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)

Total mortality showed no association with heavy coffee consumption in the four race-sex groups of Evans County. Deaths from coronary heart disease in WM, WF and BM showed no statistically significant differences between the two coffee consuming groups. Sex differences in cerebrovascular death rates, consistent in both races, suggest the possibility for a female excess of stroke deaths among coffee drinkers, and a "protective" effect of coffee drinking among males. Thus, in an area of the United States which has been designated the "Stroke Belt", neither the cardiovascular nor the cerebrovascular death rates seem strongly nor consistently related to coffee drinking habits. Although the number of deaths (339) is fairly large, representing a 13% mortality in this community over a four and one-half year observation period, the classification in four race-sex groups with further division into the groups with different coffee drinking habits limits each stratum to rather small numbers. In addition, 86 cases of CHD and CVD were diagnosed during lifetime already and, therefore, were excluded from the prospective mortality study. Confidently to refute or confirm the allegations of a detrimental influence of high coffee intake on ischemic heart disease one would need larger numbers. But in the light of our most important finding--that mortality from all causes is not increased in the high coffee consuming group--the finding of increased ischemic heart disease death rates with high coffee consumption would have to be compensated by a provocative, lower rate for other causes of death.
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PMID:Coffee consumption and mortality in a community study--Evans Co., Ga. 96 3

The objective of this study was to assess the potential of gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA) to identify myocardial ischemia and reperfusion in the isolated rat heart model. Ischemia was induced by reducing the perfusion pressure from 80 to 30 mm Hg for 2 hours. Hearts were not reperfused, or were reperfused for 20 minutes or for 2 hours. Perfusion was performed with Evans blue dye and/or Gd-DTPA for 3 minutes. Twenty isolated rat hearts were perfused according to the Langendorff method, and divided into five groups according to the perfusion status and the use of Gd-DTPA and/or Evans blue as perfusion markers. The Evans blue distribution in the hearts was assessed by point-counting volumetry. The Gd-DTPA distribution was assessed by magnetic resonance microimaging at 6.3 T field strength. Evans blue staining clearly identified areas with "no flow" or "no reflow." Perfusion with Gd-DTPA enhanced signal intensity significantly, both in ischemic and reperfused myocardium. Signal intensity in hearts reperfused for 2 hours was increased significantly compared to nonreperfused ischemic hearts, but not to ischemic hearts reperfused for 20 minutes. Magnetic resonance imaging with the aid of Gd-DTPA can identify ischemia and reperfusion in the isolated rat heart, dependent on residual perfusion.
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PMID:Gadolinium-DTPA-enhanced magnetic resonance imaging of the isolated rat heart after ischemia and reperfusion. 176 38

The threshold dose of the selective thromboxane receptor antagonist SQ 30,741 for increasing reflow during thrombolysis was identified and then evaluated in a model of myocardial ischemia with reperfusion. In anesthetized cynomolgus monkeys, stenotic carotid arteries were occluded with a platelet-rich thrombus by electrical stimulation and recanalized with streptokinase (680 U/min intraarterially for 1 h) and heparin (200 U/kg + 120 U/h intravenously for 3 h). Concurrent administration of SQ 30,741 (2.1 mg/kg + 0.5 mg/kg per h intravenously for 3 h; n = 4) enhanced the extent of reflow 174% compared with saline solution (n = 4; p less than 0.05) during the third hour, when lower doses were ineffective. This threshold dose was tested in anesthetized African green monkeys subjected to 90 min of left circumflex coronary artery occlusion and 5 h of reperfusion. SQ 30,741 (n = 8) or saline solution (n = 11) was administered 2 min before reperfusion and continued throughout reperfusion. The heart was removed on termination of reperfusion and perfused in vitro with Evans blue and triphenyltetrazolium chloride dyes to stain tissue at risk and infarcted tissue, respectively. The percent of left ventricle at risk did not differ between saline- (37 +/- 4%) and SQ 30,741-treated (35 +/- 3%) monkeys. In contrast, infarcted tissue expressed as percent of the left ventricle at risk was less (p less than 0.01) in monkeys receiving SQ 30,741 (31 +/- 2%) than in those receiving saline solution (49 +/- 5%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The thromboxane receptor antagonist SQ 30,741 reduces myocardial infarct size in monkeys when given during reperfusion at a threshold dose for improving reflow during thrombolysis. 230 99

