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 Copenhagen Male Study is a prospective, cardiovascular cohort study initiated in 1970 and consisting of 5249 employed men aged 40-59 years. A total of 4710 men, who had reported their smoking habits and were free of ischaemic heart disease, had their mortality recorded over a 17-year period: 585 men suffered a first incident of ischaemic heart disease (IHD), and 248 cases were fatal. There was a strong social gradient in the risk of IHD (Kendall's Tau B = 0.12, P less than 0.001). Adjusting for age, blood pressure, physical activity, body mass index and alcohol consumption in a multiple logistic regression equation, men in the lowest social class had a relative risk (95% confidence interval) of IHD of 3.6 (2.5-5.3) compared to men in the highest social class. We determined whether differences in smoking habits could explain at least some of this large increase in risk. Adjustment for the above factors and also inclusion of the form of tobacco smoked, the amount of tobacco smoked and presence or absence of inhalation, had very little effect on the estimate: the relative risk was 3.5 (2.4-5.2). There was no social gradient in age at the start of smoking. According to smoking habits, comparing social class V with social class I, the relative risk was 7.7 (2.6-22.4) in cigarette smokers, 6.0 (1.1-32.1) in pipe smokers, 3.5 (1.7-7.1) in mixed smokers, 2.25 (0.4-12.9) in cheroot smokers, 3.8 (2.4-5.9) in all smokers, 1.95 (0.8-4.6) in ex-smokers, and 4.7 (1.01-22.2) in non-smokers. In the upper social classes, 50-75% of IHD events could be ascribed to smoking, and in the lowest classes only about 20%. We conclude that the substantial social inequalities in risk of ischaemic heart disease are not accounted for by differences in smoking habits.
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PMID:Ischaemic heart disease incidence by social class and form of smoking: the Copenhagen Male Study--17 years' follow-up. 160 85

The role of hemodialysis (HD) as an arrhythmogenic event has recently been emphasized. We studied 18 patients by Holter monitoring, comparing the arrhythmogenic effect of acetate dialysis (AHD) and bicarbonate dialysis (BHD). The frequency of ventricular arrhythmias was 93 +/- 66/h in AHD and 32 +/- 26/h in BHD (p less than 0.005). According to the classification of Lown and Graboys, classes III and IV were more often to be found in AHD than in BHD and no patient on BHD was in class IVB and class V. Five patients affected with ischemic heart disease had more frequent and dangerous ventricular arrhythmias than the others; a significant difference between buffers was recorded in all cases but 1. Intradialytic changes in body weight, hematocrit, osmolarity, ionized calcium and potassium during AHD and BHD were similar. The two methods only differed in the quickness and degree of correction of acidosis, and this was related to a significant difference in intraerythrocytic potassium at the end of the session. The quicker and more regular correction of acidosis with BHD and the consequent difference in ionic flows between the intra- and extracellular spaces, as demonstrated by changes in intraerythrocytic potassium at the end of the session, could account for the seemingly less arrhythmogenic effect of BHD.
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PMID:Hemodialysis-associated cardiac arrhythmias: a lower risk with bicarbonate? 186 78

The Copenhagen Male Study is a prospective, cardiovascular cohort study initiated in 1970 and consisting of 5249 employed men aged from 40 to 59 years. A total of 4710 men, who had reported their tobacco habits and were initially free of ischaemic heart disease (IHD), had their mortality and morbidity recorded over a 17-year period: 585 men suffered a first incident of ischaemic heart disease, and 248 cases were fatal. There was a strong social gradient in the risk of IHD, Kendall's Tau B = 0.12, p < 0.001. After adjusting for age, blood pressure, physical activity, body mass index and alcohol consumption in a multiple logistic regression equation, men in the lowest social class had a relative risk (95% confidence interval) of IHD of: RR = 3.6 (2.5- 5.3) compared to men in the highest social class. We determined whether differences in smoking habits could explain at least some of this large increase in risk. Adjusting for the above factors as well as the form of tobacco smoked, the amount of tobacco smoked and presence or absence of inhalation had very little effect on the estimate: the relative risk was 3.5 (2.4-5.2). There was no social gradient in age at the start of smoking. When comparing social class V to social class I according to smoking habits, the relative risk was 7.7 (2.6-22.4) in cigarette smokers, 6.0 (1.1-32.1) in pipe smokers, 3.5 (1.7-7.1) in mixed smokers, 2.25 (0.4-12.9) in cheroot smokers, 3.8 (2.4-5.9) in all smokers, 1.95 (0.8-4.6) in exsmokers and 4.7 (1.01-22.2) in never smokers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Social inequalities as a risk of ischemic heart disease--a matter of smoking habits? 17 years' follow-up in the Copenhagen Male Study]. 831 56

Familial hypercholesterolaemia (FH) is the most common inherited metabolic disease characterized by elevated serum levels of low-density lipoprotein cholesterol (LDL-C) and ischaemic heart disease early in life. Early diagnosis and treatment are essential to prevent premature atherosclerosis in FH patients. The aim of our study was the evaluation of the effects of genetic [class of the LDL receptor (LDLR) gene mutation, apolipoprotein (apo)E, apoA-IV and cholesterol ester transfer protein gene polymorphisms] and environmental factors (age, sex, smoking habit and body mass index) on the lipid-lowering response to statin therapy in patients with molecularly defined FH. Atorvastatin 20 mg/day was prescribed in 49 patients with heterozygous FH. The lipid profile was examined before and after 12 weeks of therapy. Statin therapy resulted in a decrease of 37% and 36% in LDL-C and apoB levels, respectively. The study population was then divided into 2 groups according to the class of the LDLR mutation [patients sharing a class V mutation (the G1775A mutation, n=21) and patients sharing class II mutations (the G1646A and the C858A mutations, n=28)]. In both groups, the percentage decrement in LDL-C and apoB levels were correlated with the initial LDL-C and apoB levels, respectively. The class of the LDLR mutation affected the LDL-C and apoB-lowering response of heterozygous FH patients to statin therapy. In detail, heterozygotes sharing a class V mutation of the LDLR showed a higher percentage decrement in LDL-C and apoB levels after atorvastatin administration compared to patients sharing class II mutations (49+/-9% versus 34+/-9%, P=0.001 for LDL-C and 42+/-16% versus 35+/-20%, P=0.001 for apoB). The influence of the classes of the LDLR gene mutations on the change of LDL-C and apoB levels to atorvastatin was still significant in a multivariate analysis. None of the other genetic and environmental factors studied affected the lipid-lowering response to atorvastatin therapy in patients with heterozygous FH in a multivariate analysis. Our data indicate that the class of the LDLR gene mutation affects the LDL-C and apoB-lowering response of heterozygous FH patients to statin therapy. Specifically, patients with a class V mutation exhibit higher percentage decrease in LDL-C and apoB levels after statin therapy compared to patients sharing class II mutations.
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PMID:Genetic and environmental factors affecting the response to statin therapy in patients with molecularly defined familial hypercholesterolaemia. 1586 14