Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0004153 (atherosclerosis)
77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred eighteen patients with idiopathic hypertrophic subaortic stenosis were studied with cardiac catheterization and coronary arteriography. In 112 a gradient across the left ventricular outflow tract was present in the resting state. Seventeen of the 61 patients who had right heart catheterization had a mild resting gradient across the right ventricular outflow tract, that was considered clinically and hemodynamically insignificant. Ninety-five patients (80 percent) had a left ventricular end-diastolic pressure greater than 10 mm Hg; 60 percent had mitral regurgitation that was of mild degree in most cases. Almost 20 percent had coexistent coronary atherosclerosis (25 percent incidence rate in subjects aged 40 years or older). Patients with associated severe coronary atherosclerosis had a lower intraventricular gradient at rest than other patients. Coronary atherosclerosis appears to be a coincidental condition. The need for objective evaluation of the coronary circulation is emphasized.
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PMID:Hemodynamics and coronary angiography in idiopathic hypertrophic subaortic stenosis. 56

A case of non endocarditic mitral insufficiency in a 76 years old woman is described. After an extensive pathogenetical introduction, a comparison is made between clinical features of this case an its pathogenetical possibilities. The conclusion is drawn that there are most probabilities for an atherosclerosis of the antero-medial limbus of the mitral valve, arising from a coexisting atherosclerotic mild stenosis of the aortic valves.
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PMID:[Non-endocarditic mitral insufficiency]. 68 70

Coronary- and LV-angiography in coronary heart disease are indicated I) to clarify whether or not surgery is required (e.g. aorto-coronary-bypass operation, aneurysmectomy) in 1) drug resistent angina pectoris, 2) myocardial aneurysms (or the suspicion of), 3) VSD following myocardial infarction and/or 4) as preoperative investigations in mitral regurgitation or 5) other valve lesions. II) These investigations are furthermore indicated in the under-50-yr.-old considering their prognosis and diagnosis 1) following myocardial infarction 2) to clarify a pathological exercise test with or without angina pectoris 3) in the differential diagnosis of myocardial diseases and 4) occasionally in patients with a number of risk factors or exposed to particular occupational hazards or from families with a high incidence of early deaths from heart disease. Coronary- and LV-angiography are contraindicated in 1) generalized stenosing atherosclerosis, 2) acute myocardial infarction, 3) failure from other organ-systems (e.g. kidney), 4) drug resistent endogenous risk factors and/or relevant obesity, 5) biological age over 60-65.6) continued nicotine dependence. In many cases the specific diagnostic investigations will include the assessment of coronary flow at rest and during maximal drug induced coronary dilatation. This enables us to estimate the coronary reserve and to diagnose coronary insufficiency in patients with normal coronary angiograms.- Instructive morphological and/or functional results illustrate this presentation.
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PMID:[Indications for coronary arteriography and left ventriculography in coronary heart disease (author's transl)]. 125 Nov 19

Homozygous familial hypercholesterolaemia is characterized by cutaneous xanthoma development from infancy, precocious and accelerated atherosclerosis with clinical signs of ischemic heart disease and frequent involvement of left heart valves resulting in stenosis and/or incompetence. Two cases are described of this condition, both associated with aortic stenosis. In one case mitral incompetence and thromboembolic pulmonary hypertension were also found. The mitral valve is involved in the atherosclerotic process at the level of the cusps. These become thickened and stiff. Aortic stenosis is mainly due to atheromas infiltrating the Valsalva sinuses and the ascending aorta. Pulmonary hypertension, never reported before in this disease, is probably due to concomitant atheromatosis involving the pulmonary artery with secondary fatty embolism.
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PMID:[Involvement of the heart valves and great vessels in homozygote familial hypercholesterolemia]. 129 17

A 70-year-old woman presented with anular and progressive intramyocardial calcification within a five-year period. She had become increasingly symptomatic with mitral regurgitation and coronary insufficiency during the same period. The subvalvular (mitral) calcified intramyocardial mass was found to be "grumous atherosclerosis." This was obliterated while the mitral valve was replaced with a prosthetic valve and the coronary arteries were bypassed x3. She is surviving and well four years postoperatively.
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PMID:Intramyocardial calcification in the elderly. A diagnostic and therapeutic puzzle. 162 83

