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Does mitral prolapse occur in mitral stenosis?
'ABSTRACTS
TUESDA Y, MARCH 13, 1979 AM STUDIES OF MITRAL PROLAPSE 8:30-10:00 LEFT VENTRICULAR DYsFuNcTION IN MITRAL VALVE PROLAPSE Joh__n S.Gottdiener , MD; Jeffrey S.Borer, MD, FACC, Stephen L.Bacharach, PhD; Michael V. Green, MS; Kenneth M. Kent, MD, PhD; Douglas R. Rosing, MD; Stephen E. Epstein, MD, FACC; NHLBI, Bethesda, Maryland Abnormalities of left ventricular (LV) function have been noted in pts with mitral valve prolapse. In order to d e ~ K m i n e systolic LV function in mitral valve prolapse, Tc ..... gated equilibrium radionuclide cineangiography was performed at rest and during maximal supine bicycle exercise in 25 pts with mitral prolapse who did not have coronary artery disease. Chest pain was noted by 15 pts, and arrhythmia was documented by ambulatory ECG monitoring and/or exercise electrocardiography in i0 pts. Ejection fraction (EF) at rest was normal in all pts (average 0.57+0.02 SEM; normal 0.57+O.01, NS). Although 13/19 pts with trivial or no mitral regurgitation increased ejection fraction during exercise, the average exercise EF for this group of 13 pts (0.60+0.02) was below normal (0.71+0.02, p<0.O01). The remaining 6 pts without mitral regurgitation evidenced a decline in EF with exercise (average 0.57+0.05) including 2 pts with an exercise EF <0.55. Of the 6 pts with mitral regurgitation, EF at rest was normal (average 0.56+0.04) but declined with exercise in 4/6 pts (0.50+0.07). Left ventricular end-diastolic dimension by echocardiogram was normal in all pts without mitral regurgitation. Chest pain and arrhythmia, though commonly present, did not predict LV dysfunction. While many pts with mitral valve prolapse have normal left ventricular function, there is a subgroup with diminished LV functional reserve. In those pts with mitral regurgitation, decrease in LV function may represent, in part, the effects of chronic volume overload. In the absence of mitral regurgitation, LV dysfunction is suggestive of a cardiomyopathic process.
THE CLOSING SNAP OF MITRAL VALVE PROLAPSE. J.Y. Wei, MD; N.J. Fortuin, MD. The Johns Hopkins University School of M e d i c i n e Baltimore, Maryland.
DOES MITRAL PROLAPSE OCCUR IN MITRAL STENOSIS? Byron Beas!ey, M.D; Richard Kerber, MD, FACC, CV Cent, Dept of Med, Univ of lowa Hosp, Iowa City, lowa Rhdumatic heart disease is often l i s t e d as a cause of mitral valve prolapse (MVP), but the frequency with which these two conditions coexist is unknown. We searched for MVP in 20 patieqts with cath-proven mitral stenosis (MS), using four d i f f e r e n t diagnostic c r i t e r i a . M-mode echocardiograms were defined as positive for MVP i f there was >2 mm posterior displacement of the s y s t o l i c echo beyond a line connecting the C and D points. 2-D sector scans were judged to.be positive for MVP i f the mitral echo arched cephaloposteriorly beyond a l i n e joinin'g the post e r i o r mitral valve annulus at the posterior mitral leafl e t and the junction of the a n t e r i o r mitral l e a f l e t and posterior a o r t i c wall. Left v e n t r i c u l a r angiograms (RAO projection) were evaluated subjectively for s y s t o l i c bulging of the mitral valve l e a f l e t s beyond the mitral annulus and o b j e c t i v e l y using the posterior medial scallop index (PMSLI) of Smith, et al (AJC 41:432, 1978)- A l i n e is drawn j o i n i n g the posterior aortic root and the l e f t v e n t r i c u l a r f o r n i x ; in MVP the posterior mitral valve l e a f l e t maximum distance from this l i n e divided by LV minor axis exceeds 0.27. Results" Echo Vent r i cu 19gram M-mode 2-D Subjective PMSLI MVP 13 4 5 8 No MVP 7 16 15 12 Only 2 MS patients were positive for MVP by all c r i t e r i a ; one patient was positive by 3 of 4 c r i t e r i a . Conclusion' MVP does occur in MS patients, but is uncommon. M-mode echo is p a r t i c u l a r l y unreliable to diagnose MVP when MS is present, because of the multiple s y s t o l i c echoes from the thickened, fused valve l e a f l e t s . The coexistance of MVP and MS is most r e l i a b l y defined when both echo and angio c r i t e r i a are s a t i s f i e d .
