Echocardiographic detection of scar tissue in patients with coronary artery disease

Echocardiographic detection of scar tissue in patients with coronary artery disease

ABSTRACTS ECHOCARDIOGRAPHIC DETECTION OF SCAR TISSUE IN PATIENTS WITH CORONARY ARTERY DISEASE. Betty C. Corya, MD; Susan Rasmussen, RN; Harvey Feigen...

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ABSTRACTS

ECHOCARDIOGRAPHIC DETECTION OF SCAR TISSUE IN PATIENTS WITH CORONARY ARTERY DISEASE. Betty C. Corya, MD; Susan Rasmussen, RN; Harvey Feigenbaum, MD, FACC; Mary J. Black, BA; Suzanne B. Knoebel, MD, FACC. Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana. The purpose of this study was to determine if septal thickness and echo density on M-mode echocardiography (ECHO)

represents

scar.

Sector scans of the left ventricle were made from as many intercostal spaces as possible. Among 275 coronary artery disease patients (pts), 53 (19%) had septal areas which were thin (less than the 7 mm lower limit of the normal range) and dense, compared to the opposing posterior wall. Q waves were present in the anterior electrocardiographic leads in 52 of these 53 pts (98%). Twenty-six of these 53 pts were examined either by surgery (18 pts) or by autopsy (8 pts) and septal scar was confirmed in each case. This group was compared to normal and to pts with acute infarction. In 19 pts there were continuous sector scans from areas of normal septum to the thin dense areas; in 7 pts the septum was thin and dense in all areas examined by ECHO. Septal thickness in the area of suspected scar ranged from 3-6 mm with a mean of 5 mm and was significantly less than the normal range of 7-12 mm with a mean of 9 mm (p
EFFECT OF THE BETA ADRENERGIC RECEPTOR UPON POTASSIUM UPTAKE IN SKELETAL MUSCLE Jim C. Costin, M.D., Lawrence S. Cohen, M.D., FACC, Barry L. Zaret, M.D., FACC, Yale University School of Medicine, New Haven, Connecticut. The role of the beta adrenergic receptor in the control of potassium uptake by skeletal muscle was evaluated in 17 dogs utilizing the vascularly isolated, innervated gracilis muscle and hindlimb. The uptake of potassium (43K or 42K) following intravenous injection was assessed from tissue activity and local arterio-venous (A-V) K differences in pairs of muscle either at rest or post-contraction (PC). Either local beta adrenergic blockade with propranolol (6AB) or stimulation with isoproterenol (BAS) was carried out in each state. Studies were performed in both the controlled blood flow and autoperfused states. In the control state potassium uptake was 8.7 times greatBeta adrenergic blockade deer PC than at rest (pc.01). creased uptake by 64.3% PC (pc.001) and by 27.9% at rest In all studies there was no difference between (pc.01). autoperfused and constant perfused muscles. Returning contraction strength to control (increased voltage stimulation) in the@B muscles had only minor effects on K uptake. BAS resulted in significantly greater K uptake both at rest (77.8%, pc.001) and PC (605.1%, pc.001). K kinetics offered additional support for the muscle uptake data, showing significantly less A-V difference in the SAB muscles (pc.001). Thus the beta adrenergic receptor plays a significant role in skeletal muscle potassium uptake, which is most marked post-contraction. This role is independent of local blood These findings may have flow and contraction strength. clinical relevance in the muscle fatigue associated with propranolol therapy.

DETECTION

OF MYOCARDIAL

INFARCTION

EARLY

AFTER

CORONARY ARTERY BYPASS GRAFT SURGERY Michael Crawford, MD; Albert0 Righetti, MD; Robert O’Rourke, MD,

FACC;

Thordur

Hardarson,

MD;

Pat Daily,

MD;

DeLuca, PhD; William Ashburn, MD; John Ross, Jr., University of California Medical Center, San Diego,

Marlene MD, FACC, California.

To evaluate methods for detecting myocardial infarction (Ml) after coronary artery bypass graft surgery (CABG), we studied 39 patients (pts) before and serially during the first 48 hrs. after CABG with ECGs, VCGs and serum MB-CPK isoenzymes. In addition, 99Tc pyrophosphate (P) myocardiol scans were obtained in 27 pts 4 to 5 days after CABG. Twenty-two pts (57%) had no ECG or VCG changes post CABG (group I); all 16 P scans in these pts were negative and only one pt hod an elevated MB-CPK area (4 samples over 48 hrs). Eleven pts (28%) had ECG and VCG evidence of new MI (group II); 7 of 8 P scans in these pts were positive and MB-CPK was elevated in all. Six pts (15%) had diffuse ST-T wave changes (group Ill); of 4 P scans done, all were negative, but MB-CPK was increased in 4 pts (2 with negative P scans). Meon MB-CPK area was 953?288(SE) IU/L in group II pts compared to 77*36 IU/L in group I pts and 147*36 IU/L in group III pts (both p<.Ol). The preoperative radioisotopeejection fraction,the severityof coronary artery disease and the number of grafts inserted were not different in the groups. However, the total aortic cross clamp time was longer in group II pts, 41: 18 vs 25t5.1 min in group I and III pts (p<.O2). We conclude that MB-CPK determinations are useful for confirming transmural MI post CABG and for detecting subendocardial Ml; in contrast, P scans appear to be specific, but less sensitive for detecting post CABG infarction. Factors other than coronary anatomy and LV performance appear to define the incidence of Ml post CABG.

EVOLUTION OF REGIONAl POSTEXTRASYSTOLIC POTENTIATION DURING EXPERIMENTAL MYOCARDIAL INFARCTION Bertrand Crozatier, MD; Pierre Theroux, MD: Shigetake SaF ayama, MD; Dean Franklin; John Ross,Jr.,MD, FACC,Univ. of Calif.,San Diego,School of Medicine, La Jolla, California Regional postextrasystolic potentiation (PEP) following coronary artery occlusion (CO) was studied serially in 9 dogs (5 conscious) instrumented with a cuff around the circumflex coronary artery and pairs of ultrasonic crystals implanted subendocardially in ischemic segments that showed no significant return of shortening (IS) and in marginal segments that showed eventual return of active (% shortening (MS). The percent shortening or bulging AL) of each segment during systole was measured in each region before a spontaneously occurring premature ventricular contraction (PVC) and in the beat following the PVC. Within 1 minute after CO (20+5 sec,SEM), in the MS, %AL was 8.05.8 in the contraction preceding a PVC and 16.2+ 2.8 in the beat following the PVC (~~0.05). In the IS, systolic expansion (%AL -1.6+2.3%)in the beat before the PVC was replaced by shortening (%AL=19.5+6.5) ($0.05) in the beat after the PVC. Within the firsil 15 minutes following CO (9.30+2min) %AL in MS was 0.0+2.1before the WC and 9.0+1.5 after the PVC (~~0.05) while PEP was less in the IS,-%AL being -6.0+1.5 in the beat before the PVC and -1.2+1.9 in the beat aFter the PVC (~~0.05). Only slight further decreases in PEP in IS and MS occurred during the subsequent 1.5 hours and there were no further changes in PEP during the ensuing 2 days. Thus, there is extreme and persistent reduction of PEP in severely ischemic myocarduim within minutes after CO, even when function can be restored by reperfusion. In contrast, PEP persists over a prolonged period in marginally ischemic myocardium. These findings suggest caution in interpreting the significance of minimal PES after CO but indicate that viable myocardium can be identified by PES when accompanied by active shortening.

January 1976

The American Journal of CARDIOLOGY

Volume 37

129