ABSTRACTS
utilization varied. Increased myocardial O2 demand by L-NE was met by a rise in myocardial blood flow as well as Oa extraction. In the presence of normal myocardial metabolic findings L-NE caused a shift in substrate utilization. Extraction of lactate decreased ; that of FFA strikingly increased. If myocardial metabolism was abnormal before drug administration, the response to L-NE varied. Whereas L-NE further decreased lactate, pyruvate and FFA utilization in most patients, myocardial metabolism markedly improved in others. This study suggests that in selected patients Prop may improve myocardial OZ availability and be beneficial during AMI. Is Coronary Sinus Monitoring in Acute Myocardial Infarction Useful? Studies in 25 Patients HILTRUD MUELLER, MD, FACC: JAMES T. MAZZARA. New York, New York
FACC’; STEPHEN M. AYRES, MD, MD: WILLIAM J. GRACE. MD. FACC.
Prognosis after acute myocardial infarction is related to the oxygen availability and contractile state of the noninfarcted myocardium. Infarcted areas are poorly perfused in the acute state so that mixed coronary sinus (CS) blood is dominated by the metabolic state of the noninfarcted myocardium, suggesting that CS sampling might provide useful information regarding prognosis and efficacy of therapeutic interventions. We evaluated myocardial metabolism in 25 patients in the acute state of transmural infarction and related these findings to clinical and hemodynamic observations. Sequential metabolic measurements were made at 12 to 24 hour intervals for up to 72 hours in 20 patients. Coronary blood flow and myocardial O3 consumption values (mean, range) were, respectively, 87 (57, 111) and 10.6 (5.7, 13.9) ml/100 g per min ; extraction ratios for oxygen, lactate, pyruvate and free fatty acids were 68.9% (53, 82), 10.2% (-44, 38), 1.1% (-96, 38) and 12.6 Y0 (-20, 39)) respectively. Eleven patients had lactate extraction ratios below 12% for at least 24 hours and were tentatively considered to exhibit “abnormal” myocardial metabolism. Most patients who changed from abnormal to normal metabolism demonstrated evidence of arrhythmias, left ventricular failure, or hypotension; in 2 or 4 patients who remained abnormal during 48 to 72 hours shock developed, and they died. All but 1 of the patients who had normal metabolism during the entire observation period did well. The following initial measurements were significantly different (P <0.05) comparing abnormal to normal groups: pulse pressure -32 mm Hg; diastolic arterial pressure -23 mm Hg; mean arterial pressure -29 mm Hg; left ventricular work index -2.5 kg-m/min per m2. Pulmonary arterial wedge pressure and arteriovenous 0, difference were 5 mm Hg and 2.1 ml/100 ml higher in the abnormal group, but clear statistical significance was lacking. These observations suggest that CS monitoring in complicating infarction may be useful for prognosis and management. Tritiated Digoxin Uptake by the Normal and Hypertrophied Rabbit Myocardium MARVIN L. MURPHY, MD, FACC, Little Rock, Arkansas
FACC*;
JAMES
E. DOHERTY,
MD,
The relative importance of myocardial mass compared to serum levels of digoxin for achieving maximal conVOLUME
29, FEBRUARY
1972
centration of digoxin is undetermined. Left ventricular hypertrophy (LVH) was induced in 6 rabbits by a technique of banding the aorta with the production of a significant gradient. The weight of the left ventricle of the banded rabbits exceeded that of the control animals by an average of 49.6% (2.39 or 4.81). These animals are compared with 5 control rabbits. Tritiated digoxin (125 &mg) in a dose of 0.045 mg/kg was given intravenously to each animal. Serum samples were collected every 15 minutes for 2 hours at which time the animals were sacrificed and all tissues analyzed for digoxin content by a method of chloroform extraction, column chromatography and liquid scintillation counting. There was no significant difference in serum levels between the control animals and those with LVH. A significant correlation (r = 0.883) was established between the serum concentration of digoxin and the total myocardial digoxin concentration. Serum concentration rather than myocardial mass is the determining factor in myocardial tissue concentration of tritiated digoxin ; thus, the presence of cardiac hypertrophy does not undermine the usefulness of the serum level of digoxin. The Mechanism of Activation of the Canine Endocardium ROBERT J. MYERBURG, MD*; GELBAND, MD, Miami, Florida
