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or echocardiographic evidence of mitral valve prolapse
ABSTRACTS
MITRAL VALVE PROLAPSE SYNDROME- EV IDENCE FOR A HYPERADRENERGIC STATE. P~risios Boudoulas, MD, FACC; Charles F. Wooley, MD, FACC; James Reynolds, MD- Ernest Mazzaferri, MD; Ohio State University, Columbus, Ohio. Symptomatic patients with mitral valve prolapse frequently mimic thyrotoxicosis, hyperadrenergic" states or hypoglycemia. Eighteen symptomatic patients with auscultatory and echocardiographic mitral valve prolapse were studied in the clinical research unit. Thirteen patients had frequent premature ventricular depolarization ( > i 0 per min) with couplets and/or triplets detected by 24 hour Holter monitoring. Corrected for heart rate QT was not different from normal before, during, or post treadmill exercise test. T3, T4, plasma cortisol and glucose tolerance test with insulin blood levels were not different from normal. Twenty-four hour urinary epinephrine (E) and norepinephrine (NE) was greater than normal (E+NE secretion, 44+2 vs 29.5+3 lug/ 24 hour/g creatinine, p~O.01.) Total plasma catecholamines were higher than normal (269~_29 vs 154+11, p~O.01). The short electromechanical systole corrected for heart rate (QS21) (529~_3.9, normal 548+_1, p~O.01) also reflected high adrenergic tone. Catecholamine secretion and frequency of premature ventricular repolarizations were parallel and both decreased significantly during the night (p~0.05). It is concluded that i) symptomatic patients with mitral valve prolapse have high adrenergic tone, 2) frequency of premature ventricular depolarizations and adrenergic activity are parallel, 3) mitral valve prolapse patients with frequent premature ventricular depolarizations usually have normal QT corrected for heart rate.
MORPHOLOGIC OBSERVATIONS O N T H E MITRAL VALVE AT NECROPSY IN PATIENTS WITH SYSTOLIC CLICKS WITH OR WITHOUT SYSTOLIC MURMURS AND/OR ECHOCARDIOGRAPHIC EVIDENCE OF MITRAL VALVE rPROLAPSE. Jeffrey M. Isner, MD, and William C. Roberts, MD, FACC, National Heart, Lung, and Blood Institute, Bethesda, Maryland . Mitral valve prolapse (MVP) in the vast majority of patients (pts) is a benign valvular heart disease. Conseuqently, little information is available on the morphology of those mitral valves that produce classic ausculatory (A) or echocardiographic (E) abnormalities of MVP in the absence of associated chordal rupture or superimposed infective endocarditis. Accordingly, qualitative and quantitative analysis was performed on the mitral valves of i0 pts, all of whom died non-cardiac deaths and had no history of cardiac surgery, and all of whom had A and/or E evidence of MVP in life. At necropsy, the mitral valves in 4 were judged to be only borderline abnormal (mild hooding, mildly thickened); in the other 6 pts, the valves were clearly abnormal (moderate to severely thicked, and moderate to severe hooding). Each pt with mild or more hooding had E evidence of MVP. Absolute measurements or leaflet surface area and length of chordae tendineae did not differ significantly from 67 control pts. Furled chordae (excessive length relative to left ventricular dimensions),~however, were associated with systolic clicks, except in 3 pts where clinical evaluation suggested moderate mitral regurgitation. Thus, in pts with FMV, mitral valve hooding appears to be the primary morphologic substrate of an abnormal echocardiogram; 2) relative redundancy of chordae tendineae appears to be the primary morphologic substrate of a systolic click; and 3) when valvular dysfunction causes significant mitral regurgitatation, the click may be absent in spite of redundant chordae.
368
February 1979
The American Journal of CARDIOLOGY
TUESDA Y, MARCH 13, 1979 AM CARDIAC SURGERY AND VALVULAR DISEASE 10:30-12:00
HYPERTROPHIC CARDIOMYOPATHY FOLLOWING,.AORTIC VALVE REPLACEMENT Richard Thompson, MRCP; Mohammed Ahmed, MRCP; Ronald Pridie, FRCR and Magdi Yacoub, FRCS, Harefield Hospital, Middlesex, England. The association of hypertrophic cardlomyopathy (HOCM) and aortic valve disease is well documented. The development of the syndrome however, arising de novo, late after valve replacement has not been previously described. We present 6 cases, all in females aged between 50 - 71 years who developed evidence of HOCM 3 - 5 years after successful valve replacement. The preoperative haemodynamic lesion was aortic stenosis in 4 and aortic regurgitation in 2. Prior to operation no patient showed evidence of HOCM as judged by the absence of: 1) asymetrlc septal hypertrophy (ASH) (septal/posterior wall ratio was in each case less than 1.4/1). 2) systolic anterior mitral valve motion (SAM), 3) L.V. cavity obliteration at angiography, 4) intraventricular gradient. Following valve replacement no patient had significant aortic regurgitation and none were hypertensive. Four patients subsequently developed recurrence of symptoms including dyspnoea in 4, angina in 3 and syncope in 2. ECG showed reappearance of LVH in 4 patients and LBBB in 1. Echocardiography showed ASH in 5 (septal/posterior wall ratio greater than 1.8/1) SAM in 3 and evidence of inflow obstruction in 3. At cardiac catheterisation an intraventricular gradient of 36-60mm Hg.was demonstrated at rest in 3 patients, on provocation in 1 patient, whilst 2 patients showed no gradient. Angiography showed cavity obliteration in all 6 patients (ejection fraction 0.84-0.93) Two patients had coronary artery disease. No patient had a transvalvar gradient at rest or on exercise.
