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Persistent hemodynamic abnormalities following intracardiac repair of tetralogy of fallot
ABSTRACTS
SERIAL
PRECORDIAL
MYOCARDIAL Philip Pitt,
Reid, MD
ST SEGMENT
MAPPING
MD,
Dean Taylor,
MD,
Johns Hopkins University
Precordial
IN ACUTE
INFARCTION David Kelly, and Hospital
MD,
Bertram
Baltimore,
Md.
ST segment mapping has been used to evaluate acute
myocardial
injury.
We have performed serial
ment mapping to detect infarct
extension.
precordial
Precordial
ST seg-
ST segment
mapping was performed in 14 normal subjects using a 48 lead system with
1 mv=20mm
The mean elevation in males was in females. Individual vari-
deflection.
+42.2 +17.8mm and +9.2+5.0mm
ation v&s less than 10 mm on consecutive days. Daily ST segment mapping was done in 15patients with acute myocardial infarction. In 9 patients
with transmural
and 6 patients farction,
anterior
with nontransmural
initial
myocardial
anterior
ST sums were +143.8+91.8mm
mm, respectively. normal (p<.OOl).
(TAM)
myocardial
infarction (NAM)
Those values were%gnificantly After an average of 10.9days
differen from in the TAM group
and 7.3days in the NAM group, ST segment values had fallen in normal limits. Seven of the 9 patients with TAM infarction demonstrated infarct days with further
extension
elevation
on an average of 5.7+2.5
values from the previous day (mean increase+65.4mm, to +190mm).
The infarct
extensions
with
hospital
of ST segment sums when%mpared
events and subsequent elevation
in-
and -81.5+49.2
to
range+17
were confirmed by clinical
of serum creatinine
phosphokinase
One of these patients died. Only two of the patients values. with NAM were found to have infarct extension which occurred on the 6th and 1 lth
hospital day with an average of -5Omm of further
ST segment depression. Infarct extension may be more frequent than previous1 recognized, particularly for transmural anterior infarctions. Seria Y precordial ST segment mapping offers a mpid, assessing m);ocardial
simple,
ischemia and infarct
noninvasive
means of
Between January, 1964 and December, 1971, 123 patients had an intrapericardial ascending aorta-right pulmonary artery @PA) anastomosis for a variety of cyanotic malformations in which there was pulmonary stenosis or atresia. 20 deaths occurred in the first week after operation - 12 from congestive heart failure (CHF), 5 from severe hypoxemia, and 3 from causes unrelated to the surgery. Among the 103 immediate survivors there were 17 late deaths (between 1 month and 5 years postoperative) from CHF (4), hypoxemia (5) and unrelated causes (8). The total shunt-related mortality was 21% with the mortality for patients under 1 year of age being 24% (17 of 70) and for those over 1 year of age 17% (9 of 53). 74 of the 86 survivors have had continued follow-up, 36 of whom have required therapy for CHF. At postoperative cardiac catheterization in 57 patients, 12 (21%) had a nonfunctioning anastomosis and an additional 13 (23%) had stenosis of the RPA proximal to the anastomosis site. 8 patients with RPA stenosis developed RPA hypertension 040 mm Hg) and 2 of them also had main pulmonary artery (MPA) hypertension. 28 patients had intracardiac repair and 14 of these have had repeat cardiac catheterization. One patient had occlusion of the RPA and 4 had MPA to RPA gradient greater than 20 mm Hg (20-70 mm Hg). Ascending aorta-right pulmonary artery anastomosis improves pulmonary blood flow in the cyanotic child but may be followed by complications requiring repair at the time of total correction. Residual changes may remain after total correction.
