Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty patients with systemic hypertension were classified into 4 types based on the left ventricular echocardiographic findings. Patients with normal left ventricular echogram, type I, showed little clinical symptoms and signs of hypertensive involvement. Higher systolic pressure and marked hypertensive retinal and renal changes were observed in patients with symmetric hypertrophy of the left ventricle, type II. Congestive heart failure was dominantly present in those with dilatation of the left ventricle, type IV. High voltages and marked ST-T changes in electrocardiogram were usually found in patients with asymmetric septal hypertrophy, type III, while retinal and renal damages were mild. Left ventriculograms obtained from 6 cases in type III also revealed hypertrophy of the interventricular septum and one of them demonstrated left ventricular outflow tract obstruction. These cardiac features in type III, which are quite similar to those in hypertrophic cardiomyopathy, seemed to be a secondary change induced by systemic hypertension on the basis of some predisposition.
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PMID:Echocardiographic classification of hypertensive heart disease. A correlative study with clinical features. 12 53

Echocardiography is an extremely useful noninvasive technic in the differential diagnosis of a large heart. It may show whether a large heart is due to left ventricular hypertrophy or dilatation, or if it is due to a pericardial effusion. The hypertrophied heart may be further characterized by determining whether it is symmetrical, as caused by aortic stenosis or hypertension, or whether it is assymmetrical, which is characteristic of hypertrophic cardiomyopathy. Similarly, dilatation of the heart may be due to volume overload of the left ventricle secondary to valvular insufficiency, congestive cardiomyopathy or ischemic heart disease; these can be distinguished by echocardiography. As certain types of mitral insufficiency are associated with specific valvular dysfunction, the possible etiology of the mitral insufficiency and therefore of the volume overload of the left ventricle may be determined using echocardiography. Finally, mediastinal tumors may simulate a large heart, and demonstration of normal cardiac dimensions and wall motion can exclude a cardiac etiology for the "large heart."
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PMID:Echocardiography in the differential diagnosis of the large heart. 13 5

Myocardial fiber disarray was found at necropsy in each of 53 hearts, 33 from patients with cardiovascular disease--systemic hypertension (12 patients), coronary heart disease (17 patients) or cor pulmonale (4 patients)--and 20 from patients with a normal heart. The myocardial fiber disarray was of mild degree in all 53 patients and, although similar to that observed by others in hearts of patients with hypertrophic cardiomyopathy, the amount of myocardial fiber disarray per heart was considerably less than that observed in patients with hypertrophic cardiomyopathy.
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PMID:Muscle fiber disarray in common heart diseases. 14 8

This report reviews the clinical features of 80 patients with roentgenographically proved mitral annular calcification. The mean age of the group was 73 years, and there was a 2.5 to 1 female to male ratio. Evaluation for underlying cardiovascular disease revealed six patients with severe calcific valvular aortic stenosis; five patients with hypertrophic cardiomyopathy, 11 with mitral prolapse and 33 with significant arterial hypertension (blood pressure greater or equal to 150/96 mm Hg). Eighty-five per cent of the group (68 of 80 patients) had an underlying cardiac disorder associated with either chronically increased left ventricular systolic pressure or abnormal leaflet motion. Other cardiovascular abnormalities occurring as complications secondary to the mitral ring calcification included subacute bacterial endocarditis (three cases), arterial emboli (five episodes) and high grade atrioventricular block (16 cases). Twelve patients had severe mitral regurgitation; successful mitral valve replacement was carried out in four patients (all with myxomatous mitral tissue). Evidence of diffuse conduction system disease, not limited to the area of the cardiac fibrous skeleton, was found frequently (44 patients). Nine patients had sinus node dysfunction and 35 patients had electrocardiographic evidence of distal intraventricular (fascicular) block. Twenty-one patients eventually required pacemakers for management of symptomatic bradyarrhythmias. Atrial fibrillation was present in 23 patients. In this review it was found that calcification of the mitral annulus is frequently associated with or induces serious cardiovascular disease. Since some of these disorders may be modified by appropriate therapy, calcification of the mitral annulus should no longer be ignored as a benign marker of the elderly heart.
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PMID:Calcification of the mitral annulus: etiology, clinical associations, complications and therapy. 15 99

To determine whether hypertrophic cardiomyopathy is associated with a human leukocyte antigen (HLA) phenotype, we tissue-typed 70 unrelated afflicted patients and 86 of their asymptomatic family members (from nine separate kindreds). Forty-five per cent of the white patients had B-12 antigen as compared to 23 per cent in matched control subjects; 69 per cent of black patients had a B-5-complex antigen as compared to 33 per cent in matched controls. Patients with a B-12 or B-5-complex antigen were nonhypertensive and had family members with the disease. Patients without these antigens were severely hypertensive and had no affected family members. Linkage analysis of six families revealed a lod score of 7.7 for asymmetric septal hypertrophy and the HLA region of chromosome 6. We conclude that there is a heritable, nonhypertensive form of hypertrophic cardiomyopathy linked to the HLA loci on chromosome 6 and that a sporadic form is associated with severe, systemic hypertension.
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PMID:Hypertrophic cardiomyopathy and human leukocyte antigen linkage: differentiation of two forms of hypertrophic cardiomyopathy. 634 49

