M. Ziad Sinno

Cardiac Conduction in Patients with Symptomatic Sinus Node Disease

Cardiac conduction was investigated at the time of pacemaker insertion in 15 patients with symptomatic sinus node disease. Techniques included recording of His bundle potentials, atrial pacing at various heart rates, and atropine administration. Atrioventricular (AV) conduction was impaired in eight patients who manifested one or more of the following: P-R prolongation, P-H prolongation, and development of second degree AV block with atrial pacing at heart rates below 130 beats/min. Five patients had intraventricular conduction defects diagnosed electrocardiographically; none of these had H-Q prolongation. One of these five, with left bundle-branch block, subsequently developed complete heart block and had a calcific lesion involving the His bundle. Depression of cardiac automaticity was noted in four patients, with asystolic periods greater than 2 sec after sudden cessation of atrial pacing at rates of 100-160 beats/min. Responses to 1 mg of intravenous atropine were varied, but no patient developed sinus rates greater than 90 beats/min, suggesting the presence of primary sinus node dysfunction.In conclusion, abnormalities of conduction and automaticity in specialized tissue in addition to the sinus node are common in patients with symptomatic sinus node disease. These abnormalities should be recognized when present, so that the ideal site for permanent pacing may be chosen.

Relationship of Pulmonary Artery to Left Ventricular Diastolic Pressures in Acute Myocardial Infarction

We have measured pulmonary artery (PA) and left ventricular diastolic pressures (LVDP) in patients with acute myocardial infarction to establish the relationships of PA pressure to LVDP. Paired determinations for the various parameters showed (mean difference in mm Hg): left ventricular end-diastolic pressure (LVEDP)-LVDP pre-a + 7.9, P < 0.001; LVEDP-mean PA wedge + 6.0, P < 0.001; mean PA wedge-LVDP pre-a, + 0.8, P > 0.2; PA end-diastolic pressure (PAEDP)-mean PA wedge (in all patients) +3.3, P < 0.001; PAEDP-mean PA wedge (patients with pulmonary vascular resistance ≦2 units) +1.3, P < 0.1; LVEDP-PAEDP +4.7, P < 0.001; and LVEDP-mean PA −2.0, P < 0.02. The relationship of LVEDP to mean PA wedge was: LVEDP (y) = 1.12 mean PA wedge (x) +4.69; Sy.x = 3.42; r = 0.92.After acute myocardial infarction, PA pressures did not accurately reflect LVEDP because atrial contraction made a large contribution to ventricular filling pressure. In addition, PAEDPs were not the same as mean PA wedge pressures because of some increase of pulmonary vascular resistance in many patients. Thus, PA pressures only provided reliable information about the level of pulmonary venous pressure. LVDP pre-a correlated well with mean PA wedge pressure, and therefore measurement of LVDP (pre-a and EDP) yielded information not only about pulmonary edema, but also about LV performance.

Site of Heart Block in Acute Myocardial Infarction

Bundle of His electrograms were recorded in eight patients with acute myocardial infarction and heart block. Three patients with diaphragmatic myocardial infarction (DMI) and one with subendocardial infarction were characterized by slowing or block above the bundle of His and A-V junctional escape rhythms during periods of advanced or complete block. An additional patient with DMI had block in the His bundle itself. Intraventricular conduction in the above patients was characterized by normal H-Q intervals (35 to 60 msec) and absence of widened QRS. In contrast, three patients with anterior infarction (AMI) manifested complete block below the bundle of His and idioventricular escape. P-H intervals were normal (80 to 140 msec) and A-V conduction was considered unaffected. Our electrophysiologic observations coupled with previous clinical, anatomic, and pathologic findings suggest that the heart block in DMI is usually due to an ischemic lesion of the A-V node, while heart block in AMI is due to necrosis involving both bundle branches.

