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)

The pathophysiology and prognosis of coronary heart disease in women are the subject of intensive epidemiological and clinical investigations due to sex specific considerations. We have estimated the prevalence of modifiable coronary risk factors in 36 consecutive women (mean age 59.7 years) with suspected coronary heart disease in whom coronary angiography was performed due to unclear chest pain. Seventeen women revealed angiographically normal coronary arteries (gr. I) and 19 women showed coronary vessels with initial arteriosclerosis (luminal diameter reduction < 35%) (gr. II). Mean age was 59.1 years in gr. I and 60.3 years in gr. II (p = ns). No woman received lipid lowering drugs within the last 6 months. A hormone replacement therapy was not performed in any case. Women in gr. I showed significantly higher total and LDL cholesterol levels (271.6 +/- 34.3 vs 243.5 +/- 44.8 mg/dl; p < 0.005 and 190.5 +/- 36.8 vs 149.7 +/- 45.1 mg/dl; p < 0.025, respectively) and significantly lower HDL cholesterol values (57.8 +/- 16.5 vs 72.8 +/- 19.1 mg/dl; p < 0.0125) compared to women in gr. II. The total/HDL cholesterol ratio was 3.6 +/- 1.2 in gr. I and 5.1 +/- 1.7 in gr. II (p < 0.005). The positive predictive value for the existence of initial coronary atherosclerosis and a total cholesterol/HDL ratio > 4 was 76.5%. The negative predictive value and a ratio < 4 was 81.3%. Women in gr. I revealed 1.2 +/- 0.9 and in gr. II 1.6 +/- 0.8 risk factors (smoking, hypertension, body mass index > 30 kg/m2, diabetes mellitus, hyperlipidemia) (p < 0.10). The 10-year risk for the occurrence of a coronary event was 9.1 +/- 3.7% in gr. I and 14.2 +/- 5.8% in gr. II (p < 0.005). The positive predictive value for the existence of initial coronary atherosclerosis and a 10-year risk > 10% was 90%. The negative predictive value and a 10-year risk < 10% was 64.0%. Our investigation indicates that women with a mean age of 60 years, unclear chest pain and without exercise induced ischemia are highly suspected to have initial coronary arteriosclerosis, when a distinct risk factor profile and a 10-year cardiac event risk > 10% are present. For this high risk group of women, intensive secondary prevention measures are necessary.
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PMID:[Coronary risk profile in women with angiographically normal coronary arteries or initial coronary arteriosclerosis]. 1145 97

In the process of atherosclerosis sex steroids play a complex role in the vascular vessel wall system. Although a number of experimental studies have clearly documented an atheroprotective effect of estrogens, in recent clinical studies, estrogen replacement therapy has failed to reduce cardiovascular mortality. The effects of androgens on the cardiovascular system and cardiovascular diseases are even more controversial. Whereas in the past, androgens were mainly believed to exert adverse effects on the cardiovascular system, recent studies in men have documented a number of beneficial actions of testosterone in the arterial vascular system. Androgens affect lipid metabolism (e.g., LDL and HDL cholesterol, Lp(a)) and hemostasis (e.g., platelet aggregation and fibrinolytic activity). In addition, several other physiological and pathophysiological processes in the arterial vessel wall are influenced by androgens. Acute hemodynamic effects of testosterone on coronary vasomotion and stress-test-induced ischemia were reported. Additionally, recent animal and in vitro studies have further documented an inhibitory effect of androgens on neointimal plaque formation. This review discusses different and, in part, contradictory effects of androgens on the cardiovascular system including potential signal transduction pathways in androgen target cells.
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PMID:Cardiovascular effects of androgens. 1239 66

