Opening Snap Research Articles

Extent of mitral calcific deposits determined by cineangiography in mitral stenosis and their effect on valve motion, hemodynamics and clinical signs

The relation between the degree of leaflet calcium in a stenotic mitral valve and several parameters of valve mobility, hemodynamics and clinical signs was determined in 105 patients with relatively pure mitral stenosis (MS). The amount of mitral valve calcific deposits was determined by grading cineangiograms. Compared to 71 patients with no or minimal valvular calcium, the 23 patients with heavy valve leaflet calcium were significantly older, more likely to be men and more likely to be in atrial fibrillation. These patients also had a significant reduction of valve mobility in that their M-mode measurements of valve excursion and rate of valve opening were significantly reduced compared to those of patients without heavy valvular calcium. Two-dimensional echocardiograms also documented a significant reduction in valve mobility and progressive restriction in doming of the anterior mitral leaflet as the level of calcium increased. The prevalence of an opening snap was significantly decreased in patients with heavy vs no or light valvular calcium, and patients without an opening snap had reduced valve mobility. However, a considerable number of patients with moderate to heavy valve calcium retained an opening snap.

Monoclonal antibodies in the diagnosis of renal disease: A preliminary report

A 74-year-old, previously healthy woman sought medical advice because of multiple erythematous pustular skin lesions, which had started on her hands and had progressed to her arms, back, abdomen, chest, and legs. The patient had no history of renal dysfunction, renal stones, diabetes mellitus, hypertension, urinary tract infections, or analgesic abuse. She was taking no medications. She had no history of documented hypotension, fever, or chills. The patient denied sore throat, swollen glands, chest pain, shortness of breath, arthritis, and seizures. She had had rheumatic fever when she was a child. Physical examination on admission revealed a blood pressure of 140/ 70 mm Hg; pulse, 80 beats per minute and regular; temperature, 98.6F, and an estimated central venous pressure of 8 cm H20. Numerous pustular lesions, most of which were crusted, were noted on the hands, arms, trunk, buttocks, and soles. No adenopathy was present. The chest was clear. Cardiac examination disclosed an S4, with no S3 or pericardial friction rub. A grade TI/VI blowing diastolic murmur was present at the left sternal border. No opening snap was heard. The abdomen was soft and nontender without evidence of guarding or rebound. The kidneys, liver, and spleen were not palpable. Moderate left costovertebral angle tenderness was present. Rectal and pelvic examinations were unremarkable, The stool was guaiac negative. There was no peripheral edema and no evidence of active synovitis. The patient was alert, oriented, and had full range of motion in a11 extremities; she had no localizing neurologic abnormalities. All reflexes were equal and reactive throughout, with bilateral plantar responses. Laboratory data on admission showed a hematocrit of 39.4%, a white blood cell count of 17,300/mm3 with a normal thiferential, and a sedimentation rate of 90 mm/hr. Sodium was 138 mEq/liter; potassium,

Tricuspid stenosis. Atrial systolic murmur, tricuspid opening snap, and right atrial pressure pulse

