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

In a retrospective study, 29 patients at least 20 years of age with known aortic stenosis are reported who had the peak systolic gradient (PSG) measured on at least two occasions without an intervening surgical procedure or episode of endocarditis. In these 29 patients, there were 31 intervals available for evaluation with a mean follow-up time of 43.5 months (1 week to 120 months). In 16 of the 31 intervals, the PSG increased by 50% or more and in 15, it did not. In the group where the PSG increased, the average rate of increase was 1.3 mm. Hg/month with the most rapid gradient increase at 3.8 mm. Hg/month. Progression to high gradient was correlated with the development of angina pectoris or left ventricular hypertrophy by voltage and ST-T wave changes. In this study, other symptoms were not helpful in predicting an increase in severity. It is still recommended, however, that any patient with aortic stenosis and the development of symptoms of congestive heart failure or exertional syncope should be suspected of having progressed to severe aortic stenosis and should be restudied.
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PMID:Rate of progression of severity of valvular aortic stenosis in the adult. 49 18

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

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

Complications after heart valve replacement remain a substantial source of morbidity and mortality despite continuing advances in surgical care and prosthetic design. Infectious endocarditis occurs in about 4 percent of patients and may appear early (within 60 days) or late after operation. Endocarditis of early onset is commonly due to staphylococcal, fungal or gram-negative organisms and is fatal in 70 percent or more of cases. Infection of late onset is more often of streptococcal origin and the mortality rate is lower, about 35 percent. With either type, prompt recognition, vigorous and appropriate antimicrobial therapy and early consideration of surgical intervention are crucial. The postperfusion and postpericardiotomy syndromes are relatively common and relatively benign syndromes associated with postoperative fever. Their recognition is important to prevent confusion with endocarditis or sepsis and thus to reassure the patient and physician. Treatment is primarily symptomatic. Intravascular hemolysis occurs with most prosthetic heart valves but is more common with certain prostheses and with paraprosthetic valve regurgitation, with significant hemolytic anemia in 5 to 15 percent. Oral iron replacement therapy is effective in the majority of patients, but occasionally blood transfusion or reoperation for leak around the prosthesis is necessary. Prosthesis dysfunction due to thrombus may be recognized clinically by recurrence of heart failure, syncope, cardiomegaly and altered prosthetic valve sounds or new murmurs. Hemodynamic studies verify the diagnosis, and prompt reoperation is indicated for this potentially lethal problem. Systemic embolization has decreased markedly with the introduction of cloth-covered prostheses and is frequently related to erratic or ineffective anticoagulant therapy. We continue to recommend anticoagulant therapy for all patients with prosthetic heart valves unless there is a major contraindication.
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PMID:Diagnosis and management of complications of prosthetic heart valves. 109 75

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

Based on our experience and the experience of others, the following classification of patients with mitral valve prolapse has been proposed. Mitral valve prolapse - Anatomic includes patients with a wide spectrum of mitral valve abnormalities from mild to severe. Symptoms, physical findings and laboratory abnormalities in these patients are directly related to mitral valve dysfunction and progressive mitral regurgitation. Complications related to abnormal mitral valve include infective endocarditis, thromboembolic events, cardiac arrhythmias, progressive mitral regurgitation, rupture of chordae tendineae and congestive heart failure. Individuals with thick mitral leaflets and mitral systolic murmur are at higher risk of developing complications. The term mitral valve prolapse syndrome refers to the occurrence of symptoms such as palpitation, chest pain, fatigue, poor exercise tolerance, dyspnea, orthostatic phenomena and syncope or presyncope in patients with mitral valve prolapse which cannot be explained on the basis of mitral valve abnormality alone. The pathogenesis of these symptoms in patients with mitral valve prolapse syndrome appears to be related to metabolic neuroendocrine abnormalities. Preventing infective endocarditis is a major consideration in patients with mitral valve prolapse. Significant mitral regurgitation with the development of congestive heart failure often requires mitral valve surgery. The most important therapeutic approach in patients with mitral valve prolapse syndrome is to explain the mechanisms of symptoms and to reassure the patient.
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PMID:Mitral valve prolapse: etiology, clinical presentation and neuroendocrine function. 134 25

