Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an effort to compare the effects of anesthetics on cardiac functions and metabolism, mongrel dogs were anesthetized with morphine (3 mg/kg, N2O 50% in oxygen) or halothane (0.7%, N2O 50% in oxygen). Hb, Ht, pO2, pCO2, pH, O2 content, lactate, and pyruvate in the arterial and coronary sinus blood were measured and ECG, LVP, CVP, AP, and CO were recorded. Aorta was cross-clamped for 30 min under cardiopulmonary bypass (CPB). Hemodynamic and metabolic survey were continued until 120 min of recovery period. Results were as follows: Hemodynamics, such as LVP, AP, and CO, were depressed after CPB, then gradually returned to control level. Subendocardial ischemia observed through ST depression and QRS widening on ECG, as well as DPTI/TTI ratio under 1.0, disappeared in the recovery period. Lactate was produced by the heart after anoxic arrest and was extracted at 120 min after CPB. Halothane and morphine did not show any significant differences of effects on cardiac function and metabolism in this study.
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PMID:Effects of morphine and halothane on canine cardiac function before and after cardiopulmonary bypass. 103 47

Subendocardial ischemia is a common cause of death following ischemic cardiac arrest. We studied relationships among myocardial water content (WC), left ventricular function, coronary blood flow, and myocardial metabolism following ischemic cardiac arrest. Under cardiopulmonary bypass with hypothermia, 120 min of aortic occlusion was employed, and myocardial temperature was kept around 20 degrees C in 10 mongrel dogs. Left ventricular function (peak LVP, max dp/dt, LVEDP, LVSWI), coronary blood flow, myocardial enzymes (m-GOT, total CPK, MB-CPK), myocardial ATP and creatine phosphate (CP), and WC of the subendocardium of the left ventricle were measured. Data were obtained in the control state and immediately and 30 and 60 min after aortic unclamping. Significant negative correlations were obtained between WC and max dp/dt (r = -0.8384), coronary blood flow (r = -0.9928), ATP (r = -0.7038), and CP (r = -0.7835). Significant positive correlations were obtained between WC and LVEDP (r = 0.7525), m-GOT (r = 0.7638), and total CPK (r = 0.7079). These data suggest that myocardial edema results in depression of left ventricular function and metabolism.
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PMID:Correlation among water content, left ventricular function, coronary blood flow, and myocardial metabolism after hypothermic ischemic cardiac arrest. 685 73

There is a strong relation of carotid atherosclerosis to coronary artery disease and left ventricular hypertrophy. In addition, abnormalities of carotid structure are strongly associated with abnormal left ventricular geometry and structure. However, little is known regarding the relation of exercise-induced ST depression to carotid atherosclerosis, carotid, or left ventricular structure in the absence of apparent coronary disease. The relationship of exercise ECG myocardial ischemia to the presence of carotid atherosclerosis and to carotid and left ventricular structure was assessed in 204 asymptomatic subjects free of clinical evidence of cardiovascular disease. Myocardial ischemia on the exercise ECG, defined by a chronotropically adjusted ST/HR slope of >3.47 microV/bpm, was associated with a nearly threefold greater likelihood of discrete carotid atherosclerosis (50% [6 of 12] versus 17% [29 of 192], P=.007) and with older age, male sex, higher systolic and diastolic blood pressures, greater left ventricular mass and mass index, and greater common carotid artery intimal-medial thickness and cross-sectional area index. Stepwise logistic regression analyses, including standard risk factors, revealed that only carotid artery cross-sectional area index (P=.0007) and systolic blood pressure (P=.005) independently predicted an abnormal chronotropically adjusted ST/heart rate slope. Moreover, among 132 subjects with > or = 10 microV of ST-segment depression, only left ventricular mass index and carotid artery cross-sectional area index were significant predictors of the chronotropically adjusted ST/heart rate slope response. Subendocardial ischemia on the exercise ECG is strongly associated with the presence of carotid atherosclerosis and is related to systolic blood pressure, carotid artery cross-sectional area index, and left ventricular mass index, independent of age, sex, and other cardiac risk factors. These findings provide additional insights into the relation between coronary and carotid atherosclerosis and suggest that an association among ischemia and left ventricular and carotid structural abnormalities may contribute to the pathogenesis of coronary events.
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PMID:Relation of exercise-induced myocardial ischemia to cardiac and carotid structure. 940 57

