- Email: [email protected]
Sinus node responses to atrial extra-stimulus in 36 patients without apparent sinus node disease
ABSTRACTS
IMPROVED
QUANTIFICAT1ON
OF MYOCARDIAL
Burton E. Sobe\,
MD,
FACC,
Washington
University,
SINUS NODERESPONSESTO ATRIAL EXTRA-STIMULUSIN 36 PATIEtCS WITHOVTAPPAREM SINUS NODEDISEASE Kenneth H. Rosen, MD, FACC; Ramesh Dhingra, MD; Christopher Wyndham, MD; Fernando Amat-y-Leon, MD; Delon Wu. MD; Pablo Dense, Ml, University of Illinois, ChFcago, Illinois.
INFARCTION
BASED ON ANALYSIS OF SERUM CPK ISOENZYMES Robert Roberts, MD; H. Dieter Ambos; Elaine M. Carlson, St.
MS; Louis,
Missouri.
Thirty-six patients (pts) without sinus node disease were scanned with an atria1 extra-stimulus (A21 during sinus rhythm with sinus cycle length (CL) mesrrured in msec, Zones of non-reset due to interference (ZNR), reset (ZR), interpolation (211, and sinus echoes (ZE) were defined by noting the timing of the first response following A2. The tones were defined in tenna of their longest and shortest Al-A2 coupling interval6 (in mace). ZNR was found in 12 of 12 pts in whan A2 was delivered late. Mean CL in these 12 was 779, with marn ZNR of 779 to 585 (25X of CL). All 36 pta (100%) had ZR. Mean CL in these 36 was 803 with ZR frQl 692 to 311 (47% of CL). Seven of 36 pts (192) had 21. Mean CL in thrbse 7 was 739. with mean ZI of 344 to 279 (9% of CL). Four of 36 pts (11%) had ZB. Mean CL in these 4 wan 855, with mean ZE from 350 to 313 (4% of CL). Calculated rino-atria1 conduction time ranged from 40 to 153 (mean + SEH of 92 + 5 msec).
Prognosis after myocardial infarction correlates with infarct size estimated from serum CPK changes. However, noncordioc CPK may influence serum activity, particularly after i .m. injections, hypotension,
or shock.
Accordingly,
we estimated infarct size an isoenzymr relatively specific to myocardium. MB CPK was assayed quantitatively with a fluorimctric procedure recently developed. Infarct size was estimated from the relation previously validated for total CPK as fol-
from serial changes in serum MB CPK,
lows: (Infarct size) = (CPK released) x K x (body weight). K was calculated from MB activity measured in myocardium. The MB disappearance rate (kd) was obtained from terminal portions of serum curves. MB CPK release (CPK,) was calculated fram hourly serum MB CPK values in 17 patients with infarction. Myocordial MB CPK averaged 121 f 16 (SE, n = 7) 1U/g. kd avemged 0.2 t .Ol%. Insignificant amounts of MB were detected in skeletal muscle, brain, intestines, lung, and kidney. With uncomplicated infarction, MB released into serum paral!sled total CPK released. (CPK, = (7.7 x MB CPK,) - 4.5, n = 12, SD of slope = .6) and infarct size calculated from MB and from total CPK caorrelatd clasely (r = .97). With infarction compf icated by shock, noncardiac CPK led to spuriously high estimates, and infarct size estimated from MB CPK was significantly less (p < .Ol, n = 5), Thus, analysis of serial changes in serum MB CPK activity pennits accurate evaluation of the extant of infarction even in patients with shock accompanied by release of CPK from organs besides the heart.
In conclusion, ZNR and ZR were found in all pts with nor-1 sinus node function, while ZI and ZE were less c-on. Calculated sine-atria1 conduction tbne was rurprfringly long.
MITRAL VALVEABNORMALITIES ASSOCIATEDWITH TRANSPOSITION OF THE GREATARTERIES Glenn C. Rosenquist, M. D.; J. Stark, M. D.; J. F. N. Taylor, M. D. The Johns Hopkins University, Baltimore, Md. and The Hospital for Sick Children, London, England
RUPTUREOF THE LEFT VENTRICUUR FREE WALL (LVFW) OR VENTRICULARSEPTUM(VS) SECONDARY TO ACUTEMYOCARDIAL INFARCTION(AMI): AN OCCURRENCE VIRTUALLYLIMITED TO TNE FIRST TRANSMURAL AM1 IN A HYPERTENSIVE INDIVIDUAL William C. Roberts, MD, FACC; James A. Ronan, Jr., ND, PACC; W. Proctor Harvey, MD, PACC, Georgetown University, Washington, D.C. Among patients (pte) with fatal AM1 studied at nectopsy, 23 had rupture of the LVFWand 18, rupture of the VS. The 41 pts ranged in age from 43 to 84 years (avg 60); 26 were men and 15 were women. The rupture occurred vithln the first 7 days in 29 pta. Evidence of previous ayatamic hypertension was preeent in 33 pta; at necropay, however, cardiomegaly (heart weight z 400 gms) was preeent in 37 pts and all 41 had thickened LV walls. Only 3 pts had questionable historical evidence of previous AM1 and 4, angina pet tor is. At necropey, only 3 pts had groes myocardial fibbtosis and in each it wae subendocardial. Prior congestive cardiac failure was absent In all 41 pts. At necropsy, the LV cavity was dilated in only 11 pta, and in each of them it appeared to have developed during the ANI. The AMI wa8 anterior in 21 and posterior in 20 pte. _ Phonocatdiographic and hemodynamic observationa in 5 pts with rupture of the VS discloeed the followfug in each: wide (0.05 to 0.07 set) splitting of the second heart sound; loud, usually holosyetolic, murmurs decreasing in late systole because of reduced left ventricular ejection time indices (304-356 mfeec); atria1 and ventricular filling sounds; and palpable thrills at the lower left sternal borders. Kn summgry, rupture of the LVFWor VS is primarily 8 complication of nystemic hypertenefon, of the first AM1, and of hypertrophied, previously wellcontracting, hearts.
