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

Patients with mitral valve prolapse (MVP) frequently experience chest pain which may, expecially in older subjects and males, be difficult to differentiate from angina pectoris. Electrocardiographic (ECG) changes, ventricular arrhythmias, metabolic abnormalities and rare reports of myocardial infarction and sudden death further suggest the presence of an ischemic process in these patients. The recognition of accompanying coronary artery disease (CAD) and exclusion of other causes of ischemia, therefore, may be important in determining the prognosis and appropriate therapy for such patients.
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PMID:Myocardial perfusion scintigraphy in patients with mitral valve prolapse: Its advantage over stress electrocardiography in diagnosing associated coronary artery disease and its implications for the etiology of chest pain. 61 88

First heart sound (S1) energy spectra in isovolumic systole, hemodynamics, and angiographic left ventricular wall motion (LVWM) at rest and with atrial pacing were compared in 27 patients who underwent diagnostic cardiac catheterization and angiography because of chest pain. Eighteen patients were found to have coronary artery disease (CAD) and nine patients, normal coronary arteries. Eleven of the 18 CAD patients (61%) had a mean reduction in the spectral energy of S1 of 6.5 +/- 1.4 (SEM) dB below control (-52%), during interruption of ischemic stress of rapid atrial pacing, compared to only one of nine patients without CAD (P less than 0.05). Only five CAD patients (28%) had an abnormal rise (greater than or equal to 5 mm) in left ventricular end-diastolic pressure (LVEDP) either during or upon interruption of pacing, and six (33%) had ischemic ST-segment depression greater than or equal to mv in the ECG. Similarly two patients free of CAD (22%) had an abnormal increase in LVEDP, and none had ECG evidence of ischemia. Seventeen CAD patients (94%) had segmental LVWM abnormalities at rest or with interruption of pacing, while three patients with normal coronary arteries (33%) had abnormal angiographic LVWM (P less than 0.01). Thus, reduction is S1 spectral energy is a common accompaniment of myocardial ischemia. In the present study, it was more frequently observed than abnormalities in either the ECG or LVEDP, but was not was consistently seen as segmental left ventricular wall motion abnormalities.
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PMID:Spectral energy of the first heart sound in acute myocardial ischemia. A correlation with electrocardiographic, hemodynamic, and wall motion abnormalities. 62 70

Myocardial ischemia at rest occurs only late in the course of coronary artery disease, but transient ischemia can often be induced by increasing myocardial oxygen demand with exercise or atrial pacing. Myocardial ischemia causes a series of physiologic abnormalities that can be detected by assessment of myocardial perfusion, regional mechanical function, electrophysiology, and metabolism. Methods of assessment vary widely in sensitivity, specificity, cost, and ease of application. Although the appropriate choice of diagnostic test may be difficult, the morbidity and mortality that result from myocardial ischemia and infarction and the demonstrated potential of coronary artery bypass surgery to reverse myocardial ischemia before the development of permanent sequellae make the detection of ischemia an important clinical problem. Present methods for quantitating myocardial ischemia are imprecise and difficult to apply but have been used successfully to evaluate the efficacy of therapies designed to reduce the size of myocardial infarction.
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PMID:Myocardial ischemia: detection and quantitation. 62 55

In 12 patients with coronary artery disease and typical exercise-induced angina pectoris hemodynamic and ECG studies were performed at rest and during ergometer load in supine position. During the attacks of angina there was a significant ST-depression in all cases accompanied by elevated pulmonary capillary wedge pressures (PCP) and pulmonary artery mean pressures (PAM). Intravenous administration of 40 mg furosemide showed consistent hemodynamic changes. Cardiac output (CO) dropped significantly by 15.9 per cent at rest (p is less than 0.001) and by 6.9 per cent during exercise (p is less than 0.005). The PCP during exercise following furosemide decreased from 32.9 mmHg to 11.8 mm Hg (p is less than 0.001) and was paralleled by a significant decrease of PAM, indicating reduction of ischemia-related hemodynamic impairment. Furthermore, there was a striking improvement of Ecg findings during ergometer load in 9 of 12 patients as well as a relief of anginal pain in 11 of 12 patients. The present demonstration of antianginal properties of furosemide may be explained by the reduction of ventricular volumes and pressures, resulting in a decrease of myocardial wall stress. These effects are suggested to be related to the peripheral venodilator capacity of furosemide in conjunction with its diuretic properties. Thus, in patients with left ventricular dysfunction secondary to ischemia, intravenous furosemide may have salutary effects on myocardial oxygen requirements resembling the action of nitroglycerin, but without its oxygen-wasting effects on tachycardia.
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PMID:[Effects of furosemide on hemodynamic, electrocardiographic, and symptomatic responses to exercise in patients with angina pectoris (author's transl)]. 63 18