Few disorders ever provoked more interest and controversy than mitral valve prolapse (MVP). Past echocardiographic over-diagnosis led to it becoming a whipping boy for otherwise unexplained chest pain, palpitation, arrhythmias and emboli. Surgical centres reported a high incidence of endocarditis and severe regurgitation. Most investigators who have studied the prevalence of arrhythmias in MVP have concluded that they are more common in this syndrome than in the general population and that there is a causal rather than a fortuitous relationship. However, the prevalence of arrhythmias in reported studies is probably higher than in unselected MVP patients. Multiple ventricular premature beats, ventricular tachycardia and sudden death have been reported. Suggested mechanisms have included a focal cardiomyopathy with incoordinate contraction and relaxation, QRS dispersion, a long QT, traction on papillary muscles by prolapsed leaflets, interference with the blood supply of the papillary muscles, stimulation of the endocardium by the chordae and diastolic depolarisation of muscle fibres in redundant leaflets with triggered repetitive automaticity. MVP has been associated with pre-excitation giving rise to atrioventricular re-entry tachycardia. Autonomic dysfunction and a hyperadrenergic state has been claimed and this may also be responsible for supraventricular arrhythmias including atrioventricular nodal re-entry tachycardia, flutter and fibrillation. Electrophysiological studies have yielded contradictory results which may be due to the heterogeneity of the patients studied and variability of the mechanisms. Whatever the true prevalence, arrhythmias in MVP are usually benign. Syncope and sudden death are rare. Anti-arrhythmic therapy is only warranted in patients with frequent and distressing symptoms shown to be due to the arrhythmias or when arrhythmias are judged potentially life threatening.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitral valve palpitations. 144 39

Mitral valve prolapse is a common cardiac disorder that can readily be diagnosed by characteristic auscultatory and echocardiographic criteria. Although many diseases have been associated with mitral valve prolapse, most affected individuals have the primary form of the disorder. Mitral valve prolapse is an inherited condition commonly associated with myxomatous degeneration of the mitral valve and its support structures. Complications of mitral valve prolapse, including cardiac arrhythmias, sudden death, infective endocarditis, severe mitral regurgitation (with or without chordae tendineae rupture), and cerebral ischemic events, occur infrequently considering the wide prevalence of the disorder. Panic disorder is a specific type of anxiety disorder characterized by at least three panic attacks within a 3-week period or one panic attack followed by fear of subsequent panic attacks for at least 1 month. It too is a common condition with a prevalence and age and gender distribution similar to that of mitral valve prolapse. Panic disorder and mitral valve prolapse share many nonspecific symptoms, including chest pain or discomfort, palpitations, dyspnea, effort intolerance, and pre-syncope. Chest pain is the symptom in both conditions that most commonly brings the patient to medical attention. The clinical description of chest pain in patients with mitral valve prolapse is highly variable, possibly reflecting multiple etiologies. Chest pain in panic disorder is usually characterized as atypical angina pectoris and as such bears resemblance to the chest pain commonly described by patients with mitral valve prolapse. Multiple investigative attempts to elucidate the mechanism of chest pain in both conditions have failed to identify a unifying cause. Review of the literature leaves little doubt that mitral valve prolapse and panic disorder frequently co-occur. Given the similarities in their symptomatology, a high rate of co-occurrence is, in fact, entirely predictable. There is, however, no convincing evidence of a cause-effect relationship between the two disorders, nor has a single pathophysiologic or biochemical mechanism been identified that unites these two common conditions. Until specific biologic markers for these disorders are identified, it may be impossible to do so. The lack of a proven cause-and-effect relationship between mitral valve prolapse and panic disorder and the absence of a unifying mechanism do not diminish the clinical significance of the high rate of co-occurrence between the two conditions. Primary care physicians and cardiologists frequently encounter patients with mitral valve prolapse and nonspecific symptoms with no discernible objective cause who fail to respond to beta-blockade. Panic disorder should be considered as a possible explanation for symptoms in such patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mitral valve prolapse, panic disorder, and chest pain. 189 9

