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 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The availability of basic and reliable data on cardiovascular problems in Africans is limited and this hinders the presentation of a comprehensive review of the subject. Nevertheless, there is a strong suggestion that the spectrum and pattern of cardiovascular disorders in Africa is rapidly becoming indistinguishable from that observed in developed countries. The classic risk factors appear to be on the rise and smoking may attain levels equal to or exceeding those in many developed countries. Infectious and inflammatory cardiovascular conditions may still be the most common, although limitations in the technology available for accurate diagnosis make this difficult to verify. Rheumatic fever and rheumatic heart disease remain common, and the potential for educational and other preventive strategies is being realized in many countries. Hypertension at frequencies exceeding 5-10% in most rural areas and 12% in most urban areas, together with complications such as stroke, heart failure and renal failure, are leading causes of morbidity and mortality. Hypertension is the major public health problem in most African countries. The cardiomyopathies are a common problem, and the limited availability of specific diagnostic procedures is matched by limited therapeutic options for most Africans. The prevalence of atherosclerosis and coronary artery disease and its complications, such as myocardial infarction and other degenerative disorders, remains low, but the situation is rapidly changing, especially in urban areas where appropriate diagnostic capabilities exist. It is thought that changes or modifications in lifestyle, risk-prone behaviour, diet, cultural attitudes and certain other consequences of rapid urbanization and demographic tendencies largely explain the observed trends.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular disorders in Africa. 830 7

Myocardial infarctions which are derived from embolic source have an incidence of 5-13%. They are at risk of systemic embolism. The pathogenesis of myocardial infarction is similar to that of those myocardial infarction whose etiology is atherosclerosis. This make it susceptible to thrombolysis. We report 3 patients with either inactive rheumatic heart disease, coarctation of the aorta or mechanical valvular prosthesis as the probable causes of an embolic infarction. It was located in the posterior-inferior region with a dorsal extension. These patients were treated with intravenous streptokinase. The three of them fulfilled criteria for myocardial reperfusion. Two of them suffered post-infarction angina. In the first case reocclusion of the righ coronary artery was observed; thus a saphenous vein graft was undertaken. In the second, the persistence of thrombus required three month treatment with anticoagulants. The third patient showed not coronary lesions. In conclusion, thrombolytic therapy with streptokinase in acute infarction of embolic origin prevents the progression of ischemic damage and betters the clinical outcome of the patient. Furthermore such disease should be suspected in patients that have risk factors for systemic embolism and normal coronary arteries and with obstruction of a single vessel.
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PMID:[Thrombolysis in acute myocardial infarct of embolic origin]. 876 29

Among 407 patients with rheumatic heart disease studied in our department, we found 8.3% with coronary atherosclerosis: 2.7% with mitral stenosis and 2.4% with aortic stenosis, lower figures than those reported in the literature. In our patients with coronary atherosclerosis, the male to female ratio was 1.6:1. The mean age of men and women with coronary atherosclerosis were 58.9 +/- 8.48 years and 60.33 +/- 5.75 years respectively. The cumulated relative frequency curve of the age was shifted to the right in the patients with coronary atherosclerosis, compared with the age frequency curve of the patients with normal coronary arteries: 50% of the cases with coronary atherosclerosis were < or = 60 years old; on the other hand, 50% of the patients with normal coronary arteries were < 53 years old. We only discovered 3 patients younger than 50 years old with coronary atherosclerosis. In order of frequency, the coronary arteries more affected were the anterior descending, right and circumflex. The mean coronary stenosis was 75.2 +/- 21.2%. Disease of one vessel was observed more frequently. We believe that age is not a good parameter to indicate coronarography in patients with valvular heart disease. If coronarography would be performed in all patients with valvular disease > or = 30 or 40 years old, would result in a great number of normal studies, with the consequent misspend of supplies and the increased risk of complications. On the other hand, restricting the coronarography indication, would miss the diagnosis in patients that might need myocardial revascularization. To restrict or to increase the indication of coronarography in patients with valvular disease will depend of the frequency between rheumatic heart disease and associated coronary atherosclerosis, and also on the atherosclerosis risk factors present in each patient. We recommend not to use the age of the patients as an index to indicate coronarography.
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PMID:[Indications for coronarography in heart valve diseases]. 876 24

