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

Seven patients with aortic regurgitation, manifesting diastolic flutter of the aortic valve cusps (DFAVC) in the echograms, are described. Five patients with infective endocarditis revealed coarse or fine, irregular DFAVC. Two patients with severe aortic regurgitation and a musical murmur manifested regular DFAVC with a frequency identical to that of a simultaneously recorded diastolic murmur. Of the 5 patients with infective endocarditis, 4 required urgent aortic valve replacement and 1 died. The 2 patients with musical murmurs are clinically stable without surgery. This report extends the clinical spectrum of patients with DFAVC and describes the character of the flutter in patients with muscial murmurs. Furthermore, it suggests that DFAVC is a sign of severe aortic regurgitation.
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PMID:Diastolic flutter of aortic valves in aortic regurgitation: a report of seven cases. 44 98

Systolic flutter of the mitral valve was observed in 11 cases during the past 3-1/2 years. All patients had mitral regurgitation due to mitral valve prolapse or flail leaflets, and nine of the 11 (82%) had prior or concurrent bacterial endocarditis. Systolic flutter is uncommon in the absence of endocarditis and was observed in only two of 15 patients (13%) with proven chordae tendinae or papillary muscle rupture without historical and pathological evidence of infection involving the mitral valve. Systolic flutter was also not seen in a large number of patients with mitral regurgitation due to other causes. It is postulated that the regurgitation jet of blood across the edge of a structurally abnormal but flexible mitral leaflet is important for the development of flutter.
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PMID:Systolic flutter of the mitral valve. 67 75

Three patients with aortic valve endocarditis were studied. The single beam M-mode echocardiographic findings comprised the appearance in diastole of a cluster of shaggy echoes at the aortic valve in all three patients. Mitral flutter was seen in two patients and premature closure of the mitral valve in one patient. At multiple beam two-dimensional echocardiography, the echo cluster could in all three patients be seen to move perpendicular to the sound beams, ascending into the aorta in systole and descending in diastole. At valve replacement, vegetations were found that explained the abnormal echo cluster. The multiple beam echocardiography facilitated the interpretation of the single beam findings and increased the confidence therein. By applying the non-invasive modality of echocardiography in these patients with their high risk of embolism, cardiac catheterization may possibly be avoided.
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PMID:Single and multiple beam echocardiography in aortic valve endocarditis. Report of three cases. 69 30

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

We have described a 28-year-old male sheepfarmer who had fever, headache, chills, malaise, and aortic insufficiency. Echocardiography revealed a tricuspid aortic valve with a large vegetation on the right cusp, an enlarged left ventricle, and diastolic flutter of the mitral valve. Repeated blood cultures were negative. Seroconversion of IgG and IgM to Rickettsia typhi was found on the 13th day of hospitalization. The patient was treated with tetracycline for 1 year and remained afebrile and free of symptoms for 9 months, when he was lost to follow-up. IgM and IgG fluorescent antibodies to R typhi remained positive during 8 months of the follow-up period. We believe this to be the second reported case of endocarditis due to R typhi and the first not treated surgically.
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PMID:Murine typhus endocarditis. 163 93

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

From 1976 through 1986, 188 patients (female/male ratio: 2/1, age 20-77 years, mean 58 years) with isolated mitral valve disease underwent valve replacement using the Carpentier-Edwards porcine bioprothesis (CEPB). Nine hospital deaths (4.8%) were excluded from further analysis. Follow-up was 0.2-11.3 years (mean 5.2 years); preoperatively, 74% had atrial flutter/fibrillation, and 75% were in NYHA-classes III-IV. All patients were put on life-long coumadin treatment. Preoperative predictability of long-term survival and prosthesis-related complications was examined using Cox regression analysis. Five preoperative variables were found to have independent predictive value as regards long-term survival: myxomatous degeneration of the valve (p = 0.002), chronic regurgitation (p = 0.003), age (p = 0.004), NYHA-class III-IV (p = 0.05), and atrial flutter/fibrillation (p = 0.05). A prognostic index calculated form the final Cox model identified six risk groups (I-VI) having cumulative 10-year survivals +/- SE of: I (n = 9) 100%, II (n = 10) 90 +/- 9%, III (n = 30) 73 +/- 10%, IV (n = 70) 51 +/- 9%, V (n = 43) 17 +/- 10%, and VI (n = 17, 7-year survival) 16 +/- 13% (p less than 0.0001). The incidence of late valve-related complications (%/patient-years) were: hemorrhage, 1.2; thromboembolism, 0.5; Endocarditis, 1.0; paravalvular leak, 0.2; and primary tissue failure, 1.5. Previous closed comissurotomy adversely influenced the occurrence of hemorrhage, while calcified mitral annulus were predictive of endocarditis. Younger age (less than or equal to 45 years) had a strong predictive influence of primary tissue failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Isolated mitral valve replacement. With Carpentier-Edwards bioprosthesis :independent risk factors for long-term survival and prosthesis failure. 276 73

