Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect selenium in the form of sodium selenite on central hemodynamic conditions and coronary artery flow was studied in pig hearts infarcted by a ligature of the ramus interventricularis anterior. Infusions of sodium selenite solutions at levels of 1-3 mg/kg body wt improved the survival of infarcted pigs. Both short-term and long-term protective effects of selenite could be demonstrated. It is of potential therapeutic importance that sodium selenite administration suppresses the electrical vulnerability of the cell membrane, notably the occurrence of ventricular late potentials in the ischemic border zone. Coronary blood circulation, as evidenced by an increase of heart rate and coronary artery dilatation and peripheral vasodilation was also improved. The pulsatile coronary blood flow thus is altered, increasing total perfusion of the infarcted heart. Initial observations with human subjects suggest that selenium deficiency is a factor in the pathogenesis of ischemic and arteriosclerotic heart disease. In 54 hospitalized patients with clinical diagnosis of acute myocardial infarction, serum selenium levels were 670 +/- 266 nmol/L, as compared to 981 +/- 209 nmol/L in 93 healthy controls. In 32 patients with general arteriosclerosis, the serum Se level was 375 +/- 85 nmol/L, in 64 patients with arteriosclerotic occlusional disease in the leg region, 366 +/- 85 nmol/L, respectively. Serum selenium levels of healthy subjects were found to be age- and sex dependent. In men, the selenium concentrations reached maximum levels of 1083 nmol/L in the 41-50 y age group. In women in the same age group, the serum Se level was 1385 nmol/L. Evidence is presented to suggest that selenium is preventing oxidative damage of heart cell membranes by lipid peroxidation.
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PMID:Selenium in cardiology and angiology. 248 14

Cytochrome-c-oxidase, the terminal enzyme of the respiratory chain, was studied in 140 hearts from men obtained at autopsy revealing randomly distributed cardiomyocytes without enzyme activity. The expression of the defect was independent of an underlying heart disease and was observed both in normal hearts and in hearts with hypertrophy and/or coronary arteriosclerosis. In contrast, age was a discriminating factor: The defects occurred sporadically in the second decade, but were regularly present from the sixth decade on. Also, the number of defects/sq cm (defect density) increased with age from 2 to 3 in the second and third decade, to about 50 defects in advanced age. Irrespective of the defect density, the enzyme defect always affected isolated cardiomyocytes and ended abruptly at the intercalated disc of neighboring heart muscle cells, as revealed by ultracytochemistry. The results indicate that cytochrome-c-oxidase deficient heart muscle cells represent a degenerative lesion associated with cellular ageing and may be involved in the reduction of myocardial contractile ability in senescence.
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PMID:Cytochrome-c-oxidase deficient cardiomyocytes in the human heart--an age-related phenomenon. A histochemical ultracytochemical study. 254 14

We are studying the genetic factors underlying the common forms of heart disease by identifying genes that affect normal variations in plasma lipid, lipoprotein, and apolipoprotein concentrations in baboons. For these studies we are using cloned human gene probes to identify restriction fragment length polymorphisms (RFLPs) at loci encoding the proteins of cholesterol metabolism. In this report we present the identification and mapping of a polymorphic Ava II cleavage site in intron 17 of the baboon low density lipoprotein (LDL) receptor gene. We determined genotypes for this RFLP on a population of 253 pedigreed baboons and assessed the effect of LDL receptor RFLP genotypes on serum concentrations of LDL cholesterol (LDL-C) and apolipoprotein B (apo B). These measures were obtained for each baboon on each of two diets: a low cholesterol, low fat (basal) diet and a high cholesterol, high saturated fat (atherogenic) diet. Statistical analysis detected a significant association between LDL receptor genotype and serum LDL-C and apo B concentrations on both diets. Homozygotes for the rarer allele had lower serum concentrations of LDL-C and apo B than did homozygotes for the common allele, and with the exception of apo B levels on the basal diet, intermediate levels were observed in heterozygotes. The LDL receptor RFLP accounted for approximately 3% to 7% of the variation in serum LDL-C and apo B concentrations on both diets.
Arteriosclerosis
PMID:Identification of LDL receptor gene marker associated with altered levels of LDL cholesterol and apolipoprotein B in baboons. 257 32