The causes, clinical indications and diagnosis and differential diagnosis of cardiac disorders which may lead to cerebral symptoms are illustrated on the basis of a review of the present day level of scientific research. Principally involved are cerebral ischaemias arising from cerebral embolisms or from reduction of cardiac output in cardiovalvular and myocardial disorders. The incidence of all embolisms of cardiac origin makes up 10% of all ischaemic cerebral infarcts, with auricular fibrillation, irrespective of its origin, mitral stenosis, myocardial infarct, mitral insufficiency and combined mitral valve defects, and, in younger patients, mitral valve prolapse, being, in this order of frequency, of primary clinical significance. The other cardiovalvular and myocardial disorders have, in comparison, a relatively low incidence of cerebral embolisms. Haemodynamically induced cerebral ischaemias frequently occur in the form of complications following acute cardiac arrest, in myocarditis and in case of primary cardiomyopathies resulting from cardiac insufficiency or complicating bradyarrhythmia. They are clinically apparent in the form of syncope, and other impairments of consciousness of various levels of seriousness with and without indications of cerebral origin, extending up to coma. In view of the high incidence of 25% of acute cerebral ischaemias in cases of cardiac disease, not only neurological but also detailed cardiological investigation is vital in all cases for a correct diagnosis and for the selection of a suitable course of treatment. Cerebral complications in bradyarrhythmia and endocarditis are discussed in the context of a review of the relevant literature together with consideration of their epidemiology, aetiology, pathophysiology and clinical profile. Pathological sinus-bradycardia, bradyarrhythmia absoluta, sinu-atrial and atrio-ventricular blockages, carotid-sinus and sick-sinus node syndrome, paroxysmal atrial tachycardia, AV-node tachycardias, and auricular fibrillation and flutter, taken as a whole, lead to cerebral complications affected patients in 5 to 10% of afflictions of the central nervous system occur in 50% of patients suffering from complete AV blockage and, at a not precisely definable frequency, in patients suffering from other bradyarrhythmias. In addition to transitory, uncharacteristic symptoms such as dizziness, vertigo, impairment of vision and balance, presyncope, syncope and Adams-Stokes syndrome dominate the clinical profile. Endocarditis, with an incidence of 0.01 to 0.05% in the overall population, results in central nervous system complications in 12 to 25% of cases on average.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Heart diseases as a cause of cerebral symptoms and syndromes]. 222 59

Despite different aetiologies, acquired aortic stenosis is a self-maintaining, slowly progressive process with good long-term prognosis. In 142 patients with mild stenosis, there was clinical progression within 10 years of the initial diagnosis in only 12% of patients. Twenty-five years after the diagnosis had been established, the severity of aortic stenosis was clinically unchanged in 38%, while 25% of patients had moderate stenosis and 35% had undergone valve replacement. Progression of moderate aortic stenosis was more rapid: the average time interval between the manifestation of moderate aortic stenosis and surgery was 13.4 years. Age at the onset of initial symptoms was related to aetiology: 39 +/- 18 years with rheumatic aortic stenoses, 48 +/- 6 years in patients with bicuspid valves who had no history of rheumatic fever, infective endocarditis or myocarditis, and 66 +/- 12 years in degenerative, calcific stenoses of tricuspid aortic valves. Patients with haemodynamically severe stenosis who had refused the recommended operation (n = 55) had an overall poor prognosis: mean survival averaged 23 +/- 5 months and the five-year probability of survival was 18 +/- 7%. All these patients died within 12 years of observation. Mean survival after the occurrence of angina pectoris was 45 +/- 13 months, after syncope 27 +/- 15 months, and after first occurrence of left heart failure 11 +/- 10 months.
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PMID:The natural history of aortic valve stenosis. 304 4


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