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 purpose of this study was to determine the coexistence of idiopathic hypertrophic cardiomyopathy (IHC) and atheromatous coronary artery disease. We studied forty six patients with IHC documented by complete clinical study and also by left heart catheterization. The diagnosis was considered established, when the patient had a significant left intraventricular pressure gradient (LIPG) and by angiographic and or echocardiographic demonstration of systolic anterior movement of the mitral valve and asymmetric septal hypertrophy. In 15 patients a selective coronary angiography was performed because ischemic myocardial disease was suspected. There were eight patients with significant atherosclerotic obstruction (greater than 75% narrowing). There was one vessel disease in 13%, two vessels in 37% and three vessels in 50% of the patients. The LIPG was 43 +/- 20 mmHg, the left ventricular and diastolic pressure (LVEDP) was 18 +/- 11 mmHg in patients with atheromatous disease and there was no significant difference with the patients with normal coronary arteries with LIPG 52 +/- 31 mmHg and LVEDP 21 +/- 9 mmHg. Our data demonstrate that ischemic heart disease in patients with idiopathic hypertrophic cardiomyopathy is related not only to increase of the cardiac mass and/or the ventricular wall stress, but in some of them atherosclerosis plays a role in its pathogenesis. Significant differences were found between the aged in both groups. In the patients who had coronary atherosclerosis the mean age was 54 years; on the other hand in the patients with normal coronary arteries the mean age was 44 years. This last fact could explain the high frequency of atherosclerosis in the older patients.
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PMID:[Obstructive hypertrophic myocardiopathy and coronary atherosclerosis]. 294 24

Asymmetric septal hypertrophy is considered by many to be pathologic but its presence in a number of states associated with left ventricular overload indicates that it may develop as an adaptive feature in the overloaded heart. This hypothesis implies that initially in these states a greater systolic stress and thus energy metabolism occurs in the ventricular septum than in the left ventricular free wall. It was previously demonstrated that in the early stages of ischemia regional differences in energy metabolism could be determined by comparisons of tissue high energy phosphate depletion and lactate accumulation. In the present study these measurements were made in an animal model of left ventricular overload. In open chest dogs aortic insufficiency was produced, which served to provide both volume overload to the left ventricle and regional myocardial ischemia. In addition to regional metabolite levels, measurements of regional blood flow were determined using radioactive microspheres. Tissue samples were taken from the left ventricle and interventricular septum, freeze clamped, divided transmurally into thirds and analyzed for creatine phosphate, adenosine triphosphate and lactate. Animals with myocardial ischemia after aortic insufficiency were classified into two groups: those in which ischemia was limited to the inner left ventricle and left side of the septum and those with more extensive ischemia transmurally. In the latter group, creatine phosphate depletion and lactate accumulation were greater in the septum, but myocardial blood flow was also more depressed in the septum than in the left ventricle. In the former group, where ischemia was more restricted, metabolite changes were also more severe in the left septum than in the inner left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional blood flow and metabolite levels in the left ventricular free wall and septum during aortic insufficiency: implications for the development of asymmetric septal hypertrophy. 294 41

Sixty four children with isolated congenital aortic stenosis (39 valvular, 16 fixed subvalvular, 4 supravalvular and 5 multiple) were operated at a mean age of 11,5 years. Valve repair was possible in all but three patients who had to undergo valvular replacement. Myotomy was associated in 18 cases (28 p. 100). The mean systolic pressure gradient was 79,9 mmHg (+/- 17,8); there was associated aortic regurgitation in 21 patients but this was minimal except in one case. Twenty children (31 p. 100) had symptoms on effort and the basal ECG showed ST-T wave changes in the left precordial leads in 30 cases (47 p. 100). Several preoperative exercise ECGs were performed in 29 patients without ST-T changes on the resting ECG. The exercise ECG was positive in 15 patients, providing one of the arguments for surgery; a poor blood pressure response to exercise was observed in 12 patients with a negative test. Out of the 28 patients with a positive preoperative exercise ECG, 7 (25 p. 100) went on having a positive result after surgery (p less than 0,05). The maximal heart rate was not significantly higher after surgery but the total work was significantly greater (p less than 0,01) and the increase in systolic blood pressure was even more significant (p less than 0,001). Out of 14 patients undergoing repeat catheterisation for a continuing positive exercise ECG or for ST-T wave changes on the resting ECG, there were 6 residual severe stenoses, 3 severe aortic regurgitations, 3 hypertrophic cardiomyopathies which were obstructive in 2 cases. The exercise ECG is a means of appreciating the consequences of the stenosis which are the cause of the complications (myocardial ischemia and poor blood pressure adaptation). This justifies its use in assessing the surgical indications and for the follow-up of the surgical result. A persistantly positive exercise ECG and continuing ST-T wave changes on the resting ECG are signs of a poor surgical result and hemodynamic revaluation should be considered; besides severe postoperative aortic regurgitation, residual or recurrent stenosis and, above all, asymmetric septal hypertrophy, obstructive or not, are the main causes of poor postoperative results.
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PMID:[Importance of the exercise test in the follow-up of surgically treated congenital aortic stenoses]. 641 51