Evans County black males had lower ischemic heart disease (IHD) prevalence, incidence, and mortality than white males. High-density lipoprotein (HDL) cholesterol was lower in IHD cases than in subjects without IHD. HDL cholesterol and apolipoprotein A-I (Apo A-I) were higher and low-density lipoprotein (LDL) cholesterol, very low-density lipoprotein (VLDL) cholesterol, and Apo C-II were lower in black than white males. Of the black-white male HDL cholesterol difference, 22% was statistically explained by Apo A-I. Controlling for Apo C-II reduced the black-white differences in total cholesterol 87%, LDL cholesterol 44%, VLDL cholesterol 83%, and total triglyceride 83%. There were negative associations between Apo A-I and age, Quetelet index, and cigarettes smoked; the association between Apo A-I and alcohol was positive. Only body mass index and race were strong correlates of Apo C-II. The ratios of Apo A-I to Apo A-II and of HDL cholesterol to Apo A-II were higher in black than white males with adjustment for age, body mass, and cigarette and alcohol consumption. Thus black-white differences in total lipids, lipoprotein lipids, and lipoprotein apoproteins were observed, indicating a relatively antiatherogenic profile in black males only partially explained by known correlates.
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PMID:Black-white differences in plasma levels of apolipoproteins: the Evans County Heart Study. 643 86

Ischemic heart disease (IHD) risk factors and 20-year mortality rates were studied in middle-aged Evans County black males. We hypothesized, a priori, that blood pressure, cholesterol, and smoking would be predictive of mortality in black males; that black-white differences in mortality would be due to differences in risk factor levels and not risk functions per se; and that social status would be associated with risk factor levels and would be a predictor of mortality. Multivariate analyses of cumulative risk of dying and time to death suggest that the major IHD risk factors are predictors of all-cause and IHD mortality in black males. Black-white differences in risk functions, specifically for cholesterol, were explained by social status: black males and lower social status white males had similar risk functions, different from those of higher social status white males. Black males and lower social status white males had almost identical survival curves, each less favorable than those of higher social status white males.
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PMID:Ischemic heart disease risk factors and twenty-year mortality in middle-age Evans County black males. 647 43

A survey of the rural community in Evans County, Georgia, revealed cervical arterial bruits in 72 (4.4 per cent) of 1620 persons 45 years of age of older without previous stroke, transient ischemic attacks, or overt ischemic heart disease. The prevalence of such asymptomatic bruits increased with age and was greater in women and persons with hypertension. We estimated the risk of stroke associated with cervical bruits during a six-year follow-up period, taking age and blood pressure into account. The presence of asymptomatic bruits was associated with a significantly higher risk of stroke in men but not in women, with odds ratios of 7.5 and 1.6, respectively. Despite the high risk of stroke among men with bruits, the correlation between the location of the bruits and the type of subsequent stroke was poor. Moreover, cervical bruits in men were a risk factor for death from ischemic heart disease. We suggest that asymptomatic cervical bruits are an indication of systemic vascular disease and do not themselves justify invasive diagnostic procedures or surgical correction of underlying extracranial arterial lesions.
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PMID:Risk of stroke in asymptomatic persons with cervical arterial bruits: a population study in Evans County, Georgia. 736 Jan 61

Ischemic preconditioning (PC) has been consistently observed to reduce infarct size in models of regional myocardial ischemia. However, it is also known to render the heart resistant to injury for only a finite period of time (< 2 h). Myocardial adenosine is widely believed to be one of the mediators of PC and may produce myoprotection in part through an anti-neutrophil effect during the early reperfusion period. When infarct size is assessed following a relatively short period of reperfusion (< 3 h) PC hearts may appear protected although reperfusion injury in the myocardium may be ongoing. Thus, infarct expansion may occur as the effects of PC fade. To substantiate that PC produces a sustained reduction in myocardial necrosis, 27 male Sprague-Dawley rats were anesthetized with pentobarbital and instrumented for regional coronary occlusion (30 min) and reperfusion (7 days). Animals were randomized to a control group (n = 16) or PC (n = 11), which consisted of 2 cycles of 5 min of ischemia and 5 min of reperfusion immediately prior to coronary occlusion. Successful reperfusion was confirmed visually and the occluding suture was left in the chest during recovery. Seven days later, staining for risk area was made by the injection of Evans blue dye while the occluder was in place and necrosis was detected with triphenyltetrazolium chloride staining. Planimetry was performed by a blinded investigator who found the risk area to be 27.2 +/- 1.6 and 33.6 +/- 1.7% of the left ventricle (p = NS) in PC and controls, respectively. All hemodynamic measurements were comparable between groups at all times during ischemia and reperfusion. PC reduced infarct size from 43.3 +/- 2.0% of area at risk to 20.6 +/- -2.1%, a 48% reduction (p < 0.01), and eliminated transmural necrosis which was common in the control group. From these studies we conclude that ischemic PC results in a permanent reduction in infarct size rather than a transient reduction in infarct size in the context of a gradually evolving infarction due to reperfusion injury.
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PMID:Reduction in infarct size by ischemic preconditioning persists in a chronic rat model of myocardial ischemia-reperfusion injury. 885 32

