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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Echocardiography has many attributes that are desirable for diagnostic and research studies in acute myocardial infarction patients. It does not alter the physiologic state being evaluated, is relatively inexpensive, and does not interfere with other hospital procedures. For these reasons, the test may be repeated frequently and used to monitor the changes after acute infarction. Useful information about left ventricular volume, diastolic pressure, and segmental wall motion may be obtained. Because echocarciographic estimates of stroke volume, ejection fraction, and velocity of circumferential fiber shortening are based on motion seen in only one "ice-pick" view of the heart, it is likely that they will be less reliable in patients with asynergy of contraction. Although a definite diagnosis of acute myocardial infarction cannot be made by echocardiography, abnormalities of wall motion may occur very early and support a clinical impression of infarction. An echocardiogram may also reveal changes suggesting ischemia or infarction (abnormal motion) in patients who have atypical chest pain and no other objective evidence of coronary artery disease.
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PMID:Applications of echocardiography in acute myocardial infarction. 110 66

The records of 12 patients with aortic stenosis previously studied by Fallen et al. in 1967 before and after infusion of isoproterenol were reviewed to assess the value of hemodynamic indexes in predicting myocardial ischemia--defined as less than 5 percent transmyocardial lactate extraction or lactate production. Potential subendocardial blood supply was estimated from a diastolic pressure-time index (DPTI), calculated from the tension-time index (TTI). The ratio DPTI/TTI was used to estimate the supply/demand relation. Of eight patients with aortic stenosis but without associated coronary artery disease, four (Group A) metabolized lactate normally after administration of isoproterenol, and four (Group B) had biochemical evidence of ischemia. Three of four patients (Group C) with aortic stenosis and associated coronary artery disease had abnormal glycolysis after administration of isoproterenol. Calculated aortic valve areas were comparable in all groups. In patients with aortic stenosis alone, abnormal lactate metabolism occurred whenever DPTI/TTI was less than 0.30 (P smaller than 0.01) (Group B). Two of three patients with aortic stenosis and associated coronary artery disease (Group C) showed abnormal lactate metabolism when DPTI/TTI was greater than 0.6; this ratio was below 0.3 in the third patient. These results suggest that the supply/demand relation calculated from these readily obtained indexes may be useful (1) in predicting in which patients with aortic stenosis ischemia will develop, (2) in distinguishing the role played by associated coronary artery disease, and (3) as an adjunct to calculation of valve area since the quantitation of associated aortic regurgitation is not necessary.
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PMID:Ischemia in aortic stenosis: hemodynamic prediction. 113 Feb 86

Myocardial imaging with 133-Xe and a gamma camera was employed to evaluate total and regional myocardial blood flow. The technique detected vasodilatation after injection of papaverine or diatrizoate. Contrast medium caused transient vasodilatation with return to baseline flow within five minutes. Myocardial tissue flow tended to decrease as coronary artery stenosis became more severe. There was overlap of flow measurements in patients with and without coronary artery disease. Coronary flow measurements made at rest are not considered to be an essential clinical tool. gpreater diagnostic benefit is obtained from the scintigram which distinguishes between akinesia caused by ischemia and akinesia due to extensive scarring.
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PMID:Regional Myocardial Blood Flow Measurement in the Evaluation of Patients with Coronary Artery Disease. 114 55

The occurrence of episodic painless ST segment elevation at rest was documented by continuous electrocardiographic monitoring in four patients with ischemic heart disease who did not conform to the classic description of Prinzmetal's variant angina. The degree of ST segment elevation in the absence of pain was generally similar to that seen with painful episodes. Clincopathological correlation was available in three of these patients: two were found to have severe coronary artery disease and one had a 70% obstructive lesion in the right coronary artery only. Three patients subsequently developed a myocardial infarction. Our observations suggest that transient painless ST segment elevation at rest is a serious finding reflecting severe ischemia and more likely to be "preinfarctional" than "variant" angina. Long term monitoring is useful in detecting silent severe ischemia that may sometimes occur with potentially lethal arrhythmias as demonstrated in one case.
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PMID:Case studies: Significance of episodic painless ST segment elevation at rest in ischemic heart disease. 115 Nov 96

