Murmur Of Mitral Regurgitation Research Articles

The cardiovascular manifestations of the hypereosinophilic syndrome: Prospective study of 26 patients, with review of the literature

The major cause of morbidity and mortality in patients with the hypereosinophilic syndrome is cardiac dysfunction. A review of 65 cases from the literature (historic series) revealed the following cardiovascular manifestations to be most common: dyspnea (60 per cent), signs of congestive heart failure (75 per cent), murmur of mitral regurgitation (49 per cent), cardiomegaly (37 per cent), T wave inversions on electrocardiogram (37 per cent) and pathologic findings of endocardial fibrosis, myocardial inflammation and mural thrombus formation (57 per cent). We have prospectively followed 26 patients with the hypereosinophilic syndrome for up to nine years (average follow-up prospectively was 3.3 years, retrospectively 5.7 years). Common cardiac findings in our 26 patients were dyspnea (42 per cent), chest pain (27 per cent), signs of congestive heart failure (38 per cent), murmur of mitral regurgitation (42 per cent), cardiomegaly (35 per cent) and T wave inversions (35 per cent). Thus, these patients demonstrated cardiovascular manifestations similar to those in the historic series, although the literature review showed a higher incidence of overt congestive heart failure. Of 22 patients having echocardiograms, 55 per cent demonstrated some clinical, roentgenographic or electrocardiographic evidence of cardiac involvement, but 82 per cent had echocardiographic abnormalities. This suggests that the echocardiogram is a sensitive and perhaps early indicator of cardiac involvement in this disease. Common echocardiographic findings included increased left ventricular wall thickness (68 per cent), left ventricular mass (73 per cent) and left atrial size (37 per cent). Prospective echocardiographic follow-up of 18 patients (for up to four and a half years) revealed that seven of eight untreated or inadequately treated patients had increases in left ventricular wall thickness, whereas all 10 adequately treated patients had decreases (eight of 10) or no change (two of 10) in left ventricular wall thickness. This suggests that adequate antihypereosinophilic therapy (with prednisone and/or hydroxyurea) may stabilize and, in some cases, reverse the cardiac manifestations of the hypereosinophilic syndrome. In previous studies, congestive heart failure due to eosinophilic cardiomyopathy has been reported to be very resistant to therapy. In our patients with congestive heart failure, treatment has been almost invariably effective when digitalis and diuretics were combined with adequate antihypereosinophilic therapy.

The Echocardiogram in Scleroderma Endocarditis of the Mitral Valve

Echocardiography was performed in a woman with long-standing scleroderma with the CRST syndrome in whom the murmur of mitral regurgitation had been present for one year. The echocardiogram showed an irregular shaggy thickening of the anterior mitral valve leaflet. At autopsy three months later, myocardial fibrosis, small coronary artery sclerosis, and nodular thickening of the mitral valve were found. To our knowledge, anterior mitral leaflet thickening in scleroderma has not been reported previously. In this patient, it was associated with a poor prognosis.

Demonstration of the mechanism by which mitral regurgitation mimics aortic stenosis

A case of mitral regurgitation simulating aortic stenosis is discussed. Echocardiographic and angiographie evidence is provided demonstrating the mechanism whereby the murmur of mitral regurgitation mimics aortic stenosis. This case offers direct confirmation of the hypothesis that acoustic energy derived from a mitral regurgitant jet may be transmitted to the aorta by impingement of the jet upon the portion of the left atrial wall adjacent to the aortic root.

Diagnosis and natural history of congested (dilated) cardiomyopathies.

