Mitral valve prolapse and coronary artery disease. Clinical, hemodynamic, and angiographic correlations.

Among 95 patients with angina pectoris and angiographically documented coronary artery disease (CAD), prolapse of the scallops of the posterior leaflet of the mitral valve (PLMV) was noted in 30 patients. Left ventriculograms in the right anterior oblique (RAO) projection revealed isolated prolapse of the posteromedial commissural scallop (PMCS) in 12 patients and the anterolateral commissural scallop (ALCS) in two patients. Seven patients had prolapse of both PMCS and ALCS, three had prolapse of the PMCS and middle scallop (MS), and six had prolapse of all three scallops of the PLMV. Left ventricular dilatation with increase trabeculations was observed in 19 patients. Contractility determined in a quantitative fashion by segmental motion analysis was markedly impaired in 29 patients. None of the patients had angiographic evidence of mitral insufficiency. Left ventricular dysfunction was documented in 28 patients by either elevated left ventricular end-diastolic pressure (LVEDP), low cardiac index (CI) or decreased ejection fraction (EF). In two patients in whom left ventricular contractility improved after aortocoronary by pass, previously prolapsed scallops could not be identified in the postoperative ventriculogram. Prolapsed PLMV is a frequent angiographic finding in patients with angiographically observed CAD. Impaired contractility of the ventricular myocardium and papillary muscles, left ventricular dilatation, and hypertrophy appear to play a significant role in the pathogenesis of this abnormality through distortion of the directional axis of the papillary muscles, asynergic contraction of the related free wall of the left ventricle, and changes in the normal spatial alignment necessary for mitral valve closure. The syndrome of papillary muscle dysfunction in patients with coronary artery disease represents a wider clinical spectrom than previously described.     

Mitral valve prolapse in patients with pure rheumatic mitral stenosis: an angiographic study

Of 122 adult patients suspected of having rheumatic mitral stenosis, 112 fulfilled the hemodynamic and angiographic criteria for pure, isolated mitral stenosis. There were 88 females and 24 males with an age range of 16 to 60 years. The left ventriculograms (30 degrees right anterior oblique) were subjectively assessed for gross bulging of the mitral valve leaflets beyond the mitral fulcrum into the left atrium during a beat with maximal opacification. Seventeen percent of cases had typical evidence of mitral valve prolapse, which is much higher than the 3% to 5% rate reported for the general population. This phenomenon was independent of the patients' age, sex, hemodynamic findings, and/or their underlying cardiac rhythm, thus implying the direct role of rheumatic mitral stenosis in the genesis of secondary mitral valve prolapse.     

Value of acceleration flows and regurgitant jet direction by color Doppler flow mapping in the evaluation of mitral valve prolapse

To clarify the role of color Doppler echocardiography in the evaluation of mitral valve prolapse, we studied 49 consecutive patients in whom the sites of mitral valve prolapse were confirmed at the time of operation. The study group consisted of 22 patients with anterior leaflet prolapse, 24 patients with posterior leaflet prolapse, and three patients with multiple scallop prolapse (one patient with both anterior leaflet and middle scallop prolapse, and two patients with both medial and lateral scallop prolapse). Two-dimensional echocardiographic diagnosis of anterior leaflet prolapse was correct in all patients. The diagnosis of posterior leaflet prolapse by two-dimensional echocardiography, however, was mistaken as anterior leaflet prolapse in 16 (13 patients with medial scallop prolapse and three patients with lateral scallop prolapse) of the 24 patients according to current diagnostic criteria for mitral valve prolapse. Eight patients with middle scallop prolapse were diagnosed correctly by two-dimensional echocardiography. Acceleration flows in the left ventricle were observed by color Doppler echocardiography in all 49 patients. The sites of acceleration flows detected by color Doppler echocardiography coincided with those of prolapse confirmed in all at the time of operation. There was a significant correlation between the maximum area of acceleration flow signals and severity of mitral regurgitation estimated by angiography. In the 13 patients with medial scallop prolapse and the three patients with lateral scallop prolapse, a regurgitant jet originated from a bulged portion of the posterior leaflet and was directed toward the opposite left atrial cavity to the bulged portion by short-axis images of color Doppler echocardiography.(ABSTRACT TRUNCATED AT 250 WORDS)     

