Late Systolic Murmur Research Articles

All in the family: matrimonial mitral valve clicks.

Mitral valve clicks with or without late systolic murmurs were detected in genetically unrelated marital partners of 5 families. The first family represented 2 successive nonconsanguineous marital unions with 3 generations of mitral valve clicks. The second family included 1 natural and 2 adopted children with clinical and echographic evidence of mitral valve prolapse. The third family was comprised of asymptomatic parents, both with nonejection clicks and mitral valve prolapse, whose daughter presented 3 years previously with syncope, palpitations, and combined mitral and tricuspid valve prolapse. The fourth family had 3 members with auscultatory and ultrasonic manifestations of billowing mitral valve, whereas the fourth member had "silent mitral valve prolapse." The fifth family represented a mother with auscultatory and echographic evidence of mitral valve prolapse; her 14-year-old daughter had both mitral and tricuspid valve prolapse, whereas the son had a bicuspid aortic valve. Both children were products of a prior marriage, and her husband has symptomatic mitral valve prolapse. We conclude that matrimonial mitral valve prolapse probably reflects the purported (6--10%) prevalence of this disorder in the general population. The consequences of such marital union on progeny is currently unclear and warrants future investigation.

The Click-Murmur Syndrome

AUSCULTATORY sounds of a late systolic murmur, with or without a preceding nonejection click, have been generally recognized since the late 1950s to result from abnormal movement of the mitral valve apparatus during systole. Although the mitral valvular origin of these sounds was suspected before, it was only after left ventricular angiography showed the late systolic murmur to result from mitral insufficiency, which was secondary to the abnormal billowing of the mitral leaflets into the left atrium, that the true nature of these auscultatory findings was recognized. The patient with a nonejection click, with and without a systolic murmur, has been described in the literature under a wide variety of names (Table 1). With the demonstration by echocardiography of the abnormal posterior systolic movement of both aortic and mural leaflets of the mitral valve, it has been possible to identify noninvasively the patients with an abnormally prolapsing mitral valve, even

Cardiogenic Shock Associated With Disopyramide Phosphate

To the Editor.— We would like to support the article by Story and colleagues (242:654, 1979) concerning cardiogenic shock and disopyramide phosphate. We recently had a similar case in one of our patients. Report of a Case.— A 63-year-old man was taking digoxin and had a previous history of myocardial infarction. His condition was evaluated for dyspnea and fatigue. Physical examination demonstrated summation gallops and a grade 2 to 3 late systolic murmur. The chest roentgenogram showed cardiomegaly and a mild degree of interstitial prominence. The resting ECG showed sinus tachycardia, an intravenous conduction delay of the left bundle-branch in type, and frequent multifocal premature ventricular contractions. In the presence of high-grade ventricular arrhythmia with R-on-T phenomena and multifocal ectopic activity, the patient began receiving disopyramide phosphate, 100 mg orally three times a day. Approximately 48 hours later, the patient had extreme shortness of breath, came into the emergency room,

Mitral valve prolapse: etiology, diagnosis, and management.

Mitral valve prolapse is a common cardiac anomaly in which diagnosis is generally made by auscultation. In a typical case, a midsystolic click followed by a late systolic murmur is heard, although this pattern can vary. Selected pharmacologic agents (vasopressors and vasodilators) may be useful in diagnosis, and echocardiography can be helpful in cases without auscultatory signs. In the majority of cases, mitral valve prolapse is benign and no specific treatment is needed except reassurance and perhaps endocarditis prophylaxis. Patients with chest pain and symptomatic arrhythmias may benefit from propranolol, those with ventricular tachycardia should receive antiarrhythmic therapy, and those with abnormal resting ECGs or frequent ventricular premature beats should be further tested because of increased risk of sudden death or possibility of associated ischemic heart disease.

Subxiphoid Two-Dimensional Echocardiographic Detection of Tricuspid Valve Prolapse

A patient with click and late systolic murmur syndrome originating in the right side of the heart is described. Prolapse of the anterior tricuspid leaflet was demonstrated by subxiphoid two-dimensional echocardiography alone. Neither of the mitral leaflets showed any evidence of prolapse on the echocardiogram. The prolapsed anterior tricuspid leaflet and mild regurgitation were confirmed by right heart cineangiogram.

Mitral Valve Prolapse

The syndrome of the mitral valve prolapse is being recognized more frequently in the pediatric age range. The presence of an apical midsystolic click and a late systolic murmur should suggest the diagnosis. When the diagnosis is made, a chest roentgenogram, an electrocardiogram, and an echocardiogram should be performed as a baseline. Activity can be normal. Prophylactic antibiotics are essential before oral surgery. Periodic reexaminations with an electrocardiogram, and, if indicated, a dynamic Holter tracing should be performed. Long-term prognosis remains uncertain, and some caution should be exercised in predicting the future. Because of the known familial incidence of the syndrome, echocardiograms on members of the family should be done and genetic counseling offered to the affected individuals.