Observations on the atrial systolic murmur, the tricuspid opening snap, and the right atrial pressure pulse of tricuspid stenosis are presented, based on catheter manometer intracardiac sound and pressure recordings in five patients with hemodynamically significant tricuspid stenosis. The manometer-recorded right atrial pressure pulse of tricuspid stenosis differed from the normal, with (1) elevation of right atrial pressure, (2) different morphologic features (tall, spiky A wave complete before C; small V wave with an interruption, the tricuspid opening snap notch at termination of the gradual Y descent; a diastolic plateau, the relatively flat diastolic segment of the right atrial pressure pulse following the tricuspid opening snap notch prior to the next A wave), and (3) the relative lack of right atrial pressure and right atrial pressure pulse response with normal respiration. The atrial systolic murmur, recorded in the right ventricular inflow tract, was complete by S 1; the crescendo-decrescendo atrial systolic murmur configuration paralleled the right ventricular-right atrial diastolic pressure gradient at the time of the atrial A wave. The right atrial contraction-relaxation process, as reflected by the right atrial A wave ascent and descent, was complete at the onset of ventricular systole with P-R intervals of 170 to 200 msec. Thus, the timing and configuration of the atrial systolic murmur reflected the timing and completion of the right atrial contraction-relaxation process prior to the onset of right ventricular systole and the configuration of the tricuspid diastolic pressure gradient. The tricuspid opening snap was recorded in the right ventricular inflow tract and occurred at the time of a notch at the termination of the Y descent of the right atrial pressure pulse V wave, while right atrial pressure exceeded right ventricular pressure. The sound-pressure events were consistent with angiographic and echocardiographic studies, which showed doming or ballooning of the mobile, fused, stenotic tricuspid valve into the right ventricle during the Y descent of the right atrial pressure pulse. The tricuspid opening snap occurred at the time of the termination of the diastolic movement of the fused tricuspid unit into the right ventricle. These observations are presented within the framework of previous studies in order to trace the development of medical ideas about the pathophysiologic basis for the sound and pressure events of tricuspid stenosis.

The noninvasive assessment of pulmonary capillary wedge pressure in mitral regurgitation

The interval between the aortic closure sound and the mitral opening snap (A 2-OS) has been shown to have a significant inverse correlation with pulmonary capillary wedge pressure (PCW) in mitral stenosis. The present study critically examines the relationship of several noninvasively determined diastolic intervals to PCW in patients with relatively pure mitral regurgitation (MR). Fifty-seven patients with MR of diverse etiologies were studied with echocardiograms and phonocardiograms in addition to right and left heart catheterization. Noninvasive determination of the time intervals of aortic closure sound to mitral valve opening (A 2-MO), mitral D point to E point (D-E), aortic closure sound to mitral E point (A 2-E), the interval from the onset of the QRS to mitral closure (Q-C), and the ratio Q-C A 2-E were compared to invasive measurements of mean PCW, the height of the V wave of PCW (PCW-V), and the ratio of PCW-V to left ventricular (LV) peak systolic pressure ( PCW-V LV ). Correlation between each of the five noninvasive intervals and each of the three invasive pressure measurements was then determined. Of the noninvasive intervals studied, A 2-MO had the best inverse correlation with all measures of PCW. All 18 patients having a short A 2-MO (<40 msec) had a PCW-V of ≥40 mm Hg and all seven patients having a long A 2-MO (>85 msec) had a PCW-V of <22 mm Hg. A 2-E also had a strong inverse correlation with PCW. No significant relationship was found to exist between Q-C and PCW, in contrast to what has been observed in mitral stenosis. As a result, Q-C A 2-E did not improve the correlation between A 2-E and any measure of PCW. The D-E interval had no correlation with any measure of PCW. Hemodynamic explanations for these observations are discussed.

Sudden death in primary mitral valve prolapse

Sudden unexpected death is a recognized complication of mitral valve prolapse (MVP), but well-documented cases are rare and either clinical details or necropsy findings are absent or scanty. One of our patients, a young woman with MVP who had been fully investigated’e2 and followed since childhood, died suddenly at the age of 24 years, and we were able to obtain detailed pathologic findings. At the age of 8 years a grade 216 late systolic murmur and a nonejection click were heard (see Fig. 10 of Ref. 1). Occasional ectopic beats were present, but she was asymptomatic. Chest x-ray examination was normal. The ECG (see Fig. 11 of Ref. 1) showed slight ST segment elevation with T wave inversion in leads 2, 3, and AVF. Left ventricular cineangiography (see Fig. 12 of Ref. 1) demonstrated mild mitral regurgitation and marked prolapse of the posterior leaflet. Her father had an isolated nonejection click. A diagnosis of MVP on a familial basis was made, and no treatment was given. She attended the clinic at B-month intervals and remained asymptomatic. At 13 years of age numerous multifocal ventricular premature contractions were recorded after a strenuous exercise test (See Fig. 2, a of Ref. 2). On propranolol, 80 mg daily, and diphenylhydantoin, 300 mg daily, the arrhythmia was suppressed. She was thereafter assessed at yearly intervals