Findings in 20 patients with congestive, in 14 with hypertrophic and in one with restrictive cardiomyopathy are described. In congestive cardiomyopathy, there predominated left ventricular dilatation and diffuse hypokinesis with decreased ejection fraction. The main criteria are reported for differentiating it from advanced diffuse ischaemic heart disease. More detailed characterization is presented of the type of asymmetric septal hypertrophy and of the systolic anterior motion of the mitral apparatus and the possible causes of this finding are discussed. In a patient with restrictive cardiomyopathy there predominated a symmetric thickening of the left ventricle, with diffusely decreased kinetics and increased density of all structures.
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PMID:Possibilities of two-dimensional echocardiography in cardiomyopathies. 653 93

In the winter of 1976 an examination of the composition of Eskimo food was carried out in north western Greenland. Duplicate specimens of diets collected from 50 adults, equal numbers of males and females, were analyzed for water, ash, protein, fat, individual fatty acids, cholesterol, and carbohydrate. The results are compared with those of typical Danish diets. Seal and the fish are predominant Eskimo food. Marked differences between Eskimo and Danish food were found. The Eskimo diets were richer in polyunsaturated fatty acids, the ratio to saturated fatty acids was 0.84 as compared with 0.24 in Danes. The polyunsaturated fatty acids were predominantly of the linolenic class (n-3) in Eskimos and the linoleic class (n-6) in Danes. Monoenes other than palmitoleic and oleic acids were high in Eskimo diets, but negligible in Danish. The results are related to previous examinations of the plasma lipids in Eskimos. The rarity of ischemic heart disease in Greenland Eskimos may partly be explained by the antithrombotic effect of the long-chained polyunsaturated fatty acids, especially eicosapentaenoic acid prevalent in diets rich in marine oils.
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PMID:The composition of the Eskimo food in north western Greenland. 743 33

In some patients with severe hypothyroidism thyroxine replacement therapy precipitates or aggravates angina pectoris, whereas in other patients angina pectoris is ameliorated or even disappears. The reason for this paradox is unknown. It has been attributed either to reversible endocrine cardiomyopathy in the form of asymmetric septal hypertrophy (ASH) or reversible anatomical narrowing of the coronary arteries. The results of a recent investigation, in which myocardial performance was surveyed by radionuclide ventriculography throughout early thyroxine replacement therapy in severe hypothyroidism, were compatible with the presence of reversible coronary dysfunction rather than of ASH. The aim of the present investigation was to confirm these findings. In six severely hypothyroid patients, without echocardiographic evidence of ASH or evidence of concomitant coronary artery disease (CAD), exercise and redistribution tomographic myocardial thallium-201 imaging (SPECT) was performed before thyroxine replacement therapy and repeated after 10 days and again after 2 months during therapy. In four patients substantial regional perfusion defects were demonstrated after exercise that were normalized at rest both before, and in one subject also after 10 days, on thyroxine. With restoration of euthyroidism, exercise and redistribution SPECT were normal in every patient. Determination of exact confidence limits reveals that the proportional incidence of myocardial perfusion defects in hypothyroidism, indicating myocardial ischemia, will at least be 22% with 95% probability. Despite the relatively low specificity of SPECT it seems pertinent to conclude that impaired myocardial perfusion as assessed by SPECT probably is due to reversible coronary dysfunction inherent in the hypothyroid state, and that this is not an infrequent manifestation of severe hypothyroidism.
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PMID:Silent myocardial ischemia in hypothyroidism. 880 93