Although many patients with coronary artery disease (CAD) have a positive exercise test without pain, the frequency and significance of this "silent" ischemia is unclear. Therefore, we studied 122 consecutive clinically stable patients with angiographically defined CAD (greater than 75 per cent luminal stenosis) and a positive exercise test. Seventy-eight patients had pain or anginal equivalent during or after a positive exercise test; 44 did not, including 32 (26 per cent) with no symptoms at all. Patients were evaluated as to age, sex, prior myocardial infarction, congestive failure, hypertension, diabetes mellitus, and digoxin or propranolol therapy--in addition to anginal symptoms before, during, or after the exercise itself. Extent of CAD, presence of collaterals, and left ventricular ejection fraction were also determined. All exercise tests were evaluated for evidence of ST-T abnormalities or prior infarction on the control ECG as well as peak heart rate during exercise and post-exercise degree of ST segment depression. There were no significant differences between patients with and without exercise-induced pain in regard to any of the clinical and angiographic features noted above, demonstrating that "silent" myocardial ischemia during or after exercise testing is not uncommon and is not readily attributable to any obvious clinical or catheterization findings. Further studies are necessary to determine if patients with evidence of "silent" myocardial ischemia are especially prone to sudden death.
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PMID:"Silent" myocardial ischemia during and after exercise testing in patients with coronary artery disease. 63 80

We compared ejection fraction, left ventricular end-diastolic pressure, cardiac index and the relation of left ventricular stroke work index to left ventricular end-diastolic pressure during rest and exercise in 60 patients with coronary artery disease. Left ventricular end-diastolic pressure was usually normal at rest (48/60) and abnormal during exercise (46/60) and did not correlate with ejection fraction. Cardiac index was insensitive, usually remaining normal until ejection fraction was less than 0.40. Patients with a normal left ventricular stroke work index response to exercise had higher ejection fractions than those with an abnormal response (p is less than 0.05). However, 9 patients with normal ejection fractions had an abnormal exercise response. This may reflect loss of left ventricular reserve, abnormal compliance or clinically silent ischemia during exercise. Different indices of left ventricular performance may be widely disparate in coronary artery disease, and abnormalities are frequently apparent only during exercise.
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PMID:A comparison of hemodynamic and angiographic indices of left ventricular performance in patients with coronary artery disease. 65 74

Ninety-seven patients with a prior transmural myocardial infarction who underwent coronary angiography and treadmill stress testing were studied retrospectively to assess the reliability of the exercise electrocardiogram in detecting additional disease in patients with a prior infarction. In patients with a previous inferior wall infarction, the S-T response to the treadmill stress test had a high degree of sensitivity (87 percent) and specificity (90 percent) in detecting additional significant coronary artery disease. However, in patients with a previous anteroseptal wall infarction, the S-T response had much less sensitivity (52 percent), but the degree of specificity remained high (90 percent). In this group a positive test suggested the presence of ischemia in the lateral or inferoposterior region of the myocardium, or both. A negative S-T response was of little value in distinguishing among groups of patients with single or multiple vessel coronary artery disease. The presence of an anterior ventricular aneurysm is most likely responsible for this low sensitivity rate because it generates an opposing force to the ischemic vector, thereby cancelling the S-T segment changes and producing a false negative treadmill stress test. The resting surface electrocardiogram proved useful in predicting a false negative exercise test. The presence of Q waves in the precordial leads extending to lead V4 or beyond decreased the sensitivity rate of treadmill stress testing to 33 percent.
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PMID:Comparison of S-T segment changes on exercise testing with angiographic findings in patients with prior myocardial infarction. 67 32

