Mitral Valve Echogram Research Articles

Influence of detomidine on echocardiographic function parameters and cardiac hemodynamics in horses with and without heart murmur

30 warmblood horses were examined before and after sedation with 20 micrograms/kg BW detomidine, to determine changes of cardiac function parameters, using B-mode, M-mode and Doppler echocardiography. 15 horses showed a heart murmur, but no clinical signs of cardiac heart failure, 15 horses had neither a heart murmur nor other signs of cardiac disease. After sedation with detomidine we could recognise a significant increase of end-diastolic left atrium diameter, an increase of end-systolic left ventricular diameter and aortic root diameter. The end-systolic thickness of papillary muscle and interventricular septum showed a decrease. Fractional shortening and amplitude of left ventricular wall motion was decreased after sedation. The mitral valve echogram revealed a presystolic valve closure and an inflection in the Ac slope (B-notch) in xy horses before sedation. Both increased after sedation with detomidine. Doppler echocardiography showed a decrease of blood flow velocity and velocity time integral (VTI) in the left and right ventricular outflow tract after sedation. Regurgitant flow signals were intensified following sedation in xy horses, especially at the mitral valve.

Spatial and Temporal Periodicity During Atrial Fibrillation

HomeCirculationVol. 100, No. 2Spatial and Temporal Periodicity During Atrial Fibrillation Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBSpatial and Temporal Periodicity During Atrial Fibrillation Ivan A. D’Cruz Ivan A. D’CruzIvan A. D’Cruz Director, Echocardiography Labs, VA Medical Center, Memphis and, William F. Bowld Hospital, Professor of Medicine, University of Tennessee, Memphis, Tenn Search for more papers by this author Originally published21 Mar 2018https://doi.org/10.1161/circ.100.2.211/-aCirculation. 1999;100:211–214To the Editor:The article by Skanes et al1 presented interesting evidence of spatial and temporal periodicity during atrial fibrillation, contrary to the traditional concept of totally disorganized random atrial activity in atrial fibrillation. Skanes et al referred to recent work by others23 in accord with their own.With former colleagues in Chicago, Ill, I called attention 20 years ago to the fact that some patients with ECG features of atrial fibrillation have M-mode echocardiographic findings indicating regular atrial contractions. Regular deflections on the mitral valve echogram were demonstrated in Figures 14 and 15 of that paper,4 although the ECG was typical of atrial fibrillation. At the time, we speculated that one explanation for this apparent discrepancy was one dominant circus-motion wave (producing regular atrial contractions), with smaller subsidiary irregular “eddies” of electrical activity responsible for the irregular contour of ECG atrial activity.4 Over the last 2 decades, we have noted that this phenomenon (regular diastolic mitral deflections on echocardiography concomitant with irregular atrial ECG deflections) is not very rare in clinical M-mode recordings, yet few if any similar observations have been published. References 1 Skanes AC, Mandapati R, Berenfeld O, Davidenko JM, Jalife J. Spatiotemporal periodicity during atrial fibrillation in the isolated sheep heart. Circulation.1998; 98:1236–1248.CrossrefMedlineGoogle Scholar2 Gerstenfeld EP, Sahakian AV, Swiryn S. Evidence for transient linking of atrial excitation during atrial fibrillation in humans. Circulation.1992; 86:375–382.CrossrefMedlineGoogle Scholar3 Botteron GW, Smith JM. Quantitative assessment of the spatial organization of atrial fibrillation in the intact human heart. Circulation.1996; 93:513–518.CrossrefMedlineGoogle Scholar4 Prabhu R, D’Cruz I, Cohen H, Glick G. Echocardiographic correlates of atrial contraction in normal and abnormal atrial rhythm. Prog Cardiovasc Dis.1978; 20:463–478.CrossrefMedlineGoogle ScholarcirculationahaCirculationCirculationCirculation0009-73221524-4539Lippincott Williams & WilkinsResponseMandapati Ravi, Skanes Allan, MD, Berenfeld Omer, PhD, Davidenko Jorge M., MD, and Jalife José, MD13071999We thank Dr D’Cruz for his interest in our article on spatiotemporal periodicity during atrial fibrillation (AF) in the isolated sheep heart.R1 It is reassuring to note that our experimental findings are supported by data from patients suffering from AF. Indeed, review of the manuscript cited by Dr D’CruzR2 reveals in Figures 14 and 15 that excursions of the anterior mitral leaflet (AML) show some degree of regularity. However, careful examination of the figures shows that there is some beat-to-beat change in the frequency of AML excursions. In the same article, the authors do not provide any evidence but speculate that a major or dominant wave front activating the left atrium (LA) could be responsible for the somewhat periodic motion of the AML. This is certainly a possible explanation for their findings. It is, however, important to note that such a suggestion was initially made as early as 1925 by Sir Thomas Lewis, who coined the term “impure flutter.”R3As such, the level of organization during AF may lie on a spectrum depending on the number of sources and the degree of fractionation of the periodic activity into independent wavelets, as well as their subsequent fate. It is quite possible that AF in patients with mitral valve disease is more organized than previously thought, as reported by 2 recent surgical studies.R4R5 In our experimental model, it was rare to find the entire LA being activated in a periodic manner. Usually, only a small part of the LA demonstrated periodic activity. Previous Back to top Next FiguresReferencesRelatedDetails July 13, 1999Vol 100, Issue 2 Advertisement Article InformationMetrics Copyright © 1999 by American Heart Associationhttps://doi.org/10.1161/circ.100.2.211/-a Originally publishedMarch 21, 2018 PDF download Advertisement