COMPLEMENT-RESISTANT LYMPHOCYTES IN MITRAL VALVE PROLAPSE John R. Darsee, MD; Candace L. Miklozek, MD; Steven B. Heymsfield, MD; Donald O. Nutter, MD, FACC; Emory University School of Medicine, Atlanta, Georgia
A~though the mitral valve prolapse syndrome (MVPS) is often associated with a systolic click and/or murmur, it has not been appreciated that a sound and/or murmur may also occur in diastole. We have observed 7 patients with typical echocardiographic evidence of mitral valve prolapse who were noted to have, in addition to a systolic click and/or murmur, a striking early diastolic sound. They ranged in age from 25-64 years (mean = 37 years), and 4 were women. Midsystolic prolapse of the posterior mitral leaflet was noted in all 7, and a midsystolic click coinciding with the abrupt posterior mitral leaflet movement was present in 5. Four patients had a systolic murmur, 2 late systolic and 2 pansystolic, which continued into diastole as an early diastolic decrescendo murmur that was best heard at the apex; I of the four had been referred for evaluation of "aortic regurgitation". The diastolic sound occurred between 70 and Ii0 msec (mean = 92 msec) after A2. Simultaneous echo/phonocardiograms demonstrated that this "snap" coincided with the point where the prolapsed posterior leaflet returned from the left atrium and recoapted with the anterior leaflet, 40-60 msec (mean = 55 msec) prior to the E point of the mitral valve echocardiogram and the 0 point of the apexcardiogram, and even longer before the occurrence of the ventricular rapid filling wave. These findings suggest that when a diastolic decrescendo murmur best heard at the apex is present, the possibility of MVPS should be considered; in patients with MVPS, especially those with midsystolic prolapse, an early diastolic sound may represent the closing snap of the prolapsed posterior mitral valve leaflet.
Mitral valve prolapse (MVP) is a clinical and echocardiographic syndrome of multiple etiologies. An increased number of blank or unidentifiable lymphocyte surface antigens (HLA antigens) have previously been described in patients with this disorder. In order to further clarify the cause of these unidentifiable HLA, we performed standard.typing on 70 patients (48 black, 22 white, ages 1864) with MVP diagnosed by an auscultatory click-murmur and by late-systolic prolapse on M-mode echocardiogram. Forty-six had isolated MVP; 6 also had Marfan's syndrome, 4 also had straight back syndrome, and 14 had arthritis with a positive (>1:20) serum antinuclear antibody (~qA) test. All 6 with Marfan's syndrome had a B-7 antigen and the 4 with straight back syndrome had the A-2,B-27 haplotype. In patients with isolated MVP, the frequency of the blank locus (BL) was 36% (23/64 loci) in blacks (controls=16/100 loci, p<.001) and 25% (17/28 loci) in whites (controls=9/100 loci, p<.001). The BL antigens were due to non-defined antisera in all black patients and to homozygousity or to cross-reactive antigens in all white patients. In the 14 patients with MVP and a positive ANA, the frequency of the BL was 61% (17/28 loci, p<.001) using standard typing techniques. However, by doubling the lymphocyte incubation time or the concentration of complement, and by typing cultured tissue fibroblasts from these patients, all but 1 of the BL antigens were identified as known H L A . We conclude that: i) the BL is common in patients with isolated MVP, but is due to various causes; and 2) the BL is due to relative complement resistance of peripheral lymphocytes in patients with MVP and a positive ANA.