The diagnosis of primary dilated cardiomyopathy depends on the recognition of a dilated poorly contracting left ventricle with increased end-diastolic and end-systolic volumes in the absence of a detectable cause. The diagnosis is made only after exclusion both of structural heart disease and of known causes of secondary heart muscle disorder. The natural history is still largely unknown and is probably as variable as the likely causes. The left ventricular disorder does not cause symptoms until heart failure supervenes except for occasional patients who develop an early atrial or ventricular dysrhythmia, conduction defect, chest pain or murmur of mitral regurgitation. This period of latency may be short, prolonged or even permanent since it is unlikely that all cases progess to the point of failure. A few patients recover normal or near-normal cardiac function. The interplay between high blood pressure, hypertensive heart failure and dilated cardiomyopathy is illustrated by patients who recover from heart failure to become hypertensive and vice versa and in current treatment with vasodilators and diuretics for patients at either end of the spectrum.

Successful Medical Therapy for Endocarditis due to Candida parapsilosis: A Clinical and Epidemiologic Study

A heroin addict with asymmetric septal hypertrophy and persistent fungemia with Candida parapsilosis was treated with amphotericin B and flucytosine (5-fluorocytosine). The diagnosis of endocarditis was based on the subsequent development of a murmur of mitral regurgitation and echocardiographic evidence of prolapse of the posterior leaflet of the mitral valve. Cure was effected with antifungal therapy alone. Thus, when the diagnosis of fungal endocarditis is made early in its course, open-heart surgery may not be needed. To investigate the relative frequency of isolation of C parapsilosis from particular sites, a mycologic survey was conducted in our hospital. Among the isolates of yeasts, C parapsilosis represented 8.0, 17.1, and 26.7 percent of those from all cultured sites, from contaminated intravenous catheters, and from cultures of blood, respectively. Since this trend to cluster in cases of fungemia was not seen with other yeasts, C parapsilosis appears to be more invasive than other species of Candida.

Mid-systolic click and mitral valve prolapse following mitral commissurotomy

Five patients with rheumatic mitral stenosis were observed to have mid-systolic clicks with murmurs of mitral regurgitation at various intervals after mitral commissurotomy. In two patients echocardiography showed an unusually rapid posterior deflection of the mitral valve coinciding exactly with a systolic nonejection click. It is speculated that the shortened, fused chordae tendineae, compromised by mitral commissurotomy, rigidly hold the valve leaflets fixed at the onset of systole. During systole, ventricular conformational changes, in the face of marginal coaptation of thickened and fibrotic mitral leaflets, allow the mitral valve to be forced abruptly towards the left atrium with great velocity. This is manifested by a loud systolic click and, in some patients, a near vertical posterior systolic deflection of the mitral valve on the echocardiogram. The systolic click may occur without echocardiographic or angiographic evidence of mitral valve prolapse. Unusually loud mid-systolic clicks can be heard in patients with rheumatic heart disease after mitral commissurotomy and may be accompanied by a distinctive echocardiographic appearance of the mitral valve.

Late complications of myocardial infarction.

RECOGNITION of the late complications of myocardial infarction necessitates a morphologic approach, a recognition that the pumping action of the heart is importantly affected by asynergy, aneurysm, or papillary muscle dysfunction,1,2 and the assumption that such abnormal morphology can be recognized and quantitated. Thus, congestive heart failure or dysrhythmias during acute infarction may be followed weeks or months later by recurrent pump failure. Simple description of the coronary tree, eg, critical stenosis of one, two, or three vessels, may be a wholly inadequate description of postinfarction status. It is the purpose of this review to examine the factors leading to the recognition and treatment of late complications in myocardial infarction and to attempt a separation of highand low-risk groups. Table 1 lists major and minor late complications, ie, those arising after the 14th day, in 100 patients with acute transmural myocardial infarction. Table 2 lists the frequency of abnormal clinical and laboratory indexes in those with and those without the complications listed in Table 1. A mitral regurgitant murmur, for example, was four times more common in patients shown to have either

Clinical Study on the Acoustic Phenomena in Coronary Venous System with Intracardiac Phonocardiography

