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)

A series is presented of 83 patients surgically explored for massive bowel infarction. Old men with previous heart disease and symptoms of peripheral atherosclerosis were primarily affected. Clinical presenting features were abdominal pain (100 per cent), peritonitis (57 per cent), shock (34 per cent) and hypothermia (26 per cent). A third-space syndrome with metabolic acidosis and uraemia was the most common physiological derangement. Age was the only factor that appeared to have influenced the surgeon's decision to perform massive bowel resection (71 years in non-resected versus 64 years in resected patients, P less than 0.006). The overall mortality rate was 71 per cent. Forty-four patients underwent massive bowel resection (mean length of remaining small bowel 60 +/- 40 cm) and twenty-four (54 per cent) survived the procedure. Axillary temperature was higher in survivors (36.7 degrees C versus 36.1 degrees C, P less than 0.03). Early postoperative total plasma protein and albumin concentrations were also higher in survivors (57 versus 46 g/l, P less than 0.005; 27 versus 22 g/l, P less than 0.02). Patients with previous symptoms of atherosclerotic disease and high pre-operative blood urea levels also had a bad prognosis. Survivors had a mean hospital stay of 57 days and parenteral nutrition had to be maintained for a mean of 34 days. The survival rate achieved with massive resection justifies this surgical approach in selected patients with massive bowel infarction.
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PMID:Mesenteric infarction: an analysis of 83 patients with prognostic studies in 44 cases undergoing a massive small-bowel resection. 339 20

We report semi-quantitative histological data on coronary arteries, collected at autopsy from Japanese of both sexes (Group I) who had had unstable anginal attacks and transient ST elevation or depression in ECG within 1 month before death. The cause of death in all cases was acute myocardial infarction or coronary sudden death. A control group consisted of 28 autopsied patients (Group II) who had died of causes other than heart disease and who had been free from anginal attacks. The frequency of 51-75% and 76-100% luminal narrowing in the coronary arteries in Group I was statistically higher than that in Group II (P less than 0.01). Subendothelial infiltration of monocytes/macrophages with edematous change was most evident in Group I in all segments of the coronary artery, particularly in the proximal portions of the three main branches, regardless of mural or occlusive thrombotic sites of the coronary artery. The subendothelial infiltration of monocytes/macrophages, in terms of luminal narrowing, was the most frequent in the portions with 0-50% luminal narrowing, followed by portions with 51-75% narrowing. The subendothelial infiltration of mononuclear cells with edematous change, observed mostly in the proximal portions of three main branches of the coronary artery in Group I, was attributed to increased subendothelial permeability and endothelial damage caused by coronary vasospasm of recent occurrence. We propose that repeated vasospasm may lead to further progression of coronary atherosclerosis.
Atherosclerosis 1987 Dec
PMID:Increased subendothelial infiltration of the coronary arteries with monocytes/macrophages in patients with unstable angina. Histological data on 14 autopsied patients. 342 53

Many patients with hypertrophic cardiomyopathy (HCM) have signs and symptoms or metabolic and hemodynamic evidence of myocardial ischemia and dysfunction in the absence of extramural coronary atherosclerosis. To investigate the possibility that a form of "small vessel disease" could account for these findings, a histologic analysis of left ventricular myocardium obtained at necropsy was carried out in 48 patients with hypertophic cardiomyopathy and in 68 controls with either normal hearts or acquired heart disease. In HCM, abnormal intramural coronary arteries (IMCA) were characterized by thickening of the vessel wall and an apparent decrease in luminal size (external arterial diameter less than 1500 micron; average 300 micron). The wall thickening was due to proliferation of medial and/or intimal components, particularly smooth muscle cells and collagen. Of the 48 patients with HCM,40 (83%) had abnormal IMCAs located in the ventricular septum (33 patients), anterior left ventricular free wall (20 patients) or posterior free wall (nine patients); an average of 3.0 +/- 0.7 IMCA were identified per tissue section. Altered IMCAs were also significantly more common in tissue sections having considerable myocardial fibrosis (31 out of 42, 74%) than in those with no or mild fibrosis (31 or 102, 30%; p less than 0.001). Abnormal IMCA wera also identified in 3 out of 8 infants who died of HCM before 1 year of age. In contrast, only rare altered IMCA were identified in six (9%) of the 69 control patients, and those arteries showed only mild thickening of the wall and minimal luminal narrowing (abnormal IMCA per section: 0.1 +/- 0.05: p less than 0.001). Moreover, of those patients who did show abnormal IMCA, such vessels were about twenty times more frequent in patients with HCM (0.9 +/- 0.2/cm2 myocardium) than in controls (0.04 +/- 0.02/cm2 myocardium). Hence, abnormal IMCA with markedly thickened walls and narrowed lumens are present in increased numbers in most patients with HCM at necropsy, and may represent a congenital component of the underlying cardiomyopathic process. Although the clinical significance of "small vessel coronary artery disease" in HCM is unclear, the occurrence of structurally altered IMCA within or adjacent to areas of substantial myocardial fibrosis suggests a causal role for these arteries in producing ischemia.
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PMID:Morphologic evidence for "small vessel disease" in patients with hypertrophic cardiomyopathy. 343 79

