Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of ischemic heart disease is significantly lower in southwestern American Indians than in Caucasians. To investigate this difference, the metabolism of low density lipoprotein apoprotein (apo-LDL) and plasma lipoprotein cholesterol composition were studied in 10 southwestern American Indians and 5 Caucasian controls. The plasma concentration of LDL cholesterol in American Indians was 88 +/- 5 mg/dl (mean +/- SEM) and 111 +/- 7 mg/dl in Caucasians. The corresponding values of apo-LDL concentrations were 53 +/- 3 mg/dl and 77 +/- 4 mg/dl, respectively. Conversely, high density lipoprotein cholesterol (HDL) concentrations were significantly higher in American Indians (56 +/- 4 mg/dl) than in Caucasians (37 +/- 3 mg/dl). There were no statistically significant differences in the biological half-life of apo-LDL, calculated from the second exponential of the plasma die-away curve (3.06 +/- 0.15 days vs. 3.45 +/- 0.11 days), the fractional catabolic rate of apo-LDL (0.432 +/- 0.01 vs. 0.411 +/- 0.01), or the fraction of total exchangeable apo-LDL in the intravascular space (70 +/- 1 vs. 67 +/- 3%). As derived from the absolute catabolic rate under steady-state conditions, the synthetic rate of apo-LDL in American Indians was, however, significantly lower than in Caucasians (334.6 +/- 7.8 mg/m(2) per day vs. 507.2 +/- 6.7 mg/m(2) per day; P < 0.001). These data indicate that the lower levels of plasma LDL cholesterol and apo-LDL in American Indians are due to a reduced rate of apo-LDL synthesis rather than to differences in fractional catabolic rates. These differences, in combination with higher HDL cholesterol levels, may contribute to the lower prevalence of ischemic heart disease in American Indians.
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PMID:Low density lipoprotein metabolism and lipoprotein cholesterol content in southwestern American Indians. 22 Mar 52

The 6-year cumulative incidence of ischemic heart disease (IHD) in 382 dialysis patients (mean age [SEM], 43 +/- 0.7 years) was studied. Of 101 patients with IHD, only 39 developed symptoms following dialysis (cumulative incidence, 20.8%). This group was older than those with IHD, and in 55%, IHD occurred in the first year of dialysis. Analysis by sex and race showed the rate of IHD in men and women to be similar, but the rate in whites was twice that in blacks. In men, the rate was not different from nondialysis men with similar coronary risk factors, whereas in dialysis women, the rate was twice that of nondialysis cohort. The development of IHD did not adversely affect long-term survival in patients without prior evidence of IHD. Death from myocardial infarction occurred in 3 of 320 patients ar risk. Atuopsy data in 33 patients revealed 70% stenosis of coronary arteries in 7, 4 of whom had antecedent disease. Our major conclusions are (a) the incidence of IHD during dialysis was not different from similarly matched nondialysis subjects; (b) the rate of IHD in dialysis women was greater than it was in nondialysis subjects; (c) coronary artery disease only affected long-term survival of patients with preexisting disease; (d) autopsy data did not suggest accelerated atherosclerosis.
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PMID:Ischemic heart disease in patients with uremia undergoing maintenance hemodialysis. 54 4

Twenty patients with fixed coronary artery obstruction were studied during rapid atrial pacing and methoxamine infusion. During pacing to heart rates of 142 +/- 4 (mean +/- SEM) beats per minute coronary sinus flow increased from 108 +/- 8 to 187 +/- 15 cc/min and myocardial oxygen consumption increased by + 80 +/- 11%. During methoxamine infusion that raised arterial systolic pressure to 196 +/- 5 mm Hg, similar increases in coronary sinus flow (to 179 +/- 13 cc/min) and myocardial oxygen consumption (+ 77 +/- 12%) occurred. Chest pain and ischemic ST segment changes developed in 17 and 14 patients respectively during atrial pacing, an incidence significantly greater (P less than 0.05) than during infusion of methoxamine (6 and 3 patients). Myocardial lactate extraction which averaged 26 +/- 4% during control was decreased to 10 +/- 8% during pacing and to 24 +/- 7% during methoxamine; the difference between decreases was not significant. The data show that at similar increases in myocardial oxygen consumption stress of increased heart rate results in more myocardial ischemia than stress of increased afterload.
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PMID:Effects of pharmacologically-induced hypertension on myocardial ischemia and coronary hemodynamics in patients with fixed coronary obstruction. 61 96