Physiologic concepts relating to reperfusion of ischemic areas of myocardium may be applied both to acute coronary insuficiency, manifested by angina pectoris, and to restoration of coronary blood flow by coronary bypass procedures, currently employed both in acute myocardial infarction and in chronic myocardial ischemia for relief of angina pectoris. Of the information currently available from experimental studies, much may be applicable to the clinical situation. After acutr transient coronary occlusion mechanical and electrical properties of the ischemic area rapidly return to normal, but there is prolongation of tension development and occurrence of ventricular arrhythmias; implications of these phenomena for clinical coronary ischemia deserve exploration. Following more prolonged coronary ischemia, results of experimental reperfusion appear to be variable and, although restoration of function following several hours of ischemia is possible, certain deleterious effects are often observed in the form of myocardial edema and hemorrhage. Clinical use of bypass procedures in acute myocardial infarction suggests that results may be good, but that deleterious effects are occasionally observed; occurrence of the later requires definition and explanation. Restoration of myocardial blood flow in the presence of normal left ventricular function in chronic coronary artery disease, and failure to reverse functional abnormalities when left ventricular damage has already ensued in the clinical situation, appears to be well established; however, better methods to assess the potential for recovery of function following revascularization are needed in both acute and chronic coronary artery diseases. It is anticipated that more careful exploration of pathophysiology both in the catheterization laboratory and in the operating room may aid this process.
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PMID:Effect of reperfusion in acute ischemia and infarction. 115 38

While left ventricular (LV) performance in patients with coronary artery disease (CAD) has been extensively investigated, little attention has been given to right ventricular (RV) function in this disease. For this purpose, a new geometric model for RV volume has been developed and RV end-diastolic volume index (EDVI), end-systolic volume index (ESVI), stroke volume index (SVI) and ejection fraction (EF) have been determined from biplane RV cineangiograms in 26 patients. Eight patients served as normal (control) subjects (group I). Eighteen patients with obstructive CAD comprised two other groups: six who had no significant disease of the right coronary artery (RCA) (group II) and 12 who had a high grade RCA lesion (group III). The mean values for EDVI, SVI and EF in group I were 76 +/- 11 ml/m2, 50 +/- 6 ml/m2, and 66 +/- 6%. The only significant difference between groups I and II was that SVI was lower in group II than in group I (P less than 0.01). No measurements in groups II and III were statistically different from each other. However, markedly subnormal values were found in group III (EDVI: 61 +/- 16 ml/m2, SVI: 33 +/- ml/m2 and ef: 52 +/- 7%); all values being significantly lower (SVI and EF: P less than 0.001; EDVI: P less than 0.05) than in group I. RV end-diastolic pressure was normal in all patients. These findings may related to 1) reduced RV compliance, 2) distorted LV geometry, 31 possible RV ischemia or 4) reduced Frank-Starling effect.
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PMID:Right ventricular performance in patients with coronary artery disease. 115 72

Intermittent murmurs of insufficiency (MI) associated with left atrial "V waves" often are ascribed to papillary muscle (PM) ischemia in coronary artery disease but their cause is not clear with unobstructed coronary arteries. In 49 open-chest dogs, left atrial, left ventricular, and aortic pressures and regional coronary flow (microsphere method) were measured. Subendocardial (SE) ischemia (endocardial/epicardial flow ratios less than 1.0, ischemic intracavitary electrocardiograms) was produced by lowering the SE supply/demand ratio (diastolic pressure time index times O2 content per tension time index) to below 12 with either arteriovenous fistulas, anemia, or aortic stenosis. In nonischemic hearts, O2 delivery to the PM was 20 percent more than to the SE (P less than 0.01) and rose with increasing demands. When ischemia occurred, O2 delivery per unit demand fell 35 percent (p less than 0.01) to the SE muscle, and PM O2 delivery decreased more strikingly (55 percent, p less than 0.01). This reduction in PM and SE O2 delivery often was associated with a "V wave" in the left atrium which disappeared when the intervention impairing the adequacy of O2 delivery was discontinued. We conclude that PM ischemia (1) is the probable cause of intermittent MI, and (2) can be predicted from readily obtained measurements of blood pressure and O2 content.
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PMID:Papillary muscle ischemia with patent coronary arteries. 116 9

