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)

To assess the accuracy of angiographic determinations of disease of coronary arteries and left ventricular myocardium we compared clinical with postmortem coronary arteriograms and left ventriculograms with myocardial pathology in 28 patients, all of whom died postoperatively and within three months of angiography; 19 had ischemic heart disease, four valvular heart disease, and five both. Comparison of pre and postmortem lumenal occlusion in 315 epicardial coronary segments, excluding those operated upon, showed greater than 50% narrowing discrepancies in 21 (7%). Significant coronary artery lesions were overestimated in six and underestimated in 15. Of the six overestimations, three appeared to be due to coronary spasm; of the 15 underestimations, 12 were due to overlapping images; six discrepancies were unexplained. Comparison of wall motion in 140 ventriculogram segments with myocardial pathology, excluding any post-study or perioperative injury, showed good correlation of reduced motion with 48 (34%) infarcted and 10 (7%) aneurysmal segments. However, 58 (41%) other segments had poor or absent ventriculogram motion, with structurally normal myocardium and patent coronary artery supply; 19 were on infarct margins and 39 in dilated or hypertrophied hearts. Thus, premortem coronary arteriographic occlusions generally indicate atherosclerotic narrowing; but decreased or absent segmental wall motion frequently does not indicate a myocardial lesion. It may be attributable to ischemia in the distribution of a critically narrowed coronary artery or it could be due to abnormal ventricular topography.
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PMID:Correlation of coronary arteriograms and left ventriculograms with postmortem studies. 86 69

Tricuspid regurgitation developed in two patients after inferior wall myocardial infarction. Neither patient had preexisting valvular heart disease or evidence of endocarditis, and neither had suffered chest trauma. Because abnormalities in right ventricular function may occur after inferior infarction, and because other known causes of tricuspid incompetence were not present, we postulate that these patients developed valvular regurgitation from dysfunction of the papillary muscle complex controlling tricuspid valve function, a mechanism similar to that proposed to explain mitral regurgitation seen with inferior wall ischemia.
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PMID:Tricuspid regurgitation following inferior myocardial infarction. 124 43

The QRS complex in lead V5 was studied during cardiac surgery. R wave amplitude decreased after induction of anesthesia to approximately 50% to 60% of the preanesthetic level before the institution of CPB (P < 0.001). An rS complex appeared immediately after cardioversion and changed in configuration to an Rs complex 15 to 30 minutes after aortic declamping. The R wave continued to recover toward the preanesthetic level at sternal closure. Patients with coronary artery disease had a poorer recovery of the R wave (P < 0.05) than patients with valvular heart disease; the former recovered to only 50% of the preanesthetic level at sternal closure. Nonsurvivors had much smaller R waves (26.1 +/- 20.5%) than survivors (P < 0.001). The R wave peaked 30 to 40 ms after initiation of the QRS complex, which indicates recovery of conductivity and the activation sequence of the left ventricular (LV) free wall, which is easily disturbed by hypothermia, cardioplegia, and ischemia during aortic cross-clamping. Monitoring QRS complex changes in lead V5 appears to be important on weaning from cardiopulmonary bypass to detect regional ischemia, and also to observe electrophysiologic recovery of the LV free wall.
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PMID:QRS complex changes in the V5 ECG lead during cardiac surgery. 147 59

The operating characteristics of thallium stress testing for detection of significant epicardial coronary artery disease (CAD) in hypertensive subjects with chest pain or electrocardiographic (ECG) ischemia have not been previously defined. This becomes important because of the high prevalence of both hypertensive heart disease and CAD. Ninety-two hypertensives with a history of typical or atypical chest pain or ECG myocardial ischemia underwent coronary arteriography, 2D-guided echocardiography, and thallium-201 stress testing, combined with intravenous dipyridamole if the rate-pressure product was less than 20,000. Patients with myocardial infarction, prior revascularization procedure, valvular heart disease, and chronic ethanol abuse were excluded. The mean age was 54.8 +/- 9.9 years with 55% blacks and 46% women. Eighteen patients (19.6%) had significant (greater than or equal to 50% luminal diameter narrowing) epicardial CAD at catheterization, of whom 17 had positive thallium scans. Overall, there were 17 true positives, 47 true negatives, 27 false positives, and one false negative resulting in 94.4 +/- 5.4% sensitivity (95% confidence limits [95% CL] 71 to 100%), 63.5 +/- 5.6% specificity (95% CL 51 to 74%), 38.6 +/- 7.3% positive predictive value (95% CL 25 to 54%), 97.9 +/- 2.1% negative predictive value (95% CL 88 to 100%), and 69.6 +/- 4.8% overall accuracy (95% CL 59 to 79%). For hypertensive patients with chest pain or ECG myocardial ischemia, the high sensitivity and negative predictive value and low false negative rate support the role of thallium stress testing +/- dipyridamole as an exclusion test for significant CAD.
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PMID:A negative thallium (+/- dipyridamole) stress test excludes significant obstructive epicardial coronary artery disease in hypertensive patients. 153 15

