The normal blood supply to the his bundle and proximal bundle branches

ABSTRACTS

then reduce the vascular resistance in the subepicardial more than the subendocardial vessels, resulting in a “steal” of blood flow from deep to superficial myocardium with little or no change in total coronary Aow. Acute Myocardial Infarction: Perfusion and Metabolism

Myocardial

JAMES FORRESTER, MD*; GEORGE DIAMOND. MD; WILLIAM GANZ, MD, FACC; H. J. C. SWAN, MD, PhD, FACC, Los Angeles, California

Coronary blood flow (CBF) and myocardial metabolism were evaluated in 26 patients with coronary artery disease. Ten subjects had stable coronary artery disease, 5 were hospitalized with acute coronary insufficiency without infarction and 13 had acute myocardial infarction (AMI) (2-96 hours after infarct). In the AM1 group, 5 patients had uncomplicated infarction, 5 had congestive heart failure and 2 had cardiogenic shock. CBF was measured by the thermodilution coronary sinus flow technique, and transmyocardial arteriovenous differences of lactate, serum glutamic oxaloacetic transaminase, lactic dehydrogenase, creatine phosphokinase, potassium, magnesium and calcium were determined. Although lactate metabolism at rest was abnormal in 8 of 12 with AMI, CBF in patients without shock (127 i 16 cc/min, range 71-218 cc/min) and coronary vascular resistance (6.3 -c 0.9 x lo4 dynes set cm-s) did not differ from values in the groups without infarction. Furthermore, no significant difference in arterial and coronary sinus levels of electrolytes or enzymes was found in the AMI group despite the presence of rising serum enzyme levels. The levels of CBF in the AM1 patients did not correlate well with any individual determinant of flow (arterial diastolic pressure, left ventricular (LV) filling pressure, LV AP/AT, or heart rate). Thus, despite definite evidence of reduced regional myocardial perfusion and necrosis, total CBF remained normal and did not decrease with increasing size of infarct. The absence of detectable enzyme and potassium leakage in the presence of abnormal lactate metabolism suggests that (1) the rate of release of these substances is slow relative to the sensitivity of current methods of biochemical analysis, and (2) metabolic studies in AMI may be seriously limited by this phenomenon. On the Mechanism of Diastolic Rumbles NICHOLAS J. FORTUIN, Chapel Hill, North Carolina

MD*;

ERNEST

CRAIGE,

MD,

FACC,

We used the combined techniques of phonocardiography, apex cardiography and mitral valve echocardiography in simultaneous multichannel recordings to study the apical diastolic rumbling murmur accompanying the following conditions : pure mitral regurgitation (MR, no. = 7) ; severe aortic regurgitation (AR, no. = 16) ; large left to right shunt (no. = 2) ; and mitral stenosis (no. = 12). In patients with MR, shunt or AR the rumbles were indistinguishable phonocardiographitally and occurred in mid-diastole after the period of rapid ventricular filling. In these patients the rate of mitral valve closure was excessively rapid, and the murmur occurred as the valve was closing. In patients with mitral stenosis in normal rhythm the crescendo portion of the presystolic murmur occurred after the period of atria1 systole. In patients with mitral stenosis VOLUME

29, FEBRUARY

1972

and atria1 fibrillation a crescendo presystolic murmur occurred when the duration of the preceding diastole was short. In both cases the crescendo murmur was coincident with the closing movement of the mitral valve. This occurred after the onset of isometric ventricular systole. Our findings suggest that these murmurs are due to increasing flow velocity as a result of a dynamically narrowing mitral valve orifice. The increase in flow velocity may occur even when the volume of flow is diminishing. A common denominator is thus demonstrated in the genesis of diastolic rumbling murmurs in a variety of conditions. Improved Left Ventricular Function During Nitroprusside Infusion in Acute Myocardial Infarction JOSEPH A. FRANCIOSA, MD*; NABIL H. GUIHA, MD; ERNEST0 RODRIGUERA, MD; CONSTANTINOS LIMAS, MD; JAY N. COHN, MD, FACC, Washington, D. C.

Afterload is a major determinant of myocardial oxygen consumption (MVOp) which, if decreased, should benefit an ischemic myocardium and improve ventricular performance. In 11 patients with acute myocardial infarction (AMI) nitroprusside (NP), a potent vasodilator, was infused at a rate sufficient to produce a slight reduction in arterial pressure (AP) . During NP infusion mean AP decreased from an average of 106 to 87 mm Hg, whereas heart rate was unchanged. Left ventricular filling pressure (LVFP) decreased consistently from an average of 21.6 to 10.0 mm Hg (P
The Normal Blood Supply to the His Bundle and Proximal Bundle Branches RICHARD mingham,

J. FRINK, Alabama

MD*;

THOMAS

N. JAMES,

MD,

FACC,

Bir-

Ten human hearts without coronary disease were injected with a highly colored barium gelatin mass to outline the blood supply to the His bundle (HB) and proximal bundle branches (PBB) . A different color was injected into right (R) , left anterior descending (LAD) and circumflex coronary arteries. The coloring material can withstand histologic processing and permitted histologic determination of the blood supply to these structures. The HB received a dual supply of blood from the atrioventricular nodal artery (AVNA) 263