Mitral Valve Prolapse

The syndrome of the mitral valve prolapse is being recognized more frequently in the pediatric age range. The presence of an apical midsystolic click and a late systolic murmur should suggest the diagnosis. When the diagnosis is made, a chest roentgenogram, an electrocardiogram, and an echocardiogram should be performed as a baseline. Activity can be normal. Prophylactic antibiotics are essential before oral surgery. Periodic reexaminations with an electrocardiogram, and, if indicated, a dynamic Holter tracing should be performed. Long-term prognosis remains uncertain, and some caution should be exercised in predicting the future. Because of the known familial incidence of the syndrome, echocardiograms on members of the family should be done and genetic counseling offered to the affected individuals.

A Prospective Study of Mitral Valvular Prolapse in Young Men

A cardiac history, a physical examination, an electrocardiogram, phonocardiograms in the supine and standing positions, and an M-mode echocardiogram were obtained in 100 randomly selected, presumably healthy, male medical students (mean age, 26 years). Four percent met standard echocardiographic criteria for mitral valvular prolapse. No midsystolic clicks or late systolic murmurs were appreciated in this group, and none complained of chest pain or palpitations. To elucidate further the clinical implication of the echocardiographic pattern of mitral valvular prolapse, 24-hour ambulatory ECGs, multistage exercise tests, and scintiscans of myocardial perfusion at rest and after exercise (using radioactive 13nitrogen-labelled ammonium) were obtained, with normal results. The absence of life-threatening arrhythmias and exercise-induced abnormalities in these four asymptomatic subjects without abnormal physical findings suggests that the echocardiographic pattern of mitral valvular prolapse in such individuals may represent a variant of normal which does not require extensive evaluation.

Prevalence of mitral valve prolapse in presumably healthy young men.

We determined the prevalence of mitral valve prolapse (MVP) in presumably healthy young men by studying 107 male house officers and medical students with cardiac auscultation in the supine, sitting and standing positions. Echocardiograms were performed at rest in the supine position before and after amyl nitrite inhalation and were obtainable in 101 subjects. Eleven of the 101 subjects had abnormal findings on auscultation: four had an isolated click and seven had a click and late systolic murmur. Correlation of the independent auscultatory and echocardiographic data in the 101 subjects showed that all seven of the subjects with a click and a murmur had echocardiographic evidence of prolapse. None of the 90 subjects with normal auscultation or the four with an isolated click had an abnormal echocardiogram. All seven subjects with MVP had thoracic skeletal abnormalities, but only one was symptomatic. These data suggest that the prevalence of MVP in healthy young males is similar to the reported 6-10% prevalence in healthy young females.

MITRAL VALVE PROLAPSE

Mitral valve prolapse is a relatively common condition in the general population. The syndrome appears more common in females, and is often associated with a family history. Patients may be asymptomatic or may present with a variety of symptoms ranging from mild chest aches and anxiety to severe angina-like chest pain, palpitations and dizziness. The common auscultatory features include mid-systolic clicks and a late systolic murmur, either alone or in combination. The wide spectrum of symptoms and signs may be explained by ventriculovalvular disproportion, where either the ventricle is too small for the valve, or the valve is too large for the ventricle. The long-term prognosis is very good; severe mitral regurgitation can occasionally develop, but both sudden death and bacterial endocarditis are rare. No treatment is required for asymptomatic patients, beyond antibiotic cover for dental procedures and surgery.

Origin of the basal systolic murmurs in mitral stenosis. A study with intracardiac phonocardiography

In order to study the origin of the basal systolic murmurs in mitral stenosis, left and right heart catheterization was performed in 18 patients with mitral stenosis using intracardiac phonocardiography. Our data revealed that the basal systolic murmurs originated in the aorta, the pulmonary artery, and the outflow tract of the right ventricle. In 14 cases, we noted the maximal ejection systolic murmur in the aorta near the aortic valve. However, in two cases, there was a loud systolic murmur in the pulmonary artery. These murmurs occurred in early to mid-systole and were crescendo-decrescendo in configuration. The pitch of the murmur ranged from low to medium frequency in the majority of cases. They are produced by the turbulence of blood flow in the aorta and the pulmonary artery. A late systolic murmur was also recorded in the outflow tract of the right ventricle in two patients. This is thought to occur due to functional or relative infundibular stenosis of the right ventricle. It differs in location and timing from those in the aorta and the pulmonary artery. The outflow tract of the right ventricle is regarded as the third origin of the basal systolic murmur in mitral stenosis.