KRISTINA
NILSSON;
HENRY
To determine the mechanism of the sequence of activation of the intraventricular conducting system and subendocardial muscle, we studied isolated preparations of large areas of canine endocardium, using standard microelectrode techniques and surface recordings. It was possible to stimulate the bundle branches locally, without nonspecific activation of the underlying muscle, with either intracellular stimulation or surface stimulation close to threshold. The results show that the right bundle branch gives no impulse input to the septal muscle until after passing the base of the anterior papillary muscle, at which point fibers reflect back to the anterior and posterior septum to activate the muscle. The earliest point of muscle activation occurred at the apical free wall, with the right ventricular free wall endocardium, anterior papillary muscle, and the septum from apex to base following in sequence. The left bundle branch (LBB), its proximal major divisions, and the subendocardial Purkinje fiber network of the upper portions of the left ventricular cavity generally do not provide impulse input into ordinary ventricular muscle. Rather, the propagating impulse passes from the conducting system into muscle on the lower third of the septum, the ventricular apex, the bases of the papillary muscles, and the interpapillary free wall. Muscle depolarization then occurs from the apex to base of the ventricular cavity, and from base to apex on the papillary muscles. The divisions of the LBB of the canine heart meet on the high interpapillary free wall to complete a ring of tissue having functional continuity. Second Degree Wenckebach Type Atrioventricular Block Due to Block Within the Atrium ONKAR S. NARULA, MD*; MANFRED MD, FACC, Miami Beach, Florida
Two female patients
RUNGE,
MD; PHILIPSAMET,
69 and 72 years old with a history 283
ABSTRACTS
of paroxysmal supraventricular tachycardia were analyzed by His bundle and intraatrial recordings. The electrocardiogram showed sinus bradycardia (SB) in 1 patient and SB with sinoatrial Wenckebach in the other. The conduction times through the atrioventricular (A-V) node (A-H) and His-Purkinje system (H-V) were normal in both cases. The intraatrial (P-A) conduction time was slightly prolonged (55 msec) in 1 and normal (40 msec) in the other, during normal sinus rhythm. In both cases with atria1 pacing from high right atrium (RA) the conduction time from the pacing impulse (PI) to atria1 (A) activation in the area of the A-V junction (PI-A) progressively lengthened with increase in AP rate, and finally classic second degree Wenckebach type of block was manifested at cycle lengths of 460 and 465 msec. The PI to QRS interval (PI-R) showed a progressive increase before the blocked stimulus. The lengthening of the PI-R interval was due to progressive increase in the intraatrial (PI-A) conduction time. In the dropped beats the PI was not followed by an A wave and indicated type I block within the atrium. Similarly, during induced premature atria1 be;lts the PI-A time progressively lengthened as the coupling interval was shortened. These fmdings were reproducible and were seen despite a 3-fold increase in stimulus strength and changes in electrode position along the lateral RA border. This study (1) demonstrates a hitherto undescribed site for the exhibition of second degree Wenckebach block, i.e., the atrium; (2) supports the existence of sinoatrial Wenckebach; and (3) suggests the atrium as another possible site for reentry and a cause for supraventricular tachycardia because of the degree of delay and block exhibited within the atrium.
