Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A man with known coronary heart disease underwent treadmill exercise testing to determine his functional capacity. The test was negative for ischemia. Ventricular ectopic activity was noted at rest and in the recovery period. On the same day, while viewing a sporting event at home, the patient died suddenly. An ambulatory electrocardiographic recording documented ventricular fibrillations as the terminal mechanism. Ventricular ectopic activity and heart rate increased in the two hours prior to death, and ischemic ST-segment depression was noted at the time of the terminal arrhythmia. It is postulated that myocardial ischemia and catecholamine response lowered the threshold to ventricular fibrillation, thus facilitating the emergence of the fatal arrhythmia.
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PMID:Sudden death during ambulatory monitoring. Clinical and electrocardiographic correlations. Report of a case. 83 Feb 11

Changes in myocardial carbon dioxide (PmCO2) and oxygen tension (PmO2) measured by mass spectrometry have been shown to reflect quantitatively progressive degrees of regional myocardial ischemia associated with stepwise reduction in coronary blood flow. The present study utilized mass spectrometry to assess the severity of regional myocardial ischemia developing during atrial pacing in the presence of a flow-limiting proximal critical coronary artend subendocardial layers was measured by the radioactive microsphere technique. Application of a "critical stenosis" resulted in a 6-mmHg decrease in PmO2 and a 17-mmHg increase in PmCO2 in the region of the myocardium supplied by the stenosed vessel. The addition of atrial pacing resulted in a 3-mmHg further decrease in Pmo2 and a 40-mmHg further increase in PmCO2. In the region of myocardium supplied by the critically stenosed vessel MBF increased in the subepicardial layer, but decreased or remained unchanged in the subendocardial layer. The failure of myocardial blood flow to increase in deeper myocardial layers in response to the increased myocardial oxygen demand of atrial pacing would provide a mechanism for the development of subendocardial ischemia in the presence of a critical coronary stenosis.
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PMID:Effects of atrial pacing on regional myocardial gas tensions with critical coronary stenosis. 83 20

The effects of isoproterenol and dopamine on regional myocardial blood flow were studied in 10 open-chest dogs after acute stenosis of the proximal circumflex coronary artery. Blood flow was determined by the radioactive microsphere technique. Isoproterenol led to a homogenous increase in blood flow in the normal myocardium. In the myocardium with compromised coronary blood flow, isoproterenol led to a relative subendocardial ischemia. This occurred despite increased aortic flow and peak left ventricular dp/dt. Dopamine also increased aortic flow and peak left ventricular dp/dt, but it did not cause regional myocardial ischemia. The findings suggest that dopamine is the preferable inotropic agent in managing low cardiac output in patients with significant coronary artery disease.
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PMID:The effects of isoproterenol and dopamine on regional myocardial blood flow after stenosis of circumflex coronary artery. 83 34

Although coronary angiography defines regions of potential ischemia in patients with coronary-artery disease, accurate assessment of the presence and functional importance of ischemia requires appraisal of regional and global left ventricular function during stress. To perform such assessment, we developed a noninvasive real-time radionuclide cineangiographic procedure permitting continuous monitoring and analysis of left ventricular function during exercise. In 11 patients with coronary disease who had normal regional and global ventricular function at rest, new regions of dysfunction developed during exercise (P less than 0.001), and in 10, global ejection fraction dropped 7 to 47 per cent. Fourteen age-matched normal subjects were studied; during exercise none had regional dysfunction, and each increased global ejection fraction (average increase, 23 +/- 3 per cent [+/-S.E.], P less than 0.001 as compared with patients with coronary disease). Radionuclide cineangiography during exercise permits accurate assessment of the presence and functional severity of ischemic heart disease.
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PMID:Real-time radionuclide cineangiography in the noninvasive evaluation of global and regional left ventricular function at rest and during exercise in patients with coronary-artery disease. 84 93

