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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 24-month period, 27 patients with idiopathic hypertrophic subaortic stenosis (IHSS), ages 65-80 years, were observed. Diagnoses were made by echocardiography (24 patients), cardiac catheterization (one patient), and both methods (two patients). The most common symptoms were angina (17 patients), dyspnea (13 patients), and syncope (11 patients). Two patients were asymptomatic, while another complained only of vague retrosternal chest discomfort with exertion. One asymptomatic patient had a completely normal physical examination, but electrocardiography (ECG) demonstrated a pattern of left ventricular hypertrophy. Another patient had an inconsistent apical holosystolic murmur. Two patients had alpha streptococcal endocarditis; neither was known to have pre-existing valvular disease. Fourteen patients had ECG criteria for left ventricular hypertrophy (LVH). Three patients were known to have associated aortic valve disease. The symptoms of IHSS may be nonspecific; asymptomatic patients with and without cardiac murmurs may be observed. Coexisting valvular disease, coronary artery disease, and bacterial endocarditis were documented. Patterns of myocardial infarction on ECG were not seen in these 27 patients.
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PMID:Idiopathic hypertrophic subaortic stenosis in the elderly. 56 40

Three types of small cardiac lesions were described and illustrated: (1) focal type of papillary muscle fibrosis, evidently a healed infarct of the papillary muscle present in 13% of autopsies, is a histologically characteristic lesion associated with coronary artery disease and healed myocardial infarction, (2) diffuse type of papillary muscle fibrosis, probably an aging change present in almost half of the autopsies, is associated with sclerosis of the arteries in the papillary muscle, is identifiable histologically, and apparently is not associated with any cardiac abnormality, and (3) focal cardiac myocytolysis, a unique histologic lesion, usually multifocal without predilection for any area of the heart, is associated with ischemic heard disease, death due to cancer complicated by nonbacterial thrombotic endocarditis and microthrombi in small cardiac arteries as well as with other diseases. Differentiation of the 2 types of papillary muscle fibrosis is important in the study of papillary muscle and mitral valve dysfunction. Focal cardiac myocytolysis may contribute to the fatal extension of myocardial infarcts.
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PMID:Small cardiac lesions. Fibrosis of papillary muscles and focal cardiac myocytolysis. 60 59

To determine the frequency of atrioventricular conduction disturbances in aortic valve disease, 26 consecutive patients (age 54 +/- 2 years) with symptomatic aortic valve disease were studied by His bundle electrocardiography at the time of cardiac catheterisation and were compared with a group of patients who underwent cardiac catheterisation and were found to have coronary artery or mitral valve disease but no aortic valve disease. Patients with aortic valve disease had significantly longer PR, AH, and HV intervals than cardiac patients not having this abnormality. Patients with aortic stenosis had prolonged HV, 52 +/- 6 vs +/- 42 +/- 2 ms (P = 0.06), whereas patients with chronic aortic regurgitation had prolonged PR, 245 +/- 27 vs 163 +/- 5 ms (P less than 0.001), and prolonged AH, 178 +/- 30 vs 102 +/- ms (P less than 0.001). Patients with combined lesions had significant prolongation of PR, AH, and HV intervals. Three patients with acute aortic regurgitation caused by endocarditis had normal atrioventricular conduction. Though the presence of valvular calcification did not significantly alter the pattern of atrioventricular conduction in these patients, those with calcified aortic valves had longer HV (P less than 0.005) than the control group. In addition, ventricular dysfunction or coronary artery disease did not affect the pattern of atrioventricular conduction in these patients. Thus, atrioventricular conduction disturbances are common in symptomatic aortic valve disease. With aortic stenosis the site of delay occurs more frequently below the His deflection, whereas in aortic regurgitation it is more frequent above the His deflection.
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PMID:Assessment of atrioventricular conduction in aortic valve disease. 68 91