February 1979
The American Journal of CARDIOLOGY
Volume 43
367
TUESDA Y, MARCH 13, 1979 AM STUDIES OF MITRAL PROLAPSE 8:30-10:00 LEFT VENTRICULAR DYsFuNcTION IN MITRAL VALVE PROLAPSE Joh__n S.Gottdiener , MD; Jeffrey S.Borer, MD, FACC, Stephen L.Bacharach, PhD; Michael V. Green, MS; Kenneth M. Kent, MD, PhD; Douglas R. Rosing, MD; Stephen E. Epstein, MD, FACC; NHLBI, Bethesda, Maryland Abnormalities of left ventricular (LV) function have been noted in pts with mitral valve prolapse. In order to d e ~ K m i n e systolic LV function in mitral valve prolapse, Tc ..... gated equilibrium radionuclide cineangiography was performed at rest and during maximal supine bicycle exercise in 25 pts with mitral prolapse who did not have coronary artery disease. Chest pain was noted by 15 pts, and arrhythmia was documented by ambulatory ECG monitoring and/or exercise electrocardiography in i0 pts. Ejection fraction (EF) at rest was normal in all pts (average 0.57+0.02 SEM; normal 0.57+O.01, NS). Although 13/19 pts with trivial or no mitral regurgitation increased ejection fraction during exercise, the average exercise EF for this group of 13 pts (0.60+0.02) was below normal (0.71+0.02, p<0.O01). The remaining 6 pts without mitral regurgitation evidenced a decline in EF with exercise (average 0.57+0.05) including 2 pts with an exercise EF <0.55. Of the 6 pts with mitral regurgitation, EF at rest was normal (average 0.56+0.04) but declined with exercise in 4/6 pts (0.50+0.07). Left ventricular end-diastolic dimension by echocardiogram was normal in all pts without mitral regurgitation. Chest pain and arrhythmia, though commonly present, did not predict LV dysfunction. While many pts with mitral valve prolapse have normal left ventricular function, there is a subgroup with diminished LV functional reserve. In those pts with mitral regurgitation, decrease in LV function may represent, in part, the effects of chronic volume overload. In the absence of mitral regurgitation, LV dysfunction is suggestive of a cardiomyopathic process.
THE CLOSING SNAP OF MITRAL VALVE PROLAPSE. J.Y. Wei, MD; N.J. Fortuin, MD. The Johns Hopkins University School of M e d i c i n e Baltimore, Maryland.
DOES MITRAL PROLAPSE OCCUR IN MITRAL STENOSIS? Byron Beas!ey, M.D; Richard Kerber, MD, FACC, CV Cent, Dept of Med, Univ of lowa Hosp, Iowa City, lowa Rhdumatic heart disease is often l i s t e d as a cause of mitral valve prolapse (MVP), but the frequency with which these two conditions coexist is unknown. We searched for MVP in 20 patieqts with cath-proven mitral stenosis (MS), using four d i f f e r e n t diagnostic c r i t e r i a . M-mode echocardiograms were defined as positive for MVP i f there was >2 mm posterior displacement of the s y s t o l i c echo beyond a line connecting the C and D points. 2-D sector scans were judged to.be positive for MVP i f the mitral echo arched cephaloposteriorly beyond a l i n e joinin'g the post e r i o r mitral valve annulus at the posterior mitral leafl e t and the junction of the a n t e r i o r mitral l e a f l e t and posterior a o r t i c wall. Left v e n t r i c u l a r angiograms (RAO projection) were evaluated subjectively for s y s t o l i c bulging of the mitral valve l e a f l e t s beyond the mitral annulus and o b j e c t i v e l y using the posterior medial scallop index (PMSLI) of Smith, et al (AJC 41:432, 1978)- A l i n e is drawn j o i n i n g the posterior aortic root and the l e f t v e n t r i c u l a r f o r n i x ; in MVP the posterior mitral valve l e a f l e t maximum distance from this l i n e divided by LV minor axis exceeds 0.27. Results" Echo Vent r i cu 19gram M-mode 2-D Subjective PMSLI MVP 13 4 5 8 No MVP 7 16 15 12 Only 2 MS patients were positive for MVP by all c r i t e r i a ; one patient was positive by 3 of 4 c r i t e r i a . Conclusion' MVP does occur in MS patients, but is uncommon. M-mode echo is p a r t i c u l a r l y unreliable to diagnose MVP when MS is present, because of the multiple s y s t o l i c echoes from the thickened, fused valve l e a f l e t s . The coexistance of MVP and MS is most r e l i a b l y defined when both echo and angio c r i t e r i a are s a t i s f i e d .
