Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experimental study in 69 dogs examined the effect of isolated and combined use of dibunol and verapamil (isoptin) on the course of reperfusion of ischemized myocardium after 180 minutes' coronary occlusion. Verapamil alone had no protective effect on reperfused myocardium, whereas dibunol, and particularly its combination with verapamil, essentially limited the size of necrosis, reduced plasma CPK activity and animal mortality rate and maintained ultrastructural integrity of cardiomyocytes, which was accompanied by a decrease of plasma lipid peroxidation products and a stabilization of cardiomyocyte sarcolemma. The significance of membrane damage and uncontrolled calcium entrance into cardiomyocytes for the mechanism of myocardial damage at the recovery of coronary circulation is discussed.
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PMID:[Prevention of myocardial damage during reperfusion of the coronary artery in dogs using dibunol combined with verapamil]. 365 22

In order to discuss the mechanism of onset in myocardial infarction (MI), clinical cases were reviewed and various clinical findings were analyzed according to the premise that the onset of MI requires both a predisposition and a trigger. The majority of subjects did present conditions that constituted predispositions for MI, including a history of angina pectoris (especially unstable angina), poor therapeutic results for angina pectoris, organic stenosis of the coronary artery, life changes, and overwork. Patients with multiple factors tended to develop MI without a definite trigger, i.e., onset during sleep or rest whereas, in patients with fewer predisposing factors, it was obvious effort, excitation or stress that triggered MI. However, not a few of the patients presented with no organic stenosis of the coronary artery or no history of angina pectoris. There were patients without ST segment elevation at onset of MI, and patients in whom ST elevation was recorded after onset. These findings suggest the existence of mechanisms other than coronary occlusion in onset of MI. Occlusion of the coronary artery distributed to the infarct region occurred frequently among patients with delayed CPK efflux as well as prolonged chest pain and ST segment elevation. These lines of evidence suggest extension of infarction due to secondary coronary occlusion.
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PMID:Evaluation of clinical factors involved in onset of myocardial infarction. 372 78

The causal connection between the coronary occlusion and the necrosis of the myocardium, as it is verified again and again, is not unequivocal. The favourable effects of the beta-receptorblockers in the acute phase of the infarction of the height of the ST-elevations, the later levels of the CPK and the prognosis of the patients plead for the essential causal importance of the catecholamines in the infarctional process. The catecholamines have an effect on the myocardium increasing the contraction and dissipating oxygen. Through activations of the metabolism in the vascular wall they lead to subintimal swellings and to lesions of the endothelium and increase the aggregation of the thrombocytes. With the decreasing pH, value the flexibility of erythrocytes lowers and thus the microcirculation. Via positive feed-backs the acidosis of the myocardium increases, which via activation of lysosomal enzymes leads to the necrosis of the myocardium. beta-receptorblockers reduced the myocardial contractility, the increased glycogenolysis and the increased activity of the respiratory chains. The lesion of the vascular wall, the aggregation of thrombocytes and the decrease of pH are inhibited, by means of which the spreading conditions of the necrosis deteriorate. By the early application of the beta-receptor blockers the patho-mechanisms lying still in the functional region can be inhibited, thus the danger of early disturbances of rhythm and of the early cardiogenic shock. With the deterioration of the conditions of necrotization the prognosis of the patients with infarction improves.
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PMID:[Beta-receptor blockader therapy in the acute stage of myocardial infarct pathophysiological basis]. 611 91

The time-lag between coronary occlusion and irreversible damage to the myocardium is ill-defined in man. In 10 patients the changes in left ventricular function have been studied after coronary occlusion during diagnostic or therapeutic cardiac catheterization of 1-2 hours' duration. Revascularization was achieved either surgically or through intracoronary streptokinase infusion. The interval between occlusion and onset of extracorporal circulation or reopening was 61 to 119 minutes. Despite enzyme elevation (CPK, CK-MB, SGOT) and appearance of Q-waves in 5 patients, no significant alteration of left ventricular function was noted on repeat cardiac catheterization 10 to 230 days after the accident. These observations, suggest that coronary occlusion of 1-2 hours' duration fails to produce significant irreversible damage to the myocardium despite electrocardiographic and enzymatic signs of myocardial infarction.
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PMID:[Left ventricular function following revascularization for occlusion of a coronary artery lasting 1 to 2 hours]. 665 6

To assess the significance of ST segment shift during the acute phase of non-Q myocardial infarction we studied the clinic echocardiographic, ergometric and coronarographic findings of 46 patients with a first non-Q wave myocardial infarction. The study population was subdivided in 2 subgroups on the basis of acute electrocardiographic change (Group I with ST elevation, Group II with ST depression). Patients with ST elevation had little myocardial infarction with enzymatic (early CPK peak) and coronarographic (low prevalence of coronary occlusion) signs of early spontaneous fibrinolysis. The second group had more diffuse myocardial infraction, higher prevalence of multivessel coronary disease and positive stress test. The ECG changes in this subgroup an probably due to subendocardial necrosis for the presence of collateral flow. The worse intrahospital prognosis of patients with ST segment depression may be related to cardiac function and age.
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PMID:[A non-Q wave myocardial infarct with an up or down shift of the ST segment in the acute phase: the clinical, echocardiographic, ergometric and coronary angiographic correlates]. 832 71