Insensitivity of echocardiography in detecting mitral valve prolapse in older patients with chest pain

Although echocardiography has proved useful in detecting mitral valve prolapse, its limitations have not yet been adequately defined. This study was designed to evaluate the prevalence of false negative echocardiograms in patients with angiographically proved mitral valve prolapse. Twelve patients, eight men and four women with a mean age of 47 years, were selected on the basis of the results of cardiac catheterization for chest pain. Each patient had moderate to severe mitral valve prolapse, confirmed angiographically by two observers, with no coronary artery disease or other detectable cardiac abnormalities. Clinically, a systolic click was detected in three patients, a mid-systolic murmur in five, an abnormal electrocardiogram in four and a positive maximal treadmill stress test in two of eight tested. Left ventricular angiograms exhibited anterior and posterior leaflet prolapse in five, and posterior leaflet prolapse alone in seven. High quality echocardiograms were obtained in 11 patients; one record of inadequate quality was excluded. The echocardiograms revealed mitral valve prolapse in only one case, and were “probably” negative in two, and clearly negative in eight. Although these results may reflect the well recognized variable clinical expression of this syndrome, they indicate that false negative echocardiograms are common in this selected older population of patients with angiographic mitral valve prolapse who present with chest pain and few other clinical features. Thus, caution must be exercised in the clinical interpretation of a single echocardiogram negative for mitral valve prolapse.     

Classification of the radiological morphology of the mitral valve. Differentiation between true and pseudoprolapse.

The morphology of the mitral valve apparatus was assessed on 100 normal left ventriculograms. Four distinct types of mitral valve were identified according to the position of the mitral fulcrum (the point of attachment of the leaflets to the annulus) and the configuration of the adjacent left ventricular wall (left ventricular fornix) during diastole. Types I and II closely simulated prolapse of the mitral valve (pseudoprolapse) in the right anterior oblique projection during the ejection period. Measurements showed that contraction of the ventricle failed to reduce the diameter of the mitral valve annulus in 26 per cent of normal left ventricles.     

Angiographic diagnosis of posterior mitral valve leaflet prolapse

The left ventricular cineangiograms of 22 asymptomatic, apparently healthy male aviators without noninvasive (echocardiographic or auscultatory) evidence of mitral valve prolapse were reviewed and compared with those of 12 men with noninvasive evidence of mild mitral valve prolapse. The maximal protrusion of the posterior mitral valve leaflet superior and posterior to a line perpendicular to the long axis of the left ventricle at end-systole was measured from the right anterior oblique left ventricular cineangiogram by repeated observation of left ventricular inflow. The values were 7.5 +/- 1.6 mm in patients without mitral valve prolapse and 11.2 +/- 3.4 mm in patients with mitral valve prolapse (mean +/- 1 standard deviation). This measurement did not exceed 11 mm in any patient without prolapse. It is concluded that: 1) with meticulous attention to angiographic landmarks of the left ventricular inflow area, the limits of normal systolic posterior mitral leaflet motion can be defined; and 2) systolic motion outside these limits constitutes a quantitative criterion for the angiographic diagnosis of mitral valve prolapse.     