Subendocardial ischemia as indicated by electrocardiography during exercise, in association with severe systolic anterior motion of the anterior mitral valve leaflet without left ventricular hypertrophy, has not been well described. We report the case of a 42-year-old man who presented with symptoms of exertional angina and 2-mm ST depression on treadmill electrocardiography but had a normal perfusion scan and coronary angiogram. Initially the negative angiographic results caused us to regard the treadmill results as false-positive. Subsequently, low-dose dobutamine echocardiography showed severe systolic anterior motion of the anterior mitral valve leaflet with a >144-mmHg left ventricular outflow tract gradient; we then recognized the original treadmill results to be pseudo-false-positive. Electrocardiographic changes in association with the above-described motion of the anterior mitral valve leaflet and increased left ventricular outflow tract gradient were verified by use of treadmill and supine bicycle stress echocardiography.
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PMID:Pseudo-false-positive exercise treadmill testing caused by systolic anterior motion of the anterior mitral valve leaflet. 1177 58

We quantify and provide biophysical explanations for some aspects of the relationship between the bidomain conductivities and ST-segment epicardial potentials that result from subendocardial ischemia. We performed computer simulations of ischemia with a realistic whole heart model. The model included a patch of subendocardial ischemic tissue of variable transmural thickness with reduced action potential amplitude. We also varied both intracellular and extracellular conductivities of the heart and the conductivity of ventricular blood in the simulations. At medium or high thicknesses of transmural ischemia (i.e., at least 40% thickness through the heart wall), a consistent pattern of two minima of the epicardial potential over opposite sides of the boundary between healthy and ischemic tissue appeared on the epicardium over a wide range of conductivity values. The magnitude of the net epicardial potential difference, the epicardial maximum minus the epicardial minimum, was strongly correlated to the intracellular to extracellular conductivity ratios both along and across fibers. Anisotropy of the ischemic source region was critical in predicting epicardial potentials, whereas anisotropy of the heart away from the ischemic region had a less significant impact on epicardial potentials. Subendocardial ischemia that extends through at least 40% of the heart wall is manifest on the epicardium by at least one area of ST-segment depression located over a boundary between ischemic and healthy tissue. The magnitude of the depression is a function of the bidomain conductivity values.
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PMID:The effect of conductivity on ST-segment epicardial potentials arising from subendocardial ischemia. 1607 15

The accuracy of the admission electrocardiogram (ECG) in predicting the site of acute coronary artery occlusion in patients with ST-segment elevation myocardial infarction (STEMI) and multivessel disease is not well known. This study aimed to assess whether the presence of multivessel coronary artery disease (CAD) modifies the artery-related ST-segment changes in patients with acute coronary artery occlusion. We reviewed the admission ECG, clinical records, and coronary angiography of 289 patients with STEMI caused by acute occlusion of left anterior descending (LAD; n = 140), right (n = 118), or left circumflex (LCx; n = 31) coronary arteries. All patients underwent primary percutaneous coronary reperfusion during the first 12 hours. The magnitude and distribution of artery-related ST-segment patterns were comparable in patients with single (n = 149) and multivessel (n = 140) CAD. Occlusion of proximal (n = 55) or mid-distal (n = 85) LAD artery induced ST-segment elevation in leads V1 to V5, but only the proximal occlusion induced reciprocal ST-segment depression in leads II, III, and aVF (p <0.001). Proximal and mid-distal occlusion of right (n = 45 and 73, respectively) or LCx (n = 15 and 16) coronary artery always induced ST-segment elevation in leads II, III, and aVF and reciprocal ST-segment depression in leads V2 and V3. ST-segment elevation in lead V6 >0.1 mV predicted LCx artery occlusion. In conclusion, patients with STEMI with single or multivessel CAD have concordant artery-related ST-segment patterns on the admission ECG; in both groups, reciprocal ST-segment depression in LAD artery occlusion predicts a large infarct. Subendocardial ischemia at a distance is not a requisite for the genesis of reciprocal ST-segment changes.
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PMID:Influence of the extent of coronary atherosclerotic disease on ST-segment changes induced by ST elevation myocardial infarction. 2440 7