188
.hanusry 1975
The Amefkw
Journal of CARDIOLOGY
Increasing numbers of patients with transposition of the great arteries (TGA) are undergoing successful correction with Mustard’s procedure. Although a success rate of over 90% has been reported, a knowledge of all associated lesions is desirable. For this study 163 specimens were examined. In order to determine whether the mitral valve annulus was small, its diameter was compared to that of the tricuspid annulus and length of left ventricle in the same specimen. In 38 hearts (23%) the morphology of the valve and diameter of the annulus was within normal limits. In 9 hearts (6%) the mitral valve was normal but the annulus was small. In 54 hearts (33%) the annulus was small and the valve normally formed except that chordae tendineae were attached to the midline of the anterior leaflet so that the free margin of the anterior leaflet was markedly shortened. In 62 hearts (38%) mitral valve anomalies were muscles due to underof 3 basic types: apposed papillary development of space between papillary muscles (56 hearts), poorly differentiated papillary muscles due to underdevelopment of space between papillary muscles and ventricular wall (2 hearts) and attachment of an indented anterior leaflet to the ventricular septum (4 hearts). A possible etiology for most of this spectrum is reduction in blood flow into the left ventricle in fetal life. Since the present study shows a higher incidence of mitral valve involvement than previously reported in TGA, greater clinical attention to mitral valve morphology by schocardiography and angiocardiography appears to be warranted.
Volume 35
IMPROVED
QUANTIFICAT1ON
OF MYOCARDIAL
Burton E. Sobe\,
MD,
FACC,
Washington
University,
SINUS NODERESPONSESTO ATRIAL EXTRA-STIMULUSIN 36 PATIEtCS WITHOVTAPPAREM SINUS NODEDISEASE Kenneth H. Rosen, MD, FACC; Ramesh Dhingra, MD; Christopher Wyndham, MD; Fernando Amat-y-Leon, MD; Delon Wu. MD; Pablo Dense, Ml, University of Illinois, ChFcago, Illinois.
INFARCTION
BASED ON ANALYSIS OF SERUM CPK ISOENZYMES Robert Roberts, MD; H. Dieter Ambos; Elaine M. Carlson, St.
MS; Louis,
Missouri.
Thirty-six patients (pts) without sinus node disease were scanned with an atria1 extra-stimulus (A21 during sinus rhythm with sinus cycle length (CL) mesrrured in msec, Zones of non-reset due to interference (ZNR), reset (ZR), interpolation (211, and sinus echoes (ZE) were defined by noting the timing of the first response following A2. The tones were defined in tenna of their longest and shortest Al-A2 coupling interval6 (in mace). ZNR was found in 12 of 12 pts in whan A2 was delivered late. Mean CL in these 12 was 779, with marn ZNR of 779 to 585 (25X of CL). All 36 pta (100%) had ZR. Mean CL in these 36 was 803 with ZR frQl 692 to 311 (47% of CL). Seven of 36 pts (192) had 21. Mean CL in thrbse 7 was 739. with mean ZI of 344 to 279 (9% of CL). Four of 36 pts (11%) had ZB. Mean CL in these 4 wan 855, with mean ZE from 350 to 313 (4% of CL). Calculated rino-atria1 conduction time ranged from 40 to 153 (mean + SEH of 92 + 5 msec).
Prognosis after myocardial infarction correlates with infarct size estimated from serum CPK changes. However, noncordioc CPK may influence serum activity, particularly after i .m. injections, hypotension,
or shock.