To determine the clinical value of echocardiographic evaluation of porcine bioprosthetic valves, the findings in all patients who had porcine bioprosthetic valve replacement and adequate quality echocardiographic studies from 1978 to 1982 were analyzed. The study includes 309 normal and 59 dysfunctioning valves. Valve dysfunction resulted from spontaneous cusp degeneration in 39 (34 valve regurgitations, 5 stenoses), infective endocarditis in 12, paravalvular regurgitation in 5, regurgitation of redundant cusps, mitral valve thrombi, and aortic stent stenosis in 3 others. Echocardiographic findings were correlated with gross surgical pathologic or autopsy findings in 45 of the 59 dysfunctioning valves. Echocardiographic abnormalities were demonstrated in 41 of 59 (69%) dysfunctioning valves. A systolic mitral or diastolic aortic valve flutter was diagnostic of a regurgitant valve caused by a torn or unsupported cusp margin and was observed in 28 of 34 (82%) regurgitant valves with no false-positive studies. Echocardiographic cusp thickness of greater than or equal to 3 mm correctly identified all regurgitant and stenotic valves with gross anatomic evidence of localized or generalized cusp thickening or calcific deposits. Echocardiographic valve abnormalities were observed in only 4 of 12 patients with infective endocarditis and in 1 of 5 with paravalvular regurgitation. Thus, echocardiography provides important information regarding the function of porcine bioprosthetic valves and is of value in the decision to replace these valves, especially when dysfunction is due to spontaneous cuspal degeneration. Echocardiography is neither sensitive nor specific in patients with infective endocarditis and paravalvular regurgitation.
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PMID:Echocardiographic evaluation of porcine bioprosthetic valves: experience with 309 normal and 59 dysfunctioning valves. 686 78

Echocardiographic features of acute aortic regurgitation resulting from bacterial endocarditis have been well documented (Nathan et al., 1980; Weaver et al., 1977; Wray, 1975a), and include thick shaggy echoes from aortic valve in diastole, fine diastolic flutter of aortic valves suggestive of rupture of cusps, and premature closure of mitral valves. Echocardiography being a sensitive noninvasive technique for detecting aortic valve vegetations is heavily relied on for earlier diagnosis and prompt therapy of these patients. Prognosis of echocardiographically positive endocarditis is known to be worse than for echo-negative patients. The following case is being presented because of an unusual echocardiographic manifestation with mid-diastolic aortic valve opening secondary to flail aortic valve from staphylococcal endocarditis of the aortic valve.
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PMID:Mid-diastolic aortic valve opening in bacterial endocarditis of aortic valve. 708 53

Four patients with documented flail aortic valve leaflets were studied using M-mode and two-dimensional echocardiography (2-D echo). Two had aortic valve endocarditis, one had endocarditis involving a congenital heart defect, and one had a myxomatous aortic valve. Mitral valve flutter and early mitral valve closure led to the diagnosis of severe aortic insufficiency in three patients. Diastolic aortic valve flutter, considered to be specific for a flail aortic leaflet, was present in three patients. In the fourth patient left ventricular outflow tract (LVOT) echoes were present, but did not distinguish between a flail aortic leaflet and an aortic vegetation. Two-D echo confirmed LVOT echoes in all patients. Discrimination between a flail leaflet and a vegetation(s) without leaflet disruption was accomplished by noting the hinge point of the LVOT diastolic echoes, which was the aortic wall in patients with a flail leaflet. The combination of these M-mode and 2-D echocardiographic findings permitted the diagnosis of a flail aortic leaflet to be made accurately and noninvasively. In two patients surgery was performed without prior cardiac catheterization.
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PMID:Flail aortic valve leaflets: M-mode and two-dimensional echocardiographic manifestations. 736 46


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