Lipid peroxidation contributes to myocardial reperfusion injury. The indenoindole H290/51, a lipid peroxidation inhibitor with balanced lipophilicity and a considerably higher antioxidative capacity than that of vitamin E, was tested for its myocardioprotective effect against reperfusion injury. Coronary-ligated pigs were subjected to 45 min of myocardial ischemia followed by 240 min of reperfusion. Starting five minutes prior to reperfusion, H290/51 (n = 6) or vehicle (n = 6) was retrogradely infused via a coronary vein for 30 min. The total dose of H290/51 was 1 microM in 300 ml fluid (10 ml/min). In addition to the hemodynamics, left ventricular (LV) wall segment shortening (%SS) was measured by sonomicrometry. The LV area at risk and infarct size were measured by means of Evans blue and triphenyl tetrazolium chloride staining. The hemodynamics did not change significantly during the study, and no differences were found between the two groups. In the H 290/51-treated pigs, %SS of the ischemic area recovered from 1.9% at the end of ischemia to 9.1% after 120 min (p < .05) and to 16.2% at 240 min (p < .01). There was no significant recovery in the vehicle group. The LV area at risk was approximately 20% of LV. Infarct size as a percentage of LV and of the area at risk was significantly smaller in the H290/51 group (9+/-3% and 46+/-11%) than in the control group (18+/-6%; p < .05 and 83+/-5%; p < .01). H290/51 effectively protected the myocardium at risk in the setting of myocardial ischemia followed by reperfusion. This effect was reflected by diminished infarct size and improved functional recovery.
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PMID:The lipid peroxidation inhibitor indenoindole H290/51 protects myocardium at risk of injury induced by ischemia-reperfusion. 958 2

To evaluate the extent to which the protective effect of metoprolol was accompanied by changes in myocardial oxygen consumption and metabolism, thrombotic occlusion of coronary artery followed by infusion of metoprolol or placebo was performed in twenty four German Shepherds. To restore a coronary blood flow rt-PA was administered. Plasma levels of oxygen, glucose, lactic acid, non esterified fatty acids, triacylglyceride and adenosine breakdown products were measured before and at the end of the occlusion and in the early and late reperfusion periods. Regional myocardial blood flow was measured by means of radioactive tracer microspheres. Infarct size was estimated after perfusion and staining of excised hearts with Evans blue. Plasma levels of metoprolol were determinated before the end of occlusion and during reperfusion and therapeutic concentrations were confirmed. The infarct size was smaller in dogs receiving metoprolol (21.6 +/- 20.7 vs 43.0 +/- 17.3% p. < 0.02). Coronary collateral blood flow was greater in metoprolol than in placebo dogs (18.68 +/- 7.58 vs 11.05 +/- 6.10 ml/min/100g, p. < 0.01). As a consequence of myocardial ischemia a shift toward carbohydrate utilization, the myocardial lactate release and the accompanying symptoms of diminished myocardial lipid uptake were observed. A washout of adenosine degradation products during early reperfusion was also noticed. In beta 1 blocked animals the reduction of myocardial oxygen consumption and preserved myocardial uptake of lactate and non esterified fatty acids were documented.
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PMID:Influence of an early adrenergic blockade on thrombotic infarct size and myocardial metabolism. 978 88

Radioiodinated free fatty acids are tracers that can be used to assess both myocardial perfusion and metabolism. There have been several fatty acids and structurally modified fatty acids studied since Evans' initial report of radiolabeled I-123 oleic acid in 1965. The radiolabeling of a phenyl group added to the long chain fatty acids in the omega-terminal position opposite the carboxyl terminal group prevents nonspecific deiodination and the rapid release of free iodine as the tracer undergoes beta-oxidation. The additional inclusion of a methyl or dimethyl group to the chain slows oxidation resulting in prolonged myocardial retention. The longer retention of the radiolabel permits longer image acquisitions more compatible with single photon emission computed tomography (SPECT) imaging, especially with single-detector imaging systems. Several protocols have been implemented using these compounds, particularly 15-(para-iodophenyl)-3-R,S-methyl pentadecanoic BMIPP, to detect abnormal fatty acid metabolism in ischemic heart disease as well as in nonischemic and hypertrophic cardiomyopathies. Successful management of patients with ischemic cardiomyopathies depends on the accurate identification of hibernating myocardium. The studies covered in this review suggest that both IPPA and BMIPP, especially when combined with markers of myocardial perfusion, may be excellent tracers of viable and potentially functional myocardium. Future studies with larger numbers of patients are needed to confirm the results of these studies and to compare their efficacy with that of other available imaging modalities. Cost and distribution issues will have to be resolved for these metabolic tracers to compete in the commercial marketplace. Otherwise they will likely be available only on a limited basis for research use. As progress is made with these issues and with the development of newer imaging systems, the use of radioiodinated and fluorinated fatty acids is likely to be increasingly attractive.
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PMID:Fatty acids for myocardial imaging. 1043 39


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