For half a century the systolic click and late systolic murmur lay dormant as innocent auscultatory curiosities. The thirteen years since Barlow related these phenomena to mitral leaflet prolapse have witnessed an astonishing information explosion. We have sought to bring together the accumulated data in this review. An Historical Perspective traces the evolution from the now abandoned "pericardial" or "extracardiac" phases, through the leafletchordal phase (redundancy), the myocardial phase (segmental left ventricular contraction abnormalities), to the anular phase (dilatation and faulty systolic contraction). Functional Anatomy is dealt with in terms of pathology, pathophysiology, hemodynamics, angiocardiography, echocardiography, and physical and pharmacological interventions. Clinical Manifestations are concerned with prevalence, natural history, symptoms, physical signs, electrocardiographic abnormalities and roentgen fingings. The four Major Complications- sudden death, infective endocarditis, spontaneous rupture of chordae tendineae, and progressive mitral regurgitation- are examined. Associated Cardiac Diseases, i.e., Marfan's syndrome, ostium secundum atrial septal defect and atherosclerotic coronary artery disease, are discussed, and a section on Treatment deals chiefly with prophylaxis for infective endocarditis and the management of arrhythmias and chest pain. A final section on Evolving Information considers etiologic concepts, the nature of left ventricular contration abnormalities, the cause of chest pain, the relationship to Marfan's syndrome and ostium secundum atrial septal defect, and the effect of aging and sex differences on leaflet chordal redundancy.
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PMID:Mitral valve prolapse. 77 40

Mitral valve prolapse is a condition that is being recognized with increased frequency. It is not known whether its incidence is increasing, or whether we are better able to diagnose it today. In the idiopathic or familial variety, the mitral valve pathology is almost always that of myxomatous degeneration. Some authors have suggested the presence of a cardiomyopathy because of significant left ventricular dysfunction in many cases. Idiopathic prolapse occurs predominantly in females, often at a young age, and may be associated with chest pain, dyspnea, fatigue, presyncope, syncope, and/or sudden death. The clinical findings are variable and typically consist of a nonejection click and/or late systolic murmur, heard best at the cardiac apex. Diagnosis can be confirmed by echocardiography and/or ventricular cineangiography, the latter permitting accurate recognition of the anatomy of the prolapsed leaflets. The complications of infective endocarditis, severe mitral insufficiency, and life-threatening ventricular arrhythmias represent the major problems of management. It is important to distinguish the idiopathic form of mitral valve prolapse from that due to coronary artery disease and to realize that mitral valve prolapse may occur in Marfan's syndrome, Turner's syndrome, or in association with secundum atrial septal defect or ruptured chordae tendineae. Typical clicks and/or murmurs have also been described in patients with a history of rheumatic fever and in hypertrophic cardiomyopathy. Although much descriptive knowledge has accumulated over the past 15 years, many unanswered questions remain regarding the idiopathic type of prolapse. What is the nature and cause(s) of myxomatous degeneration? What is the relation of the valve pathology to the left ventricular dysfunction? What is the relation of both of these factors to disabling chest pain, electrocardiographic changes, and life-threatening arrhythmias? Hopefully, answers to these and other important questions regarding mitral valve prolapse will be forthcoming.
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PMID:Mitral valve prolapse. 77 95

In conclusion, patients on chronic maintenance dialysis have an increased incidence of death from cardiovascular disease. Hypertension plays a major role, and these patients must be carefully monitored for complete control of blood pressure. Adequacy of ultrafiltration to maintain normal extracellular volume is an essential part of the dialytic treatment. Hypertensive patients should be screened for excessive renin secretion because of its possible role in unresponsive hypertension in patients on dialysis. Nephrectomy should be used when necessary, where dialysis and antihypertensive medication have not adequately controlled blood pressure. Patients must be monitored for the presence of pericardial disease to avoid subsequent pericardial effusion and the development of constrictive pericarditis with its adverse effect on myocardial function. When constrictive pericarditis is present, it obviously should be relieved by appropriate surgery. Efforts should be made to minimize cardiac output in hemodialysis patients. Whether or not routine transfusions to maintain a higher hematocrit are indicated is a question that cannot yet be answered. However, patients with marginal cardiovascular function who are accepted on hemodialysis and must have an arteriovenous shunt should be supported in any manner to minimize an increase in cardiac output. Early and aggressive treatment of known episodes of sepsis is important in the elimination of valvular endocarditis in this patient population. Perhaps one of the finer indicators of adequacy of hemodialysis will be K rate and peak immunoreactive insulin levels. Continued abnormality of these parameters may contribute to cardiovascular disease. Clearly, further study of the effect of abnormal carbohydrate metabolism on lipid metabolism is in order. Serum triglyceride, serum cholesterol and lipid electrophoretic pattern should be followed to evaluate the beneficial effects of drug therapy and changes in dialytic technique on the development of cardiovascular disease. Careful monitoring of calcium, phosphorus, bone films and parathyroid hormone levels is indicated to assess parathyroid status. The use of aluminum binders and parathyroidectomy to prevent vascular and myocardial calcification is important in the therapy of these patients. The use of cardiac catheterization, coronary artery arteriography, and possibly cardiac vascular repair, should be considered in the chronic hemodialysis patient with coronary artery disease if he is otherwise well. Adequacy of hemodialysis perhaps can be evaluated through its effect on all of the above parameters. Whether or not changes in artificial kidney treatments can correct the final vascular disease remains to be seen.
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PMID:Cardiovascular disease in uremic patients on hemodialysis. 109 1