These recommendations for secondary prevention of clinical coronary cardiopathy are the result of a symposium attended by 46 experts belonging to the councils on arteriosclerosis, clinical cardiology, epidemiology, and prevention and rehabilitation of the International Society and Federation of Cardiology. Secondary prevention of coronary cardiopathy refers to measures designed to prevent deterioration or death in patients with clinical manifestations of coronary cardiopathy. Such measures in addition to drugs include health actions that may improve the status of various coronary risk factors: the patient's life style should stress maintenance of proper weight, regular physical exercise, reduction of saturated fats and cholesterol in the diet, and elimination of smoking and excessive alcohol consumption. It is considered reasonable to control hypertension through the most innocuous means possible, but findings of the few existing controlled studies of effects of treatment of hypertension in coronary cardiopathy are complex. Drug treatment may be necessary for most patients, but nondrug measures should be added when possible. Various proofs including results of some controlled studies justify the recommendations for reducing elevated levels of serum cholesterol and low density lipoprotein cholesterol through dietary measures. Optimum plasma cholesterol levels are 5.2 mmol/1 or less, and the upper limit is 5.7 mmol/1. The rules for secondary prevention are the same for diabetics as for nondiabetics, but some special precautions are necessary in diabetics. Habitual and vigorous physical activity has been associated with a decline in the incidence of coronary cardiopathy in different population studies, although there has been no demonstration that exercise can alter the progression of atherosclerosis or improve collateral circulation. Stress should be recognized as a risk factor and included in secondary prevention, but the concept that stress is the key risk factor in coronary events is in conflict with a large body of scientific evidence. Oral contraceptives (OCs) tend to increase boood pressure and weight as well as serum triglyceride levels, and to reduce glucose tolerance and high density lipoprotein cholesterol in some formulations. OCs also affect the integrity of the vascular endothelium and alter blood coagulation, fibrinolysis, and platelet function. These thrombogenic changes are intensified with age, especially after 35, and with smoking. OCs are innocuous in women under 35 with no history of venous or arterial disease or pulmonary embolism and who have normal blood pressure and serum cholesterol levels. Patients using OCs should control their blood pressure and weight and be alert to any symptoms of thrombotic episodes. The risk/benefit ratio of longterm estrogen treatment in meno- and postmenopausal women with coronary cardiopathy has not yet been established. Apart from 1 study in primates, there is no evidence that vasectomy should be considered either indicated or contraindicated for coronary patients. Beta blockers, platelet function inhibitors, anticoagulants, and other drugs are under active study for secondary prevention of coronary cardiopathy.
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PMID:[Recommendations for secondary prevention of the clinical coronary cardiopathy]. 285 11

To assess effects of beta-adrenergic blockade on ventricular tachycardia (VT) of various mechanisms, electrophysiology studies were performed before and after intravenous infusion of propranolol (0.2 mg/kg) in 33 patients with chronic recurrent VT, who had previously been tested with intravenous verapamil (0.15 mg/kg followed by 0.005 mg/kg/min infusion). In the verapamil-irresponsive group, 10 patients (group IA) had VT that could be initiated by programmed ventricular extrastimulation and terminated by overdrive ventricular pacing, and 11 patients (group IB) had VT that could be provoked by isoproterenol infusion (3-8 micrograms/min) but not by programmed electrical stimulation, and that could not be converted to a sustained sinus rhythm by overdrive ventricular pacing. Notably, in the group IA patients, all 10 patients had structural heart disease (coronary arteriosclerosis or idiopathic cardiomyopathy); beta-adrenergic blockade accelerated the VT rate in one patient but exerted no effects on the VT rate in the remaining 9 patients, and VT remained inducible in all 10 patients. By contrast, in the group IB patients, 7 of the 11 patients had no apparent structural heart disease; beta-adrenergic blockade completely suppressed the VT inducibility during isoproterenol infusion in all 11 patients. There were 12 patients with verapamil-responsive VT (group II). 11 of the 12 patients had no apparent structural heart disease. In these patients, the initiation of VT was related to attaining a critical range of cycle lengths during sinus, atrial-paced or ventricular-paced rhythm; beta-adrenergic blockade could only slow the VT rate without suppressing its inducibility. Of note, 14 of the total 33 patients had exercise provocable VT: two in group IA, five in group IB, and seven in group II. Thus, mechanisms of VT vary among patients, and so do their pharmacologic responses. Although reentry, catecholamine-sensitive automaticity, and triggered activity related to delayed afterdepolarizations are merely speculative, results of this study indicate that beta-adrenergic blockade is only specifically effective in a subset group (group IB) of patients with VT suggestive of catecholamine-sensitive automaticity.
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PMID:Effects of beta-adrenergic blockade on verapamil-responsive and verapamil-irresponsive sustained ventricular tachycardias. 289 8