AORTIC STENOSIS AND CORONARY ARTERY DISEASE: LONG TERM SURVIVAL AFTER VALVE REPLACEMENT Geun C. Jang, MD; E. William Hancock, MD, FACC, Cardiology Division, Stanford University Medical Center, Stanford, CA. There is little information on the long term clinical value of coronary bypass surgery (CABG) performed in combination with aortic valve replacement (AVR). Therefore, 114 patients (pts), over 40 years old, who had coronary arteriography before valve replacement for aortic stenosis (AS) during 1970-73 were followed for 5-8 years or until death. Coronary artery disease was absent or minimal in 56 pts and moderate to severe in 58. Operative mortality was 12% (4/34) in AVR with CABG, 4% (1/24) in AVR alone in the presence of CAD, and 0% in AVR with minimal or absent CAD. Late mortality was 33% (10/30) in AVR-CABG, 38% (9/24) in AVR only with CAD, and 20% (11/56) in AVR without CAD. Five year survival was 63%, 64%, and 81% (p<0.01) in these three groups; 7 year survival was 50%, 44%, and 67% respectively. Seventynine percent (20/24 of late d e a t h s w e r e cardiac in nature. Late mortality was not significantly different in age groups j59, 60-69, ~70 if the higher prevalence of CAD in older pts was corrected for. Long term survival following AVR for AS is strongly influenced by the presence of significant CAD prior to surgery. In this series survival at 5 years was not significantly different with and without CABG performed with AVR.
Volume 43
MITRAL VALVE PROLAPSE SYNDROME- EV IDENCE FOR A HYPERADRENERGIC STATE. P~risios Boudoulas, MD, FACC; Charles F. Wooley, MD, FACC; James Reynolds, MD- Ernest Mazzaferri, MD; Ohio State University, Columbus, Ohio. Symptomatic patients with mitral valve prolapse frequently mimic thyrotoxicosis, hyperadrenergic" states or hypoglycemia. Eighteen symptomatic patients with auscultatory and echocardiographic mitral valve prolapse were studied in the clinical research unit. Thirteen patients had frequent premature ventricular depolarization ( > i 0 per min) with couplets and/or triplets detected by 24 hour Holter monitoring. Corrected for heart rate QT was not different from normal before, during, or post treadmill exercise test. T3, T4, plasma cortisol and glucose tolerance test with insulin blood levels were not different from normal. Twenty-four hour urinary epinephrine (E) and norepinephrine (NE) was greater than normal (E+NE secretion, 44+2 vs 29.5+3 lug/ 24 hour/g creatinine, p~O.01.) Total plasma catecholamines were higher than normal (269~_29 vs 154+11, p~O.01). The short electromechanical systole corrected for heart rate (QS21) (529~_3.9, normal 548+_1, p~O.01) also reflected high adrenergic tone. Catecholamine secretion and frequency of premature ventricular repolarizations were parallel and both decreased significantly during the night (p~0.05). It is concluded that i) symptomatic patients with mitral valve prolapse have high adrenergic tone, 2) frequency of premature ventricular depolarizations and adrenergic activity are parallel, 3) mitral valve prolapse patients with frequent premature ventricular depolarizations usually have normal QT corrected for heart rate.