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

Achilles tendon thickness (ATT) of 112 patients with familial hypercholesterolemia (FH) with and without ischemic heart disease (IHD) was measured radiographically and was compared with that of normal subjects. The mean and SD of serum cholesterol in the heterozygotes (107 cases), the homozygotes (5 cases) and the normal subjects (36 cases) were 347 +/- 63, 589 +/- 69 and 187 +/- 30 mg/dl, respectively. The mean and SEM of ATT in the heterozygotes, the homozygotes and the normal subjects were 12.5 +/- 0.4 mm, 18.6 +/- 6.6 mm, and 6.3 +/- 0.2 mm, respectively. Cutaneous xanthomas were observed in 34 out of 112 patients (30.4%). Increased ATT was observed in 95 (84.8%). IHD was diagnosed in 39 (34.8%). The ATT of FH with IHD was significantly thicker than that of FH without IHD (P less than 0.05) and that of normal subjects (p less than 0.001). Thus, the increased ATT evaluated by x-ray was the earliest clinical sign of FH and the measurement of ATT seems to be a useful adjunctive procedure for detecting familial hypercholesterolemic patients and predicting IHD in them.
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PMID:Achilles tendon thickness and ischemic heart disease in familial hypercholesterolemia. 70 7

The etiology of chest pain in patients with the anginal syndrome and normal coronary arteriograms has not been established. There has been no explanation for the association of electrocardiographic, hemodynamic, and myocardial metabolic abnormalities consistent with myocardial ischemia observed in some patients with this disorder. Historical, clinical, laboratory, and hemodynamic data of 45 patients (24 females, 21 males), mean age 47.5 years, with chest pain and normal coronary arteriograms are reviewed. Left ventriculograms were analyzed utilizing the single-plane cineangiographic measurement of left ventricular volume. Systolic ejection fractions for the 45 patients ranged from 0.66 to 0.91 (mean 0.80 +/- 0.01 SEM). Ventricular volumes determined angiographically revealed mean end-diastolic and end-systolic volumes of 83 +/- 5 ml and 18 +/- 2 ml, respectively. The mean changes in longitudinal and transverse segmental axis shortening that occurred during ventricular systole were 28.8% and 50.7%, respectively. These elevated values for ejection fraction, and reduced measurements of ventricular volumes, indicate that some patients with chest pain and normal coronary arteriograms may have small hearts with hyperdynamic ventricular contraction. These findings suggest that hyperdynamic ventricular contraction may play a causative role in the development of transient, angina-like chest pain in these patients. The etiology of the proposed hyperdynamic ventricle is unknown, but it may be attributable to increased beta-sympathetic stimulation of the myocardium.
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PMID:Elevated ejection fractions in patients with the anginal syndrome and normal coronary arteriograms. 73 29

Angiographically determined changes in segmental wall motion (SWM) and ejection fraction (EF) are sensitive indices of left ventricular (LV) function. To compare the effects of exercise on LV function, first pass radionuclide angiocardiography was used before and during maximal upright bicycle stress in patients with nonsignificantly stenosed coronary arteries, and in those with greater than 75% stenosis. Gamma camera acquisitions were made in the 30 degree RAO projection using a 20 mCi I.V. bolus of 99mTc-pertechnetate. In the control group (seven normals, one nonsignificant (CAD) the EF significantly increased between rest and exercise (0.65 +/- 0.03 to 0.81 +/- 0.03 (mean +/- SEM), p less than 0.005). In this group SWM measured over the two anterior and two inferoposterior segments uniformly increased. In the 11 patients with a history of angina and significant coronary artery obstruction, the EF did not change in three and significantly decreased in the remaining eight (0.57 +/- 0.04 to 0.45 +/- 0.03, p less than 0.005). In all 11 patients SWM either decreased or did not increase in the areas supplied by the significantly stenosed coronary arteries. Upright maximal stress angiocardiography appears to be well-suited for diagnosing ischemic heart disease and localizing the area of ischemic dysfunction.
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PMID:Effects of maximal exercise stress on left ventricular function in patients with coronary artery disease using first pass radionuclide angiocardiography: a rapid, noninvasive technique for determining ejection fraction and segmental wall motion. 75 25