Noninvasive study of the presystolic component of the first heart sound in mitral stenosis

Echophonocardiography and pulsed Doppler echocardiography were performed in 30 patients with mitral stenosis (19 with atrial fibrillation and 11 with sinus rhythm) to investigate the genesis of the presystolic component or small apical vibrations preceding the first heart sound in mitral stenosis. In 27 patients, mitral valve closure preceded or coincided with tricuspid valve closure regardless of the preceding RR interval. Of three patients whose tricuspid valve closed prematurely, two had a prolonged PR interval. The soft apical vibrations, which were recorded during the final rapid closing motion of the mitral valve echogram (B-C slope), began with the upstroke of the apexcardiogram. During this event the pulsed Doppler echocardiogram revealed a deceleration in the velocity of mitral inflow. In two exceptional patients with a prolonged PR interval, this apical sound was separated from a presystolic rumble that occurred during an accelerated phase of mitral inflow or at the A wave of mitral valve echograms. In conclusion, the tricuspid valve is not a factor contributing to the genesis of the small apical vibrations preceding the first heart sound in mitral stenosis. These vibrations are caused by acceleration of left ventricular contraction and deceleration of mitral inflow in the presence of a stenotic valve.

Hemodynamic evaluation by M-mode echocardiography in acute myocardial infarction

We assessed the relationship between echocardiographic and hemodynamic parameters in 28 patients with documented acute myocardial infarction (AMI), who underwent M-mode echocardiography and Swan-Ganz catheterization during the same hospitalization. Patients with valvular heart disease were excluded from the study. On mitral valve echogram, DE interval was measured and the area enclosed by mitral valve echogram during DE interval (DE subarea) was calculated in each echocardiogram. DE subarea/DE interval ratio was computed for each measurement set. Hemodynamic parameters were obtained in the usual fashion. Patients with pulmonary artery wedge pressure (PWP) < 18 mm Hg showed a DE interval markedly longer than patients with PWP > 18 mm Hg: 81.72 ± 15.23 vs 55.12 ± 9.85 msec ( p < 0.001). Patients with cardiac index > 2.2 L min −1 m −2 had a DE subarea/DE interval ratio greater than patients with cardiac index < 2.2 L min −1 m −2: 0.169 ± 0.035 vs 0.094 ± 0.017 dm 2 sec −1 ( p < 0.001). Echocardiographic and hemodynamic data were then correlated in the whole study group, and it was found that DE interval was significantly ( p < 0.001) and inversely correlated to PWP; stroke index more than cardiac index was correlated ( p < 0.005) both to DE subarea/DE interval ratio and to DE interval itself; DE interval was not affected by heart rate. We were able to categorize the patients into four subsets on the basis of echocardiographic measurements. Our findings suggest the possibility of providing, through M-mode echocardiography, a noninvasive and accurate evaluation of PWP and stroke index.