COMPLEMENT-RESISTANT LYMPHOCYTES IN MITRAL VALVE PROLAPSE John R. Darsee, MD; Candace L. Miklozek, MD; Steven B. Heymsfield, MD; Donald O. Nutter, MD, FACC; Emory University School of Medicine, Atlanta, Georgia
A~though the mitral valve prolapse syndrome (MVPS) is often associated with a systolic click and/or murmur, it has not been appreciated that a sound and/or murmur may also occur in diastole. We have observed 7 patients with typical echocardiographic evidence of mitral valve prolapse who were noted to have, in addition to a systolic click and/or murmur, a striking early diastolic sound. They ranged in age from 25-64 years (mean = 37 years), and 4 were women. Midsystolic prolapse of the posterior mitral leaflet was noted in all 7, and a midsystolic click coinciding with the abrupt posterior mitral leaflet movement was present in 5. Four patients had a systolic murmur, 2 late systolic and 2 pansystolic, which continued into diastole as an early diastolic decrescendo murmur that was best heard at the apex; I of the four had been referred for evaluation of "aortic regurgitation". The diastolic sound occurred between 70 and Ii0 msec (mean = 92 msec) after A2. Simultaneous echo/phonocardiograms demonstrated that this "snap" coincided with the point where the prolapsed posterior leaflet returned from the left atrium and recoapted with the anterior leaflet, 40-60 msec (mean = 55 msec) prior to the E point of the mitral valve echocardiogram and the 0 point of the apexcardiogram, and even longer before the occurrence of the ventricular rapid filling wave. These findings suggest that when a diastolic decrescendo murmur best heard at the apex is present, the possibility of MVPS should be considered; in patients with MVPS, especially those with midsystolic prolapse, an early diastolic sound may represent the closing snap of the prolapsed posterior mitral valve leaflet.
Mitral valve prolapse (MVP) is a clinical and echocardiographic syndrome of multiple etiologies. An increased number of blank or unidentifiable lymphocyte surface antigens (HLA antigens) have previously been described in patients with this disorder. In order to further clarify the cause of these unidentifiable HLA, we performed standard.typing on 70 patients (48 black, 22 white, ages 1864) with MVP diagnosed by an auscultatory click-murmur and by late-systolic prolapse on M-mode echocardiogram. Forty-six had isolated MVP; 6 also had Marfan's syndrome, 4 also had straight back syndrome, and 14 had arthritis with a positive (>1:20) serum antinuclear antibody (~qA) test. All 6 with Marfan's syndrome had a B-7 antigen and the 4 with straight back syndrome had the A-2,B-27 haplotype. In patients with isolated MVP, the frequency of the blank locus (BL) was 36% (23/64 loci) in blacks (controls=16/100 loci, p<.001) and 25% (17/28 loci) in whites (controls=9/100 loci, p<.001). The BL antigens were due to non-defined antisera in all black patients and to homozygousity or to cross-reactive antigens in all white patients. In the 14 patients with MVP and a positive ANA, the frequency of the BL was 61% (17/28 loci, p<.001) using standard typing techniques. However, by doubling the lymphocyte incubation time or the concentration of complement, and by typing cultured tissue fibroblasts from these patients, all but 1 of the BL antigens were identified as known H L A . We conclude that: i) the BL is common in patients with isolated MVP, but is due to various causes; and 2) the BL is due to relative complement resistance of peripheral lymphocytes in patients with MVP and a positive ANA.
February 1979
The American Journal of CARDIOLOGY
Volume 43
367