High density lipoprotein (HDL) is the major plasma lipoprotein found in mice fed normal laboratory chow containing 4% fat. When female mice from some inbred strains, such as C57BL/6, are fed a high fat diet (1.25% cholesterol, 15% fat, and 0.5% cholic acid), the levels of HDL-cholesterol decrease by about 50%, and lipid staining lesions form in the aorta within 14 weeks. In other strains of mice, such as C3H and BALB/c, HDL-lipid levels decrease only slightly, and few or no aortic lesions are observed at 14 weeks. The genetic basis of these phenotypic differences was analyzed by using recombinant inbred strains derived from C57BL/6 and BALB/c and also from C57BL/6 and C3H/He. The two phenotypes segregated as simple Mendelian traits, and no recombination was observed between them. Thus, HDL-cholesterol levels and susceptibility to atherosclerosis appear to be determined by the same gene (or by two closely linked genetic factors that are a maximum of 1.7 centimorgans apart). This gene was named Ath-1, for atherosclerosis susceptibility, with alleles r for resistance and s for susceptibility. Ath-1 maps on chromosome 1 near Alp-2, a gene that determines the structure of apolipoprotein A-II, one of the two major proteins found in HDL. Ath-1 is clearly separable from Alp-2, and the distance between these genes is 6.0 centimorgans with a standard error of 4.2 centimorgans. In humans, levels of HDL are inherited and are inversely correlated with atherosclerosis; familial hyperalphalipoproteinemia is associated with high levels of HDL-cholesterol and decreased risk of heart disease. The human trait phenotypically resembles Ath-1 in the mouse.
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PMID:Ath-1, a gene determining atherosclerosis susceptibility and high density lipoprotein levels in mice. 347 81

Cardiovascular diseases responsible for sudden unexpected death in highly conditioned athletes are largely related to the age of the patient. In most young competitive athletes (less than 35 years of age) sudden death is due to congenital cardiovascular disease. Hypertrophic cardiomyopathy appears to be the most common cause of such deaths, accounting for about half of the sudden deaths in young athletes. Other cardiovascular abnormalities that appear to be less frequent but important causes of sudden death in young athletes include congenital coronary artery anomalies, ruptured aorta (due to cystic medial necrosis), idiopathic left ventricular hypertrophy and coronary artery atherosclerosis. Diseases that appear to be very uncommon causes of sudden death include myocarditis, mitral valve prolapse, aortic valve stenosis and sarcoidosis. Cardiovascular disease in young athletes is usually unsuspected during life, and most athletes who die suddenly have experienced no cardiac symptoms. In only about 25% of those competitive athletes who die suddenly is underlying cardiovascular disease detected or suspected before participation and rarely is the correct clinical diagnosis made. In contrast, in older athletes (greater than or equal to 35 years of age) sudden death is usually due to coronary artery disease, and rarely results from congenital heart disease.
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PMID:Causes of sudden death in competitive athletes. 351 Feb 33

In clinical practice, arteriosclerotic heart disease has not been recognized as a complication of long-term corticosteroid treatment. Yet, an increasing body of evidence suggests that prolonged corticosteroid therapy accelerates the development of atherosclerosis. An important element in this process may be the fact that corticosteroids induce or exacerbate several known coronary risk factors, including hypertension, hypercholesterolemia, hypertriglyceridemia, and impairment of glucose tolerance. One group of patients that is often exposed to long-term corticosteroid treatment is that with rheumatoid arthritis. These patients have an increased mortality, with cardiovascular disease appearing to be a major contributor to this decreased survival. The weight of evidence relates the development of atherosclerosis to corticosteroid use. However, no long-term epidemiologic or morphologic studies have been performed to elucidate this issue. Until these are accomplished, prolonged therapy with this medication, particularly in younger persons, should be avoided whenever possible.
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PMID:Is atherosclerosis a complication of long-term corticosteroid treatment? 351 40

The prevalence and incidence ratios of cerebrovascular disease, with special reference to transient ischemic attack (TIA), were studied in the towns of Daisen and Ama in western Japan. There have been no previous reports on this subject in Japan. The prevalence ratios of TIA were estimated to be 4.4 in Daisen and 2.0 in Ama per 1,000 people over 40 years old. The ratio of carotid arterial system TIA to vertebrobasilar arterial system TIA was about 1 to 1. The incidence ratios of stroke were 319.6 in Daisen and 314.5 in Ama per 100,000 people of all ages. The prevalence ratios of stroke were estimated to be 14.8 in Daisen and 13.5 in Ama per 1,000 people of all ages. The prevalence ratio of TIA in Japan is about one-third to one-half of that in Western countries. However, the prevalence of complete stroke is much higher in Japan compared with that in Western countries. Therefore, the ratio of TIA to stroke is much lower in Japan than in Western countries. The obstruction of small intracranial arteries, in addition to heart disease, might play an important role in TIA in Japan, whereas in Western countries TIA might be mostly caused by heart disease or the atherosclerosis of extracranial arteries.
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PMID:An epidemiologic study of cerebrovascular disease in western Japan: with special reference to transient ischemic attacks. 356 95