In order to study the intracardiac murmurs in coronary venous system, right heart catheterization was carried out on 35 patients with or without mitral regurgitation. The double-lumen phonocatheter of A. E. L. was used for 33 cases but for 2 the microtip phonocatheter of Millar was employed. As a rule, simultaneous recording of intracardiac and external phonocardiograms was made with the pressure tracing in the majority of cases. The examined subjects were divided into 3 groups; 9 cases with mitral regurgitation confirmed by left ventriculography (Group I), 20 without mitral regurgitation (Group II), and 6 with functional systolic murmur (Group III). In Group I, a loud systolic murmur was recorded in 7 cases (MR 5, MR + AR 1, ECD 1), but in none of IHSS in the coronary sinus or great coronary vein. In Group II, no systolic bruit was noted in VSD and other lesions except ASR in the coronary venous system. The same was true in patients with functional systolic murmur (Group III). Intracardiac phonocardiography is thought to be useful to record mitral regurgitant murmurs in the coronary venous system, since the latter is in the close proximity to the mitral posterior commissure or mitral annulus.

Mitral valve prolapse in children with secundum ?Type atrial septal defect (ASD II)

A left ventricular angiocardiogram for evaluation of the mitral valve in patients with uncomplicated secundum type atrial septal defect has been proposed in a recent paper by Victoria et al. (1974). These authors observed 8 children with a ballooning mitral valve and ASD II. They stressed the necessity of performing a left ventricular angiocardiogram in every patient with ASD II. To challange their proposal, the angiocardiograms of 78 children with secundum type ASD were reviewed. Of these 89 angios 34 were performed using the left ventricle (LV) as injection site while 55 times the injection was made in other parts of the heart, e.g. left atrium, pulm. art., right ventricle, right atrium. All 34 LV angios, but only 12 of the others allowed an evaluation of function and morphology of the mitral valve. Of the 46 angiocardiograms 27 (58.7%) revealed an intact, normally closing and opening mitral valve. In the remaining 19 (41.3%) various grades of ballooning or mild prolapsing of one or two leaflets of the mitral valve could be detected. The "scallops" were minimal in 12, moderate in 4 and pronounced in 3 cases. A mild regurgitation was seen in 1 patient only. No patient had the pronounced ballooning observed by Victoria et al. On auscultation only 1 case had the apical murmur of mitral regurgitation. The ECG of our 19 "positive" cases did not show signs of left atrial or left ventricular hypertrophy. A left axis deviation was found in 1 patient. During surgery no structural abnormality of the mitral valve was noted. Postoperative reevaluation of the mitral valve (including left ventricular contrast injection) in 10 cases revealed no change of mitral valve appearance in 8, a decrease of the ballooning in one, and an increase in another patient. It is concluded that prolapses of the mitral valve are seldom of such a degree as to cause dysfunction in children with secundum type ASD. The indications for performing a left ventricular injection of contrast material are the clinical signs of mitral valve regurgitation and/or left axis deviation in the ECG.

Herniation of mitral leaflets in the ehlers-danlos syndrome

A 47 year old patient with the Ehlers-Danlos syndrome (hypermobility of the joints, hyperextensibility of the skin and atrophic cutaneous scars) was evaluated because of a mitral regurgitant murmur and paroxysmal atrial tachycardia. Angiocardiography and echocardiography demonstrated marked systolic herniation of the posterior leaflet of the mitral valve. An echocardiogram from the patient's daughter, who also had paroxysmal atrial tachycardia, revealed the same abnormality. Although a “floppy” valve is common in Marfan's syndrome, this report emphasizes that it may also occur in patients with other heritable disorders of connective tissue.

Embolization of the Anterior Leaflet of the Mitral Valve

A young woman presented to our hospital in florid pulmonary edema and with the stigmata of acute bacterial endocarditis. Murmurs of mitral regurgitation and aortic regurgitation were present. While on antibiotic therapy, the patient developed signs and symptoms of left femoral artery occlusion. Pathologic examination revealed that the specimen removed at embolectomy contained tissue from the mitral valve. Prompt surgical intervention with mitral valve replacement was required in attempting to correct the hemodynamic derangements.

