Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With use of semiselective xenon-133 injections and gamma camera recording, myocardial scintigrams were obtained in a series of 20 patients with angina pectoris, abnormal exercise electrocardiograms and normal coronary arteries. Ten patients (Group I) exhibited localized perfusion defects and the other 10 (Group II) a hjemogenous uptake of the tracer. Group I was characterized by more past myocardial infarctions and, most significantly, by male preponderance (P less than 0.001). Computer analysis of regional xenon-133 washout curves revealed that every patient in Group I had a reduced flow rate in the area of the perfusion defect (P less than 0.001). A comparison of this group with 26 patients with similarly abnormal scintigrams but coronary arterial obstruction revealed that myocardial perfusion was 16 to 18 percent greater in the group with normal coronary arteries. In three patients of this group, myocardial perfusion rates were not augmented by atrial pacing in contrast to the response in patients with coronary arterial obstruction. The data demonstrated localized perfusion abnormalities in half of the patients with angina pectoris and normal coronary arteries and constitute evidence that a metabolic disorder is not the sole mechanism for ischemia in this syndrome.
Am J Cardiol 1977 Mar
PMID:Regional myocardial perfusion abnormalities on xenon-133 imaging in patients with angina pectoris and normal coronary arteries. 84 56

Although technetium-99m stannous (99mTc[Sn]) pyrophosphate has been shown to be a specific and sensitive index of myocardial infarction, abnormal images have been reported in patients with unstable angina or ventricular aneurysm. Sixty-one subjects--33 patients subjected to maximal treadmill stress testing, 23 normal subjects and 5 patients with a calcified aortic or mitral valve--underwent imaging with 99mTc(Sn) pyrophosphate to determine whether abnormal images are associated with (1) exercise-induced ischemia, (2) delayed clearance of tracer from the blood pool, or (3) calcified intracardiac structures. Myocardial injury was excluded on the basis of normal MB creatine kinase (CK) values in all patients with stress testing. All eight patients with an abnormal exercise stress test had normal images. Four of 25 patients with a normal exercise stress test had diffusely abnormal images. In some normal subjects diffusely abnormal images were present 60 minutes after injection of the tracer, but became normal 90 to 120 minutes after injection. Variations in clearance of tracer from the blood pool were noted in this group. Patients with a calcified aortic or mitral valve had normal images. We conclude that (1) exercise-induced ischemia is not associated with abnormal 99mTC(SN) pyrophosphate images; (2) images are not necessarily abnormal in patients with a calcified valve; and (3) delayed removal of tracer from the cardiac blood pool may result in diffusely abnormal images even in normal subjects; in these cases, repeat images should be obtained at least 2 hours after injection of the tracer to avoid false abnormal images.
Am J Cardiol 1977 Mar
PMID:Technetium-99m stannous pyrophosphate scintigrams in normal subjects, patients with exercise-induced ischemia and patients with a calcified valve. 84 57

Fifty-six patients who subsequently underwent selective coronary angiography were studied noninvasively with relative myocardial perfusion scintigraphy with rubidium-81 and graded stress electrocardiography in an attempt to evaluate the ability of these tests to identify the presence of significant ischemia and, indirectly, coronary stenosis. Both the sensitivity (0.91) and specificity (0.91) of perfusion scintigraphy were impressive and better than the sensitivity (0.79) and specificity (0.64) of stress electrocardiography, the specificity of scintigraphy significantly so (P less than 0.05). Additionally, perfusion scintigraphy yielded excellent localizing information and was reliable even in the presence of drug effect, conduction abnormalities and nonspecific electrocardiographic abnormalities. Rare cases of triple vessel disease, prior myocardial infarction or single vessel disease with widespread collateral vessels were causes of scintigraphic misdiagnosis. Although ribidium-81 perfusion scintigraphy with the scintillation camera requires special collimation and significant quality control, it provides well resolved images and may prove particularly useful in facilitating quick successive multiple scintigraphic cardiac studies.
Am J Cardiol 1977 Mar
PMID:Myocardial stress perfusion scintigraphy with rubidium-81 versus stress electrocardiography. 84 58