January
1973
The American
Fifty patients have undergone clinical, hemodynamic. and angiographic evaluation l-6 years following intracardiac repair of Tetralogy of Fallot. The age range was 6-20 years. All but two were asymptomatic (NYHA Class I). The RVEDP was elevated in 32 (64%); the peak systolic RV pressure wae greater than l/2 the simultaneous systemic pressure in 13 (30%) and the LVEDP was greater than 12 mmHg in 10 of 40 (25%). Eighteen of those studied had a patent foramen ovale. There was left to right atria1 shunting present In one. Residual ventricular defects were noted in 8 (16%) with 1 having a QP/OS greater than 2/l. Pulmonary insufficiency was judged by angiogrsphy to be mild in 9/30 (30X), moderate in 12/30 (40%). and severe in 2/30 (6%). Tricuspid insufficiency was seen in 5 (10%). Aortic insufficiency was present angiographicallv in 12 of 25 (48%) in whom it was assessed. In 2 it was severe with an aortic pulse pressure greater than 50 mmHg, in 2 it was moderate, and in 8 it was felt to be minimal. Resting cardiac indices ranged from 2.4 to 6.2 L/d,.,/,,,2 with an average of 4.3. Of the fifty patients, 2 have undergone re-operation, 1 for pulmonary stenosis, and 1 for a residual ventricular defect. Therefore, while intracardiac repair of Tetralogy of Fallot dramatically improves the functional ability of these children, repeat catheterization has demonstrated residual ventricular septal defects, pulmonary stenosis, pulmonary insufficiency, tricuspid insufficiency, and aortic insufficiency. Long-term follow-up including hemodynamic evaluation appears warranted.
extension.
RESULTS OF ASCENDING AORTA TO RIGHT PULMONARY ARTERY ANASTOMOSIS IN 123 PATIENTS Milton J. Reitman, MD, Frank M. Galioto, Jr, MD, Gala1 El-Said, MD, FACC, Denton A. Cooley, MD, FACC, Grady L. Hallman, MD, FACC, and Dan G. McNamara, MD, FACC, Baylor College of Medicine, Houston, Texas
154
PERSISTENT HEMODYNAMIC ABNORMALITIES FOLLOWING INTRACARDIAC REPAIR OF TETRALOGY OF FALLOT Michael A. Berman, M.D., Robert P. Rieker. M.D., David I. Robbins, M.D., Norman S. Talner, M.D., FACC, H.C. Stansel, Jr., M.D. Yale University School of Medicine, New Haven, Connecticut
Journal
of CARDIOLOGY
QUANTIFICATION
OF CREATINE
PHOSPHOKINASE
ISOZYMES IN SERUM Robert Roberts, MD; Philip D. Henry, FACC, UCSD, La Jolla, California. Three serum creatine
phosphokinase
(CPK)
MD; Burton E. Sobel,
(CPK) isozymes (MM,
MD,
MB,
and
BB) with different electrophoretic mobilities have been recognized. MB C PK is found primarily in myocardium. lsozyme differentiation by electrophoresis
is only semi-quantitative
the basis for enzymatic
quantification
CPK isozymes with a new method. Aquaside II,
and thus,
of infarct
Serum was concentrated
isozymes in 51~1 samples containing
were separated by cellulose ml of an NADPH
acetate electrophoresis,
37’ for 20 min.
generating
CPK activity
with
0.5 mlU CPK and regions
of the strips encompassing each isozyme were cut out, 0.5
to improve
size we measured
immersed in
assay medium and incubated at
was determined by assay of fluores-
cence in the incubating medium at 25OC in an Aminco-Bowman fluorometer. The assay was linear with respect to incubation time and enzyme concentration (verified
with
radioactively
(3 to 2000 mlU/ml, labeled CPK
n = 200).
Recovery
isozymes) averaged 86 r
2% (S.E .) for each isozyme (n = 35), and reproducibility of isozyme activity in the same sample was within 2%. MB averaged 2 i 1 mlU/ml (S .E.) in normal individuals (n = 15), less than 10 mlU/ml
in 30 patients with
marked CPK elevations
without
Ml,
and 64 -c 13 (n = 11) in samples with Peak total CPK after Ml. In contrast to the 12 hour serum half life of total CPK, MB CPK exhibited a half life of only 5.8 hours. The sensitive method described permits accurate determination
of MB CPK
and thus, is of potential value in the quantitative myocardial infarction by serum enzyme analysis,
Volume
31
in serum samples assessment of
SERIAL
PRECORDIAL
MYOCARDIAL Philip Pitt,
Reid, MD
ST SEGMENT
MAPPING
MD,
Dean Taylor,
MD,
Johns Hopkins University
Precordial
IN ACUTE
INFARCTION David Kelly, and Hospital
MD,
Bertram
Baltimore,
Md.
