ABSTRACTS

SERIAL PRECORDIAL ST SEGMENT MAPPING IN ACUTE

MYOCARDIAL INFARCTION

Philip Reid, MD, Dean Taylor, MD, David Kelly, MD, Bertram

Pitt, MD Johns Hopkins University and Hospital Baltimore, Md.

Precordial ST segment mapping has been used to evaluate acute

myocardial injury. We have performed serial precordial ST seg-

ment mapping to detect infarct extension. Precordial ST segment

mapping was performed in 14 normal subjects using a 48 lead system

with 1 mv=20mm deflection. The mean elevation in males was +42.2 +17.8mm and +9.2+5.0mm in females. Individual vari-

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 anterior myocardial (TAM) infarction

and 6 patients with nontransmural anterior myocardial (NAM) in-

farction, initial ST sums were +143.8+91.8mm and -81.5+49.2

mm, respectively. Those values were%gnificantly differen from

normal (p<.OOl). After an average of 10.9days in the TAM group

and 7.3days in the NAM group, ST segment values had fallen with

in normal limits. Seven of the 9 patients with TAM infarction

demonstrated infarct extension on an average of 5.7+2.5 hospital

days with further elevation of ST segment sums when%mpared to

values from the previous day (mean increase+65.4mm, range+17

to +190mm). The infarct extensions were confirmed by clinical

events and subsequent elevation of serum creatinine phosphokinase

values. One of these patients died. Only two of the patients

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, simple, noninvasive means of

assessing m);ocardial ischemia and infarct 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

Between January, 1964 and December, 1971, 123 patients had an intrapericardial ascending aorta-right pulmonary artery @PA) anastomosis for a variety of cyanotic mal- formations 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 nonfunc- tioning 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 im- proves 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.

PERSISTENT HEMODYNAMIC ABNORMALITIES FOLLOWING INTRACAR- DIAC REPAIR OF TETRALOGY OF FALLOT Robert P. Rieker. M.D., Michael A. Berman, 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

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 angiograph- icallv 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.

QUANTIFICATION OF CREATINE PHOSPHOKINASE (CPK)

ISOZYMES IN SERUM

Robert Roberts, MD; Philip D. Henry, MD; Burton E. Sobel, MD,

FACC, UCSD, La Jolla, California.

Three serum creatine phosphokinase (CPK) isozymes (MM, 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 and thus, to improve

the basis for enzymatic quantification of infarct size we measured

CPK isozymes with a new method. Serum was concentrated with

Aquaside II, isozymes in 51~1 samples containing 0.5 mlU CPK

were separated by cellulose acetate electrophoresis, and regions

of the strips encompassing each isozyme were cut out, immersed in

0.5 ml of an NADPH generating assay medium and incubated at

37’ for 20 min. CPK activity 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 (3 to 2000 mlU/ml, n = 200). Recovery

(verified with radioactively labeled CPK isozymes) averaged 86 r

2% (S.E .) for each isozyme (n = 35), and reproducibility of iso-

zyme 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 ex-

hibited a half life of only 5.8 hours. The sensitive method de-

scribed permits accurate determination of MB CPK in serum samples

and thus, is of potential value in the quantitative assessment of

myocardial infarction by serum enzyme analysis,

154 January 1973 The American Journal of CARDIOLOGY Volume 31