Particulate matter air pollution (PM) has been associated with morbidity and mortality from ischemic heart disease and stroke in humans. It has been hypothesized that alveolar inflammation, resulting from exposure to PM, may induce a state of blood hypercoagulability, triggering cardiovascular events in susceptible individuals. Previous studies in our laboratory have demonstrated acute lung injury with alveolar inflammation in rats following exposure to residual oil fly ash (ROFA), an emission source particulate. In addition, increased mortality has been documented following exposure to ROFA in rats with preexistent cardiopulmonary disease. ROFA's toxicity derives from its soluble metal content, which appears also to drive the toxicity of ambient PM. The present study was conducted to test the hypothesis that exposure of rats to a toxic PM, like ROFA, would adversely alter hemostatic parameters and cardiovascular risk factors thought to be involved in human epidemiologic findings. Sixty-day-old male Sprague-Dawley rats were exposed by intratracheal instillation (IT) to varying doses (0.3, 1. 7, or 8.3 mg/kg) of ROFA, 8.3 mg/kg Mt. Saint Helen's volcanic ash (MSH, control particle), or 0.3 ml saline (SAL, control). At 24 h post-IT, activated partial thromboplastin time (APTT), prothrombin time (PT), plasma fibrinogen (PF), plasma viscosity (PV), and complete blood count (CBC) were performed on venous blood samples. No differences from control were detected in APTT and PT in ROFA-exposed rats; however, ROFA exposure did result in elevated PF, at 8.3 mg/kg only. In addition, PV values were elevated in both ROFA and MSH-exposed rats relative to SAL-control rats, but not significantly. Although no changes were detected in APTT and PT, alteration of important hematologic parameters (notably fibrinogen) through PM induction of an inflammatory response may serve as biomarkers of cardiovascular risk in susceptible individuals.
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PMID:Oil fly ash-induced elevation of plasma fibrinogen levels in rats. 1086 47

Coronary ischemic events increase significantly following a "bad air" day. Ambient particulate matter (PM10) is the pollutant most strongly associated with these events. PM10 produces inflammatory injury to the lower airways. It is not clear, however, whether pulmonary inflammation translates to a systemic response. Lipopolysaccharide (LPS) is a proinflammatory molecule often associated with the coarse fraction of PM. It was hypothesized that PM>2.5 from coal plus LPS induce pulmonary inflammation leading to a systemic inflammatory response. Mice were intratracheally instilled with saline, PM (200 microg), PM + LPS10 (PM + 10 microg LPS), or PM + LPS100 (PM + 100 microg LPS). Eighteen hours later, histologic analysis was performed on lungs from each group. Pulmonary and systemic inflammation were assessed by measuring the proinflammatory cytokines tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 in the pulmonary supernatant and plasma. In a follow-up study, the effects of LPS alone were assessed. Histologic analysis revealed a dose-dependent elevation in pulmonary inflammation with all treatments. Pulmonary TNF-alpha and IL-6 both increased significantly with PM + LPS100 treatment. Regarding plasma, TNF-alpha significantly increased in both PM + LPS10 and PM + LPS100 treatments. For plasma IL-6, all groups tended to rise with a significant increase in the PM + LPS100 group. The results of the follow-up study indicate that the responses to PM + LPS were not due to LPS alone. These results suggest that coarse coal fly ash PM>2.5 combined with LPS produced pulmonary and systemic inflammatory responses. The resulting low-level systemic inflammation may contribute to the increased severity of ischemic heart disease observed immediately following a bad air day.
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PMID:Instillation of coarse ash particulate matter and lipopolysaccharide produces a systemic inflammatory response in mice. 1796 67

Hypertrophic cardiomyopathy (HCM) is a common cardiac condition caused primarily by sarcomeric protein mutations with several distinct phenotypes, ranging from asymmetric septal hypertrophy, either with or without left ventricular outflow tract obstruction, to moderate left ventricular dilation with or without apical aneurysm formation and marked, end-stage dilation with refractory heart failure. Sudden cardiac death can occur at any stage. The phenotypic variability observed in HCM is the end-result of many factors, including pre-load, after-load, wall stress and myocardial ischemia stemming from microvascular dysfunction and thrombosis; however, tissue level inflammation to include leukocyte-derived extracellular traps consisting of chromatin and histones, apoptosis, proliferation of matrix proteins and impaired or dysfunctional regulatory pathways contribute as well. Our current understanding of the pathobiology, developmental stages, transition from hypertrophy to dilation and natural history of HCM with emphasis on the role of tissue-level inflammation in myocardial fibrosis and ventricular remodeling is summarized.
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PMID:Tissue-level inflammation and ventricular remodeling in hypertrophic cardiomyopathy. 3189 71