Vectorcardiography was performed on 2,449 subjects, aged six years and older, in the Tucson (Ariz) Epidemiological Study of Airway Obstructive Diseases (AOD), 95 percent of the white non-Mexican Americans in the stratified cluster population sample. The objectives were to confirm previous relationships and to determine if hypothesized changes in the vectorcardiogram (VCG) could predict AOD. Trained nurse technicians performed the VCGs, which were read and interpreted by a cardiologist. Vectorcardiographic results were broadly interpreted for abnormalities. Also, calculated vector means and angles were compared to standard questionnaire responses for medical history, to maximum expiratory flow-volume variables, and to values for blood pressure; these were all corrected for sex, age, height, weight, and the ponderal index. Values were expressed as percentages of predicted. Over 80 percent of the VCGs were found to be normal. Measured hypertrophy was related to disease; there were significantly more abnormalities in those with histories of heart disease, hypertension, arteriosclerosis, and AOD, when examined by types of ventricular hypertrophy and VCG-identified heart disease or hypertension; findings of AOD and heart disease were also correlated significantly. Of all the ventricular hypertrophy, right ventricular hypertrophy (RVH), type C, was confirmed to be the predominant type associated with decreased pulmonary function in all smoking groups. Systolic blood pressure was related to RVH, type A, and diastolic 4 and 5 blood pressure with RVH, types A and B. The vectors' magnitude and angles were related to abnormality of pulmonary function in those with and without heart disease and AOD.
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PMID:Vectorcardiographic and blood pressure correlates of obstructive pulmonary diseases in a community population. 293 31

Milk consumption is related to arteriosclerosis. Recent landmark studies confirm a previously suspected close correlation between milk intake and arteriosclerotic heart disease. Support is therefore provided for a recently proposed novel hypothesis that arteriosclerosis is a chronic infectious disease caused by blue-green bacteria and that milk is a carrier vehicle for these contaminant organisms. A revisionist view of diet and milk in the causation of arteriosclerosis is developed. Previous hypotheses relating milk consumption to arteriosclerosis and advances in pasteurization techniques are discussed and integrated with this infection theory.
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PMID:Milk and arteriosclerosis. 309 97