Cardiovascular disease, the major cause of death in the elderly, is mostly ascribable to complications of coronary atherosclerosis: angina pectoris, myocardial infarction, and sudden death. However, other degenerative diseases involving several cardiac structures exist, and should be distinguished from age-related cardiac changes. Extensive dystrophic calcification determines aortic stenosis, and may affect either a normally tricuspid or a congenitally bicuspid valve. Surgical valve replacement is now a low risk option, even in elderly persons, whereas the efficacy of balloon valvuloplasty is questionable. Aortic incompetence in adults and aged persons is mostly the consequence of aortic tunica media atrophy with anular ectasia, in the setting of nearly normal aortic leaflets. Mitral valve prolapse is the main cause of mitral incompetence; spontaneous cordal rupture is a late complication in the natural history of this disease, thus warranting prompt surgical valve repair or replacement. The entire spectrum of cardiomyopathies is observed in the elderly: dilated, hypertrophic, restrictive, arrhythmogenic. Cardiac amyloidosis is by far the most frequent secondary form and leads to congestive heart failure by impairing ventricular compliance. Idiopathic fibrosis of the specialized AV junction or dystrophic calcification of central fibrous body are the usual substrates of AV block, which requires pace-maker implantation. Nonrheumatic atrial fibrillation, due to fibro-fatty degeneration of the atrial musculature or dilated left atrium, carries a high risk of thromboembolic complications and cerebral accidents; oral anticoagulants have proven to be effective in preventing stroke. Aortic dissecting aneurysm is a spontaneous laceration, and usually a complication of longstanding systemic hypertension; exceptionally, spontaneous dissection may primarily occur in the coronary arteries. In conclusion, longevity at present is mostly threatened by cardiovascular disease, among which the role of degenerative, non-atherosclerotic disorders may be greater than thought.
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PMID:Degenerative, non-atherosclerotic cardiovascular disease in the elderly: a clinico-pathological survey. 209 63

After an extensive analysis of the world literature (121 references), beginning from the first reported case by Antopol and Kugel, 1933, the general review of the problem stressed especially the following morphologic characteristics and clinical significance of the anomalous origin of the left circumflex coronary artery (LCxA) from the right coronary artery (RCA): The place of the anomalous origin of LCxA from RCA among all other variations and anomalies of LCxA. The anatomical and topographical characteristics of LCxA originating from RCA in normal heart as well as in congenital heart diseases--CHD (especially complete transposition of great arteries--TGA). The formal genesis of LCxA from RCA according to original new Ogden's theory, taking into account the dual origin of the coronary arteries and the peritruncal angioblastic ring that surrounds the developing aorta and pulmonary artery. The frequencies of the origin of LCxA from RCA in autopsy and coronarography series. The importance of LCxA (by its origin and/or caliber) in determination of the right, left or codominance of the coronary arteries including the peculiarities in cases of isolated aortic stenosis and bicuspid aortic valve. The importance of recognizing LCxA from the RCA during implantation of artificial aortic, mitral and tricuspid heart valves, during mitral valve anuloplasty, closure of ostium primum defect as well as during aorto-coronary venous bypass. The LCxA from RCA, especially its proximal segment, shows more frequent and an earlier, faster and heavier obstructive atherosclerosis, causing different manifestations of coronary heart disease and sudden death. Also, mitral insufficiency can be caused by ischemia of the papillary muscles of the left ventricle. The awareness of the possibility that LCxA may arise from the RCA can prevent many complications during cannulations of the coronary arteries for diagnostic coronarography and myocardial perfusion during heart operations. The authors presented their 30 autopsied cases of LCxA from RCA, analysing morphological and topographic data as well as their clinical significance and association with other CHD. There were 6 isolated cases and 24 cases associated with other CHD (20 with TGA and 4 with other CHD). Our first autopsied case of LCxA from RCA was diagnosed as associated with tetralogy of Fallot in 1964. During the period 1964-1985 we had 1015 cases of CHD (including 132 cases of TGA).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathologic morphology and clinical significance of the anomalous origin of the left circumflex coronary artery from the right coronary artery. General review and autopsy analysis of 30 cases]. 213 27

Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. While myocarditis is commonly noted at autopsy, it is often silent clinically. Diagnosis during life can be confirmed only by endomyocardial biopsy. Electrocardiographic changes are often nonspecific. Endocarditis with superimposed nonbacterial verrucous vegetations (Libman-Sacks) is noted in more than 40% of hearts at autopsy, but is rarely diagnosed during life. Valve dysfunctions, such as aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency, occasionally manifest during life and rarely may necessitate surgery. Atrial and ventricular arrhythmias, first degree AV block, and acquired CHB occur in association with pericarditis, myocarditis, vasculitis, and myocardial fibrosis, respectively. CCHB developing in newborns of mothers with SLE, particularly those who have an antibody to soluble tissue ribonuclear protein RO(SS-A), is increasingly being appreciated by both pediatric cardiologists and rheumatologists. Recently, severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been noted, particularly in those who had developed risk factors such as hypertension and hyperlipidemia while receiving prolonged corticosteroid therapy. Rarely, coronary arteritis may produce similar symptoms. Congestive heart failure of either single or multiple etiologies carries an ominous prognosis. It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiovascular manifestations of systemic lupus erythematosus: current perspective. 286 Jun 99