Myocardial metabolism had been studied in 54 patients with continuous sampling of arterial (A) and coronary sinus (CS) blood during 8- to 10-min periods of control in sinus rhythm, rapid atrial pacing and recovery. The results showed that 17 subjects were normal or had insignificant coronary artery disease (CAD; nonischemic group = NI); 37 patients had significant CAD (ischemic group = 1) and developed clinical, hemodynamic, and electrocardographic evidence of myocardial ischemia during pacing, characterized by angina, elevated left ventricular end-diastolic pressure, and depressed ST segments. During pacing-induced ischemia the following metabolic abnormalities were detected: (1) myocardial anaerobiosis indicated by lactate % uptake ((A-CS)/AS X 100) of -17.2 +/- 5.0% (mean +/- SE); (2) myocardial loss of K+ suggested by an A-CS difference of -0.25 +/- 0.08 mEq/liter (N=18); (3) small but significant loss of inorganic phosphorus (Pi) of -1.0 +/- 1.4% (N=18); and (4) elevation of CS blood creatine phosphokinase activity (N=5). These metabolic abnormalities were temporally related to the other manifestations of myocardial ischemia and were not seen in the NI; Lactate production and Pi loss occurred in 75 and 55% of the IG, respectively, suggesting that accelerated anaerobic glycolysis was the best indicator of myocardial ischemia in man. K+ loss was an unreliable index in this experimental situation, since tachycardia alone caused significant K+ egress from the heart. Lactate production and K+ loss were reduced by nitroglycerin, which abolished angina and improved hemodynamics and electrocardiographic manifestations. That these metabolic abnormalities were not observed in all 1 patients may have been related to methodology, the random distribution of CAD, and the fact that the chemical composition of the CS blood reflects the metabolic balance of both well oxygenated and ischemic areas of the myocardium.
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PMID:Metabolic indicators of myocardial ischemia in man. 120 71

Over the span of two or three days in August, 1972, in two separate communities in eastern Massachusetts two men, one aged 39, the other 66, each without previous overt heart disease, were stung by wasps. Each went into shock rapidly after an interval of over a half-hour developed chest pain and, later, sequential electrocardiographic changes diagnostic of acute myocardial infarction. Each survived; each had normal electrocardiograms before the sting. Though preexistent coronary artery disease can be excluded in neither, the view is favored that acute myocardial infarction in each was caused by deficient coronary perfusion secondary to anaphylactic shock induced by the wasp stings. An intriguing case was just recently reported58 of a 62-year-old man with previous angina who developed pulmonary edema but no chest pain following wasp sting and went on to show rapidly reversed electrocardiographic changes attributable to subendocardial ischemia or infarction. In a sense, this sequence fills the gap as an intermediate phase between the normal and the two individuals described here who developed pain after anaphylactic shock, then proceeded, perhaps through this phase, to develop transmural infarction.
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PMID:Acute myocardial infarction following wasp sting. Report of two cases and critical survey of the literature. 125 36

Inverted T waves due to coronary artery disease and previous myocardial infarction were observed to revert ot normal, upright position during ischemia in 38 patients. The normalization of inverted T waves was seen on the electroencephalograms of 19 patients during spontaneously occurring angina pectoris and of 11 patients when ischemia was provoked by treadmill exercise; for 8 patients, normalization occurred during the administration of isoproterenol hydrochloride and during the consequent episode of angina pectoris. The mechanism for normalization may be the algebraic sum of the extent of ST segment elevation and the amplitude of the T waves of acute ischemia plus the extent of preexisting ST segment depression and the degree of T wave inversion, to result in isoelectric ST segment and upright T wave. As with myocardial infarction, reciprocal changes may also be recorded. However, the reciprocal nature may be masked since either acute ST segment elevation of T wave inversion, or both, may not be recorded in the leads reflecting the ischemic area because of normalization.
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PMID:Normalization of abnormal T waves in ischemia. 126 47


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