The relation between myocardial release of prostaglandin and myocardial ischemia was studied in 12 selected patients with multivessel coronary artery disease. These 12 were chosen for analysis because they experienced angina pectoris, ischemic electrocardiographic changes and decreased myocardial lactate uptake during atrial pacing. Simultaneous aortic and coronary sinus blood samples were obtained at rest, during angina and after recovery and were assayed for prostaglandins F, E and A with radioimmunoassay. Cardiac release of prostaglandin F was observed during angina in 11 of 12 patients. Aortic prostaglandin levels remained constant throught each study. During angina, the mean aortovenous difference (+/- standard error) was -0.30 +/- 0.04 ng/ml (P less than 0.001) for prostaglandin F and -0.10 +/- 0.03 ng/ml (Pless than 0.001) for prostaglandin E. There was no significant release of prostaglandin A. Blood samples were also drawn at subanginal heart rates in two patients. Prostaglandin F was released only during angina. In three control patients with a chest pain syndrome and normal coronary arteries, comparable atrial pacing produced no release of prostaglandin F, E or A. These results, together with the known vascular and metabolic actions of prostaglandins, suggest that these pharmacologically active compounds may also play a physiologic role in the cardiac response to ischemia in man.
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PMID:Cardiac prostaglandin release during myocardial ischemia induced by atrial pacing in patients with coronary artery disease. 84 31

Myocardial carbon dioxide tension and intramyocardial S-T segment voltage have previously been shown to provide useful quantitative indexes of the severity of regional myocardial ischemia. This study was designed to determine if (1) changes in intramyocardial S-T segment voltage and myocardial gas tensions, with the addition of atrial pacing, could be used to assess the functional significance of a coronary stenosis, and (2) if changes in S-T voltage recorded in intramyocardial electrodes proved a more sensitive indicator of ischemia than changes recorded in epicardial electrodes. In 12 open chest dogs, a variable constrictor and an electromagnetic flow probe were placed on the proximal left circumflex coronary artery. Myocardial carbon dioxide and oxygen tensions were recorded with mass spectrometry and unipolar intramyocardial S-T segment voltage with multicontact plunge electrodes. Intramyocardial S-T voltage and myocardial carbon dioxide tension showed parallel increases with atrial pacing in the presence of subcritical, critical and supercritical coronary stenoses. In the presence of a critical stenosis, S-T segment changes recorded in deepr myocardial layers were of greater magnitude than those recorded near the epicardial surface. These findings suggest that the severity of myocardial ischemia can be assessed by measuring intramyocardial S-T voltage or myocardial gas tensions at resting and paced heart rates. They also suggest that intramyocardial S-T voltage is a more sensitive indicator of the severity of pacing-induced myocardial ischemia than epicardial S-T changes. Application of this technique to patients undergoing coronary revascularization could allow intraoperative determination of the functional significance of questionable angiographic lesions and a more rational approach to the assignment of priorities to individual arteries when multiple bypasses are being considered.
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PMID:Functional significance of coronary arterial stenoses assessed by regional changes in intramyocardial S-T segment voltage and myocardial gas tensions with atrial pacing. 84 37

The effects of various drugs on delayed activation of the ischemic myocardium and the incidence of ventricular arrhythmias were studied in 34 open-chest anesthetized dogs. The left anterior descending coronary artery was occluded for 6 minutes before and 42 minutes after administration of aprindine (2.85 mg/kg body weight), quinidine (8 mg/kg) and verapamil (0.2 mg/kg) and during infusion of isoproterenol (0.2 microng/min). The time intervals from the onset of the QRS complex to the major deflection of the bipolar electrograms recorded within the normal and ischemic zones were measured at cycle lengths of 500, 400 and 300 msec and were correlated with the development of ventricular arrhythmias. At a cycle length of 500 msec, aprindine increased by 19.5 msec the delay in activation time produced by coronary ligation alone (P less than 0.05), whereas verapamil reduced by 10 msec the extent of ischemia-induced conduction delay (P less than 0.05). The delay in activation time in the ischemic zone was not significantly altered by quinidine or isoproterenol. The incidence of ventricular arrhythmias was increased by aprindine (from 1 in 11 to 8 in 11 dogs), decresed by verapamil (from 3 in 7 to 0 in 7 dogs) and was not changes by quinidine or isoproterenol. Thus, delayed activation of the ischemic myocardium appears to play an important role in the genesis of early arrhythmias due to myocardial ischemia, and drugs that significantly depress conduction in the ischemic myocardium may predispose to the development of ventricular arrhythmia whereas those that improve conduction may be protective. Contrary to their effects on slow channel-dependent conduction, verapamil improved and isoproterenol worsened conduction during ischaemia.
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PMID:Effect of drugs on conduction delay and incidence of ventricular arrhythmias induced by acute coronary occlusion in dogs. 84 39