Incidence of Mitral Valve Prolapse in Adolescent Scoliosis and Thoracic Hypokyphosis

Seventy-four patients with adolescent scoliosis underwent cardiac examination and M-mode echocardiography to detect the presence of mitral valve prolapse (MVP). Twenty-one (28%) had echocardiographic evidence of MVP, whereas 18 had auscultatory findings of a nonejection click or late systolic murmur. A subset of 41 patients had a family history of scoliosis and 37% had MVP. The incidence of MVP increased to 41% when a first degree relative, such as a sibling, parent, or offspring, had scoliosis. Thirty-six patients with scoliosis had additional thoracic hypokyphosis (straight back) and 13 (36%) had MVP. The incidence of MVP was 48% when the scoliosis and hypokyphosis were hereditary and increased to 53% when a familial history of skeletal abnormality was present. This study indicates a high incidence of MVP in patients with scoliosis and hypokyphosis, especially when the cardiac and skeletal systems may be affected by a generalized soft-tissue defect.

Does mitral valve prolapse cause nonspecific symptoms?

I studied the prevalence and symptoms of idiopathic mitral valve prolapse by ausculation in 972 consecutive patients in an adult general medical population. Forty-five patients (4.6%) had idiopathic mitral valve prolapse defined by a nonejection click with or without a late systolic murmur. The prevalence was not significantly different in men and women. The mean age (49.9 yr) and age distribution of patients with prolapse were similar to those of patients without prolapse (47.7 yr). The prevalence of dizziness (4.1% vs. 1.5%), fatigue (4.4.% vs. 2.6%), and palpitations (4.4% vs. 1.3%), was not significantly greater in patients with or without prolapse. Atypical chest pain (13% vs. 4.3%) and chronic anxiety (8.8% vs. 2.9%) were more frequent (< 0.05) in the patients with prolapse than in those without prolapse. Of the patients with prolapse, 29 were healthy without clinically identifiable diseases while 16 had medical diseases. In the group without prolapse, 184 patients were healthy and 707 had other diseases. When patients with isolated prolapse without other associated diseases were compared to healthy patients without prolapse, the prevalence of atypical chest pain (17.4% vs. 17.2%) and chronic anxiety (7.1% vs. 10.3%) were not significantly different. When patients with prolapse and other diseases were compared to patients without prolapse and other diseases, the prevalence of atypical chest pain (6.2% vs. 1.1%) and chronic anxiety (6.2% vs. 1.7%) was again not significantly different. Thirty-two patients without prolapse were suspected but not confirmed of having disease and were not included in this analysis. The results would have been unaltered by their inclusion in the diseased group without prolapse. Thus, the prevalence of commonly attributed nonspecific symptoms in patients with idiopathic mitral valve prolapse is not significantly different between healthy patients without or with prolapse without other diseases. These findings suggest a coincidence of a common syndrome with frequently occurring symptoms, rather than cause and effect.

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

Cross-Sectional Echocardiographic Observations on the Mechanism of Preservation of the Opening Snap in Calcific Mitral Stenosis

Cross-sectional echocardiography (CSE) was performed on 19 patients with mitral stenosis (MS). Nine patients (group 1) had little or no mitral valve (MV) calcification; ten patients (group 2) had heavy MV calcification. An opening snap was present in each of the patients in group 1. Of the group 2 patients, five (group 2A) had an opening snap and five (group 2B) did not. CSE in the long axis revealed in group 1 patients a mobile MV with sharp anterior arching of the anterior leaflet in early diastole; in group 2A, dense echoes suggestive of calcification were noted near the tip of the MV, while the body of the leaflet was relatively thin and it arched anteriorly sharply in early diastole; and in group 2B, dense echoes were noted at the tip and body of the MV with reduction in mobility of the valve, and the sharp anterior arching of the anterior leaflet in early diastole was absent. Preservation of the OS in calcific MS depends on the distribution of calcification. Heavy calcification confined to the tip of the MV allows the anterior leaflet to arch anteriorly in early diastole, allowing preservation of the OS, whereas heavy calcification of the tip and body of the MV reduces the pliability of the valve with consequent disappearance of the OS.