Bundle Branch and Ventricular Activation in Man A Study Using Catheter Recordings of Left and Right Bundle Branch Potentials

His (H), right bundle branch (RB), and left bundle branch (LB) potentials were recorded by electrode catheters passed into the left and right ventricles in seven patients without conduction defects. In another three patients, H and LB were recorded. Initial ventricular activation was considered to coincide with the onset of the QRS (Q). The following intervals were measured in milliseconds: H-Q, LB-Q, RB-Q, H-LB, H-RB, and LB-RB. The average and range of these was as follows: H-Q 46 (39-54), LB-Q 27 (24-30), RB-Q 25 (20-27), H-LB 20 (14-28), H-RB 21 (15-29), and LB-RB 2 (1-10). LB-RB was 3 msec or less in six of seven patients. Coupled atrial pacing produced delays in H-RB without effect on H-LB and LB-Q. The production of incomplete and complete right bundle branch block was related to increase in the LB-RB interval. One patient developed left bundle branch block (LBBB) during coupled pacing with delay of LB while RB-Q remained unchanged. H-Q intervals were measured in three additional patients with rate related LBBB during both control and block. Prolongation of H-Q was less than 3 msec during LBBB. It is concluded that the proximal left and right bundle branches are usually activated simultaneously in man, and that block of either bundle without contralateral bundle delay does not significantly delay the onset of ventricular activation.

Effects of ouabain on impaired left ventricular function in acute myocardial infarction.

Abstract The effects of intravenous ouabain were assessed in 16 patients with a recent acute myocardial infarction. The mean ± S.E.M. of the values, before and one hour after ouabain, were as follows: left ventricular end-diastolic pressure, 24.8 ± 2.1 and 16.1 ± 2.5 mm Hg; left ventricular stroke work, 65.8 ± 9.5 and 80.9 ± 14.3 g-m per beat; peak first derivative of left ventricular pressure, 1798 ± 150, and 2081 ± 150 mm Hg per second; maximum velocity of contractile element shortening, 1.20 ± 0.04 and 1.41 ± 0.06 muscle lengths per second; and pre-ejection period corrected for heart rate, 135.0 ± 5.0, and 128.8 ± 3.6 msec. These changes were significant (p less than 0.05 for paired determinations). There were no significant changes in cardiac index, heart rate and mean arterial pressure. Although ouabain does not change cardiac output in patients with acute myocardial infarction, it causes significant improvement in other indexes of left ventricular performance.

Failure of rapid atrial pacing in the conversion of atrial flutter

Abstract Rapid atrial pacing, at rates of 150 to 600/min with stimulus strength up to 15 ma, was attempted in 15 patients with atrial flutter. In 13 of the patients, atrial capture was achieved with changes in both atrial and ventricular rates. In 7 of these, flutter resumed upon cessation of pacing. In the other 6, rapid atrial pacing produced atrial fibrillation which persisted until cardioversion. In 2 patients, atrial capture could not be obtained because of increased atrial refractoriness secondary to flutter. Thus, rapid atrial pacing was ineffective in converting atrial flutter to normal sinus rhythm in all 15 patients. This was in contrast to direct-current cardioversion which was successful in 12 of the patients, in all of whom stable sinus rhythm developed. The 3 patients who did not undergo cardioversion subsequently experienced spontaneous conversion to sinus rhythm. These results suggest that rapid atrial pacing has little place in the management of atrial flutter.

Effects of Ouabain on Impaired Left Ventricular Function during Convalescence after Acute Myocardial Infarction

The effects of intravenous ouabain (0.015 mg/kg body weight) were assessed in 13 patients 3-5 weeks after an uncomplicated acute myocardial infarction. The patients were not in clinical cardiac failure and were not having anginal pain.The mean ± SEM of the values prior to (C) and 1 hour after ouabain (A) were: left ventricular end-diastolic pressure (LVEDP), C 18.6 ± 1.5, A 10.2 ± 1.4; stroke index, C 35.8 ± 3.9, A 39.5 ± 4.8; left ventricular stroke work (LVSW), C 99.4 ± 15.8, A 120.3 ± 19.5; mean rate of LV ejection (MRE), C 237.3 ± 21.9, A 274.5 ± 28.9; peak LV dp/dt, C 1,614 ± 141, A 2,145 ± 230; preejection period corrected for heart rate (PEPc), C 135.8 ± 8.7, A 125.1 ± 9.2; left ventricular ejection time corrected for heart rate (LVETC), C 407.9 ± 10.3, A 389.5 ± 9.2. These changes were significant (P < 0.05 for paired determinations). There were no significant changes in cardiac index, heart rate, mean arterial pressure, and systemic resistance.The reductions of LVEDP, PEPc, and LVETc and increases in SI, LVSW, MRE, and peak LV dp/dt show improvement of ventricular performance after ouabain and suggest that digitalis therapy could contribute to the management of patients convalescing after uncomplicated acute myocardial infarction.