MORPHOLOGIC OBSERVATIONS O N T H E MITRAL VALVE AT NECROPSY IN PATIENTS WITH SYSTOLIC CLICKS WITH OR WITHOUT SYSTOLIC MURMURS AND/OR ECHOCARDIOGRAPHIC EVIDENCE OF MITRAL VALVE rPROLAPSE. Jeffrey M. Isner, MD, and William C. Roberts, MD, FACC, National Heart, Lung, and Blood Institute, Bethesda, Maryland . Mitral valve prolapse (MVP) in the vast majority of patients (pts) is a benign valvular heart disease. Conseuqently, little information is available on the morphology of those mitral valves that produce classic ausculatory (A) or echocardiographic (E) abnormalities of MVP in the absence of associated chordal rupture or superimposed infective endocarditis. Accordingly, qualitative and quantitative analysis was performed on the mitral valves of i0 pts, all of whom died non-cardiac deaths and had no history of cardiac surgery, and all of whom had A and/or E evidence of MVP in life. At necropsy, the mitral valves in 4 were judged to be only borderline abnormal (mild hooding, mildly thickened); in the other 6 pts, the valves were clearly abnormal (moderate to severely thicked, and moderate to severe hooding). Each pt with mild or more hooding had E evidence of MVP. Absolute measurements or leaflet surface area and length of chordae tendineae did not differ significantly from 67 control pts. Furled chordae (excessive length relative to left ventricular dimensions),~however, were associated with systolic clicks, except in 3 pts where clinical evaluation suggested moderate mitral regurgitation. Thus, in pts with FMV, mitral valve hooding appears to be the primary morphologic substrate of an abnormal echocardiogram; 2) relative redundancy of chordae tendineae appears to be the primary morphologic substrate of a systolic click; and 3) when valvular dysfunction causes significant mitral regurgitatation, the click may be absent in spite of redundant chordae.
368
February 1979
The American Journal of CARDIOLOGY
TUESDA Y, MARCH 13, 1979 AM CARDIAC SURGERY AND VALVULAR DISEASE 10:30-12:00
HYPERTROPHIC CARDIOMYOPATHY FOLLOWING,.AORTIC VALVE REPLACEMENT Richard Thompson, MRCP; Mohammed Ahmed, MRCP; Ronald Pridie, FRCR and Magdi Yacoub, FRCS, Harefield Hospital, Middlesex, England. The association of hypertrophic cardlomyopathy (HOCM) and aortic valve disease is well documented. The development of the syndrome however, arising de novo, late after valve replacement has not been previously described. We present 6 cases, all in females aged between 50 - 71 years who developed evidence of HOCM 3 - 5 years after successful valve replacement. The preoperative haemodynamic lesion was aortic stenosis in 4 and aortic regurgitation in 2. Prior to operation no patient showed evidence of HOCM as judged by the absence of: 1) asymetrlc septal hypertrophy (ASH) (septal/posterior wall ratio was in each case less than 1.4/1). 2) systolic anterior mitral valve motion (SAM), 3) L.V. cavity obliteration at angiography, 4) intraventricular gradient. Following valve replacement no patient had significant aortic regurgitation and none were hypertensive. Four patients subsequently developed recurrence of symptoms including dyspnoea in 4, angina in 3 and syncope in 2. ECG showed reappearance of LVH in 4 patients and LBBB in 1. Echocardiography showed ASH in 5 (septal/posterior wall ratio greater than 1.8/1) SAM in 3 and evidence of inflow obstruction in 3. At cardiac catheterisation an intraventricular gradient of 36-60mm Hg.was demonstrated at rest in 3 patients, on provocation in 1 patient, whilst 2 patients showed no gradient. Angiography showed cavity obliteration in all 6 patients (ejection fraction 0.84-0.93) Two patients had coronary artery disease. No patient had a transvalvar gradient at rest or on exercise.
AORTIC STENOSIS AND CORONARY ARTERY DISEASE: LONG TERM SURVIVAL AFTER VALVE REPLACEMENT Geun C. Jang, MD; E. William Hancock, MD, FACC, Cardiology Division, Stanford University Medical Center, Stanford, CA. There is little information on the long term clinical value of coronary bypass surgery (CABG) performed in combination with aortic valve replacement (AVR). Therefore, 114 patients (pts), over 40 years old, who had coronary arteriography before valve replacement for aortic stenosis (AS) during 1970-73 were followed for 5-8 years or until death. Coronary artery disease was absent or minimal in 56 pts and moderate to severe in 58. Operative mortality was 12% (4/34) in AVR with CABG, 4% (1/24) in AVR alone in the presence of CAD, and 0% in AVR with minimal or absent CAD. Late mortality was 33% (10/30) in AVR-CABG, 38% (9/24) in AVR only with CAD, and 20% (11/56) in AVR without CAD. Five year survival was 63%, 64%, and 81% (p<0.01) in these three groups; 7 year survival was 50%, 44%, and 67% respectively. Seventynine percent (20/24 of late d e a t h s w e r e cardiac in nature. Late mortality was not significantly different in age groups j59, 60-69, ~70 if the higher prevalence of CAD in older pts was corrected for. Long term survival following AVR for AS is strongly influenced by the presence of significant CAD prior to surgery. In this series survival at 5 years was not significantly different with and without CABG performed with AVR.
Volume 43