The isovolumic index: A new noninvasive approach to the assessment of left ventricular function in man

Both a high ratio of preejection period (PEP) to left ventricular ejection time (LVET) and a prolonged isovolumic relaxation time are associated with left ventricular dysfunction. In pilot studies in instrumented dogs, we measured a combined isovolumic index, defined as (isovolumic contraction + isovolumic relaxation time)/LVET and found an inverse correlation with changes in fractional shortening. To test the utility of this index in human subjects, we used the electrocardiogram, mitral valve (MV) echogram, and indirect carotid arterial tracing to calculate isovolumic index as (time from R wave to MV opening — LVET)/LVET × 100%. Normal subjects had isovolumic index values that averaged 24 ± 7% (standard deviation), in contrast to patients with cardiomyopathy who averaged 5 ±14% ( p < 0.001 versus normal values) and patients with coronary artery disease who averaged 40 ±15% (p < 0.001 versus normal values and patients with cardiomyopathy). All normal subjects had an isovolumic index of < 32% and all patients with cardiomyopathy had values >32%. Of patients with coronary artery disease, 72% (21 of 29) had an isovolumic index >32%. An isovolumic index >32% identified 20 of 22 patients (91%) with a reduced ejection fraction and 12 of 14 (86% ) with a segmental wall motion abnormality, and it was a more sensitive marker of these abnormalities than abnormal E point-septal separation. In 6 patients with coronary artery disease who had simultaneous echocardiograms and measurements of left ventricular pressure by micromanometer tip catheter, the time constants of isovolumic pressure decrease were uniformly increased in association with an isovolumic index >32%. In contrast, all had normal PEP/LVET ratios. The isovolumic index is thus a sensitive, potentially useful noninvasive marker of left ventricular dysfunction that is easily obtained from the routine echocardiogram.

Echocardiographic assessment of the aortic root in syndromes with left ventricular hypoplasia

Echocardiograms and angiograms of six infants with left ventricular hypoplasia were examined. Three observations were made: (1) A normal-sized aortic root echogram may be seen in infants with mitral atresia, intact ventricular septum and normally related great arteries. (2) A recognizable mitral valve echogram may be seen in mitral atresia. (3) The true echocardiographic left ventricular dimension may be exceedingly difficult to measure, the tendency being to overestimate it. Awareness of these pitfalls with aid in the echocardiographic diagnosis of left ventricular hypoplasia in infants.

Forward stroke volume calculated from aortic valve echograms in normal subjects and patients with mitral regurgitation secondary to left ventricular dysfunction

A clinically applicable method was developed for calculating aortic valve stroke volume using the echocardiographically recorded initial and late aortic cusp separation, ejection time and amplitude of posterior aortic root motion during ejection. The formula was tested prospectively in 55 patients for whom 65 Fick [n = 26]or thermodilution [n = 39]cardiac output determinations were performed simultaneously with echocardiography. Aortic valve echograms were recorded in all patients and mitral valve echograms were also recorded in 48 of the 55 patients. Twenty patients had nonrheumatic mitral regurgitation. For the 65 studies, linear correlation (r) was excellent between the aortic valve method and Fick or thermodilution method for stroke volume (r = 0.96, standard error of the estimate [SEE]± 6 cc) and for cardiac output (r = 0.92, SEE ± 0.44 liters). Differences between cardiac output values obtained from aortic valve echograms and either Fick or thermodilution techniques ranged from −1.4 to +1.5 liters/min and were normally distributed. Ninety percent of the computed aortic valve data was within 15 percent of the Fick or thermodilution data. Aortic valve stroke volume correlated well (r = 0.93) with stroke volume derived from mitral valve echograms in the patients without mitral regurgitation but did not correlate well (r = 0.78) in the patients with mitral regurgitation. Mitral valve stroke volume exceeded aortic valve stroke volume by more than 20 percent in 19 of the 20 patients with mitral regurgitation compared with 1 of 28 patients without mitral regurgitation. The presence or absence of ventricular dyssynergy did not alter statistical findings. Data from this study show that (1) aortic valve echograms can be used clinically to measure forward stroke volume, and (2) the difference between mitral valve and aortic valve volume should be a measure of mitral regurgitant flow.