Macrovascular complications in diabetics create a high risk for cardiovascular disease (CVD). Generally, the main risk factors for CVD include age, men's sex, elevated LDL-cholesterol and reduced HDL-cholesterol, elevated fibrinogen, hypertension, smoking, and diabetes mellitus. Clinical manifestation of coronary disease is determined by number, area, and severity of coronary stenoses, myocardial function, and presence of induced ischemia. Routine pharmacological treatment of ISHD concentrates on risk factors and hasn't been yet focused on changes in energy metabolism during ischemic situation which are important factors contributing to ischemic damage. Substances able to optmize energy metabolism of heart muscle offer a very tempting way both for ISHD treatment and for treatment of following cardiovascular complications. Optimal use of energy source in heart muscle can favour heart activity so that comparable amount of contractile work requires less oxygen. The most beneficial way of getting energy for myocardium while low consumption of oxygen is oxidation of glucose. Because of a large amount of free fatty acids (FFAs) in diabetics a more demanding way of oxidation takes place in them, the oxidation of FFAs. Therefore myocardium of a diabetic needs under normal perfusion conditions more oxygen to provide energy. Besides increase in demand of oxygen, FFAs separate glycolysis from glucose oxidation and increase undesirable production of lactate and protons. An ischemic myocardium of a diabetic has primarily bigger demand of oxygen then myocardium of a non-diabetic. Development of cell ischemia, with all the known consequences in forms of lactate acidosis, calcium overload, and depletion of ATP, leads to considerable contractile disorder. Unfavourable position of metabolic activities in myocardium of diabetics and faster and more serious progression of atherosclerosis result in a big risk of CVD in diabetics. Incidence of coronary events in diabetics without history of ISHD is as big as in non-diabetics with history of coronary events.
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PMID:[The heart in diabetics]. 1504 Jan 56

Heavy coffee consumption has been associated with increased coronary heart disease (CHD) risk although many studies have not observed any relation. We studied the effect of coffee consumption, assessed with a 4-d food record, on the incidence of nonfatal acute myocardial infarction or coronary death in a cohort of 1971 men who were 42 to 60 y old and free of symptomatic CHD at baseline in 1984-1989. During a mean follow-up of 14 y, 269 participants experienced an acute coronary event. After adjustment for age, smoking, exercise ischemia, diabetes, income, and serum insulin concentration, the rate ratios (95% CIs) in daily nondrinkers and light (375 mL or less), moderate (reference level), and heavy (814 mL or more) drinkers were 0.84 (0.41-1.72), 1.22 (0.90-1.64), 1.00, and 1.43 (1.06-1.94). To address time dependence of the effect, the analysis was repeated for 75 CHD events that occurred during the first 5 y; the respective rate ratios were 0.42 (0.06-3.10), 2.00 (1.16-3.44), 1.00, and 2.07 (1.17-3.65). Further adjustment for serum HDL and LDL cholesterol concentration, diastolic blood pressure, maximal oxygen uptake, and waist-hip ratio slightly increased the rate ratio for heavy coffee intake. Neither the brewing method (boiling vs. filtering) nor the serum LDL cholesterol concentration had any impact on the risk estimates for coffee intake. In conclusion, heavy coffee consumption increases the short-term risk of acute myocardial infarction or coronary death, independent of the brewing method or currently recognized risk factors for CHD.
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PMID:Coffee drinking is dose-dependently related to the risk of acute coronary events in middle-aged men. 1533 32

The purpose of this study was to test whether the insulin sensitivity, lipid metabolism and the susceptibility of the heart to ischemia/reperfusion injury are modulated by the chronic estrogen status. Rats were ovariectomized (OVX), not ovariectomized (sham) or ovariectomized and treated with subcutaneous 17 -estradiol (30 mug/kg/day, OVX+E2) (n=14-17 per group). Within 3 months after operation, body weight, the serum levels of estrogen, glucose, insulin, total cholesterol (T-chol), HDL-chol, LDL-cholesterol (LDL-chol), triglycerides (TG) and lipoprotein a (Lp(a)) were monitored. Three months after operation, hearts of partial rats (n=6-8 per group) were isolated and allowed an initial 20-min stabilization period, and then cardiac function was recorded and creatine kinase (CK) release in the coronary effluent was measured after 4 h of hypothermic ischemia in isolated rat hearts. The experimental results showed that from 2 weeks after ovariectomy to the end of the study, body weights of OVX were significantly higher compared with the other two groups (p<0.05). On weeks 5 and 9, insulin level of OVX was significantly higher than that of the other two groups (p<0.05), whereas it was not different among the three groups on weeks 12 and 13 (p>0.05). Blood glucose on week 13 was significantly higher in OVX (p<0.05). Consequently, Insulin Sensitivity Index (ISI) of OVX was lower than that of the other two groups on weeks 5 and 9 (p<0.05), but not on weeks 12 and 13. Serum values for T-chol, HDL-chol and LDL-chol were not significantly different among the three groups within the observing period. On week 13, TG level in ovariectomized group was significantly lower than in the sham- and E2-treated groups (p<0.05). Compared with sham, Lp(a) level was slight increased in OVX rats (p<0.05), while it was further increased in E2-treated rats (p<0.05). Cardiac function (left ventricular pressure (LVP) and +/-dp/dtmax) of hearts removed from OVX rats was depressed, and CK release was markedly increased (p<0.05). However, treatment with E2 significantly improved cardiac function, as shown by increasing left ventricular pressure,+dp/dtmax and -dp/dtmax, and decreased CK release. In conclusion, chronic E2 treatment has some beneficial effects on cardiovascular disease (CVD), which come from the results of improvement of insulin sensitivity and post-ischemia cardiac function. However, the mechanism did not include changes in lipids and lipoproteins. The change in Lp(a) level shows that estrogen does not confer cardiovascular protection and may increase the risk of stroke.
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PMID:Influence of ovariectomy and 17beta-estradiol treatment on insulin sensitivity, lipid metabolism and post-ischemic cardiac function. 1556 37