Dispersion of the effective refractory period was measured in anesthetized dogs using a computerized system and bipolar epicardial electrodes or, alternatively, transmural plunge electrodes. Measurements were made at 1 minute intervals during short (5 minute) and long (15 minute) periods of coronary arterial ligation and for 3 to 5 minutes after release of the ligatures. Both transepicardial and transmural temporal dispersion of refractoriness correlated well with the increased vulnerability to spontaneous ventricular fibrillation during short periods of ligation and the relative electrical stability observed toward the end of the longer periods of ligation. During reperfusion, transmural dispersion increased somewhat after ligature release in the longer-term experiments but the increase did not appear adequate to explain the associated large incidence of spontaneous arrhythmias after release. Effective refractory periods measured at one nonischemic and five ischemic electrode sites at intervals as short as 20 seconds revealed abrupt shortening of the refractory period at all ischemic sites during the 1st minute of reperfusion, resulting in a large but short-lived electrical gradient between the ischemic and nonischemic myocardium. This increased dispersion between the ischemic and nonischemic myocardium occurred at a time of maximal vulnerability to reperfusion arrhythmias. However, this increased dispersion was greater after the 5 minute than after the 15 minute periods of ligation and thus does not fully explain the greater incidence of reperfusion arrhythmias after ligature release in the longer-term studies. Although arrhythmias of acute ischemia are associated with increased dispersion of refractoriness within theischemic segment and reperfusion arrhythmias with dispersion between ischemic and nonischemic segments, other electrophysiologic alterations probably play an important role in the genesis of the arrhythmias of reperfusion.
Am J Cardiol 1977 Mar
PMID:Dispersion of effective refractory period during abrupt reperfusion of ischemic myocardium in dogs. 84 60

Angina with "normal coronary arteries" might best be thought of as "angina with coronary dysfunction". It seems likely that this syndrome is due to inadequate regional myocardial perfusion with manifestations similar to those seen when ischemia results from occlusive coronary artery disease. The prognosis of the disorder is favorable, but occasional catastrophic events occur. It appears likely that maldistribution of perfusion results from dynamic changes affecting proximal, and perhaps distal coronary vessels, potentially mediated by vasoactive substances released from platelets precipitating or exacerbating coronary arterial spasm. Clarification of the pathogenesis of the syndrome should permit implementation of more effective therapy and prevention of the rare malignant sequelae of this disorder.
Adv Cardiol 1977
PMID:Angina with "normal coronary arteries". A misnomer. 84 83

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.
Am J Cardiol 1977 Apr
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.
Am J Cardiol 1977 Apr
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

To determine the sequence of changes in segmental myocardial function, regional lactate metabolism and global left ventricular function induced by mild regional ischemia, blood flow in the left anterior descending coronary artery of 10 dogs was reduced by 10 percent decrements with use of a screw clamp. At each level of flow, segmental mechanical function and regional metabolism were assessed, the former with use of a mercury-in-Silastic length gauge and the latter with transmyocardial lactate balance measurements obtained with sampling from the anterior interventricular vein. Coronary arterial flow at the onset of regional lactate production was 48 +/- 4 percent (mean +/- standard error of the mean) of the control value. The onset of segmental mechanical dysfunction coincided with the onset of lactate production. Epicardial S-T segment abnormalities over the ischemic zone usually could not be detected until coronary flow was further reduced. After the onset of regional ischemia there was a linear correlation between coronary arterial flow and regional lactate production. At the onset of mild regional ischemia, defined as the onset of regional lactate production, no significant or directionally consistent changes were noted in standard measurements of global left ventricular performance, including heart rate, mean aortic pressure, left ventricular end-diastolic pressure, cardiac output, stroke volume, stroke work and peak positive dP/dt (maximal rate of rise of pressure). However, peak negative dP/dt (maximal rate of pressure decrease) decreased from 99 +/- 2 to 89 +/- 3 percent of the control value (P less than 0.0005) coincident with the onset of ischemia. It is hypothesized that dyssynchronous wall motion in the ischemic zone during isometric relaxation accounts for this decrease in peak negative dP/dt.
Am J Cardiol 1977 Apr
PMID:Early changes in regional and global left ventricular function induced by graded reductions in regional coronary perfusion. 84 38

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.
Am J Cardiol 1977 Apr
PMID:Effect of drugs on conduction delay and incidence of ventricular arrhythmias induced by acute coronary occlusion in dogs. 84 39

Six men, clinically diagnosed as having coronary heart disease, had postexertional ventricular fibrillation after maximal exercise testing. The common featureof their treadmill performance was "exertional hypotension," that is, a decrease or a limited increase (10 mm Hg) in systolic blood pressure. All six men were successfully resuscitated with electircal defibrillation. The major indication for electrocardiographic monitoring is the detection of major ventricular arrhythmias and changes in QRS-ST-T of acute myocardial infarction or severe ischemia, all of which are urgent indications for stopping exertion. Close supervision both during and after exercise testing is essential, particularly in men with severe coronary artery disease; monitoring of changes in systolic pressure during and shortly after exercise testing is as important as searching for changes in the -S-T segment.
Am J Cardiol 1977 May 26
PMID:Exertional hypotension and postexertional ventricular fibrillation in stress testing. 86 Jun 95


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