M mode and cross-sectional echocardiographic features of flail posterior mitral leaflets

Seventeen patients with accepted M mode echocardiographic criteria for flail mitral leaflet were studied. M mode echocardiograms revealed characteristic disordered mitral valve motion: (1) 16 (94 percent) had chaotic diastolic mitral motion; (2) 14 (82 percent) had systolic mitral flutter; (3) 14 (82 percent) had systolic left atrial echoes; and (4) 12 (71 percent) had systolic mitral valve prolapse. In 8 patients (47 percent) all four findings were present, with three findings present in 16 (35 percent) and two findings present in 13 (18 percent); none had fewer than two findings. Cross-sectional echocardiographic studies in 10 patients revealed a systolic whipping motion of the posterior mitral leaflet into the left atrium in all, abnormal systolic mitral coaptation in all and an abnormal mass of systolic left atrial echoes in 4. None of the first three M mode criteria were observed in 230 patients with uncomplicated “mid systolic click-late systolic murmur” syndrome; cross-sectional echocardiography in 30 of 230 patients revealed normal systolic mitral coaptation and no systolic whipping of the tip of the posterior mitral leaflet into the left atrium.     

Mitral valve prolapse in coronary artery disease.

Mitral valve motion, left ventricular segmental contraction and severity of arterial stenosis were analyzed in 92 patients with coronary artery disease and 28 patients with "atypical chest pain" and normal coronary arterio-rams. Mitral valve motion was evaluated for the presence or absence of leaflet prolapse. Segmental contraction was evaluated by calculating the percent shortening of six chords of the left ventricle measured from right anterior oblique ventriculograms. The severity of disease in each coronary vessel (left anterior descending, left circumflex and right coronary) was graded on a scale of 1 (0 to 30 percent stenosis) to 5 (complete occlusion). Mitral valve prolapse was not suspected clinically but observed angiographically in 15 of 92 patients with coronary artery disease and in 5 of 28 patients with normal coronary arteriograms. In nine patients with coronary artery disease, the prolapse was restricted to the posterior leaflet, in five it was in both the anterior and the posterior leaflets and in one patient in the anterior leaflet only. Mitral regurgitation was noted in seven patients with coronary artery disease; it was mild in six and moderate in one. Among the patients with coronary artery disease, 12 of the 15 (80 percent) with mitral valve prolapse had left ventricular asynergy compared with 63 of the 77 (82 percent) without valve prolapse. The mean scores for severity of disease in the left anterior descending, circumflex and right coronary arteries were, respectively, 4.2, 2.5 and 3.2 in the patients with valve prolapse and 4.2, 2.2 and 3.5 in those without prolapse. In summary, there was no significant correlation between mitral valve prolapse and distribution of coronary arterial obstructions or abnormal patterns of left ventricular segmental contraction. There was a high frequency of mitral valve prolapse in patients with severe coronary artery disease and in those with normal coronary arteriograms and atypical chest pain.     

Mitral valve prolapse in patients with coronary artery disease. Echocardiographic-angiographic correlation.

Echocardiography was performed in 25 consecutive patients with angina pectoris and angiographically demonstrable coronary artery disease. Left ventricular echograms detected late or pansystolic mitral valve bowing suggesting of mitral valve proplapse in 6/25 (24%). Left ventricular angiography showed prolapse of the posterior mitral leaflet in 15/25 (60%), including 5 detected by echocardiography. Significant triple vessel coronary disease was present in 11 of 15 patients with prolapsed mitralvalve. In each of the latter a greater than 90 per cent obstructive lesion was noted in at least one coronary artery: right coronary artery, 9 subjects (82%); left circumflex coronary artery, 5 patients (33%); and left anterior descending coronary artery, 4 patients (27%). Of 15 subjects with angiographic evidence of mitral valve prolapse, 13 had left ventricular asynergy-inferior or inferoposterior in 8 subjects (62%) and anterior or anteroapical in 5 subjects (38%). Eleven subjects had vectorcardiographic evidence of transmural myocardial infarction-inferior or inferoposterior in 9 (82%) and anteroseptal in 2 (18%). A single subject with mitral valve prolapse had mild mitral regurgitation. It is concluded that: (1) coexisting prolapse of the posterior mitral valve leaflet and coronary artery disease is usually associated with triple vessel obstructive lesions, (2) severe right coronary disease, inferior left ventricular wall asynergy, and inferior myocardial infarction are important angiographic and vectorcardiographic correlates, and (3) echocardiography will detect such mitral valve prolapse in only one-third of affected cases.     

