Because exercise induced pulmonary hypertension may disturb optimal coupling between the right ventricle and pulmonary artery in coronary artery disease, high fidelity pulmonary artery and right ventricular pressure and electromagnetic pulmonary artery flow velocity data were recorded at rest and during supine exercise in 10 control subjects free of detectable cardiovascular disease and in 11 patients with coronary artery disease. The pulmonary artery impedance and power spectra were calculated from Fourier analysis of pressure and flow waveforms. Total hydraulic power expended per unit of forward flow was computed as an index of right ventricular-pulmonary artery coupling. In coronary artery disease exercise produced substantial increases in pulmonary artery pressure, pulmonary artery characteristic impedance, and total power per unit flow. These changes did not occur in control subjects. Despite a significant exercise increase in right ventricular end diastolic pressure and peak right ventricular dP/dt, and independent of the presence of right coronary artery involvement, the right ventricular stroke output response during exercise was significantly blunted in the coronary artery disease patients. Pulmonary vascular resistance was unchanged by exercise in either group. Exercise induced ischaemia presents an increased pulsatile hydraulic load to the right ventricle. Increased pulmonary artery input impedance impairs the hydraulic efficiency of right ventricular-pulmonary artery coupling and may contribute to the limitation of right ventricular ejection performance in coronary artery disease.
The electrocardiographic response of digoxin-induced fascicular tachycardia to Fab fragments was evaluated in two patients. In addition, we documented the response of the fascicular tachycardia to spontaneous premature ventricular depolarizations during different tachycardia rates, the response to a nonsustained episode of ventricular tachycardia, and the mode of spontaneous initiation and termination of short-lived episodes of the tachycardia during the treatment process. The following findings were noted: slowing of the tachycardia in response to Fab administration; change in the morphologic characteristics of the tachycardia from multiform to uniform; resetting of the tachycardia by spontaneous premature ventricular depolarization with the return cycle equal to the observed tachycardia cycle length; acceleration of the tachycardia in response to five beats of a faster nonsustained ventricular tachycardia; and initiation and termination of the tachycardia, both by spontaneously occurring premature ventricular depolarizations and in the absence of premature ventricular depolarizations. Both tachycardias resolved completely within 20 and 40 minutes, respectively, of Fab administration. We conclude that Fab administration can promptly resolve fascicular tachycardias precipitated by digoxin toxicity and that the observed electrocardiographic phenomena strongly suggest triggered activity as the electrophysiologic mechanism of fascicular tachycardia in man.
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