Nonejection clicks and associated mitral systolic murmurs are common in routine cardiologic practice and can result from multiple etiologic factors affecting the complex mitral valve mechanism. Such factors include a specific syndrome the essential feature of which is that the mitral leaflets or part thereof, primarily the posterior one, are voluminous. The syndrome has stimulated widespread interest and study during the last decade and various descriptive terms, including the "billowing mitral leaflet syndrome" (BMLS), have been applied to it. A familial occurrence of the BMLS may be detected and symptoms include chest pain, palpitations, syncope, and anxiety. Arrhythmias, conduction defects, and ECG abnormalities which mimic occlusive coronary artery disease are important features which remain ill understood. It is suggested that there is a possible relationship between the so-called "athlete's heart" and the BMLS. We also postulate that the entity of acute myocardial infarction without demonstrable occlusive coronary artery disease is, in at least some instances, a complication of the BMLS-possibly on the basis of coronary spasm. More severe mitral regurgitation, infective endocarditis, or, rarely, sudden death may supervene in the BMLS but we conclude, from published data and our own experience, that the prognosis is generally good.
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PMID:The problem of nonejection systolic clicks and associated mitral systolic murmurs: emphasis on the billowing mitral leaflet syndrome. 119 42

The Toronto SPV is a Dacron covered stentless porcine aortic prosthesis used for aortic valve replacement (AVR). We implanted this valve in 53 patients with a mean age of 58 years. The predominant valve lesion was aortic stenosis in 39 patients, insufficiency in 13 and a failed bioprosthesis in one. Six patients also had mitral valve disease and 18 had coronary artery disease. There was one operative death. Patients have been followed for four to 58 months, mean 27 months. There have been two late deaths but neither one was valve related. The actuarial survival at four years was 92% +/- 5%. Two patients required reoperation for reasons other than failure of the stentless aortic valve. There have been no thromboembolic complications. No patient had had infective endocarditis. Doppler echocardiographic assessment of the stentless valve revealed excellent effective valve areas and low transvalvular gradients. A few patients developed mild aortic insufficiency after implantation of the valve, but this problem has been practically eradicated by correct sizing of the prosthesis. AVR with the Toronto SPV provides excellent functional and hemodynamic results. This bioprosthesis seems to be associated with an extremely low rate of valve related complications. These findings justify its continued use, but further follow up is needed to determine its durability.
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PMID:Aortic valve replacement with the Toronto SPV bioprosthesis. 134 36

The antiphospholipid syndrome has been associated with multiple cardiac abnormalities. The earliest reports were of valvular disease, including verrucous endocarditis, as well as valvular thickening and insufficiency. Subsequently, antiphospholipid antibodies were implicated in coronary artery disease manifested by premature myocardial infarction and coronary artery bypass graft occlusion. In addition, there have been rare reports of intracardiac thrombi and diffuse cardiomyopathy in association with antiphospholipid antibodies. In this review, we discuss the nature and prevalence of the cardiac manifestations of the antiphospholipid antibody syndrome as well as some of the proposed pathophysiologic mechanisms. We also provide examples from our own experience. The expanding spectrum of cardiac disease associated with antiphospholipid antibodies suggests an important role for these antibodies in certain types of cardiac pathology.
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PMID:Cardiac manifestations of the antiphospholipid syndrome. 144 4

Chlamydiae are common human pathogens, causing a broad spectrum of infectious diseases. Chlamydial infections involving the heart have been described in numerous previous reports. These organisms are documented to cause endocarditis, myocarditis and pericarditis. Furthermore, Chlamydia pneumoniae, the recently discovered respiratory pathogen, has also been implicated in coronary artery disease. For the first time the literature on involvement of the heart in chlamydial infections is reviewed. Information on the discovery of Chlamydia species is also included and the problem of the species determination of Chlamydia in interpretation of the older literature is mentioned.
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PMID:Chlamydial infections of the heart. 148 83


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