Echophonocardiographic Findings in a Patient With Aortic and Mitral Prostheses

A 33-year-old woman had undergone aortic and mitral valve replacement with Bjork-Shiley prostheses in 1973 because of rheumatic valvular disease. She has been receiving digoxin and warfarin sodium since then. In November 1978, she noted the gradual onset of exertional dyspnea and orthopnea, which prompted her admission to the hospital. Physical examination disclosed a regular heart rate of 96 beats per minute, blood pressure of 120/70 mm Hg, and a grade 3/6 midsystolic murmur at the apex. A third sound of variable timing was noted. The ECG indicated left ventricular hypertrophy and left atrial enlargement only. A chest roentgenogram was compatible with congestive heart failure. Figure 1 is a simultaneous recording of the ECG, apical phonocardiogram (PCG), and mitral prosthetic valve echogram (PVE). What is your diagnosis? Diagnosis. —Malfunction of Bjork-Shiley Mitral Prosthesis. Figure 2 is a higher paper-speed recording of the same graphics as in Fig 1. Note

Hemodynamics and Echocardiograms Before and After Cardioversion of Atrial Fibrillation to Normal Sinus Rhythm

Hemodynamic and echocardiographic measurements were obtained in 15 patients prior to cardioversion and immediately, one, three, and five hours after cardioversion of atrial fibrillation to normal sinus rhythm. At five hours after cardioversion, there was improvement in cardiac index (P less than 0.005), in stroke index (P less than 0.005), and in stroke work index (P less than 0.025), but no significant change in heart rate, mean pulmonary capillary wedge pressure, left atrial dimemsions (LAD), left ventricular end-diastolic dimensions (LVEDD), or left ventricular end-systolic dimension (LVESD). At follow-up one week to nine months after cardioversion, 10 of the 15 patients (67 percent) remained in normal sinus rhythm. Neither the size of the left atrium, changes in hemodynamics, LAD, LVEDD, or LVESD, nor the presence or amplitude of the A-wave on the mitral valve echogram correlated with the persistence or normal sinus rhythm.

Echographic evaluation of acquired valvular diseases of the heart.

The mitral valve is one of the easiest structures to identify echographically. The valve is located along the left sternal border at the third to fifth intercostal space. The normal mitral valve follows a characteristic motion pattern during ventricular diastole (Fig. 1). Although the anterior mitral leaflet echo is most prominent, the posterior leaflet may also be detected ultrasonically and shows a pattern opposite in direction to that of the anterior leaflet. At the onset of ventricular diastole, there is a rush of blood across the valve that results in a peak excursion that terminates at point e of the mitral valve echogram depicted in Fig. 1. Following rapid ventricular filling, the mitral valve coasts toward a position of closure at point f and then reopens (point a) with atria1 systole. The mitral valve echogram thus reflects phasic flow across its orifice.14 When rheumatic fever results in mitral stenosis, the slope of the anterior leaflet from point e-f is reduced below the normal range of 80-150 mm/set, the response to atria1 systole is obliterated, and the posterior leaflet tends to follow the anterior in diastole (Fig. 2).3*7 M-mode echocardiography has been of limited value in assessing severity of mitral stenosis; the abnormal echographic pattern may also be found in patients with left ventricular failure and pulmonary hypertension.” The newer two-dimensional

Assessment of left ventricular function during myocardial ischemia from the mitral valve echogram

Assessment of left ventricular function during myocardial ischemia from the mitral valve echogram

Noninvasive assessment of left ventricular function from the mitral valve echogram. Relation of final anterior mitral leaflet closing velocity to peak dp/dt and aortic velocity.