To determine whether patients with syndrome X suffer from myocardial ischemia, coronary sinus oxygen saturation was continuously measured during pacing loading in 31 patients. Subjects were categorized by groups as syndrome X (11 patients), effort angina (14), and old myocardial infarction and valvular heart disease (6). Pacing loading induced evidence of ischemia in all syndrome X patients and in eight of the 11 patients with effort angina, while there was no such evidence in those with old myocardial infarction and valvular heart disease. Coronary sinus oxygen saturation in syndrome X decreased significantly from 44.2 +/- 5.8% to 33.5 +/- 4.4% (p less than 0.01), and it decreased from 47.0 +/- 4.9% to 31.2 +/- 4.0% (p less than 0.01) in effort angina with induced ischemic evidence, indicating that a significant reduction in coronary sinus oxygen saturation reflects the presence of myocardial ischemia. In the group with old myocardial infarction and valvular heart disease, coronary sinus oxygen saturation remained nearly unchanged during pacing. The pattern of depression of coronary sinus oxygen saturation during pacing was steeper in effort angina than in syndrome X. Therefore, we conclude that, although syndrome-X may not be a homogeneous group of patients, most of them may develop myocardial ischemia due to reduced vasodilator reserves of the small coronary artery.
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PMID:[Continuous monitoring of coronary sinus oxygen saturation during pacing loading in patients with syndrome X]. 209 60

Intraoperative use of transesophageal echocardiography (TEE) to detect ischemia is more predictive of a postoperative myocardial infarction than is ECG, and two-dimensional (2-D) TEE has been shown to be more sensitive than ECG in detecting regional wall-motion abnormalities, which are highly suggestive of ischemia. More recent studies have demonstrated that postbypass TEE ischemia is predictive of an adverse outcome. Other potential diagnostic uses of TEE include evaluation and identification of intraoperative ventricular aneurysms and assessment of papillary muscle function. Intraoperative detection of thrombus and atrial myxoma has been significantly enhanced using 2-D TEE and, in the postoperative period, TEE is a more sensitive measure of pericardial tamponade than changes in hemodynamic variables. In cardiac surgery, contrast TEE has been reported to be useful in evaluating the adequacy of the delivery of cardioplegia as well as aiding in the detection of air emboli. The incorporation of Doppler into TEE probes now enhances the clinician's ability to diagnose and treat patients with valvular heart disease. The value of TEE must be weighed against cost-effectiveness and outcome as it becomes more widely used.
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PMID:Transesophageal echocardiography: is it for everyone? 213 50

The causes of chest pain in patients found to have angiographically normal coronary arteries during cardiac catheterization remain controversial. Cardiac sensitivity to catheter manipulation, pacing at various stimulus intensities and intracoronary injection of contrast medium was examined in several groups of patients who underwent cardiac catheterization. Right heart (especially right ventricular) catheter manipulation and pacing and intracoronary contrast medium provoked chest pain typical of that previously experienced in 29 (81%) of 36 patients with chest pain and angiographically normal coronary arteries and 15 (46%) of 33 symptomatic patients with hypertrophic cardiomyopathy. In contrast, only 2 (6%) of 33 symptomatic patients with coronary artery disease experienced their typical chest pain with these sensitivity tests (p less than 0.001). None of 10 patients with valvular heart disease but without a chest pain syndrome experienced any sensation with these tests. Cutaneous pain threshold testing demonstrated that patients with chest pain and normal coronary arteries had a higher pain threshold to thermal stimulation compared with patients who had coronary artery disease or hypertrophic cardiomyopathy. No relation existed between cardiac sensitivity and cutaneous sensitivity testing. Thus, patients who have chest pain despite angiographically normal coronary arteries may have abnormal cardiac sensitivity to a variety of stimuli. This increased sensitivity may be of causal importance to their chest pain syndrome or may contribute to their perception of ischemia-induced pain. The same phenomenon was also commonly seen in symptomatic patients with hypertrophic cardiomyopathy. Whether this phenomenon represents abnormal activation of pain receptors within the heart or abnormal processing of visceral afferent neural impulses in the peripheral or central nervous system is unknown.
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PMID:Abnormal cardiac sensitivity in patients with chest pain and normal coronary arteries. 222 87