The pathogenesis of nonrheumatic calcification of the mitral valve was investigated by analyzing the clinical and echocardiographic characteristics of patients with mitral valvular calcification without any findings suggestive of rheumatic heart disease or infective endocarditis. Calcification of the mitral valve was observed in nine patients, who all had calcified stenotic (aortic valve area < 1 cm2) bicuspid aortic valve. Calcification of the mitral valve was localized to the basal portion of ventricular aspect of the anterior mitral leaflet and contiguous to that of the aortic valve. Mobility and thickness of the mitral leaflet was normal except for the calcified portion. Calcification of the mitral valve was not contiguous to posterior mitral annular calcification nor was related to direction of aortic regurgitant flow. In patients with calcified stenotic bicuspid aortic valve, calcification of the mitral valve was not associated with location of the two aortic cusps, aortic valve area, aortic valvular peak pressure gradient, direction of the left ventricular outflow, end-diastolic left ventricular outflow tract dimension, end-diastolic dimension of the aortic annulus, incidence of aortic regurgitation, calcification of the aortic arch, or risk factors of atherosclerosis. Six patients with mitral valvular calcification had aortic valve replacement. Preoperative coronary angiogram of these patients was normal. Calcification of the aortic valve was on the ventricular and aortic aspects. The calcification of the aortic valve, anterior mitral ring, or anterior mitral leaflet was not rheumatic in these six patients. Rheumatic disease, risk factors of atherosclerosis, mechanical stress by left ventricular outflow or aortic regurgitant flow, or mitral annular calcification did not appear to be related to mitral valvular calcification. The distribution of aortic and mitral valvular calcification suggested that the calcification of the mitral valve was due to progression of calcification of the bicuspid aortic valve.
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PMID:[Nonrheumatic calcification of the mitral valve in patients with stenotic calcified bicuspid aortic valve]. 893 38

We analysed the causes of 67 deaths, over a 4 y period, in our oriental population with systemic lupus erythematosus (SLE). The median disease duration was 48 +/- 60.5 months (range 1-250 months). The mean age at diagnosis and death were 30 and 35.1 y respectively. SLE alone accounted for death in 30 patients (44.8%), infection in 27 (40.3%), pulmonary embolism in 5 (7.5%), malignancy in 4 (5.9%) and rheumatic heart disease in 1 (1.5%). The major organ involvement in those with active disease at death were SLE related thrombocytopenia (n = 23/44, 52.3%), nephritis (n = 21/44), 47.7%), cerebral lupus (n = 16/44, 36.4%), and pulmonary haemorrhage (n = 12/44, 27.3%). As in other series, SLE and infection were the principal causes of death in our population. During this 4 y period, there was no late death due to atherosclerosis.
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PMID:SLE mortality in an oriental population. 911 15

This histological study of endocardial thickening in human hearts revealed that as in adult hearts, the proliferation in fetal, neonatal, and infant hearts consisted of collagen, elastin, and smooth muscle cells. Variation in severity from chamber to chamber and site to site indicated that severity is not an aging phenomenon and that predominantly local blood flow conditions determine localization and progression of proliferation. The similarity to endocardial thickening of cardiac valves and to intimal proliferation in blood vessels was remarkable. In old age and in chronic rheumatic heart disease the proliferation exhibited hyalinization, cell depletion, loss and fragmentation of elastin, lipid accumulation, and thrombosis, indicative of a similar pathogenesis to atherosclerotic changes in valvular endocardium and blood vessels. It was concluded that these chronic hemodynamically induced degenerative changes in the endocardium, including cardiac valves, should be classified as endocardial atherosclerosis analogous to that in arteries and veins and that severity is aggravated by high blood pressure, cardiac malformations, and dysfunction or damage caused by other disease processes.
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PMID:The histopathology of endocardial sclerosis. 1098 16