Ischemia is traditionally considered a cause of intermittent left bundle-branch block (LBBB), and some patients have right precordial T-wave inversion in the normally conducted beats. Clinical correlates of T-wave abnormalities were examined in 46 consecutive patients with intermittent LBBB. Thirty-three patients (72%) had at least transient right precordial (V-14) T-wave inversion suggesting ischemia in normally conducted beats. Seventeen such patients had no evidence of coronary heart disease, including five with normal arteriograms. During LBBB conduction, T-wave abnormalities (upright T-waves I, aVL, V5-6) were frequent (48%) and more common than among patients with permanent LBBB (p less than 0.005). The T-wave abnormalities during LBBB conduction occurred in the absence of coronary heart disease in nine patients, including two with normal arteriograms. Thus, right precordial T-wave inversion may result from recent LBBB itself, associated with T-wave abnormalities during the LBBB, in the absence of coronary artery disease.
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PMID:T-wave abnormalities of intermittent left bundle-branch block. 67 81

Experimental work has shown that even small reductions in myocardial perfusion impair contractile performance. We, therefore, studied the relationship between regional perfusion, assessed by thallium-201 scintigraphy and segmental wall motion, quantitated on biplane contrast ventriculograms, in patients with coronary artery disease. We evaluated 270 segments in 54 patients, including 27 without evidence of myocardial infarction. Most normally perfused regions (125 of 140) contracted normally, whereas those with scintigraphic defects at rest were usually asynergic (42 of 46). Surprisingly, 57% (48 of 84) of regions with exercise-induced perfusion defects were also asynergic, including 48% (25 of 52) of those in patients without myocardial infarction. In 22 patients who had intervention ventriculograms, improvement of perfusion abnormalities at rest correlated closely with reversibility of asynergy. Although there was an association between the location and severity of coronary artery stenosis and segmental wall motion, myocardial perfusion during exercise was a significantly better predictor of asynergy. These findings suggest that resting asynergy may occur even in patients without previous infarction, predominantly in regions with jeopardized perfusion. Asynergy in regions with exercise-induced perfusion abnormalities may, therefore, be an indicator of resting ischemia and may be reversible by coronary artery revascularization.
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PMID:Relationship of regional myocardial perfusion to segmental wall motion: a physiologic basis for understanding the presence and reversibility of asynergy. 70 71

Cardiokymography is a technique to assess myocardial wall motion by means of an electromagnetic field induced over the left precordium. The normal cardiokymogram (CKG) is characterized predominantly by systolic inward movement. An abnormal contraction pattern--either at rest or provoked by a stress test--reveals a different tracing with decreased or absent systolic inward motion and/or systolic outward motion (bulging). In 50 patients with suspected coronary artery disease (CAD) the CKG was recorded before and after treadmill exercise test and the results compared to coronary angiography. Out of 33 patients with angiographically documented CAD (more than 50% luminal narrowing) 25 showed an abnormal CKG after exercise. There was one false positive postexercise CKG in the group of 17 patients without angiographically documented CAD. The CKG allows the qualitative assessment of regional myocardial wall motion, which is a sensitive and specific marker of ischemia. In conjunction with an ECG-stress test the CKG helps to detect the evolving ischemic abnormalities of myocardial contraction. The CKG represents a marker of ischemia independent of the ECG and helps to improve the diagnostic accuracy of stress testing for detection of CAD. The stress CKG is especially advantageous in those cases in which the interpretation of the stress ECG is difficult or even not possible. Its simple and inexpensive technique makes it a useful adjunct to the stress ECG in the diagnosis of CAD.
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PMID:[Cardiokymography: noninvasive assessment of the regional myocardial wall motion in the detection of coronary artery disease (author's transl)]. 73 85


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