Accordingly,
we estimated infarct size an isoenzymr relatively specific to myocardium. MB CPK was assayed quantitatively with a fluorimctric procedure recently developed. Infarct size was estimated from the relation previously validated for total CPK as fol-
from serial changes in serum MB CPK,
lows: (Infarct size) = (CPK released) x K x (body weight). K was calculated from MB activity measured in myocardium. The MB disappearance rate (kd) was obtained from terminal portions of serum curves. MB CPK release (CPK,) was calculated fram hourly serum MB CPK values in 17 patients with infarction. Myocordial MB CPK averaged 121 f 16 (SE, n = 7) 1U/g. kd avemged 0.2 t .Ol%. Insignificant amounts of MB were detected in skeletal muscle, brain, intestines, lung, and kidney. With uncomplicated infarction, MB released into serum paral!sled total CPK released. (CPK, = (7.7 x MB CPK,) - 4.5, n = 12, SD of slope = .6) and infarct size calculated from MB and from total CPK caorrelatd clasely (r = .97). With infarction compf icated by shock, noncardiac CPK led to spuriously high estimates, and infarct size estimated from MB CPK was significantly less (p < .Ol, n = 5), Thus, analysis of serial changes in serum MB CPK activity pennits accurate evaluation of the extant of infarction even in patients with shock accompanied by release of CPK from organs besides the heart.
In conclusion, ZNR and ZR were found in all pts with nor-1 sinus node function, while ZI and ZE were less c-on. Calculated sine-atria1 conduction tbne was rurprfringly long.
MITRAL VALVEABNORMALITIES ASSOCIATEDWITH TRANSPOSITION OF THE GREATARTERIES Glenn C. Rosenquist, M. D.; J. Stark, M. D.; J. F. N. Taylor, M. D. The Johns Hopkins University, Baltimore, Md. and The Hospital for Sick Children, London, England
RUPTUREOF THE LEFT VENTRICUUR FREE WALL (LVFW) OR VENTRICULARSEPTUM(VS) SECONDARY TO ACUTEMYOCARDIAL INFARCTION(AMI): AN OCCURRENCE VIRTUALLYLIMITED TO TNE FIRST TRANSMURAL AM1 IN A HYPERTENSIVE INDIVIDUAL William C. Roberts, MD, FACC; James A. Ronan, Jr., ND, PACC; W. Proctor Harvey, MD, PACC, Georgetown University, Washington, D.C. Among patients (pte) with fatal AM1 studied at nectopsy, 23 had rupture of the LVFWand 18, rupture of the VS. The 41 pts ranged in age from 43 to 84 years (avg 60); 26 were men and 15 were women. The rupture occurred vithln the first 7 days in 29 pta. Evidence of previous ayatamic hypertension was preeent in 33 pta; at necropay, however, cardiomegaly (heart weight z 400 gms) was preeent in 37 pts and all 41 had thickened LV walls. Only 3 pts had questionable historical evidence of previous AM1 and 4, angina pet tor is. At necropey, only 3 pts had groes myocardial fibbtosis and in each it wae subendocardial. Prior congestive cardiac failure was absent In all 41 pts. At necropsy, the LV cavity was dilated in only 11 pta, and in each of them it appeared to have developed during the ANI. The AMI wa8 anterior in 21 and posterior in 20 pte. _ Phonocatdiographic and hemodynamic observationa in 5 pts with rupture of the VS discloeed the followfug in each: wide (0.05 to 0.07 set) splitting of the second heart sound; loud, usually holosyetolic, murmurs decreasing in late systole because of reduced left ventricular ejection time indices (304-356 mfeec); atria1 and ventricular filling sounds; and palpable thrills at the lower left sternal borders. Kn summgry, rupture of the LVFWor VS is primarily 8 complication of nystemic hypertenefon, of the first AM1, and of hypertrophied, previously wellcontracting, hearts.
188
.hanusry 1975
The Amefkw
Journal of CARDIOLOGY
Increasing numbers of patients with transposition of the great arteries (TGA) are undergoing successful correction with Mustard’s procedure. Although a success rate of over 90% has been reported, a knowledge of all associated lesions is desirable. For this study 163 specimens were examined. In order to determine whether the mitral valve annulus was small, its diameter was compared to that of the tricuspid annulus and length of left ventricle in the same specimen. In 38 hearts (23%) the morphology of the valve and diameter of the annulus was within normal limits. In 9 hearts (6%) the mitral valve was normal but the annulus was small. In 54 hearts (33%) the annulus was small and the valve normally formed except that chordae tendineae were attached to the midline of the anterior leaflet so that the free margin of the anterior leaflet was markedly shortened. In 62 hearts (38%) mitral valve anomalies were muscles due to underof 3 basic types: apposed papillary development of space between papillary muscles (56 hearts), poorly differentiated papillary muscles due to underdevelopment of space between papillary muscles and ventricular wall (2 hearts) and attachment of an indented anterior leaflet to the ventricular septum (4 hearts). A possible etiology for most of this spectrum is reduction in blood flow into the left ventricle in fetal life. Since the present study shows a higher incidence of mitral valve involvement than previously reported in TGA, greater clinical attention to mitral valve morphology by schocardiography and angiocardiography appears to be warranted.
Volume 35