Haemodynamic explanation of why the murmur of mitral regurgitation in independent of cycle length.

Haemodynamic explanation of why the murmur of mitral regurgitation in independent of cycle length.

Silent Mitral Regurgitation Complicating Silent Myocardial Infarction: Hemodynamic and Morphologic Documentation

Clinical, hemodynamic and anatomic findings are described in a 71-year-old man with “silent” acute myocardial infarction. Hemodynamic evidence of mitral regurgitation resulting from papillary muscle necrosis was obtained both before and after the appearance of the murmur of mitral regurgitation.

Physical diagnosis of coronary artery disease and its sequelae.

ABSTRACT:Physical examination tends to be regarded negatively in the diagnosis of coronary artery disease (CAD). A resurgence of current interest in the physical diagnosis of CAD and its sequelae results from the availability of surgical techniques for their treatment and is made possible by a systemic clinical‐physiological‐angiographical correlative approach. An accentuated first sound (S1) in association with presystolic and diastolic gallops in the absence of congestive heart failure is highly suggestive of papillary muscle dysfunction (PMD) and/or ventricular aneurysm (VA), two of the most common sequelae of CAD. When S1 in VA is not accentuated, mural thrombosis should be suspected. The murmurs of PMD are much more common in CAD than generally believed and can be either ejection‐type, early systolic, midsystolic, pansystolic, or late systolic. A late systolic murmur (LSM) in CAD represents a mild form of PMD and may be distinguished from the murmur of the “auscultatory‐electrocardiographic” syndrome by its responses to amyl nitrite and the squatting position. Murmurs of PMD can be differentiated from other mitral regurgitant murmurs by their changing configurations, post‐extrasystolic diminution and inspiratory accentuation. Paradoxical splitting of the second sound in CAD is more an auscultatory illusion than an actual reversal of the sequence of closure of the aortic and pulmonic valves. Diastolic murmurs in CAD may be due to either VA or segmental coronary artery stenosis. It is concluded that physical examination gives valuable clues to the existence of CAD or its sequelae and to the functional status of the underlying myocardium. It constitutes the single most useful non‐invasive tool available to every physician.

Atrial fibrillation and hyperthyroidism in a 14-year-old boy

<h2>Summary</h2> Atrial fibrillation is reported in a 14-year-old boy with juvenile hyperthyroidism, who also developed congestive heart failure and mitral regurgitation. The atrial fibrillation and congestive heart failure responded to treatment with digitalis, diuretics, quinidine, and antithyroid therapy. The murmur of mitral regurgitation resolved after the hyperthyroidism was brought under control. Hyperthyroidism should be included in the differential diagnosis of the pediatric patient with unexplained atrial fibrillation and unexplained congestive heart failure.

The Use of Isometric Exercise As a Diagnostic Maneuver in Patients with Heart Disease.

Meeting Abstracts1 May 1971The Use of Isometric Exercise As a Diagnostic Maneuver in Patients with Heart Disease.Wayne Siegel, M.D., D. O. Nutter, M.D., R. C. Schlant, M.D., F.A.C.P., J. W. Hurst, M.D., F.A.C.P.Wayne Siegel, M.D.Search for more papers by this author, D. O. Nutter, M.D.Search for more papers by this author, R. C. Schlant, M.D., F.A.C.P.Search for more papers by this author, J. W. Hurst, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-74-5-822_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIsometric handgrip exercise has been employed to induce acute elevation of blood pressure and heart rate in 81 patients with valvular or coronary atherosclerotic heart disease. Pressor responses occurred in all patients and normals. Handgrip exercise altered murmur intensity in 19 patients with documented valvular lesions. The murmurs of aortic stenosis (six patients) and subaortic stenosis (one patient) decreased in intensity during exercise. The murmurs of aortic regurgitation (six patients), mitral regurgitation (four patients), mitral stenosis (three patients), and pulmonic regurgitation (two patients) increased during handgrip exercise. In 27 patients with atherosclerotic heart disease the responses to maximal handgrip exercise... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Atlanta, Ga. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1971Volume 74, Issue 5Page: 822-822KeywordsBlood pressureCardiovascular therapyCoronary heart diseaseExerciseHeart rateLesionsMitral insufficiencyMitral stenosisStable coronary artery diseaseStenosis Issue Published: 1 May 1971 PDF downloadLoading ...