A 53-year-old-man afflicted with combined valvular heart disease and atrial fibrillation was admitted to our department complaining of chest pain. ST elevation on ECG (II, III, aVF) and elevated CPK value were recognized. He was diagnosed as having acute myocardial infarction, and percutaneous transluminal coronary recanalization was performed immediately. The coronary angiogram showed occlusions at the proximal left branch (#12). But these lesions could not be recanalized by 960000 IU urokinase administration. The cineangiogram after one month revealed perfect recanalization of these occlusions. Mitral stenosis with neovascularity to the left atrium and aortic regurgitation were recognized. We supposed this infarction caused by coronary embolism originated from left atrial thrombi. Acute myocardial infarction associated with mitral stenosis has been reported in fifteen cases previously in Japan, but only three cases revealed coronary occlusion in the acute phase with normal coronary artery in the chronic stage. However, there has been no report, except for this case, demonstrating occlusion in two coronary arteries at the same time. So, our case is the first report of the involvement of two coronary artery occlusions.
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PMID:[A case of coronary artery embolism associated with combined valvular heart disease]. 843 64

The present study indicates that iv tetrandrine may transiently decrease blood pressure, while other hemodynamic parameters such as LVP, +/- dp/dtmax, LVEDP, HR and CO may not be significantly altered. During coronary occlusion three of five dogs developed ventricular fibrillation (VF) and died in the control group, i.e. incidences of VF and mortality were 60%. While tetrandrine (Tet) appeared to reduce the severity of ischemic injury. It may alleviate arrhythmia and prevent VF and death in four of the five dogs. Tet also attenuated Ca2+ accumulation in myocardial cell, reduced melondialdehyde (MDA) production in ischemic myocardial and decreased CPK release in comparison with the control. It appears that Tet may have significant protective effects against ischemia induced cardiac damage in anesthetized dogs.
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PMID:[Protective effects of tetrandrine on ischemic myocardia in anesthetized dogs]. 870 39

Angiotensin II (Ang II) and apoptosis contribute significantly to myocardial ischemia-reperfusion (I-R) injury. Evidence indicates that Ang II may activate apoptosis in myocytes. The present study was undertaken to investigate the effects of angiotensin receptor blockers (ARBs), candesartan, on the apoptosis of cardiac myocytes in rats after I-R. Rats were divided into a control group, a candesartan group I (0.015 mg/kg), and a candesartan group II (0.03 mg/kg). Candesartan was intravenously administered 30 min before ischemia. All rats were subjected to 30 min of coronary occlusion followed by 3 h of reperfusion. The data showed that left ventricular (LV) systolic pressure and LV +dp/dt was decreased after administration of candesartan, but increased after reperfusion in the candesartan group II, compared with those in the candesartan group I and control group. LV -dp/dt was decreased after candesartan administration in candesartan group II. The number of apoptotic cells in the candesartan groups (497+/-204 and 543+/-254, respectively) was higher than that in the control group (287+/-166; p<0.05). There was no significant difference in infarct size among the three groups. However, plasma CPK was lower in the candesartan groups than in the control group. Northern blot analysis showed that p53 mRNA was upregulated in the candesartan groups, in association with increased expression of bax mRNA. Immunohistochemical analysis showed that p53 and bax immunoreactivity were increased in both of the candesartan groups. In conclusion, candesartan increased apoptosis in the rat hearts after acute I-R, and this increase was possibly mediated by upregulation of p53 and bax gene expressions. In addition, candesartan was shown to improve LV function, in association with reduction of CPK release.
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PMID:An angiotensin II type 1 receptor blocker, candesartan, increases myocardial apoptosis in rats with acute ischemia-reperfusion. 1140 58

The aim of the present study was to compare the effects of genetic mPGES-1 loss and COX-2 inhibition on myocardial damage after coronary occlusion. mPGES-1(-/-) mice and their wild-type littermates were injected with vehicle or COX-2 inhibitor (celecoxib), and 30min later the left coronary artery was surgically occluded. At 24h, myocardial infarct (MI) volume was measured histologically. Post-MI survival was reduced in WT mice receiving celecoxib (12/20) compared with vehicle-treated controls (12/12) or the loss of mPGES-1 (13/13) together with increased phosphokinase (CPK) and cardiac troponin-I release. Endogenous mPGES-1 expression was unchanged by ischemia in WT mice and absent in mPGES-1(-/-) hearts. COX-2 expression was markedly increased at 24h after MI in WT hearts; this upregulation was largely attenuated in mPGES-1(-/-) mice. We conclude that loss of mPGES-1 prevents the upregulation of COX-2 after myocardial infarct, and in contrast to inhibition of COX-2, does not increase ischemic myocardial damage.
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PMID:Comparison of microsomal prostaglandin E synthase-1 deletion and COX-2 inhibition in acute cardiac ischemia in mice. 1955 11


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