ST segment mapping has been used to evaluate acute
myocardial
injury.
We have performed serial
ment mapping to detect infarct
extension.
precordial
Precordial
ST seg-
ST segment
mapping was performed in 14 normal subjects using a 48 lead system with
1 mv=20mm
The mean elevation in males was in females. Individual vari-
deflection.
+42.2 +17.8mm and +9.2+5.0mm
ation v&s less than 10 mm on consecutive days. Daily ST segment mapping was done in 15patients with acute myocardial infarction. In 9 patients
with transmural
and 6 patients farction,
anterior
with nontransmural
initial
myocardial
anterior
ST sums were +143.8+91.8mm
mm, respectively. normal (p<.OOl).
(TAM)
myocardial
infarction (NAM)
Those values were%gnificantly After an average of 10.9days
differen from in the TAM group
and 7.3days in the NAM group, ST segment values had fallen in normal limits. Seven of the 9 patients with TAM infarction demonstrated infarct days with further
extension
elevation
on an average of 5.7+2.5
values from the previous day (mean increase+65.4mm, to +190mm).
The infarct
extensions
with
hospital
of ST segment sums when%mpared
events and subsequent elevation
in-
and -81.5+49.2
to
range+17
were confirmed by clinical
of serum creatinine
phosphokinase
One of these patients died. Only two of the patients values. with NAM were found to have infarct extension which occurred on the 6th and 1 lth
hospital day with an average of -5Omm of further
ST segment depression. Infarct extension may be more frequent than previous1 recognized, particularly for transmural anterior infarctions. Seria Y precordial ST segment mapping offers a mpid, assessing m);ocardial
simple,
ischemia and infarct
noninvasive
means of
Between January, 1964 and December, 1971, 123 patients had an intrapericardial ascending aorta-right pulmonary artery @PA) anastomosis for a variety of cyanotic malformations in which there was pulmonary stenosis or atresia. 20 deaths occurred in the first week after operation - 12 from congestive heart failure (CHF), 5 from severe hypoxemia, and 3 from causes unrelated to the surgery. Among the 103 immediate survivors there were 17 late deaths (between 1 month and 5 years postoperative) from CHF (4), hypoxemia (5) and unrelated causes (8). The total shunt-related mortality was 21% with the mortality for patients under 1 year of age being 24% (17 of 70) and for those over 1 year of age 17% (9 of 53). 74 of the 86 survivors have had continued follow-up, 36 of whom have required therapy for CHF. At postoperative cardiac catheterization in 57 patients, 12 (21%) had a nonfunctioning anastomosis and an additional 13 (23%) had stenosis of the RPA proximal to the anastomosis site. 8 patients with RPA stenosis developed RPA hypertension 040 mm Hg) and 2 of them also had main pulmonary artery (MPA) hypertension. 28 patients had intracardiac repair and 14 of these have had repeat cardiac catheterization. One patient had occlusion of the RPA and 4 had MPA to RPA gradient greater than 20 mm Hg (20-70 mm Hg). Ascending aorta-right pulmonary artery anastomosis improves pulmonary blood flow in the cyanotic child but may be followed by complications requiring repair at the time of total correction. Residual changes may remain after total correction.