Severe valvular aortic stenosis in patients over 65 years of age: A clinicopathologic study

Clinical and anatomic data are presented in 21 autopsy cases of patients over 65 years of age with severe valvular aortic stenosis. Attention is called to the unusual nature of the valvular lesion in the elderly compared to its manifestations in younger adults. The degree of aortic stenosis even in the very elderly may be extreme. The aortic valve in 2 patients was congenitally bicuspid, and in 19, tricuspid. The latter valves usually were characterized by the uniform distribution of nodular calcific deposits on the aortic aspects of the cusps and by the lack or near lack of commissural fusion. Calcification of the mitral annulus occurred in 16 of the 21 patients. Clinically, aortic stenosis in the elderly is characterized by several features that are either absent or more prominent than in younger subjects with this valvular lesion: The systemic arterial pulse pressure may be increased due to systolic hypertension; a harsh right basal systolic murmur may be relatively inconspicuous, whereas a pure musical systolic murmur may be prominent at the apex; a coexisting apical systolic murmur of mitral regurgitation may be related to mitral annular calcification and not to left ventricular failure; and systemic systolic hypertension can result in a comparatively small pressure gradient despite severe left ventricular outflow obstruction.

The effect of pregnancy on the murmurs of mitral and aortic regurgitation.

The effect of pregnancy on the intensity of murmurs of aortic and mitral regurgitation has not been reported previously. Twenty-five women with these murmurs, singly or in combination, were examined when pregnant as well as when not pregnant. During pregnancy the murmur of aortic regurgitation decreased in intensity or became inaudible in 10 patients, remained unchanged in four, and increased in one. The murmur of mitral regurgitation decreased in intensity or became inaudible in eight patients, became shorter in duration in two, was unchanged in three, and became louder in one. Three of the patients who did not show a decrease in intensity of the mitral or aortic regurgitation murmur and the patient whose murmurs increased during pregnancy had the appearance or persistence of systemic hypertension during pregnancy. Phenylephrine consistently increased the loudness of the murmurs, usually to the level present in the nonpregnant state. The diminished intensity of these murmurs may be related to the decrease in peripheral resistance known to occur during pregnancy. It is apparent that (1) aortic regurgitation or mitral regurgitation may be missed during pregnancy, since these murmurs may become inaudible, and (2) the severity of these cardiac lesions may be underestimated clinically because of a decrease in intensity of these murmurs during pregnancy. It is important to determine the existence of valvular heart disease, since endocarditis is a hazard during parturition, and prophylactic antibiotic therapy should be given to these patients.

A Clinical Study on the Pattern of Mitral Valvular Disease in a Peripheral Tertiary Hospital in Bangladesh