Noninvasive gated cardiac blood pool imaging with technetium-99m autologous erythrocytes was employed to differentiate reversible verus irreversible abnormal ventricular segmental contraction by regional wall and pump responses to sublingual nitroglycerin in 25 patients with chronic coronary heart disease. In 12 patients without ECG infarctions compared to 13 with infarctions, radioisotopic images demonstrated significantly greater percent decreases in end-systolic volumes (33.8 +/- 6.7 SEM vs 187 +/- 4.4; P less than 0.05) without differences in percent reductions in end-diastolicvolumes (13.7 +/- 3.9 vs 11.6 +/- 6.1; NS) and thereby significantly greater percent increases in ejection fractions (9.3 +/- 1.6 vs 4.1 +/- 2.0; P less than 0.05). In the 22 patients with regional dyssynergy, improvement in disordered pattern and extent of localized dyssynergy following antianginal action of nitroglycerin was related to ECG absence of prior infarction. These obsevations demonstrate the clinical accuracy of atraumatic scintigraphy in the detection of reversible localized dyssynergy due to myocardial ischemia in coronary heart disease.
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PMID:Radionuclide assessment of nitroglycerin influence on abnormal left ventricular segmental contraction in patients with coronary heart disease. 81 50

Recent studies have shown that after total coronary artery occlusion, there is impaired "reflow" of blood accompanied by myocardial and capillary endothelial cell swelling. To investigate the effect of prolonged low flow myocardial ischemia on coronary vascular resistance, regional hypoperfusion of the distal left anterior descending coronary artery was studied in 31 autonomically blocked dogs on right heart bypass. Heart rate, aortic pressure, and, during ischemia, left ventricular end-diastolic pressure were held constant. The distal left anterior descending coronary artery was perfused at a substantially reduced perfusion pressure which resulted in an antegrade coronary blood flow that usually was between 3% and 7% (0.5-1 ml/min) of control. When relative hypothermia (33-34 degrees C) was induced in nine dogs, left anterior descending coronary artery vascular resistance did not change during 2.5-3 hours of low flow ischemia. Under euthermic conditions (37-40 degrees C) in 17 dogs there was a consistent progressive increase in distal left anterior descending coronary artery vascular resistance starting at 90 minutes (median) after onset of ischemia. By 110-140 minutes ischemic antegrade flow decreased by 35 +/- 4% (SEM) (P less than 0.01). Directionally similar flow changes were observed in six euthermic experiments using the krypton-85 washout technique. Light microscopy did not reveal hemorrhage as a cause of the increased vascular resistance. The perfusion impairment did not occur in two euthermic, nonischemic hearts. In five dogs elevation of serum osmolality by 23 +/- 11 mOsmol/liter with mannitol attenuated the progressive decrease in flow. Thus, a progressive perfusion defect exists in the ischemic low flow state in the heart which presumably contributes to the extent of eventual necrosis.
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PMID:Progressive perfusion impairment during prolonged low flow myocardial ischemia in dogs. 93 13

1. The National Blood Pressure Study (NBPS) is a single blind trial designed to test the efficacy of active drug treatment in reducing complications from mild hypertension (mean diastolic pressure = 95-109 mmHg). 2. Between 1973 and 1975, four centres screened about 104 000 subjects aged 30-69 years, yielding an estimated prevalence of hypertension (greater than or equal to 95 mmHg diastolic) of 16% and of moderate-to-severe hypertension (greater than of equal to 110 mmHg diastolic) of 1-3%. 3. Some 4000 subjects selected for untreated uncomplicated mild hypertension were randomized to either active treatment (cholorothiazide +alpha-methyldopa and/or a beta-adrenoreceptor antagonist as required) or to matching placebos. 4. At 1 year mean pressures had fallen significantly below entry pressures in both groups but in the active group the fall was greater by a margin of 14-4+/-1-3 (SEM) mmHg systolic and 7-1+/-0-7 mmHg diastolic. At 1 year 5% of subjects in the placebo group had been placed on active treatment on the ethical grounds that pressure had exceeded the mild hypertension limit. 5. Trial end-points (death, morbidity from stroke, hypertensive heart and renal disease, and ischaemic heart disease) number 106 (nine deaths) thus far, of which ischaemic heart disease accounts for 71% and stroke 19%. 6. The duration of trial may need to be extended beyond the original estimate of 5 years.
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PMID:Report on progress in the Australian National Blood Pressure Study (NBPS). 107 98


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