January
1973
The American
Fifty patients have undergone clinical, hemodynamic. and angiographic evaluation l-6 years following intracardiac repair of Tetralogy of Fallot. The age range was 6-20 years. All but two were asymptomatic (NYHA Class I). The RVEDP was elevated in 32 (64%); the peak systolic RV pressure wae greater than l/2 the simultaneous systemic pressure in 13 (30%) and the LVEDP was greater than 12 mmHg in 10 of 40 (25%). Eighteen of those studied had a patent foramen ovale. There was left to right atria1 shunting present In one. Residual ventricular defects were noted in 8 (16%) with 1 having a QP/OS greater than 2/l. Pulmonary insufficiency was judged by angiogrsphy to be mild in 9/30 (30X), moderate in 12/30 (40%). and severe in 2/30 (6%). Tricuspid insufficiency was seen in 5 (10%). Aortic insufficiency was present angiographicallv in 12 of 25 (48%) in whom it was assessed. In 2 it was severe with an aortic pulse pressure greater than 50 mmHg, in 2 it was moderate, and in 8 it was felt to be minimal. Resting cardiac indices ranged from 2.4 to 6.2 L/d,.,/,,,2 with an average of 4.3. Of the fifty patients, 2 have undergone re-operation, 1 for pulmonary stenosis, and 1 for a residual ventricular defect. Therefore, while intracardiac repair of Tetralogy of Fallot dramatically improves the functional ability of these children, repeat catheterization has demonstrated residual ventricular septal defects, pulmonary stenosis, pulmonary insufficiency, tricuspid insufficiency, and aortic insufficiency. Long-term follow-up including hemodynamic evaluation appears warranted.
extension.
RESULTS OF ASCENDING AORTA TO RIGHT PULMONARY ARTERY ANASTOMOSIS IN 123 PATIENTS Milton J. Reitman, MD, Frank M. Galioto, Jr, MD, Gala1 El-Said, MD, FACC, Denton A. Cooley, MD, FACC, Grady L. Hallman, MD, FACC, and Dan G. McNamara, MD, FACC, Baylor College of Medicine, Houston, Texas
154
PERSISTENT HEMODYNAMIC ABNORMALITIES FOLLOWING INTRACARDIAC REPAIR OF TETRALOGY OF FALLOT Michael A. Berman, M.D., Robert P. Rieker. M.D., David I. Robbins, M.D., Norman S. Talner, M.D., FACC, H.C. Stansel, Jr., M.D. Yale University School of Medicine, New Haven, Connecticut
Journal
of CARDIOLOGY
QUANTIFICATION
OF CREATINE
PHOSPHOKINASE
ISOZYMES IN SERUM Robert Roberts, MD; Philip D. Henry, FACC, UCSD, La Jolla, California. Three serum creatine
phosphokinase
(CPK)
MD; Burton E. Sobel,
(CPK) isozymes (MM,
MD,
MB,
and
BB) with different electrophoretic mobilities have been recognized. MB C PK is found primarily in myocardium. lsozyme differentiation by electrophoresis
is only semi-quantitative
the basis for enzymatic
quantification
CPK isozymes with a new method. Aquaside II,
and thus,
of infarct
Serum was concentrated
isozymes in 51~1 samples containing
were separated by cellulose ml of an NADPH
acetate electrophoresis,
37’ for 20 min.
generating
CPK activity
with
0.5 mlU CPK and regions
of the strips encompassing each isozyme were cut out, 0.5
to improve
size we measured
immersed in
assay medium and incubated at
was determined by assay of fluores-
cence in the incubating medium at 25OC in an Aminco-Bowman fluorometer. The assay was linear with respect to incubation time and enzyme concentration (verified
with
radioactively
(3 to 2000 mlU/ml, labeled CPK
n = 200).
Recovery
isozymes) averaged 86 r
2% (S.E .) for each isozyme (n = 35), and reproducibility of isozyme activity in the same sample was within 2%. MB averaged 2 i 1 mlU/ml (S .E.) in normal individuals (n = 15), less than 10 mlU/ml
in 30 patients with
marked CPK elevations
without
Ml,
and 64 -c 13 (n = 11) in samples with Peak total CPK after Ml. In contrast to the 12 hour serum half life of total CPK, MB CPK exhibited a half life of only 5.8 hours. The sensitive method described permits accurate determination
of MB CPK
and thus, is of potential value in the quantitative myocardial infarction by serum enzyme analysis,
Volume
31
in serum samples assessment of