Since final mitral valve (MV) closure and aortic ejection velocity are mediated by the same forces in early left ventricular (LV) contraction, the rate of final MV closure (BC slope) should reflect LV performance. We first verified whether peak final closing velocity (ds/dt) of the anterior MV leaflet (AMVL) is related to peak aortic ejection velocity (V) and LV dp/dt in 18 open-chest dogs. We then checked the validity of the relations in man. Our approach was to measure peak ds/dt, peak aortic acceleration (dV/dt) and peak LV dp/dt using electronic differentiation of analog signals of the AMVL echogram, V and LV pressure. In dogs, resting ds/dt averaged 26.9 +/- 9.0 (SD) cm/sec and changed significantly (P less than 0.001) after isoproterenol, propranolol, coronary ligation and aortic cross-clamping. We found good (P less than 0.001) correlations between ds/dt and V (r = 0.82), dV/dt ( r = 0.67) and dp/dt (r = 0.73). In man, resting ds/dt averaged 25.5 +/- 1.6 cm/sec in six normals. In 40 patients with coronary artery disease, restind ds/dt was lower (15.7 +/- 4.4 cm/sec; P less than 0.001) in the 19 with resting LV end-diastolic pressure (LVEDP) greater than 12 mm Hg. Resting ds/dt correlated closely with V (r = 0.82, N = 10), dp/dt (r = 0.93, N = 6), resting LVEDP (r = -0.67, N = 40), angiographic ejection fractions (r = 0.62, N = 40) as well as manually obtained BC slopes (r = 0.93, N = 40). Thus, final MV closing velocity provides a useful and simple means for the objective noninvasive assessment of LV performance.

Echocardiographic features of congenital mitral stenosis

To determine the echocardiographic features of congenital mitral stenosis, echoeardiograms were obtained in 2 children with Isolated mitral stenosis and 28 with mitral stenosis in assoclation with other congenital heart defects. The diagnosis was confirmed at cardiac catheterization in all 30 patients and also at operation or autopsy in 12. The pattern of mitral valve motion was assessed qualitatively, and the amplitude of excursion of the anterior leaflet and the rate of early diastolic closure (E-F slope) were measured. The values were compared with those from 145 normal children, 22 children with Isolated ventricular septal defect and 16 children with Isolated coarctation of the aorta. In patients with congenital mitral stenosis, the echocardtographic findings included dlastollc anterior motion of the posterior leaflet of the mitral valve, absence of the A wave and reduction of the E-F slope. Diastollc vibration of the mitral leaflets occurred in 21 of the 30 patients with mitral stenosis and in 8 of the 145 normal children, but in none of the patients with coartation of the aorta. From the mitral valve echogram, It was not possible to determine whether the site of the inflow obstruction was the leaflets themselves, the chordae tendbleae, the papillary muscles or a supravalve membrane. Patients with severe stenosis tended to have a greater decrease in E-F slope and exhibited abnormal motion of the posterior mitral leaflet more frequently than patients with mild or only moderately severe mitral stenosis. However, the mitral valve echogram was more useful in detecting the presence of mitral stenosis, even in the presence of other cardiac malformations, than in determining the precise anatomy of the mitral valve lesion or estimating Its severity.

Stroke volume calculated from the mitral valve echogram in patients with and without ventricular dyssynergy.

A formula was derived for calculating mitral valve stroke volume (MVSV) using the rate of mitral valve (MV) opening (DE slope on the MV echogram), the vertical disease between the mitral leaflet echoes early in diastole (EE), the electrocardiographic PR interval and heart rate. The formula was tested prospectively on 80 consecutive patients from whom 95 simultaneous MV echograms and either thermodilution (45) or Fick (50) cardiac outputs were obtained. Sixteen patients were normal; 54 had coronary artery disease; three had cardiomyopathy; and seven had nonrheumatic mitral regurgitation (MR). Linear regression for stroke volume was r = 0.90, SEE +/- 6, and for cardiac output r = 0.83, SEE +/- 0.5 liter for the 73 patients without MR. The presence or absence of ventricular dyssynergy did not alter statistical findings. MVSV consistently overestimated forward stroke volume for the seven patients with MR. This study shows that the MV echogram provides an accurate, widely applicable method for calculating MVSV.

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.