To elucidate the incidence and natural history of valvular heart disease in Kawasaki syndrome, we analyzed patients who were found to have a new heart murmur after the onset of the disease. Among 1215 patients we found 13 (1.1%) with valvular disease (12 with mitral regurgitation and one with aortic regurgitation). We compared these patients with 30 who did not have valvular lesions. The duration of fever was longer and the incidence of coronary artery lesions significantly higher than in those without valvular disease. Heart murmurs disappeared within 2 months after the onset of valvular heart disease in five patients, whereas in another six, all involving valve prolapse, they persisted for 2 years or more. We postulate that two different mechanisms may be responsible for the variation in the duration of valvular heart disease: one, which disappeared spontaneously, was attributed to pancarditis; the other, which persisted, was due to dysfunction in valve and papillary muscles as a result of ischemia.
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PMID:Valvular heart disease in Kawasaki syndrome: incidence and natural history. 238 13

Cardiac ischemia and myocardial infarction continue to be major causes of perioperative morbidity and mortality, despite aggressive intraoperative monitoring. Intraoperative TEE is evolving as a helpful noninvasive monitor in patients with coronary artery disease and valvular heart disease. Early detection of ischemia and evaluation of valve function with continuous imaging has allowed the use of TEE as a dynamic tool to optimize therapeutic management of cardiac dysfunction that was not always readily available by conventional invasive techniques. As new equipment and techniques are developed, this monitoring method will undoubtedly find even more frequent intraoperative use.
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PMID:Transesophageal echocardiography. A technique for intraoperative monitoring. 278 5

To characterize the ultrastructural and metabolic changes occurring in the hypertrophied ventricle during cardiac operations in man, we studied 36 patients with valvular heart disease undergoing valve replacement, during which multiple doses of cold potassium cardioplegic solution were administered (Group I). Each patient had substantial ventricular hypertrophy according to measurements made of left ventricular mass, with a mean of 232.1 +/- 19.8 gm/m2 (normal: 92 +/- 16 gm/m2). Serial biopsy specimens were obtained from the left ventricular apex at the initiation of bypass, during the cross-clamp interval, and during reperfusion. Each specimen was scored from 0 to 4 according to ischemic changes in nuclear chromatin, mitochondrial swelling, myofibrillar edema, glycogen depletion, and overall cell morphology. Myocardial pH and temperature were measured continuously in the left ventricular free wall. During the cross-clamp period, ischemic injury was evidenced by changes in nuclear chromatin (0.38 +/- 0.10 to 1.25 +/- 0.21, p less than 0.0001), intracellular edema (0.43 +/- 0.06 to 0.97 +/- 0.14, p less than 0.002), overall cell morphology (0.37 +/- 0.06 to 0.97 +/- 0.14, p less than 0.001), and mitochondria (0.10 +/- 0.05 to 0.19 +/- 0.07, p less than 0.0001). During reperfusion, mitochondrial swelling increased further (0.19 +/- 0.07 to 0.35 +/- 0.08, p less than 0.0001) and glycogen stores were depleted (0.63 +/- 0.13 to 0.96 +/- 0.17, p less than 0.02), while the other structures remained unchanged. Myocardial pH declined during ischemic arrest from 6.89 +/- 0.04 to 6.40 +/- 0.04 (p less than 0.001). The changes in myocardial pH in Group I were compared to changes in myocardial pH in 10 patients (Group II) with no left ventricular hypertrophy undergoing isolated coronary bypass graft operations with the same protective techniques. In contrast to Group I, myocardial pH did not fall in Group II during ischemic arrest (6.98 +/- 0.06 to 6.94 +/- 0.05, p = not significant). Thus, with the use of current myocardial protective techniques, ultrastructural and metabolic changes indicative of ischemia are produced in the hypertrophied myocardium. The structural alterations consist of changes in nuclear chromatin and intracellular edema during the ischemic phase and by mitochondrial swelling during reperfusion.
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PMID:Structural and metabolic correlates of cell injury in the hypertrophied myocardium during valve replacement. 295 40


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