Estrogen stimulates endothelial nitric oxide (NO) production and attenuates endothelial dysfunction in ischemia/repurfusion and menopause. Recent studies have shown that phytoestrogens from dietary sources improve endothelial function and reduce cardiovascular risks. The Thai medicinal plant Pueraria mirifica (PM) contains many potent phytoestrogens including miroestrol and deoxymiroestrol but no study on vascular function has been established. Ground powder of PM was orally given to ovariectomized White New Zealand rabbits (OVX + PM group) (n = 4) weighing 3.2-4.0 kg at the dose of 100 mg/kg for 90 days. Saline-treated ovariectomized rabbits were assigned as a control group (OVX group) (n = 5). At the end of treatment thoracic aorta was isolated for functional evaluation. Maximal relaxant response to acetylcholine (ACh) was significantly increased (24%) with 3.5-fold decrease in EC50 while no change in relaxant response to sodium nitroprusside was observed Minimal and maximal responses to 17beta-estradiol (E2) were increased in the OVX + PM group and L-NAME (100 mM) attenuated Emax of E2. PM significantly decreased maximal contractile responses to norepinephrine (NE), but no change in EC50 was observed. In addition to vascular study, the authors found no significant alteration in serum cholesterol, LDL, triglyceride, HDL, ALT AST alkaline phosphatase, and lipid peroxidation in OVX + PM rabbits. These data demonstrate that PM (100 mg/kg/d) improved endothelial function through NO-dependent pathway and increased response to E2 while sensitivity to NE was reduced. In addition, it had no impact on lipid profile, liver enzymes, and ALP activities. PM is a potential source of phytoestrogens for postmenopausal women to improve cardiovascular function or reduce cardiovascular risks.
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PMID:Effects of Pueraria mirifica on vascular function of ovariectomized rabbits. 1686 67

Elevated plasma levels of LDL and lipoprotein (a) [Lp(a)] are associated with an increased risk of atherosclerosis and coronary heart disease. However, it is not known whether Lp(a) would enhance the atherogenic effect of LDL on coronary atherosclerosis and myocardial infarction. To address this issue, we cross-bred human Lp(a) transgenic (Tg) rabbits with Watanabe heritable hyperlipidemic (WHHL) rabbits and evaluated the long-term (at the age of 2 years) effects of Lp(a) on the development of coronary atherosclerosis. Compared to non-Tg WHHL rabbits, Tg WHHL rabbits did not show significant changes in plasma total cholesterol, triglycerides, or HDL-C. However, Tg WHHL rabbits showed significantly larger lesions in the right coronary arteries (p<0.05). Immunohistochemical staining revealed that the lesions of Tg WHHL rabbits were enriched in the extracellular matrix contents whereas the cellular components were not different from those in non-Tg WHHL rabbits. Increased atherosclerosis in the coronary arteries in Tg WHHL rabbit hearts was also associated with a higher incidence of chronic ischemia and myocardial infarction. These results suggest that increased plasma levels of Lp(a) enhance coronary atherosclerosis and myocardial infarction in the setting of hypercholesterolemia.
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PMID:Lp(a) enhances coronary atherosclerosis in transgenic Watanabe heritable hyperlipidemic rabbits. 1704 71