Cellular consequences of myocardial ischemia were studied in anesthetized dogs. Confirmation of myocardial ischemia was provided by electrocardiographic and biochemical indexes. Prostaglandin F2alpha release into coronary venous blood was significantly elevated during myocardial ischemia, whereas indomethacin treatment prevented this increase in coronary venous prostaglandin F2alpha concentrations. No significant increase in prostaglandin E2 release was observed in response to myocardial ischemia, but indomethacin treatment significantly reduced coronary venous prostaglandin E2 concentrations below those of control values. Within one hour after occlusion of the coronary artery, the S-T segment was significantly altered, and coronary venous prostaglandin F2alpha had increased significantly above the control concentration. These changes persisted during four hours of myocardial ischemia. Plasma creatine phosphokinase activity increased significantly after two hours of myocardial ischemia and remained elevated for the subsequent two hours of ischemia. After four hours of myocardial ischemia, myocardial creatine phosphokinase activity of ischemic myocardium was significantly reduced, and labilization of myocardial treatment prevented increases in prostaglandin release but did not influence other biochemical changes or the electrocardiographic response to ischemia. Thus, prostaglandin release by ischemic myocardial tissue is an early response to the ischemic stimulus.
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PMID:Early prostaglandin release from the ischemic myocardium in the dog. 85 Aug 57

This study was undertaken to determine if computerized tomography (CT scanning) with an EMI cranial scanner could detect edema associated with myocardial ischemia in canine hearts. A localized area of decreased density in the posterior papillary muscle and surrounding myocardium was detected on serial 8 mm CT scan slices of each heart after 60 min of circumflex artery occlusion and 45 min of reflow of blood. The wet/dry weight ratios and previous electron microscope studies of the ischemic posterior papillary muscles revealed edema accumulation. After 1 hour of arterial occlusion and 12 hours of reflow (which produces extensive necrosis and a decrease in the wet/dry ratio) lesions were still discernible but were less consistently as severe. Permanent ligation of the left anterior descending coronary artery and major collateral arteries for 6 hours also resulted in a lesion of decreased density in the distribution of the occluded arteries. Thus, CT scanning can detect, and is a potential means for sequential noninvasive quantitation of myocardial edema associated with ischemia.
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PMID:Detection of edema associated with myocardial ischemia by computerized tomography in isolated, arrested canine hearts. 85 70

Recent studies emphasize the importance of heart rate in the genesis of ventricular arrhythmias during myocardial ischemia. The role of alterations in rhythm has not previously been systematically investigated. In 20 dogs subjected to acute myocardial ischemia and crushing of the sinus node, standard electrocardiographic leads were recorded, as well as His bundle and epicardial electrograms from the normal and ischemic areas. Abrupt pauses in regular atrial pacing did not cause arrhythmias prior to the onset of ischemia; however, during ischemia, atrial pacing with intermittent abrupt pauses resulted in the induction of ventricular arrhythmias beginning after the second conducted beat following each pause (ventricular premature beats, 20/20; ventricular tachycardia, 19/20; and ventricular fibrillation, 8/20). Onset of the arrhythmia was associated with increased delay in activation of ischemic epicardium and fractionation of the electrogram potential of the second conducted impulse. Typical Gouaux-Ashman phenomenon was an incidental observation. Unlike the Gouaux-Ashman phenomenon, which is restricted to the His-Purkinje system, the phenomenon we observed orginated within ischemic myocardium. In vitro studies indicate that the underlying mechanism may be related to postrepolarization refractoriness induced by ischemia.
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PMID:The induction of ventricular arrhythmias in acute myocardial ischemia by atrial pacing with long-short cycle sequences. 85 60


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