Four year follow-up of Black schoolchildren with non-ejection systolic clicks and mitral systolic murmurs

In 1972 we conducted a survey of 12,050 urban Black schoolchildren and detected 168 (prevalence rate of 14 per 1,000) with a non-ejection systolic click (NESC), a late systolic murmur, or both. The etiology of the mitral valve abnormality was unknown but we considered that a significant proportion might have early rheumatic heart disease. The ausculatory features four years later of 139 of the original 168 subjects as well as those of 139 age- and sex-matched controls are presented in this study. No cardiac abnormality was detected in as many as 55 of the subjects. Five children now had pansystolic murmurs but the mitral regurgitation was assessed as mild in four. Twenty-five (17.9 per cent) of the controls, 23 of whom had NESCs, had auscultatory features compatible with mitral valve prolapse. These findings do not support our earlier suggestion that a large number of the 1972 subjects have mild rheumatic heart disease. The results are in accord with other studies which have indicated that auscultatory features compatible with mitral valve prolapse are common in “normals” and also that the prognosis of the specific “billowing mitral leaflet syndrome” is generally benign.

Effects of gravitational stresses on mitral valve prolapse. I. Changes in auscultatory findings produced by progressive passive head-up tilt.

The effects of passive head-up tilt on systolic time intervals were assessed in 18 patients with mitral valve prolapse. In addition to causing prolongation of the pre-ejection period and shortening of left ventricular ejection time, this circulatory stress led to progressive shortening of the Q to click interval. In 1 patient, a systolic click became audible which had not been heard in the supine posture. In 7 patients the click disappeared during head-up tilt, usually at 60 degrees or 90 degrees. In 2 patients without a murmur while supine, a mid-late systolic murmur appeared with tilt; 1 of these 2 as well as another patient who had a soft late systolic murmur while supine developed loud systolic whoops at greater angles of tile. The correlations between Q to click interval and aortic valve opening to click interval, and both the angle and the sine of the angle of tilt were highly significant.

Ultrasono-cardiographic diagnosis of the prolapsed mitral valve.

The characteristic ultrasono-cardiographic (UCG) findings of prolapsed mitral valve were studied in 9 cases by means of ultrasonocardiotomography (UCT). The changes in degree and shape of the prolapsed valve were examined and the leaflet involved was identified. Of the 9 cases, 5 had prolapse of anterior, 3 had that of posterior leaflet and 1 had both. In all cases with midsystolic click and late systolic murmur or pansystolic murmur with late systolic accentuation, the prolapse of anterior leaflet was observed on UCT, and though UCG disclosed midsystolic buckling it was difficult to determine the exact timing of the prolapse by UCG alone. In the cases with rheumatic mitral regurgitation, the prolapse of posterior leaflet and the ballooning of anterior leaflet could easily be found on UCT, but the detection of the above-mentioned 2 findings was difficult by UCG alone. Three of the 9 cases were found to have prolapse of posterior leaflet by left ventriculography, whereas these 3 had prolapse of anterior leaflet on UCT. Hence, the diagnosis of prolapsed mitral valve based on the cineangiography may require re-evaluation.

Mitral valve prolapse and infective endocarditis

This study describes the clinical features, laboratory findings and follow-up of 25 patients with bacterial endocarditis found to have mitral valve prolapse. Mitral valve prolapse was confirmed by echocardiography (17 patients), angiocardiography (nine patients) or by pathologic study of the mitral valve (10 patients). There were no associated cardiac lesions except for atrial septal defect in two patients. Physical examination at the time of endocarditis revealed holosystolic murmurs in 22 patients (five with late systolic crescendo) and mid-systolic click with late systolic murmur in three. Six patients with holosystolic murmurs were known to have had only late systolic murmurs prior to endocarditis. Causative organisms included alpha Streptococcus in 12 patients, Strep. group D in five, Staphylococcal aureus in four, and Strep. hemolyticus, Bacteroides, Hemophilus aphrophilus, Strep. pneumoniae and Moraxella in one patient each. Nine patients, six of whom had ruptured chordae tendineae, subsequently required mitral valve replacement. In two additional patients congestive heart failure developed which responded to medical therapy. Cerebral embolism occurred in five patients. Three patients had second episodes of endocarditis. One death occurred from cerebral hemorrhage secondary to thrombocytopenia. Ten of these 25 patients were found in a review of 87 consecutive patients with infective endocarditis seen over a five-year period at Stanford University Hospital. Twenty-eight of the 87 had isolated mitral regurgitation, suggesting that mitral valve prolapse is the basis for about one third (10 of 28) of the instances of bacterial endocarditis associated with isolated mitral regurgitation in our hospital. The high incidence of holosystolic murmurs suggests either that endocarditis leads to more severe mitral regurgitation and ruptured chordae in some instances or that patients with holosystolic murmurs are more susceptible to bacterial endocarditis than those with less striking auscultatory findings.