Clinical features and investigative findings in presence of mitral leaflet prolapse. Study of 85 consecutive patients.

In a 14-month period mitral leaflet prolapse was diagnosed in 85 patients by echocardiography or cineangiography. Chest pain alone was the presenting complaint in 30 patients and linked with palpitation, dyspnoea, or syncope in 9. Eleven presented with major neurological disturbances (9 had transient ischaemic attacks), 10 with palpitation, 4 with undue and persistent fatigue, 2 with dyspnoea, and 2 with dizziness. Seventeen were referred not because of symptoms but because of clicks and murmurs. Overall, chest pain affected 61 patients and unless associated with coronary artery disease was not anginal. Palpitation was admitted by 42 patients; dizziness, lightheadedness, or paraesthesiae by 15, and syncope by 12. Systolic auscultatory abnormalities were noted in 69: 25 had single clicks, 3 had multiple clicks, 19 had both click(s) and murmur, and 22 had a murmur alone. Electrocardiography revealed ST segments flat for greater than 0-10 s in 21, prolonged QTc in 18, and T wave flattening or inversion in inferior limb and lateral chest leads in 14. The exercise stress test was abnormal in 13 of 27 patients. Mitral valve echograms showed definite mitral leaflet prolapse in 61, 'possible' prolapse in 14, and were normal in 8 patients with angiographic proof of mitral leaflet prolapse. Cardiac catheterization with left ventriculography showed prolapse of posterior mitral leaflet in 36, of both leaflets in 2, and left ventricular wall motion abnormalities in 16 cases. Selective coronary arteriography in 31 cases showed major vessel narrowing of larger than or equal to 80 per cent lumen diameter in 4, all with angina. This consecutive series indicates that the physical event of mitral leaflet prolapse is more common than hitherto appreciated, is priminently associated with non-anginal chest pain, palpitation, and neurological disturbances, and in 90 per cent of cases could be shown echocardiographically.     

Clinical features and investigative findings in presence of mitral leaflet prolapse. Study of 85 consecutive patients.

In a 14-month period mitral leaflet prolapse was diagnosed in 85 patients by echocardiography or cineangiography. Chest pain alone was the presenting complaint in 30 patients and linked with palpitation, dyspnoea, or syncope in 9. Eleven presented with major neurological disturbances (9 had transient ischaemic attacks), 10 with palpitation, 4 with undue and persistent fatigue, 2 with dyspnoea, and 2 with dizziness. Seventeen were referred not because of symptoms but because of clicks and murmurs. Overall, chest pain affected 61 patients and unless associated with coronary artery disease was not anginal. Palpitation was admitted by 42 patients; dizziness, lightheadedness, or paraesthesiae by 15, and syncope by 12. Systolic auscultatory abnormalities were noted in 69: 25 had single clicks, 3 had multiple clicks, 19 had both click(s) and murmur, and 22 had a murmur alone. Electrocardiography revealed ST segments flat for greater than 0-10 s in 21, prolonged QTc in 18, and T wave flattening or inversion in inferior limb and lateral chest leads in 14. The exercise stress test was abnormal in 13 of 27 patients. Mitral valve echograms showed definite mitral leaflet prolapse in 61, 'possible' prolapse in 14, and were normal in 8 patients with angiographic proof of mitral leaflet prolapse. Cardiac catheterization with left ventriculography showed prolapse of posterior mitral leaflet in 36, of both leaflets in 2, and left ventricular wall motion abnormalities in 16 cases. Selective coronary arteriography in 31 cases showed major vessel narrowing of larger than or equal to 80 per cent lumen diameter in 4, all with angina. This consecutive series indicates that the physical event of mitral leaflet prolapse is more common than hitherto appreciated, is priminently associated with non-anginal chest pain, palpitation, and neurological disturbances, and in 90 per cent of cases could be shown echocardiographically.     