Little is known of the clinical significance of myocardial bridges, which may be recognized angiographically as systolic coronary artery narrowing (SCAN). A retrospective review of a 1 year's experience (313 consecutive coronary arteriograms) revealed 5 patients with SCAN, an incidence of 1.6%. SCAN involved the proximal and/or middle segments of the left anterior descending coronary artery in all patients. It is of particular note that the administration of nitroglycerin noticeably accentuated the SCAN phenomenon in each of 3 patients to whom it was administered. Four of the 5 patients had left ventricular hypertrophy due to hypertrophic cardiomyopathy (2), aortic stenosis (1), and hypertension (1). All 5 patients with the SCAN phenomenon had anginal chest pains, and critical obstructive coronary atherosclerosis was observed in only 2 cases. The other 3 patients showed, otherwise normal coronary arteriograms. Thus, myocardial bridges appear to be angiographically manifest predominantly in patients with cardiac hypertrophy. Nitroglycerin, which accentuates SCAN, might be useful as a provocative test to enhance the angiographic recognition of this phenomenon. The possible role of myocardial bridges in the production of myocardial ischemia warrants further investigation.
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PMID:Myocardial bridges in man: clinical correlations and angiographic accentuation with nitroglycerin. 40 19

This case report documents the co-existence of valvar aortic stenosis and hypertrophic obstructive cardiomyopathy with systemic hypertension and calcific mitral annulus, a combination which has not hitherto been reported. It is the purpose of this paper to help assess the true incidence of the co-existence of aortic stenosis and hypertrophic cardiomyopathy.
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PMID:Valvar aortic stenosis with unusual features. 56 Jun 91

We compared the histologic picture of myocardial fiber disarray in thin (4 mu) and thick (25 mu) sections of tissues obtained at autopsy from 18 adults and eight infants with clinically normal hearts, from 10 hearts with concentric hypertrophy (hypertensive patients), nine with myocardial infarction and four with hypertrophic cardiomyopathy (HCM). In the thick sections, so-called bizarre myocardial fiber disarray in thin sections was seen as a bizarre fascicle disarray. Therefore, the usual fiber disarray reported in cases of HCM is actually a fascicle disarray with a three-dimensional complex network. There was no marked difference in distribution and frequency of fascicle disarray among normal adult and infant hearts, and diseased hearts with hypertension and myocardial infarction. In the four hearts with HCM, diffuse bizarre fascicle disarray in the thick section was detected in the septum and anterior and posterior walls of the left ventricles in all cases, and in the lateral walls in one case. In the portions without the diffuse fascicle disarray, the distribution of disarray was the same as that in hearts with no HCM. Such fascicle disarray, including that of HCM, is probably congenital.
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PMID:Myocardial fascicle and fiber disarray in 25 mu-thick sections. 57 11

To determine the prevalence and characteristics of disproportionate ventricular septal thickening (septal-free wall ratio of greater than or equal to 1.3) in a population of patients with severe chronic hypertension, which was unassociated with coronary arterial disease, 33 patients were studied at necropsy. The overall prevalence of disproportionate septal thickening was relatively low, ie, two (6 percent) of the 33 patients. The septal-free wall ratio in both of these patients was 1.3. Disproportionate septal thickening appeared to be secondary to the left ventricular pressure overload, rather than to coexistent genetically transmitted hypertrophic cardiomyopathy. This conclusion was based on the following facts: (1) numerous disorganized cardiac muscle cells, characteristic of hypertrophic cardiomyopathy, were not present in the ventricular septum of either patient with disproportionate septal thickening; and (2) echocardiographic studies performed in first-degree relatives of one of the two patients did not disclose disproportionate septal thickening. Hence, disproportionate septal thickening may occur as a secondary manifestation of left ventricular pressure overload that is present in patients with systemic hypertension, but this association appears to be relatively uncommon.
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PMID:Disproportionate ventricular thickening in patients with systemic hypertension. 63 Sep 63

Two patients, both women, one with "lupus-like" disease, age 51 years, the other a 45-year-old with systemic lupus erythematosus (SLE), developed symptoms and echocardiographic signs of hypertrophic cardiomyopathy. One patient had a family history of sudden maternal death. Neither patient had a history of sustained hypertension and there were no significant valvular lesions detectable to account for the septal and ventricular hypertrophy. The association of SLE or any related condition with hypertrophic cardiomyopathy has not been recorded. In one patient the question of a hereditary cardiomyopathy remains a possibility. The diagnosis of the condition was based on clinical and echocardiographic grounds alone. No endomyocardial biopsies were performed.
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PMID:Hypertrophic cardiomyopathy in systemic lupus erythematosus and "lupus-like" disease. Chance association? A report of 2 cases. 129 51


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