Clicks due to Swan-Ganz Catheter

Nonejection systolic and diastolic clicks appeared when a Swan-Ganz catheter was positioned in the proximal portion of the right pulmonary artery. The clicks disappeared on inflation of the catheter's balloon. Initial impressions included secondary prolapse of the mitral leaflets, an accentuated third heart sound, and the exposure of an occult opening snap. These high-frequency sounds are thought to be generated by the forward and backward movement of the catheter against either the proximal portion of the pulmonary artery or the right ventricular outflow tract or by a whipping action of the catheter itself.

Noninvasive study of early diastole in mitral stenosis.

Cardiac events of early diastole were studied in 50 normal subjects and 46 patients with mitral stenosis (MS) by simultaneous recordings of the mitral valve echogram (MVE), phonocardiogram, and apexcardiogram (ACG). Left ventricular isovolumic relaxation time (IRT), measured between A2 and onset of the MVE opening motion, had almost the same values in normals 54 +/- 7 msec, and MS 51 +/- 16 msec. The interval between A2 and the ACG "O" point was approximately double that of IRT: 99 +/- 11 msec in normal subjects, 109 +/- 20 msec in MS. The normal MVE opening motion had a velocity 293 +/- 76 mm/sec and duration 45 +/- 6 msec, values significantly different (P less than 0.001) from 536 +/- 271 mm/sec, 23 +/- 7.5 msec found in MS patients. In atrial fibrillation the length of the cardiac cycle did not affect A2-O interval or mitral valve opening movement duration; however cycle length was clearly related to isovolumic relaxation time. This resulted in a variation in the interval between completion of the mitral valve opening (opening snap) and O point. This interval was longer after a short diastole and vice versa.

“Mitral stenosis” secondary to combined “massive” mitral anular calcific deposits and small, hypertrophied left ventricles: Hemodynamic documentation in four patients

Certain observations are described in four elderly women with massive mitral anular calcific deposits, small thick-walled left ventricles and diastolic gradients between pulmonary artery wedge position (or left atrium) and left ventricle. All four patients had some degree of obstruction to left ventricular outflow. Examination at necropsy (two patients) or at operation (one patient) disclosed only focal fibrous thickening of the mitral leaflets without commissural or chordal fusion. By auscultation, none had mitral opening snaps, only two had loud first heart sounds and only one had a mitral diastolic rumble. Hemodynamic documentation of a diastolic gradient between pulmonary artery wedge position (or left atrium) and left ventricle in the presence of massive mitral anular calcific deposits and in the absence of diffuse disease of the mitral leaflets has not been demonstrated previously. The diastolic gradients are considered to result from the combination of the large mitral anular calcific deposits and the small, thick-walled, noncompliant left ventricles.

Diastolic Rumbles in Normally Functioning Porcine Mitral Valves

Fourteen of 22 patients (64%) with normally functioning porcine prosthetic valves in the mitral position had apical diastolic rumbles on phonocardiogram and by auscultation. Six (27%) had opening snaps. Factors necessary for the production of a diastolic rumble appear to include central flow, a flexible stent, and the presence of biologic material. Clinicians should be aware that diastolic murmurs and snaps occur in the normally functioning porcine valve.

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.

Tricuspid Opening Snap in Tricuspid Insufficiency

An opening snap is most frequently heard in the presence of acquired mitral or tricuspid stenosis. A normally mobile atrioventricular valve is capable of producing an opening snap when excessive blood flows across it.1-4 This would explain the occasional finding of a tricuspid opening snap in atrial septal defect5,6 and Ebstein's anomaly.7 The purpose of this report is to describe this finding in two patients with severe tricuspid insufficiency secondary to pulmonary hypertension.