ABSTRACTS

and penetrating branches from the anterior septum in 90% of cases. The HB and PBB were supplied wholly by AVNA in 10:/c. The proximal right bundle branch and anterior fascicles of left bundle branch (LBB) received a dual supply in 50% and were supplied by anterior septal branches alone in another 40%. The posterior fascicles of the LBB received a blood supply from the AVNA in 50% and a dual supply from AVNA and anterior septal arteries in 40%). In 10% the posterior fascicles were supplied by the LAD. We conclude that the blood supply to most portions of the HB and PBB is frequently dual, with the most anterior and posterior portions being commonly supplied by the anterior septal and AVN arteries, respectively. These 2 vascular systems generally arborize in the mid-portion of the HB. New England Regional Infant Cardiac Program DONALDC. FYLER, MD*; LUCY PARISI, MD; MICHAEL BERMAN, MD, Boston, Massachusetts and New Haven, Connecticut

A regional program encompassing all 11 New England hospitals which provide definitive care for infant cardiac patients was begun in 1969. The purposes of this program are to increase case finding, to encourage early referral and to improve transportation, diagnosis and treatment. Data referrable to any infant ill with cardiac disease have been tabulated and results covering a 36 month period (circa 1,200 infants) will be available within weeks. To date experience with 826 critically ill infant cardiac patients seen between July 1968 and June 1970 is available. During the first year of program activity 457 babies underwent cardiac catheterization or cardiac surgery or died, compared to 369 in the prior year. Three hospitals managed 70$? of the infants; 30% were managed in 8 smaller hospitals. Overall hospital mortality for the 2 year period was 360/c. Whereas 115 patients underwent surgical procedures (29 “4, mortality) in 8 smaller hospitals, an additional 31 babies were transferred to larger hospitals for surgery. Among the larger hospitals gross surgical mortality was 405; (32-56s). Medical management of 455 patients resulted in 367; mortality. The hospital using surgical treatment most aggressively (54 “/c surgical management) produced the lowest overall mortality rate (3254) ; the hospital that used conservative treatment most often (555% medical management) produced the highest overall mortality rate (49 ‘/o). From these preliminary experiences, it is our impression that an aggressive approach to case finding, early diagnosis and treatment results in improved survival among infants critically ill with cardiac disease. Alterations in the Left Ventricular Contractile State During Isometric Exercise in Patients with Coronary Artery Disease WILLIAM H. GAASCH, MD*; MIGUEL EFRAIN WAISSER, MD; HANS G. THIEL, ANDER, MD, FACC, Houston, Texas

A. QUINONES, MD; MD; JAMES K. ALEX-

The effects of isometric exercise (IE) on myocardial function were evaluated in 8 patients. Two normal subjects and 6 patients with angiographically documented coronary artery disease (CAD) were studied before

264

and at 3 minutes of IE (2576 maximal voluntary contraction). Using isovolumic pressure measurements (SF-l, catheter tip micromanometer), contractile elein see I) at 0 load ment velocity (V,-,,: = ldp/dt1/24P (Vmax) and peak V(., were derived. Left ventricular (LV) max dp/dt, heart rate (HR), blood pressure (BP), and arteriovenous oxygen (A-V 0,) differences were measured. During IE all 8 patients had similar increases in HR (22 % ) and mean BP (18 f$ ) . In 2 normal subjects and 1 patient with CAD, LV end-diastolic pressure (EDP) and A-V OZ differences remained unchanged ; Vmax increased 38% (2.1 r_ 0.2 to 2.9 t 0.3), peak Vc7iGincreased 4356 (1.6 2 0.2 to 2.3 & 0.2), and max dp/dt increased 22%. In 5 patients with CAD the A-V 0, difference widened 12% (4.1 c 0.3 to 4.6 2 0.2 vol %), LVEDP increased 69% (16 ? 3 to 27 -C 6 mm Hg) and max dp/dt increased 16%. In this group, Vmax averaged 1.6 2 0.1 and peak V(.,< averaged 1.1 2 0.2 (control state) ; during IE there was no change in Vmax or peak Vc.r in 3 of the 5 ; angina developed in the other 2, and in both patients Vmax and peak V,, fell (18% and 20 %, respectively). Thus, it appears that in normal subjects LV performance improves during IE by a shift to an augmented ventricular function curve (improved contractile state, no change in perload), whereas in some patients with CAD this transition does not occur (increased preload, no change in contractile state). When angina occurs preload increases and a decrease in contractility may occur. IE, as a test of myocardia! function, has been used to gain further insight into altered ventricular dynamics in patients with CAD. Manifest and Concealed Reentry: A Mechanism of Atrioventricular Nodal Wenckebach in Man JOHN J. GALLAGHER, MD*; JACOB VARGHESE, MD; SUN York

ANTHONY N. DAMATO, MD; P. H. LAU, MD, Staten Island, New

Previous explanations of the atrioventricular nodal (A-VN) Wenckebach phenomenon have centered around the concept of decremental conduction. Recent animal studies from this laboratory suggest that A-VN reentry may provide an alternate mechanism of conduction delay and block during A-VN Wenckebach cycles. The present study documents similar findings in man. Four patients were studied using electrograms recorded from the high right atrium (HRA) and His bundle (HBE) during stimulation of the atrium (A) and ventricle. During sinus rhythm, a normal sequence of atria1 depolarization from high (HRA) to low (HBE) atrium was noted. Ventricular pacing (S) was associated with a reversal of atria1 depolarization. In addition, a retrograde His (HR) was seen in 2 patients. The ventricle was paced at a cycle length sufficient to produce retrograde Wenckebach. At a critical degree of retrograde A-VN delay, manifest reentry (reciprocal beat) occurred. Decreasing the cycle length of stimulation concealed the reentry. The presence of concealed reentry can be confirmed by noting an antegrade His deflection with a shorter S-H interval than the otherwise constant S-H,, during ventricular pacing. Both concealed and manifest reentry occurred after the last retrograde atria1 complex of the Wenckebach cycle. The mechanism by which the last ventricular impulse

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