The aim of this study was to evaluate the causes of death in individuals who died suddenly in Addis Ababa, Ethiopia. The selection of the cases was based on police reports, which contained a description of sudden unexpected or instantaneous death. The study was performed on necropsies of the Medico legal Department of Menelik II Hospital, in Addis Ababa during the years 1998 and 1999. According to the pathological features of the heart, we classified 92 dead bodies in 3 groups: Group A: Hearts showing adequate morphological changes to explain sudden death (n = 63). Group B: Hearts showing some structural changes, but inadequate to explain sudden death (n = 20). Group C: Normal hearts (n = 7). In two bodies the general autopsy revealed an extra cardiac cause of death. The single most relevant cause of death in group A was coronary artery disease (44 cases) followed by excessive myocardial hypertrophy due to post-rheumatic valvular lesions (7 cases). While the high prevalence of rheumatic heart disease in Ethiopia is well known, the proportion of cases who died due to coronary heart disease is surprising. Though during the last years some African authors assumed that coronary atherosclerosis is on the increase in developing countries the percentage is higher than expected and higher than in other countries where similar studies exist.
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PMID:Causes of sudden death in Addis Ababa, Ethiopia. 1238 Feb 32

The avascularity of cardiac valves is abrogated in several valvular heart diseases (VHDs). This study investigated the molecular mechanisms underlying valvular avascularity and its correlation with VHD. Chondromodulin-I, an antiangiogenic factor isolated from cartilage, is abundantly expressed in cardiac valves. Gene targeting of chondromodulin-I resulted in enhanced Vegf-A expression, angiogenesis, lipid deposition and calcification in the cardiac valves of aged mice. Echocardiography showed aortic valve thickening, calcification and turbulent flow, indicative of early changes in aortic stenosis. Conditioned medium obtained from cultured valvular interstitial cells strongly inhibited tube formation and mobilization of endothelial cells and induced their apoptosis; these effects were partially inhibited by chondromodulin-I small interfering RNA. In human VHD, including cases associated with infective endocarditis, rheumatic heart disease and atherosclerosis, VEGF-A expression, neovascularization and calcification were observed in areas of chondromodulin-I downregulation. These findings provide evidence that chondromodulin-I has a pivotal role in maintaining valvular normal function by preventing angiogenesis that may lead to VHD.
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PMID:Chondromodulin-I maintains cardiac valvular function by preventing angiogenesis. 1702

Calcific aortic stenosis in the elderly is the number one cause of surgical valve replacement in the US and Europe. The incidence of calcific aortic stenosis is increasing as the general age of the population increases. For many years, rheumatic heart disease was the main cause of aortic valve disease. Over the last half century, however, there has been a change from a rheumatic etiology to a 'degenerative' mechanism because of the increase in access to health care in developed countries and the increasing age of the population in the US and Europe. For many years 'degenerative' aortic stenosis was thought to be caused by the passive accumulation of calcium on the surface of the aortic valve leaflet. Recent studies have demonstrated, however, that the etiology of aortic valve disease has a similar pathophysiology to that of vascular atherosclerosis, and that the treatment of this disease could be similar to that of chronic vascular atherosclerosis. This Review will discuss our current understanding of the pathophysiology, risk factors, cellular mechanisms, diagnosis and finally, future medical therapies for calcific aortic stenosis.
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PMID:Calcific aortic stenosis: an update. 1745 49

Rheumatic Heart Disease (RHD) is well known to be an active inflammatory process which develops progressive calcification and leaflet thickening over time. The potential for statin therapy in slowing the progression of valvular heart disease is still controversial. Retrospective studies have shown that medical therapy is beneficial for patients with calcific aortic stenosis and recently for rheumatic valve disease. However, the prospective randomized clinical trials have been negative to date. This article discusses the epidemiologic risk factors, basic science, retrospective and prospective studies in valvular heart disease and a future clinical trial to target RHD with statin therapy to slow the progression of this disease. Recent epidemiological studies have revealed the risk factors associated with valvular disease include male gender, smoking, hypertension and elevated serum cholesterol and are similar to the risk factors for vascular atherosclerosis. An increasing number of models of experimental hypercholesterolemia demonstrate features of atherosclerosis in the aortic valve (AV), which are similar to the early stages of vascular atherosclerotic lesions. Calcification, the end stage process of the disease, must be understood as a prognostic indicator in the modification of this cellular process before it is too late. This is important in calcific aortic stenosis as well as in rheumatic valve disease. There are a growing number of studies that describe similar pathophysiologic molecular markers in the development of rheumatic valve disease as in calcific aortic stenosis. In summary, these findings suggest that medical therapies may have a potential role in patients in the early stages of this disease process to slow the progression of RHD affecting the valves. This review will summarize the potential for statin therapy for this patient population.
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PMID:Medical therapy for rheumatic heart disease: is it time to be proactive rather than reactive? 1972 84


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