Mitral valve echoes in patients with mitral valve prolapse syndrome.

Echocardiology is an important tool in diagnosing patients with the mitral valve prolapse (MVP) syndrome. An unusual echocardiographic finding reported in this study was observed in 12 of 83 patients (14.5 per cent) with MVP syndrome. The finding consisted of a pattern of multiple, high-intensity parallel echoes behind the anterior mitral leaflet noted throughout diastole which in character were closely akin to those previously observed in left atrial myxoma or hemodynamically significant flail mitral valve leaflet. These latter diagnoses were excluded by other criteria. The prevalence of this finding in patients with MVP was significantly increased (P < .01 by Chi-square contingency testing) when contrasted with 44 patients without MVP. There was no identifying feature in the clinical history or physical examination which could be used to predict those in whom the diastolic echoes were observed. However, a significant increase in dysrhythmias as recorded by routine electrocardiogram or 24-hour Holter monitoring was noted. Angiographic information obtained in selected patients suggested that the posterior leaflet per se caused these diastolic echoes. Because of patulous transformation of the valve, elongation of the chordae, or loss of support of the papillary muscle from the posterior free wall, the posterior leaflet appeared drawn forward toward the anterior leaflet, perhaps from a venturi-like effect caused by the rapid ingress of blood during diastolic filling. This malpositioning of the posterior leaflet was not associated with significant mitral regurgitation and appears to represent but another facet in the spectrum of mitral valve prolapse.     

Two dimensional echocardiographic evaluation of patients with mitral insufficiency

One hundred forty patients with clinical mitral insufficiency were studied with two dimensional echocardiography. Cardiac catheterization was performed in 51 patients; all had mitral insufficiency. Thirty-three patients were surgically treated. An etiologic diagnosis was made in 133 patients. Mitral valve prolapse (41 patients) was the most common cause of mitral insufficiency; the amount of valve insufficiency did not correlate with the leaflet involved or the severity of the prolapse. Patients with rheumatic disease either had combined mitral stenosis and insufficiency (27 patients) or pure mitral insufficiency (10 patients). Echocardiographic measurement of the mitral valve area separated patients with combined lesions from those with pure insufficiency. Fourteen patients had ruptured chordae tendineae; surgical findings were confirmatory in each patient who had valve replacement. Nineteen patients had left ventricular dysfunction; angiographie findings were confirmatory in each patient who underwent cardiac catheterization. Two dimensional echocardiographic findings reliably differentiated mitral insufficiency secondary to valve disease from that secondary to ventricular or papillary muscle dysfunction. Other causes of mitral insufficiency included mitral anular calcification (11 patients), idiopathic hypertrophic subaortic stenosis (5 patients), cleft anterior mitral leaflet (5 patients) and atrial myxoma (1 patient).     

Incidence of systolic pulmonary venous flow reversal in patients with mitral valve prolapse: influence of the prolapse site]

OBJECTIVES: Systolic pulmonary venous flow reversal identified by pulsed Doppler echocardiography is useful for the diagnosis of severe mitral regurgitation. The direction of the mitral regurgitant jet in severe mitral regurgitation significantly influences the systolic pulmonary venous flow reversal in an experimental model. This study investigated the influence of the site of mitral valve prolapse on the incidence of systolic pulmonary venous flow reversal in patients with severe mitral regurgitation using transthoracic color Doppler echocardiography. METHODS: This study included 59 consecutive patients with severe mitral regurgitation (regurgitant fraction > 50%) due to mitral valve prolapse. Exclusion criteria were left ventricular ejection fraction < 45%, non sinus rhythms, associated aortic valve disease, bileaflet prolapse, and inadequate Doppler recordings. Right upper pulmonary venous flow was recorded and regurgitant fraction of mitral regurgitation measured by transthoracic color Doppler echocardiography. The sites of mitral valve prolapse were confirmed at operation in all patients. RESULTS: The incidence of systolic pulmonary venous flow reversal was 78% (14/18) in the patients with anterior leaflet prolapse, 82% (9/11) in the patients with medial commissure prolapse, 75% (12/16) in the patients with posterior middle scallop prolapse, 20% (2/10) in the patients with posterior medial scallop prolapse, and 25% (1/4) in the patients with posterior lateral scallop prolapse. There were no significant differences in regurgitant fraction between the five groups. The incidence of systolic pulmonary venous flow reversal was significantly lower in the patients with posterior medial scallop prolapse compared to the other sites of mitral valve prolapse (p < 0.01). CONCLUSIONS: Assessment of the severity of mitral regurgitation by systolic pulmonary venous flow reversal using transthoracic color Doppler echocardiography may be underestimated in patients with prolapse of the posterior medial scallop.     