This study provides the first direct comparison of the relative importance of structural versus functional aspects of social network ties as they relate to susceptibility to coronary artery disease. Data from 119 men and 40 women undergoing coronary angiography provide an opportunity to compare these associations in relation to a direct and continuous measure of atherosclerosis while controlling for age, sex, income, hypertension, serum cholesterol, smoking, angina, diabetes, family history of heart disease, Type A behavior pattern, and hostility. Regression analyses indicate that network instrumental support and feelings of being loved are more important in predicting coronary atherosclerosis than is network size, independent of all covariables (relative extent of atherosclerosis, low/high support = 1.74 and 1.5, respectively). More "problem-oriented" emotional support did not show a similarly strong association (relative extent of atherosclerosis = 1.01). These findings suggest that certain functional aspects of social network ties are more strongly associated with host resistance to coronary atherosclerosis than are structural characteristics like network size.
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PMID:Social networks and coronary artery disease: a comparison of the structure and function of social relations as predictors of disease. 361 63

The variation in background radiation levels is an important source of information for estimating human risks associated with low-level exposure to ionizing radiation. Several studies conducted in the United States, correlating mortality rates for cancer with estimated background radiation levels, found an unexpected inverse relationship. Such results have been interpreted as suggesting that low levels of ionizing radiation may actually confer some benefit. An environmental factor strongly correlated with background radiation is altitude. Since there are important physiological adaptations associated with breathing thinner air, such changes may themselves influence risk. We therefore fit models that simultaneously incorporated altitude and background radiation as predictors of mortality. The negative correlations with background radiation seen for mortality from arteriosclerotic heart disease and cancers of the lung, the intestine, and the breast disappeared or became positive once altitude was included in the models. By contrast, the significant negative correlations with altitude persisted with adjustment for radiation. Interpretation of these results is problematic, but recent evidence implicating reactive forms of oxygen in carcinogenesis and atherosclerosis may be relevant. We conclude that the cancer correlational studies carried out in the United States using vital statistics data do not in themselves demonstrate a lack of carcinogenic effect of low radiation levels, and that reduced oxygen pressure of inspired air may be protective against certain causes of death.
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PMID:Altitude, radiation, and mortality from cancer and heart disease. 368 64

Many patients with hypertrophic cardiomyopathy have signs and symptoms of myocardial ischemia and dysfunction. Although hypertrophy and increased left ventricular pressure can account for such abnormalities, altered small intramural coronary arteries have also been described in such patients. To determine the prevalence and extent as well as the clinical relevance of abnormal intramural coronary arteries, a histologic analysis of left ventricular myocardium obtained at necropsy was performed in 48 patients with hypertrophic cardiomyopathy (but without atherosclerosis of the extramural coronary arteries) and in 68 control patients with either a normal heart or acquired heart disease. In hypertrophic cardiomyopathy, abnormal intramural coronary arteries were characterized by thickening of the vessel wall and a decrease in luminal size. The wall thickening was due to proliferation of medial or intimal components, or both, particularly smooth muscle cells and collagen. Of the 48 patients with hypertrophic cardiomyopathy, 40 (83%) had abnormalities of intramural coronary arteries located in the ventricular septum (33 patients), anterior left ventricular free wall (20 patients) or posterior free wall (9 patients); an average of 3.0 +/- 0.7 abnormal arteries were identified per tissue section. Altered intramural coronary arteries were also significantly more common in tissue sections having considerable myocardial fibrosis (31 [74%] of 42) than in those with no or mild fibrosis (31 [30%] of 102; p less than 0.001). Abnormal intramural coronary arteries were also identified in three of eight infants who died of hypertrophic cardiomyopathy before 1 year of age. In contrast, only rare altered intramural coronary arteries were identified in 6 (9%) of the 68 control patients (0.1 +/- 0.05 abnormal arteries per section; p less than 0.001) and those arteries showed only mild thickening of the wall and minimal luminal narrowing. Moreover, of those patients with abnormal intramural coronary arteries, such vessels were about 20 times more frequent in patients with hypertrophic cardiomyopathy (0.9 +/- 0.2/cm2 myocardium) than in control patients (0.04 +/- 0.02/cm2 myocardium). Hence, abnormal intramural coronary arteries with markedly thickened walls and narrowed lumens are present in increased numbers in most patients with hypertrophic cardiomyopathy studied at necropsy and may represent a congenital component of the underlying cardiomyopathic process.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Intramural ("small vessel") coronary artery disease in hypertrophic cardiomyopathy. 374 99


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