During electrophysiological investigation of 22 patients with VT or aborted sudden cardiac death, arterial and RV pressures were measured. The time courses of mean arterial pressure (MAP), RV pulse pressure (RVPP), RV pulse pressure integral (RVPPI), and maximum right ventricular dP/dt (RV dP/dtmax) were followed during the first 15 seconds after VT induction. Compared to basal (preinduction) conditions, the RVPPI decreased by 41+/-10% (mean +/- SD) after 10-15 seconds of VT in 11 patients with stable VT and by 75+/-8% in 11 patients with unstable VT (MAP < 60 mmHg 15 s after VT onset). RVPP decreased by 13+/-11% after 10-15 seconds of VT in the stable VT group and by 50+/-16% in the unstable VT group. For RV dP/dtmax, these decreases were 4+/-22% in the stable VT group and 37+/-24% in the unstable VT group. There was a good correlation between percent decrease in MAP and percent decrease in RVPPI, RVPP, and RV dP/dtmax at 5-10 seconds (r = 0.86, 0.81, and 0.73, respectively) and 10-15 seconds (r = 0.84, 0.82, and 0.69, respectively) after VT onset. There was hardly any overlap of distributions of the individual values with the RVPPI parameter between the two VT groups. Comparing and correlating the percent decrease in mean arterial pressure with the RVPPI, RVPP, and RV dP/dtmax during induced VT, RVPPI demonstrated the most significant and specific changes in discriminating stable from unstable rhythms. However, by comparing RVPPI and RVPP using the area under the receiver operating characteristic curves, there was no significant statistical difference between the two parameters. By integrating rate criteria, electrogram signal analysis, and RVPPI or RVPP as a hemodynamic criterion, detection and treatment algorithms could improve the performance of future implantable defibrillators and avoiding shocks in VTs that can be terminated by antitachycardia pacing.
A new, dual-chamber temporary pacing lead was introduced via the subclavian vein in 20 patients who needed a temporary pacemaker. Stroke volume (SV) was measured continuously by combining M-mode and noninvasive Doppler echocardiography during spontaneous rhythm (SR), AV sequential pacing at a positive AV interval (DP), ventricular pacing (VP) and AV sequential pacing at a negative AV interval (VA pacing). The valvular functions were determined by Doppler echocardiography. Left ventricular dimensions and function, and left atrial size were measured by M-mode echocardiography. In the nine patients with no valvular heart disease and with no ventriculoatrial (VA) conduction (group I) the CO increased 83 +/- 11% during DP and 42 +/- 9% during VP as compared to during SR when the heart rate (HR) was increased from 34 +/- 3 to 72 +/- 1 beats/min. The CO was 29 +/- 3% higher during DP than that during VP. In the seven patients with valvular heart disease and with no VA conduction (group II), the increment in CO compared to that during SR was 53 +/- 12% during DP and 31 +/- 11% during VP; the CO was 17 +/- 4% higher during DP than that during VP. In the four patients with spontaneous VA conduction (group III), the CO during DP was 35 +/- 10% greater than that during VP, which did not result in an increase in the CO compared to that during SR in spite of an increase in HR from 52 +/- 8 to 74 +/- 2 beats/min. The study demonstrated that DP is the preferred temporary pacing mode and also that VA conduction during VP resulted in a mean decrease of 20% in CO compared to that during VP without VA conduction. The hemodynamic benefit from DP compared to SR seems to decrease when the left ventricular end-diastolic dimension increases. Furthermore, patients with large left ventricular end-systolic dimensions seem to have a lower increase in stroke index during DP as compared to that during VP than patients with smaller end-systolic dimensions.
Atrial natriuretic peptide (ANP) was measured in coronary sinus (CS) plasma in seven patients with induced tachycardia. Right atrial pressure (RAP) and femoral artery (FA) levels of ANP, noradrenaline (NA) and adrenaline (A) were measured before and after 5 min with tachycardia. During tachycardia, ANP in CS plasma increased from 381 +/- 273 (mean +/- SD) to 1376 +/- 1191 pmol l-1 (p < 0.0001), and ANP levels in FA plasma from 89 +/- 48 to 231 +/- 151 pmol l-1 (p < 0.005). A significant increase was observed for peak RAP, whereas mean RAP remained unaltered. While no correlation existed between the increase in CS plasma ANP level and RAP, significant correlations were found between the changes in FA plasma ANP and RAP, and between FA plasma levels of ANP and NA. Following tachycardia, significant correlations were found both between ANP in CS and FA plasma and between the changes in these plasma levels. Whereas the changes in FA plasma levels of ANP during tachycardia seems dependent of RAP and arterial plasma levels of NA, the CS plasma ANP level appears to be independent of the two factors, probably because CS plasma ANP are drained mainly from the left side of the heart.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.