Coronary artery spasm and mitral valve prolapse

Ten patients, representing 1.34 per cent of those patients undergoing selective coronary arteriography, were found to have unequivocal evidence of coronary artery spasm. This involved the proximal right coronary artery in eight patients, the mid-left anterior descending branch in one, and the left main coronary artery in one. Eight of these 10 patients had otherwise normal coronary arteries.Of these 10 patients with coronary artery spasm, nine had evidence of mitral valve prolapse. This involved the posteromedial scallop in six patients; the anterolateral and posteromedial scallops in one; the middle and posteromedial scallops in one; and the anterolateral, middle, and posteromedial scallops in one.These data suggest an association between coronary artery spasm and mitral valve prolapse. Coronary artery spasm may thus be an important factor in the pathogenesis of the chest pain, arrhythmias, electrocardiographic abnormalities, and sudden death, that have already been described in some patients with mitral valve prolapse.     

Left Ventricular Outflow Tract Obstruction Following Mitral Valve Replacement with Carpentier-Edwards Prosthesis

Left ventricular outflow tract (LVOT) obstruction is a rare complication of mitral valve replacement. In this article, we describe three patients in whom left ventricular outflow tract obstruction occurred following Carpentier-Edwards porcine mitral valve replacement. All three patients presented with symptomatic mitral regurgitation (angiographic grade 3–4) requiring mitral valve replacement. Preoperatively there was no evidence of hypertrophic obstructive cardiomyopathy by physical exam, echocardiography, or by cardiac catheterization. At the time of surgery all three were shown to have severe mitral valve prolapse. The native anterior mitral leaflet was left intact and pledgeted to the mitral annulus. Following surgery a new systolic murmur was appreciated. Echocardiographic exam visualized obstruction of the left ventricular outflow tract by the prosthetic strut in two cases and by a flail anterior leaflet in one case. Continuous-wave Doppler measured a calculated peak gradient of 72 to 81 mmHg across the left ventricular outflow tract. In one case simultaneous Doppler and cardiac catheterization confirmed the diagnosis and severity of left ventricular outflow tract obstruction. Mechanisms of left ventricular outflow tract obstruction following Carpentier-Edwards porcine mitral valve replacement are discussed. These three cases highlight the importance of echo-Doppler techniques in understanding the mechanism of newly detected systolic murmurs following mitral valve replacement.     

Echocardiographic features of primary pulmonary hypertension

Echocardiograms were recorded in nine patients with primary pulmonary hypertension proved at cardiac catheterization. A reduced diastolic slope of the anterior mitral valve leaflet, simulating mitral stenosis but with normal motion of the posterior leaflet, was observed in all patients. Other features found included a large right ventricular dimension (nine patients), a small left ventricular dimension (three patients), a thick interventricular septum (six patients), systolic mitral leaflet prolapse (four patients) and abnormal septal motion (four patients). The last feature was most probably due to secondary tricuspid or pulmonic insufficiency, or both. The finding of a decreased mitral valve slope, often used as a criterion for mitral stenosis, should not be accepted alone as proof of mitral stenosis; the posterior mitral valve leaflet echo must be carefully searched for and identified. This echo is often difficult to identify, but the normal motion of this structure found in all patients excludes the diagnosis of mitral stenosis as a cause for the pulmonary hypertension.     