We investigated the prevalence of carotid atherosclerosis and its association with serum lipoprotein cholesterol fractions in 412 Eastern Finnish men ages 42, 48, 54, or 60 years who were examined between February and December 1987 in the Kuopio Ischaemic Heart Disease Risk Factor Study. Carotid atherosclerosis was assessed with high-resolution B-mode ultrasonography. Of the participants, 37% had thickening of the intimal or medial layer of the arterial wall, 10% had plaques, 2% had stenosis in the right or left common carotid artery or in the carotid bifurcation, and only 51% were free of any detectable carotid atherosclerosis. The prevalence of atherosclerosis was 14.1%, 32.0%, 67.7%, and 81.9% in the four age groups, respectively. The mean age-adjusted serum low density lipoprotein (LDL) cholesterol concentration was 3.67 mmol/l (142 mg/dl) in men free of carotid atherosclerosis and 4.02 mmol/l (155 mg/dl) in those with at least intimal thickening (p = 0.003 for difference). The mean age-adjusted serum cholesterol concentration in the high density lipoprotein (HDL) fraction was 1.34 mmol/l (52 mg/dl) in the atherosclerosis-free and 1.27 mmol/l (49 mg/dl) in the atherosclerotic men (p = 0.029 for difference). There was a similar difference in both the serum HDL2 and the HDL3 cholesterol levels. Serum LDL and HDL (inverse) cholesterol were significant determinants of severity of carotid atherosclerosis in a multivariate regression model adjusting for age, obesity, plasma fibrinogen, cigarette-years, and duration of hypertension. Our data reveal the high prevalence of atherosclerosis in middle-aged Eastern Finnish men and provide further evidence of the roles of LDL and HDL cholesterol in atherosclerosis.
Arteriosclerosis
PMID:Prevalence of carotid atherosclerosis and serum cholesterol levels in eastern Finland. 319 22

Risk factors for coronary disease were assessed and noninvasive methods were used to quantitate the extent of extracranial carotid atherosclerosis in 382 patients free of cerebrovascular symptoms. The ages of the participants ranged from 27 to 80 years. There were 183 men and 199 women, 30 black and 352 white persons. All patients had heart disease symptoms and were hospitalized for coronary angiography. Correlation of risk factors with extent of extracranial carotid atherosclerosis in this series of patients undergoing coronary angiography uncovered individual variability in relationships between risk factors and carotid atherosclerosis that depended on coronary status. Risk factors for carotid atherosclerosis in patients with and without coronary disease differed. Age and hypertension were independently related to carotid atherosclerosis in patients with, as well as those without, coronary disease. However, other risk factors were related to carotid atherosclerosis in only one group or the other. Risk factors correlated strongly with carotid atherosclerosis in patients with coronary disease (r2 = 0.41) but poorly in those with no coronary disease (r2 = 0.21). Certain risk factors (age, pack years of smoking, left ventricular hypertrophy) related differently to the extent of carotid atherosclerosis in patients with, than in those without, coronary disease. Clarification of the role of coronary status in the carotid atherosclerosis response to risk factors may partly explain the results of certain population-based studies that have related race, gender, and other risk factors to carotid atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Arteriosclerosis
PMID:Individual variation in susceptibility to extracranial carotid atherosclerosis. 339 75

As an overview of cardiovascular disease in the aged, 3657 autopsy cases were analyzed for the frequency and age-wise incidence of cardiovascular disease. The three major categories, ischemic heart disease, valvular heart disease, and aortic aneurysm and dissection were described. 1. The incidence of overall cardiovascular disease increases sharply between the ages of 60 and 75. Prevention and treatment could be effectively directed at this age group. 2. The incidence of organic cardiovascular disease was: myocardial infarction 19.8 percent; valvular disease 10.0 percent; arteriosclerosis obliterans 3.5 percent; aortic aneurysm and dissection 3.3 percent; pericarditis 2.1 percent; cardiomyopathy 1.6 percent; cor pulmonale 1.4 percent; congenital heart disease 0.7 percent; and others 0.8 percent. 3. As coronary sclerosis progresses, death from ischemic heart disease increases; however, 7 out of 10 patients with 3 vessel disease still die of causes other than ischemic heart disease (pneumonia, malignancy etc.). The general management of infection and malignant neoplasms is important in addition to treatment of cardiovascular disease. 4. Except for mitral stenosis, valvular heart disease, the etiology of which is mostly non-rheumatic, increases with advancing age. 5. In aortic aneurysm, the rupture rate is relatively high in the thoracic aorta; however, this may be caused by the successful surgical repair of abdominal aneurysms. An aneurysm below 6 cm in diameter is not absolutely safe from rupture. 6. In aortic dissection, the interval from onset to the death of the patient is often too short to consider surgery.
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PMID:Cardiovascular disease in the aged: overview of an autopsy series. 341 67


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