creatine kinase (CK). Estimates of myocardial damage obtained from the visual and computer-assisted analysis of the 201Tl images showed a statistically significant correlation with the enzymatic estimates of infarct size. These results suggest that quantitative evaluation of 201Tl image defects may provide useful information regarding the degree of myocardial damage in the very early stages of acute infarction before biochemical estimates of infarct size are available, and that sequential imaging with 201Tl might provide an independent method of monitoring evolutionary changes in myocardial damage.

Importance of Heart Antibody in Infective Endocarditis

Antiheart antibody (HAb) was observed in nine of 13 patients (62%) with infective endocarditis (IE). This increased prevalence of HAb in patients with IE did not appear to be a result of a generalized immunologic disturbance. Antiheart antibody was present in seven of eight patients who had clinical heart failure as a complication of their disease. In these patients, HAb possibly reflected the degree of myocardial damage induced by the endocarditis. The disappearance of the HAb from the serum was associated with recovery of the patient from the infection. The persistence of HAb with treatment signaled a grave prognosis. ( Arch Intern Med 137:591-593, 1977)

Protection against epinephrine induced myocardial necrosis with clofibrate

To investigate the possibility that oral clofibrate interferes with catecholamine-induced platelet aggregation and myocardial necrosis, 12 dogs pretreated with oral clofibrate and 10 dogs not pretreated were infused with epinephrine, 4 μg per kilogram of body weight per minute. After killing the dogs 1 week later, the degree of myocardial damage was assessed histologically. All control dogs had myocardial necrosis, 6 with 3+, 2 with 2+, and 2 with 1+ necrosis. Seven of the 12 pretreated dogs had no necrosis, 2 had 1+, and 3 had 2+ necrosis. These differences are statistically significant (p < 0.01). Previous studies have shown that norepinephrine infusions will induce intravascular platelet aggregation in the dog heart and pretreatment with antiplatelet aggregating agents will prevent epinephrine-induced myocardial necrosis. The demonstration of oral clofibrate's protection against epinephrine-induced myocardial necrosis suggests that clofibrate may exert a similar antiplatelet aggregating effect. It is possible that oral clofibrate exerts a beneficial effect in human coronary artery disease via a similar mechanism.

Recognition of Postoperative Acute Myocardial Infarction

Routine enzymatic and electrocardiographic diagnosis of postoperative acute myocardial infarction (AMI) is frequently inconclusive. The detection and quantitation of isoenzymes of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), especially the cardiac-specific CPK-MB isoenzyme, have allowed earlier recognition of AMI in nonsurgical patients. Serial monitoring with these methods has been utilized during the postoperative period in 20 noncardiac surgical patients and 100 patients undergoing coronary artery bypass grafting (CABG). In the noncardiac surgery group, both isoenzymes were accurate in diagnosing AMI in the early postoperative period. Of the 100 patients in the CABG group, CPK-MB appearance in 21 correlated with AMI by electrocardiogram. The absence of CPK-MB postoperatively in 49 patients permitted a 73% incidence of new ECG abnormalities to be effectively resolved. Autopsy confirmation of AMI was obtained in two patients with nondiagnostic ECG, but with elevated CPK-MB. The elevated CPK-MB without ECG evidence of AMI in the remaining patients could possibly be explained by varying degrees of myocardial damage produced by intraoperative cardiac manipulation. These data demonstrate the value and sensitivity of CPK-MB isoenzyme determinations in the early recognition of postoperative acute myocardial infarction.

Myocardial revascularization by bilateral internal mammary artery implantation: Experimental and clinical data

Laboratory experimentation demonstrated widespread myocardial revascularization after bilateral internal mammary artery implantation and concomitant triple coronary ameroid occlusion. The feasibility of operating on patients with severe triple coronary artery disease and myocardial failure in need of widespread myocardial revascularization is described. The patients in this series were failing in spite of competent medical therapy and were considered from all aspects as a salvage group of patients with progressive coronary artery disease. No patient was refused operation on the basis that the disease process was too severe. There was no question before operation that these patients needed additional myocardial circulation, but we did question whether the operative risk might be prohibitive or the degree of myocardial damage too extensive to allow any worthwhile result. Unfortunately, preoperative enzyme and metabolic studies did not appear to be sufficiently accurate in determining the extent of the myocardial damage or whether sufficient functioning myocardium remained. As a consequence, operation was undertaken in this pilot group of patients to determine risk and results. It is realized that the time interval after operation is too short to allow a proper evaluation of the benefits obtained. Cineangiographic evaluation performed in 15 patients from three to five months postoperatively revealed 28 of the 30 implanted internal mammary arteries to be patent. Sixteen of these vessels demonstrated new anastomotic channels between the implant and the diseased coronary arteries. An additional 6 patients had new anastomotic channels between the extracardiac portion of the internal mammary arteries and the coronary arteries. A new cineangiographic technic for determining postoperative volume flow through the internal mammary arteries, described in detail in another article, was employed in 4 patients. A significant amount of additional blood flow to the ischemic myocardium was demonstrated by these studies.

Influence of Protein and Thiamine Intake on Pathologic and Weight Changes Produced by Atabrine.

SummaryThe hepatic damage resulting from continued atabrine administration was more severe in rats maintained on a low protein diet than in those on a high protein diet. On the other hand, the incidence and degree of myocardial damage were slightly greater in the rats fed the high protein diet. Thiamine deficiency had no effect upon the hepatic and myocardial damage produced by atabrine. The daily administration of atabrine to rats maintained on high and low protein rations resulted in a retardation of growth beyond that observed in their isocaloric controls which did not receive atabrine.