SLE affects most aspects of cardiac function, and recent studies have reported increasing cardiovascular morbidity and mortality. Pathologically, SLE is characterized by a pancarditis involving pericardium, myocardium, endocardium, and coronary arteries. In autopsy series, pericarditis has been found in 43% to 100% (mean 62%, Table I), and myocarditis was found in 8% to 78% (mean 40%, Table II), but both have been underdiagnosed clinically. Libman-Sacks lesions have been noted in 25% to 100% (mean 43%) and infective endocarditis in 1.1% to 4.9% of clinical and autopsy studies (Table III). Coronary disease may be due to arteritis, which should be treated with high-dose steroids, or it may be due to atherosclerosis, which is amenable to medical or surgical therapy. Valvular disease has been treated surgically, but with a combined surgical mortality as high as 25%. Aortic insufficiency and mitral regurgitation are the most common valvular problems, although aortic and mitral stenosis have also been reported. Hypertension has been noted in 14% to 69%, and heart failure in 5% to 44%. Evidence for a lupus cardiomyopathy, which may be subclinical, is reviewed. While steroids may ameliorate SLE pancarditis, they have also been associated with hypertension, LV hypertrophy, purulent and constrictive pericarditis, mitral regurgitation, and perhaps accelerated atherosclerosis. It remains to be seen if improved diagnosis and treatment of the cardiovascular manifestations of SLE can enhance survival.
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PMID:Cardiovascular manifestations of systemic lupus erythematosus. 390 17

Episodic mitral regurgitation due to ischaemia of one or both papillary muscles was studied in a review of 39 cases with complementary investigations and compared with previously reported data. The condition occurred after myocardial infarction in 69 p. 100 of cases (usually after inferior infarction: 54 p. 100) associated with ischaemia of the controlateral territory; there was no history of myocardial infarction in 31 p. 100 of cases. The patients were usually elderly (73 years), often hypertensive (77 p. 100) and diabetic (62 p. 100). The clinical syndrome was that of severe anginal pain, mitral regurgitation and left ventricular failure which was critical in some cases. The ECG showed typical ST depression (4.1 +/- 1.6 mm) especially in the antero-lateral leads; left bundle branch block (28 p. 100) with left axis deviation (18 p. 100), sometimes associated with changes of chronic infarction (64 p. 100) was also recorded. Mitral regurgitation and left ventricular failure regressed almost completely in typical cases between attacks, whilst the ECG showed slight residual sub-endocardial ischaemia (ST depression of 1.5 +/- 0.4 mm) in 30 cases and/or subepicardial ischaemia observed in the anterolateral leads in 13 cases. Phonomechanographic recordings (n = 32) showed moderate mitral regurgitation (1-2/6), usually parasystolic (47 p. 100) or early and mid systolic (36 p. 100) in 87.5 p. 100 of cases between attacks, aggravated by handgrip exercise and improved by trinitrin administration. Echocardiography (n = 27) only showed mitral valve changes in 2 patients (increased density of the papillary muscle in 1 case and prolapse of the anterior leaflet in 1 case); however, segmental wall hypokinetic (51 p. 100) or dyskinetic (15 p. 100) motion, was common with increased left ventricular end diastolic dimensions (mean 56.3 +/- 8.0 mm) and decreased fractional shortening (mean 0.30 +/- 0.07) (67 p. 100). Left atrial dimensions were increased (mean 39.7 +/- 6.4 mm) in 52 p. 100 of patients. Thallium 201 myocardial scintigraphy (n = 32) showed hypofixation in 57 (36 p. 100) and a lacuna in 23 (14 p. 100) of the 160 segments analysed. Left ventricular angioscintigraphy (n = 27; 135 segments) showed hypokinesia in 72 segments (53 p. 100); 2.7 segments per patient), akinesia in 19 segments (15 p. 100; 0.7 segment per patient) and dyskinesia in 2 segments (1.5 p. 100); 0.1 segment per patient). The global ejection fraction was 46 +/- 13 p. 100. Coronary angiography (n = 8) showed significant diffuse atherosclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Paroxysmal mitral insufficiency caused by ischemic dysfunction of the papillary muscles. Apropos of 39 cases]. 391 82


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