The objective of the study is to study of the fatty acids spectr of LDL and HDL of blood plasma unstuble stenocardia (US) and increace efficiency of treatment with statines. 21 patients with US were presckribed atorvastatine with the first day of treatment Patients in control group received only basis therapy. The duration of the treatment was was 21 days. The patients were observed behive and after the treatment. The change of the content of LDL and HDL was made with jafic chromotography method. Payly ECG monotoring was used to check ST segment dynamie, and heart rate disordens. It was esheblished That the use of atorvastatine normalises contents of LDL and HDL and decreases episodes of the duratuion of miocardial ischemia and the quantity of ventricular extrasystols.
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PMID:[Efficiency of early atorvastatine treatment in patients with unstable angina]. 1768 1

The lysosphingolipid sphingosine 1-phosphate (S1P) is a component of HDL. Findings from a growing number of studies indicate that S1P is a mediator of many of the cardiovascular effects of HDL, including the ability to promote vasodilation, vasoconstriction, and angiogenesis, protect against ischemia/reperfusion injury, and inhibit/reverse atherosclerosis. These latter cardioprotective effects are being shown to involve the S1P-mediated suppression of inflammatory processes, including reduction of the endothelial expression of monocyte and lymphocyte adhesion molecules, decreased recruitment of polymorphonuclear cells to sites of infarction, and blocking of cardiomyocyte apoptosis after myocardial infarction. This review article summarizes the evidence that S1P as a component of HDL serves to regulate vascular cell and lymphocyte behaviors associated with cardiovascular (patho)physiology.
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PMID:HDL serves as a S1P signaling platform mediating a multitude of cardiovascular effects. 1769 55

Hypercholesterolemia (HC) induced endothelial cell dysfunction and decreased endothelial nitric oxide formation results in impaired angiogenesis and subsequent cardiovascular disorders. Therapeutic angiogenesis is known to be a novel strategy for treatment of patients with ischemic heart disease. We have shown that secoisolariciresinol diglucoside (SDG) is angiogenic as well as cardioprotective against myocardial ischemia. In the present study, we examined the efficacy of SDG in a hypercholesterolemic myocardial infarction (MI) model. The rats were maintained on a normal and high cholesterol diet (2%) for 8 weeks followed by oral administration of SDG (20 mg/kg) for 2 weeks. The rats were divided into four groups (n=24 in each): Control (C); SDG control (SDG); HC; and HC+SDG (HSDG). Isolated hearts subjected to 30 min of global ischemia followed by 120 min of reperfusion were used to measure the cardiac functions, infarct size and to examine the protein expression profile. After treatment, MI was induced by ligating the left anterior descending artery. Echocardiographic parameters were examined 30 days after MI. Significant reduction in total cholesterol, LDL-cholesterol, triglycerides and an increase in HDL-cholesterol levels were observed in HSDG as compared to the HC. Decreased infarct size was observed in the HSDG group (43%) compared to the HC (54%). Increased phosphorylation of endothelial nitric oxide synthase (p-eNOS) (3.1-fold), vascular endothelial growth factor (1.9-fold) and heme oxygenase-1 (2.3-fold) was observed in the HSDG group as compared to the HC group. Significant improvement in left ventricular functions was also observed in the HSDG group as evidenced by increased ejection fraction (55% vs. 45%), fractional shortening (28% vs. 22%) and decreased left ventricular inner diameter in systole (8 vs. 6 mm) in HSDG compared to HC. Moreover, MI model has shown increased capillary density (2531 vs. 1901) and arteriolar density (2.6 vs. 1.8) in SDG-treated rats as compared to the HC. The increased capillary and arteriolar density along with increased left ventricular functions on SDG treatment might be due to increased HO-1, VEGF and p-eNOS expression. In conclusion, our study demonstrates for the first time that SDG treatment reduces ventricular remodeling by neovascularization of the infarcted HC myocardium.
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PMID:Secoisolariciresinol diglucoside induces neovascularization-mediated cardioprotection against ischemia-reperfusion injury in hypercholesterolemic myocardium. 1800 68


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