The variability of arterial pressure

Echocardiograms from 562 patients were examined for evidence of the pattern of tricuspid valve prolapse. Criteria for the diagnosis can be established similar to those applicable to mitral prolapse. In 500 consecutive patients without mitral valve prolapse, there were no cases of isolated tricuspid valve prolapse. Eleven of 53 (21 per cent) patients with mitral valve prolapse also had tricuspid valve prolapse. Four of six (67 per cent) patients with Marfan's syndrome and mitral valve prolapse also had tricuspid valve prolapse. The occurrence of this echocardiographic pattern as an isolated finding as well as associated with mitral valve prolapse was significantly less than previous angiographic reports. Patients with both these findings tended to be older than those with mitral valve prolapse alone, but clinically differed in no other way. Use of standardized technique can minimize errors in diagnosis.     

Mitral valve repair for extended commissural prolapse involving complex prolapse

We reviewed our experience of mitral valve repair techniques for extended commissural prolapse involving complex prolapse of either or both leaflets, due to chordal rupture or elongation. Between June 1991 and January 2005, 21 of 210 patients who underwent mitral valve repair for mitral regurgitation had extended commissural prolapse involving either or both of the anterior and posterior leaflets. There were 17 (81%) patients with degenerative and 4 (19%) with infective endocarditis. The distribution of diseased mitral commissural lesions was: posteromedial commissure in 14 (67%) patients, anterolateral in 6 (29%), and bilateral in 1 (5%). Reconstructive techniques included leaflet folding plasty in 10, resection-suture in 6, the sliding technique in 2, commissuroplasty in 2, and chordal shortening in 1. There were no perioperative deaths; postoperative mitral regurgitation was none or trivial in 19 patients and mild in 2. The mean follow-up period was 54 months (range, 2-155 months), and no patient required re-operation. There was one late death from a noncardiac cause at 103 months. Mitral valve repair for extended commissural prolapse is satisfactory. We consider leaflet folding plasty and its modification to be effective in patients who require extensive leaflet resection in the commissural area.     

M-mode and cross-sectional (2D)echocardiograms in the diagnosis of mitral valve prolpase

Forty-nine patients were studied to assess the value of M-modeand cross-sectional echocardiography in the diagnosis of mitralvalve prolapse. There were 20 normal subjects and 29 patientswith clinical and phonocardiographic evidence which suggestedprolapse. Using an arbitrary line connecting the base of theanterior and posterior leaflets at their attachment to the atrioventricularjunction, 22 of the 29 patients had abnormal arching of themitral leaflets into the left atrium on cross-sectional echocardiograms(CSE); this was not seen in the normal subjects. There were15 patients with double leaflet prolapse, five with lone anteriorand two with lone posterior leaflet prolapse. M-mode recordingsfailed to show prolapse in six of the 22 patients with positiveCSE but showed prolapse in one patient with an inadequate cross-sectionalechocardiogram. The difficulty in demonstrating prolapse onM-mode was caused by multiple systolic echoes in four subjects,and poor separation of the posterior leaflet from the posteriorleft ventricular wall echoes in two subjects. The anterior leafletwas well seen on CSE with long axis parasternal views but theposterior leaflet could not be seen on the long axis view in13 of the 29 subjects in the abnormal group; short axis fourchamber views from the apex allowed definition of the posteriorleaflet in nine of these 13 patients. We conclude that CSE is better than M-mode echocardiographyand should be used in conjunction with it for the diagnosisof mitral valve prolapse. Superior arching of the mitral leafletsinto the left atrium is the characteristic feature, and longaxis parasternal views should be supplemented by short axisfour chamber apical views.