Angiographic diagnosis of mitral valve prolapse: Correlation with echocardiography

Mitral valve prolapse is characterized clinically by a nonejection systolic click and a late systolic murmur and angiographically by end-systolic bulging of one or both mitral leaflets into the left atrium. If one accepts the end-systolic configuration of the left ventriculogram as the diagnostic standard, recent studies suggest that mitral valve prolapse may frequently be associated with certain other forms of cardiac disease. To determine the incidence of this finding in patients unselected for their primary cardiac diagnosis, the left ventricular angiograms from 336 consecutive patients (223 men and 133 women) were analyzed. Six patients had the clinical diagnosis of click-murmur syndrome, and all six had angiographic prolapse. Leaflet bulging was also present in 52 of 131 patients with ischemic heart disease (40 percent), 27 of 84 with rheumatic valve disease (32 percent), 3 of 19 with cardiomyopathy (16 percent), 5 of 12 with congenital heart disease (42 percent) and 50 of 84 with chest pain and no significant coronary artery disease (60 percent). Technically satisfactory echocardiograms were available from 140 of these patients; mitral valve prolapse was evident in the echocardiograms of 9 (6.4 percent), including 6 with the click-murmur syndrome. Thus, angiographie mitral valve prolapse was present in 43 percent of cases and occurred without predilection for any diagnostic subgroup. Echocardiographic prolapse was less common but correlated well with the presence of the click-murmur syndrome. Some end-systolic bulging of posterior mitral leaflet scallops therefore is a common angiographic finding that should probably not be considered pathologic in the absence of other features of the click-murmur syndrome.

Systolic honks in young children

Three children with-loud systolic honks were studied noninvasively with phonocardiography and echocardiography. It was shown that the precordial honk, like the late systolic mitral murmur and the clicking apical systolic sound, is part of a continuum of auscultatory sounds that result from a defect of mitral valve support and are classified under the general heading of mitral valve prolapse syndrome. Prolapse of one or both of the mitral valve leaflets is believed to cause the characteristic auscultatory findings of click, murmur or honk. The timing of these sounds in systole varies with different physiologic or pharmacologic maneuvers. Variations in the onset of prolapse are associated with changes in left ventricular end-diastolic dimensions.

Long-term prognosis of mitral-valve prolapse.

We examined the natural history of mitral-valve prolapse in 53 patients who had had a midsystolic click or late systolic murmur (or both) documented phonocardiographically a mean of 13.7 years earlier. Thirty-eight patients were alive without serious complications, and seven had died of unrelated causes. In two patients prolapse was implicated in the cause of death. Other complications were ventricular fibrillation in one patient and bacterial endocarditis in three. Progressive mitral regurgitation developed in five patients, requiring valve replacement in two. These complications occurred in a total of eight patients (15 per cent), and were significantly (P = 0.15) associated with a late systolic murmur rather than an isolated midsystolic click. Thus it appears that the diagnosis of mitral-valve prolapse should not be regarded as ominous; however, patients in whom this diagnosis is associated with a late systolic murmur should be followed carefully.

Palpitations and Late Systolic Murmur in a Young Man

A 25-year-old man was seen because of palpitations. Physical examination disclosed a slender man with a crescendo late systolic apical murmur. The ECG was normal, except for occasional premature ventricular beats. His echocardiogram and a superimposed apex phonocardiogram are shown in the Figure below. What is your diagnosis? <h3>Diagnosis.—Mitral Valve Prolapse</h3> Sharp midsystolic sounds that Gallavardin (1913) believed were due to pleuropericardial adhesions were recognized as originating in the mitral apparatus by Griffith in 1892¹and again by Reid²in 1961. Five years later, Barlow and Bosman angiographically demonstrated mitral prolapse.³Echocardiographic findings were described by Shah and Gramiak⁴in 1970 and by Dillon et al⁵and Kerber et al⁶in 1971. Careful physical examination has disclosed typical findings of mitral prolapse in 6%⁷to 17%⁸of presumably healthy young women. There often are associated skeletal deformities, such as pectus

Echocardiogram of the month: palpitations and late systolic murmur in a young man

Echocardiogram of the month: palpitations and late systolic murmur in a young man