Echocardiographic features of cor triatriatum

A patient is presented who had cor triatriatum documented with angiography and surgery. On echocardiographic study, an abnormal, dense linear echo on “sector scan” was consistently seen to traverse the left atrial cavity obliquely; the ends of the echo were attached to the posterior aortic and lateral walls of the left atrium. In addition, high frequency oscillatory movements were evident in the echo of the posterior mitral cusp. Both echocardiographic features disappeared promptly after successful resection of the intraatrial fibrinous membrane. This experience indicates that in the presence of strong evidence of mitral stenosis, an unexpectedly normal mitral valve echogram should initiate a thorough echographic search for cor triatriatum, a treatable cardiac malformation whose diagnosis can easily be missed on “routine” echocardiographic studies.

Echocardiogram in Pulsus Paradoxus

The mechanism of production of pulsus paradoxus was echocardiographically studied in a 74-year-old male with subacute effusive-constrictive pericarditis which developed to constrictive pericarditis under the observation. Echocardiography disclosed the following phenomena during inspiration: 1) mitral valve did not open until the atrial systole, probably because of the lack of antegrade mitral flow during rapid filling phase (the E wave was not observed), 2) concomitantly, aortic valve opening decreased markedly in its grade, and 3) left ventricular ejection time (LVET) decreased and pre-ejection period (PEP) increased, resulting in a higher PEP/LVET ratio (up to 1.32). The opposite was true during expiration (PEP/LVET ratio was 0.40). This is probably the first case, in which the mechanism of pulsus paradoxus was investigated by aortic and mitral valve echograms.

End-diastolic amplitude of mitral valve echogram in mitral stenosis.

By using simultaneous recordings of the mitral valve echogram and apex cardiogram, the mitral echogram amplitude was measured at the onset of left ventricular isovolumic contraction (MAIC). Twenty normal subjects and 68 patients with a reduced diastolic closure rate in the mitral valve echogram were studied. Of these patients, 53 had mitral stenosis, 6 aortic valvar stenosis, and 9 hypertrophic obstructive cardiomyopathy. In the normal subjects the MAIC ranged between 2 and 4 mm, average 2-7 mm, in the patients with aortic valvar stenosis or hypertrophic obstructive cardiomyopathy between 2 and 4 mm, average 2-9 mm, and in the patients with mitral stenosis between 6 and 17 mm, average 11-3 mm. The DE/MAIC ratio, where DE represents the opening amplitude of the mitral valve in early diastole, was between 3-3 and 6-5, average 5-1, in normal subjects; in the patients with aortic stenosis or hypertrophic obstructive cardiomyopathy the DE/MAIC ratio was between 2-7 and 6-5, average 4-2, and in the patients with mitral stenosis between 0-7 and 1-5, average 1-1. An excellent correlation was found between the DE/MAIC ratio and mitral valve area in the patients with mitral stenosis (r = 0-84, P less than 0-01) while the correlation between the diastolic closure rate and valve area was less satisfactory (4 = 0-62, P less than 0-01). These findings suggest that in cases with a reduced diastolic closure rate for reasons other than mitral stenosis, error can be avoided by using the DE/MAIC ratio.

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.

Incidence of murmurs in the aging heart.

One hundred patients aged 60 or older were studied clinically after excluding those with cardiac enlargement, definite valvular lesions or electrocardiographic (ECG) evidence of left ventricular hypertrophy. In 30 of the the 100 patients a significant systolic murmur was heard on auscultation. Phonocardiograms (PCGs), mitral echograms and pulse tracings were obtained in 28 of these 30 patients (2 had died meanwhile), and the ECGs and chest roentgenograms were reviewed. In 23 PCG patients there was an early or midsystolic murmur, best recorded at the base of the heart and often transmiteed to the apex. Mitral valve echograms and carotid and jugular pulse tracings were normal in all cases. Chest roentgenograms revealed aortic enlargement in 83 percent of the 23 patients. In the elderly with no evidence of organic heart disease, a basal systolic murmur is probably an aortic flow phenomenon caused by either moderate aortic dilatation or minimal fibrotic fusion of one or more commissures of the aortic valve.