Postexercise systolic time intervals in the midsystolic click syndrome.

Postexercise systolic time intervals (STI) were measured in ten patients (PMV group) with auscultatory evidence of the midsystolic click syndrome (i.e. one or more systolic nonejection clicks alone or in association with the late systolic murmur), and compared to eight age-matched volunteers (control group) with no evidence of heart disease. Following measurement of supine STIs, the subjects pedalled an upright bicycle ergometer at progressive work loads until a target heart rate (HR) representing 85% of the age-adjusted maximum was attained, or an abnormal end point was noted. Immediately postexercise, a repeat measurement of STIs, was obtained. A shortened or unchanged postexercise left ventricular ejection time corrected for HR (deltaLVETc) and a marked shortening of total electromechanical systole after exercise (deltaQS2c) constituted a normal STI response to stress testing and was noted in all control subjects. All of the PMV group exhibited evidence of left ventricular dysfunction characterized by a prolonged deltaLVETc. It is concluded that an abnormal STI response to exercise consistent with left ventricular dysfunction can be demonstrated in patients with prolapse of the mitral valve by the response of the STI.

Non-ejection systolic clicks and mitral systolic murmurs in black schoolchildren of Soweto, Johannesburg.

A survey was conducted on 12 050 Black schoolchildren, aged 2 to 18 years, in the South Western Townships of Johannesburg (Soweto), and the prevalence of non-ejection systolic clicks and late systolic murmurs was determined. One or both of these auscultatory findings were detected in 168 children, yielding a prevalence rate of 13-99 per 1000 in the school population. A female preponderance of 1-9:1 was present and there was a strong linear increase in prevalence with age, with a peak rate of 29-41 per 1000 in 17-year-old children. A non-ejection click was the only abnormal auscultatory finding in 123 children (73%) and a mitral systolic murmur in 8 (5%), whereas in 37 (22%) both these findings were present. Of the latter 37 children, the murmur was late systolic in 32; in 5 it was early systolic. Auscultation in different postures was important in the detection of both non-ejection clicks and mitral systolic murmurs. Experience in the detection of these auscultatory findings influenced the frequency with which they were heard. Electrocardiographic abnormalities compatible with those previously described in the billowing mitral leaflet syndrome were present in 11 of 158 children. The aetiology of these auscultatory findings in this community remains unknown. In the same survey, a high prevalence rate of rheumatic heart disease was recorded and the epidemiology of the non-ejection clicks and these mitral systolic murmurs showed similarties to that of rheumatic heart disease. Though the specific billowing mitral leaflet syndrome almost certainly accounts for some of these auscultatory findings, a significant proportion may have early rheumatic heart disease. Further elucidation of this problem is necessary.

Editorial: Mitral-valve prolapse: a clinical spectrum.

Definition of an association between non-ejection clicks and late systolic murmurs, and the observation that patients with these physical findings usually do not manifest clinically important cardi...

Prevalence of clinical mitral-valve prolapse in 1169 young women.

Eleven hundred and sixty-nine young women were prospectively examined for the presence of mitral-valve prolapse as manifested by midsystolic non-ejection click or late systolic murmur (or both). Of the 1169 women 74 (6.3%) had physical findings consistent with mitral-valve prolapse. Sixty-eight of the 74 (92%) had midsystolic non-ejection click, and in 57 the click was accompanied by a late systolic murmur. In six (8%) only a late systolic murmur was heard. Echocardiography on all patients with clinical diagnosis of mitral-valve prolapse showed patterns of prolapse in 60 of 74 (81%). Fourteen (19%) had negative echocardiograms. We conclude that mitral-valve prolapse is clinically present in approximately 6.3% of otherwise healthy young women.

Mitral valve prolapse.

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.