Bonnie J. Baker

Relation of right ventricular ejection fraction to exercise capacity in chronic left ventricular failure.

Although the left ventricle is traditionally viewed as the hearts main pumping chamber, no correlation has been shown between left ventricular (LV) ejection fraction (EF) at rest and exercise capacity in patients with chronic LV failure. Because vasodilators with venodilating activity increase exercise capacity more than predominant arterial dilators in patients with LV failure, right ventricular (RV) function may relate to exercise capacity in these patients. In 25 patients with chronic LV failure, caused by coronary artery disease in 12 patients and idiopathic dilated cardiomyopathy in 13 patients, RVEF and LVEF at rest were measured by radionuclide angiography. Maximal upright bicycle exercise testing was also performed to determine maximal oxygen consumption, which averaged only 13 +/- 4 ml/min/kg. The LVEF at rest was 26 +/- 10% and did not correlate with maximal oxygen consumption (r = 0.08). However, the RVEF was 41 +/- 12% and correlated with maximal oxygen consumption (r = 0.70, p less than 0.001) in the same patients. The correlation was stronger (r = 0.88) in patients with coronary artery disease than in those with idiopathic dilated cardiomyopathy (r = 0.60). Thus, RVEF at rest is more predictive of exercise capacity than LVEF in the same patients with chronic LV failure. These results are consistent with the clinical observation that only venodilating agents increase exercise capacity of patients with chronic LV failure.

Reevaluation of electrocardiographic criteria for left, right and combined cardiac ventricular hypertrophy

Cardiac chamber weight was determined at necropsy in 323 men to develop correlative studies of electrocardiographic criteria for ventricular hypertrophy. Thirty recommended criteria for left ventricular (LV) hypertrophy, 10 for right ventricular (RV) hypertrophy, and combinations of both criteria for combined hypertrophy were evaluated. Four methods for electrocardiographic diagnosis of LV hypertrophy were derived: (1) a modification of the Romhilt-Estes point system; (2) the presence of any 1 of 3 criteria: (a) S V1 + R V5 or V6 greater than 35 mm, (b) left atrial abnormality, or (c) intrinsicoid deflection in lead V5 or V6 greater than or equal to 0.05 second; (3) a combination of any 2 criteria or of 1 criterion (above) plus at least 1 of the following 3 additional criteria: (a) left-axis deviation greater than -30 degrees, (b) QRS duration greater than 0.09 second, or (c) T-wave inversion in lead V6 of 1 mm or more; and (4) the use of a single criterion--left atrial abnormality. Sensitivity varied from 57 to 66% and specificity from 85 to 93% among these 4 methods. Myocardial infarction increased sensitivity of the foregoing methods, but the specificity was reduced. Method 2 is preferred for the electrocardiographic diagnosis of LV hypertrophy. Two methods were useful for right ventricular (RV) hypertrophy: (1) the use of any 1 of 4 criteria: (a) R/S ratio in lead V5 or V6 less than or equal to 1; (b) S V5 or V6 greater than or equal to 7 mm; (c) right-axis deviation of more than +90 degrees, or (d) P pulmonale; and (2) use of any 2 combinations of the foregoing criteria. Sensitivity ranged from 18 to 43% and specificity from 83 to 95%. Combined hypertrophy was best diagnosed using left atrial abnormality as the sole criteria of LV hypertrophy, plus any 1 of 3 criteria of RV hypertrophy: (a) R/S ratio in lead V5 or V6 less than or equal to 1, (b) S V5 or V6 greater than or equal to 7 mm, or (c) right axis deviation greater than +90 degrees.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of propafenone on left ventricular ejection fraction

The effects of orally administered propafenone on ejection fraction (EF) determined by radionuclide angiography were studied in 2 groups of patients receiving different dosing regimens. Fourteen group A patients had no clinical evidence of left ventricular (LV) dysfunction and were not receiving digoxin therapy. In this group a mean daily dosage of 879 mg resulted in a decrease in resting LVEF from 52 +/- 9% to 48 +/- 11% (p less than 0.05). Eight group B patients had clinical radionuclide evidence of LV dysfunction and were receiving digoxin therapy. In this group, a daily dosage of propafenone of 600 mg/day resulted in no significant change in LVEF. No clinically significant effects on cardiac compensation were evident in either group. These data suggest a negative inotropic effect that is either related to propafenone dosage or at least partially attenuated by digoxin therapy. Further studies are necessary to define precisely the effects of propafenone on LV function.

Exercise increases the circulating concentration of the N-terminus of the atrial natriuretic factor prohormone in normal individuals☆

Recently two peptides consisting of amino acids (aa) 1 to 30 and 31 to 67 of the N-terminus of the 126 aa prohormone of atrial natriuretic factor (proANF), as well as atrial natriuretic factor (ANF, aa 99 to 126; C-terminus), were found to have vasodilatory and natriuretic properties. These peptides, as well as ANF, circulate in humans as part of the N-terminus of the prohormone. To determine the effect of graded exercise on the circulating concentrations of the N-terminus and C-terminus of the ANF prohormone in normal persons, 12 healthy individuals (mean age 45 +/- 2 years) were evaluated before, for 2 hours after, and during bicycle exercise at a work loads of 25, 50, 75, 100, 125, 150, and 175 W. Both the N- and C-terminus of the ANF prohormone were released simultaneously with graded exercise in direct proportion to the intensity of the work load, measured objectively via maximal oxygen consumption (VO2max), respiratory quotient, and heart rate. Both the N-terminus and C-terminus of the ANF prohormone had strong positive correlations (p less than 0.001) with blood pressure, heart rate, VO2max, and respiratory quotient. Following exercise, the C-terminus returned to preexercise levels within 30 minutes, while the N-terminus remained significantly elevated at 30 and 60 minutes postexercise, reflecting the longer half-life of the N-terminus in the circulation.