Background: Rheumatic mitral valvular disease (MVD) is a common cause of cardiovascular morbidity and mortality in Bangladesh. Many patients are diagnosed late, get maltreated, and develop complications, which can be minimized if early diagnosis could be made. Objectives: The study was carried out to determine the common symptoms and signs of mitral valvular disease in our population, to find out the incidence and pattern of complications, to list the pattern of valve lesions, to identify the common findings in different investigations and to find out the causes of delay in diagnosis. Methods: Fifty consecutive cases of isolated MVD of rheumatic origin admitted in Rajshahi Medical College Hospital, Rajshahi, Bangladesh, from July, 2002 to March, 2003 were included. Detailed history was taken, and clinical examination was performed. Chest skiagram, 12-lead ECG and echocardiography were performed in all patients. Other investigations include complete blood counts, anti-streptolysin O (ASO) titre, C-reactive protein (CRP), blood sugar, serum creatinine and routine urinalysis. Results: The peak incidence of MVD was found in the third decade (34%), 14 (28%) patients were &lt;20 years of age. Thirty two (64%) patients had poor socio-economic condition. A previous history suggestive of rheumatic fever was found in 28 (56%). Twenty six (52%) patients received treatment from the registered medical practitioners and/or from the hospitals, 11 (22%) consulted with the quacks only, 5 (10%) had treatment from both sources. Significant delay was found in 28 (56%) patients. Illiteracy and ignorance was found to be the cause in 14 (28%) cases, poverty in 12 (24%) and misdiagnosis in 7 (14%). Six (12%) patients adopted indigenous treatment. Forty three (86%) patients experienced moderate to severe limitation of day-to-day activities all had breathlessness. Palpitation, fatigue and cough were found in 49 (98%), 45 (90%) and 42 (84%) cases respectively. Nineteen (38%) patients had haemoptysis, 15 (30%) had dysphagia. Apex beat was normally situated in 32 (64%), and shifted in 16 (32%) cases. Forty two (84%) patients had left parasternal heave and palpable P2 was found in 41 (82%) patients. Diastolic thrill was palpable in 28 (56%) cases, systolic thrill in 8 (16%) patients. The first heart sound (S1) was loud in 34 (68%) and soft in 8 (16%) cases. Mid-diastolic murmur of MS was audible in 46 (92%) cases, pansystolic murmur of mitral regurgitation in 19 (38%) patients and pansystolic murmur of tricuspid regurgitation in 10 (20%). Opening snap was found in 30 (60%), and presystolic accentuation in 27 (54%) cases. Roentgenographic study revealed moderate to huge enlargement of cardiac shadow in 29 (58%), straightening of the left border of the heart with fullness or outward bulging of the pulmonary conus in 43 (86%), double contour of the right border in 35 (70%), upper lobe diversion of pulmonary vasculature in 31 (62%), Kerley B lines in 10 (20%) and pulmonary oedema in 16 (32%) patients. The ECG showed P-mitrale in 32 (64%), atrial fibrillation in 14 (28%) and atrial flutter in 2 (4%) cases. Echocardiography revealed thickening of mitral valve leaflets in all patients, changes in subvalvular apparatus in 28 (56%) and calcification in mitral valve apparatus in 3 (6%) cases. Mitral valve area was &lt;1 cm2 in 33 (66%), 1.0 to 1.4 cm2 in 14 (28%) and e”1.5 cm2 in 1 (2%) patients. The left atrial size was 41 to 50 mm in 20 (40%) and &gt;50 mm in 10 (20%) cases. Two patients had left atrial thrombus. Evidence of pulmonary hypertension was found in 34 (68%) patients. Conclusion: Rheumatic MVD and the accompanying complications can be detected with an appreciable degree of accuracy by skillful clinical assessment and judicial use of simple investigations like roentgenography, electrocardiography and echocardiography which are available in many parts of our country at affordable costs. So every effort should be made to utilize these invaluable resources to tackle this public health problem more efficiently. Key Words: Rheumatic; Mitral valvular disease; Clinical. DOI: 10.3329/cardio.v3i1.6421Cardiovasc. j. 2010; 3(1): 11-21

The Murmurs of Mitral Regurgitation

Not all murmurs of mitral regurgitation are holosystolic. Occasionally, the patient with mitral reflux will demonstrate an early systolic murmur, a late systolic murmur or a mid-systolic murmur. Rarely, a systolic murmur is absent. We have also described a patient with silent mitral regurgitation and a short diastolic rumbling murmur.