Ten Year Experience With Isolated Starr-Edwards Mitral Valve Replacement HERBERT A. OXMAN, MD’; DANIEL C. CONNOLLY, MD, FACC; DWIGHT C. McGOON, MD; ROBERT 6. WALLACE, MD; GORDON K. DANIELSON, MD, FACC; JAMES R. PLUTH, MD, Rochester, Minnesota
Between April 29, 1961 and December 31, 1970, 1,081 Starr-Edwards (S-E) mitral valves were inserted in 1,073 patients at the Mayo Clinic. Of these, 604 patients (4154) male and 597; female) underwent 608 operations for isolated S-E mitral valve replacement. The average age was 49 years, 9774 were in New York Heart Association functional class III or IV preoperatively. Thirty-four percent of the patients had had previous cardiac surgery. Early mortality (within the first 30 days) after surgery was 15yh (94/608). The most common cause of early mortality was low cardiac output, which accounted for 38’;4, of the deaths. The incidence of early thromboembolic complications was 5%. Of the 510 patients who survived the first 30 days, followup study has been possible through April 1971 in 507 (99.4%) ranging from 1 month to 114 months (mean 44 months). Late mortality thus far has been 22$. Overall total mortality thus far is 3574 (210/604). Of the entire group of 604 patients, 394 (65%) were alive in April 1971 with improved functional status. The most common cause of late death was chronic congestive heart failure in 29:4 (34/116) of the cases. Incidence of early thromboembolic complications following isolated mitral S-E replacement was 55/c (31/ 608) ; the incidence of late embolic complications was At least 1 thromboembolic episode oc28C, (145/510). curred in 287: (1701608) of the total group. Early mortality for isolated mitral valve replacement during 1961 through 1965 was 2356 (51/225) and for 1966 through 1970 was ll?;> (43/383).
A Study of the Effect of the Argus Computer System on Treatment Actions in a Coronary Care Unit G. CHARLES OLIVER, MD, FACC*; FLOYD M. NOLLE, MS; ALAN J. TIEFENBRUNN, AB; KENNETH W. CLARK, BS, St. Louis, Missouri
A prospective study was made over a 2 month period to evaluate the influence of a dedicated computer system (ARGUS) on the mode of treatment of ventricular arrhythmias. Patients admitted to the Barnes Hospital coronary care unit were divided into 2 groups (A and B) of 20 patients each. Continuous monitoring by Argus was instituted on all patients as soon as possible and continued for an average of 32 hours per patient, resulting in a total of 1,278 hours of monitoring. Both groups were also monitored by conventional methods. Argus calculated the rate of premature ventricular contractions (PVC’s) and detected the occurrence of certain premonitory combinations of PVC’s in both groups but supplied these results to the nurses for group A only. The influence of Argus was studied by noting treatment actions consisting of an initiation or an increment in rapid-acting antiarrhythmic agents. In all, 33 actions were taken, 25 in group A and 8 in group B. For these patients, an average of 3.1 actions were taken for patients in group A but an average of only 1.3 for those in group B. Thus, computer monitoring resulted in a marked increase in treatment actions with rapidacting antiarrhythmic agents.
284
Syndrome of Ventricular With Aortic Insufficiency
Septal Defect
MD; WILLIAM H. LUCY F. PARISI, MD*; ALYS M. HOLDEN, PLAUTH. MD: ALEXANDER S. NADAS, MD, Boston, Massachusetts
The course of 72 patients having ventricular septal defect (VSD) with aortic insufficiency (AI) followed up between 1950 and 1971 and involving over 600 patient years has been reviewed. The median age of onset of AI was 6.9 years (range 0.1-20.5) with male subjects comprising 61% (44/72). The median pulmonary to systemic flow ratio was 2.1 (range l-5) ; moderate to severe AI was present in 619, (44/72) ; and significant pulmonary stenosis was present in 197: (12/72). The average duration of followup study prior to onset of AI was 2.9 years (range O-15) with 3 patients experie encing AI 1.4 to 4.2 years after VSD closure. The average duration of followup after onset of AI and before operative in ervention was 4.3 years (range O-18). Surgery was performed in 57% (41172). During the followup period the condition of the patients deteriorated in 44% (32172)) improved in 6(/, (4/72) and did not change in the remainder. Whereas only 37y; (27,’ 72) were symptomatic at the onset of AI, congestive heart failure (CHF), dyspnea or fatigue subsequently developed in 57:{ (41/72). The overall mortality was
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