Predictive value of M-mode echocardiography in patients with congestive heart failure

The M-mode echocardiogram (ECHO) is widely used to follow patients with congestive heart failure (CHF), but the value of ECHO for this purpose is unclear. In 49 patients with symptomatic CHF, we obtained ECHO during baseline evaluation to determine the value of ECHO for predicting 1-year survival or maximal oxygen uptake during exercise (VOmax). The cause of CHF was coronary artery disease in 12 patients and idiopathic dilated cardiomyopathy in 37 patients. Overall mortality at 1 year was 10 of 49 (20%), but was higher in patients with coronary artery disease (42%) compared to those with idiopathic dilated cardiomyopathy (14%), p less than 0.001. ECHO indices of left ventricular contractility were greater in survivors (S) in whom shortening fraction averaged 16 +/- 8 (SD)% vs 10 +/- 4% in nonsurvivors (NOS), p less than 0.025. Velocity of circumferential fiber shortening averaged 0.53 +/- 0.25 Hz in S vs 0.35 +/- 0.15 Hz in NOS, p less than 0.05. No left ventricular dimensions, including systolic and diastolic diameters, volume, wall thickness, and mass differed significantly between S and NOS. No ECHO measure of left ventricular dimensions or contractility correlated significantly with VOmax. Thus, ECHO may be useful to predict survival but not functional capacity in patients with CHF.

Prohormone Atrial Natriuretic Peptides 1-98 and 31-67 Increase with Exercise in Congestive Heart Failure Patients

Recently two peptides consisting of amino acids (a.a.) 1-30 and 31-67 of the N-terminus of the 126 a.a. prohormone of atrial natriuretic factor (pro ANF), as well as atrial natriuretic factor (ANF, a.a. 99-126; C-terminus) were found to have vasodilatory and natriuretic properties. These peptides, as well as ANF, circulate in man as part of the N-terminus of the prohormone. To determine the effect of graded exercise on the circulating concentration of the N-terminus and C-terminus of the ANF prohormone in persons with abnormal salt and water metabolism, 12 individuals with stable congestive heart failure (CHF) were evaluated before and after bicycle exercise testing and the results were subdivided based on the maximal exercise they could achieve. In all of the CHF patients, the circulating concentration of the whole N-terminus (ie, a.a. 1-98), the midportion of the N-terminus (pro ANF 31-67), which circulates as a distinct 3900 molecular weight (m.w.) peptide after being proteolytically cleaved from the N-terminus, and the C-terminus (ANF) increased with exercise. The patients who were able to achieve 100 and 125 watts of workload had a greater maximal oxygen consumption and, in general, a greater percent increase in the circulating concentration of both the N-terminus and the C-terminus of the ANF prohormone than those who had less exercise capacity. Evaluation of the echocardiographic, radionucleotide, and the exercise parameters revealed that the circulating concentrations of these atrial peptides correlated best with left atrial dimension, but that left ventricular systolic and diastolic dimensions also correlated positively with their concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Efficacy of propafenone compared with quinidine in chronic ventricular arrhythmias

A double-blind, randomized study was designed to evaluate the efficacy of oral propafenone and oral quinidine in suppressing premature ventricular complexes (PVCs). Twenty-five men were studied for 3 weeks. Twelve were randomized to the quinidine group and 13 to the propafenone group. Small doses of the drugs were administered for 1 week (200 mg of quinidine every 6 hours or 300 mg of propafenone every 12 hours) and large doses were administered for another week (400 mg of quinidine every 6 hours or 300 mg of propafenone every 8 hours). Strict criteria were used to define responders to antiarrhythmic therapy. For more than 85% reduction in total PVCs per hour: During the low-dose week, 36% in the quinidine group and 50% in the propafenone group were responders (difference not significant [NS]), while during the high-dose week 33% and 64% were responders (NS). For more than 95% reduction of ventricular couplets per hour: During the low-dose week, 45% in each group were responders, while during the high-dose week, 56% and 60% were responders (NS). For 100% abolition of ventricular tachycardia (VT) beats per 24 hours: During the low-dose week, 60% in the quinidine group and 56% in the propafenone group were responders (NS); during the high-dose week 80% and 67% were responders (NS). There was no significant difference in the 2 groups in incidence of side effects. This study shows comparable efficacy and tolerance of propafenone and quinidine for the control of ventricular arrhythmias in ambulatory patients with diverse forms of heart diseases.

Sustained therapeutic efficacy and safety of oral propafenone for treatment of chronic ventricular arrhythmias: A 2-year experience

Thirty-two men with chronic ventricular arrhythmias responded to propafenone, a new potent antiarrhythmic agent, in short-term trials with 85% or greater reduction of total ventricular premature complexes (VPCs) per hour, 95% or greater reduction of ventricular couplets (VCs) per hour, and 100% abolition of ventricular tachycardia (VT) beats per 24 hours. These patients were continued on long-term propafenone therapy to assess sustained therapeutic efficacy and safety. Thirty patients completed 1 year and 26 patients completed 2 years of testing with this agent; one patient died of sudden death and another died of a noncardiac cause. Although there were significantly fewer patient responders at 1 and 2 years, the majority of patients (greater than 79%) continued to respond optimally to propafenone. Side effects were minor and included bitter taste, dizziness, congestive heart failure, fatigue, and significant prolongation of the PR and QRS intervals. Propafenone has sustained antiarrhythmic efficacy after 2 years without serious toxicity.