Normal and stenotic human aortic valve opening: in vitro assessment of orifice area changes with flow.

The ability to measure aortic valve area clinically has emphasized the need to understand the changes in aortic valve orifice area during flow. To compare the performance of normal and stenotic human aortic valves we used a pulsatile flow model that simulated in vivo flow conditions. Five normal autopsy specimens and 15 stenotic valves removed at operation were mounted into the model. Valve function was assessed by analysis of video recordings of valve leaflet motion during flow. Over the flow rates tested normal valves demonstrated a linear increase in orifice area. There was no resistance to leaflet opening and valve closure was rapid. The majority of stenotic valves demonstrated an increase in orifice area at low flow rates. No valve showed any increase in maximal area beyond flow rates of 3 l min-1. Increased leaflet resistance of these abnormal valves resulted in notably slower opening and closing rates. In patients with a high cardiac output and severe stenosis, overestimation of the anatomic orifice area derived by the Gorlin equation can result. This is not related to variability in maximal orifice area.

Balloon dilatation of the aortic valve in a pulsatile flow model: assessment of the mechanisms and the magnitude and duration of changes in valve area and gradient.

Eighteen stenotic aortic valves (17 removed at operation) mounted in a pulsatile flow duplicator were dilated with a balloon catheter. Sequential measurements showed that the valve area initially increased from a mean (SD) of 0.52 (0.16) to 0.78 (0.17) cm2. It was 0.73 (0.16) cm2 five minutes after dilatation and this was little changed at four weeks (0.70 (0.15) cm2). Initially the mean transvalvar gradient fell significantly from 54 (27) to 32 (8) mm Hg but increased to 35 (10) mm Hg at five minutes and to 40 (11) mm Hg at four weeks. In six valves stretching of the orifice was the only mechanism responsible for the changes while in the remainder there was tearing through commissures with a greater initial increase in area (0.31 v 0.18 cm2) and a smaller decrease in area at five minutes (0.03 v 0.08 cm2). Fractures of calcific deposits in non-commissural positions were seen in one valve only. This laboratory study of isolated aortic valves showed a significant but small increase in valve area after balloon dilatation, which was greater when commissural tearing had occurred. Recoil of the stretched orifice was complete at five minutes and there was little further change over the next four weeks.

Thermal effects of stationary "hot tip" laser coronary probes: an in vitro assessment.

Percutaneous laser thermal probe angioplasty requires sufficient laser probe flexibility to access the coronary tree. This may entail a loss of axial strength and the resultant slow advancement may lead to unwanted heating of the normal coronary artery proximal to the lesion. To assess the lateral thermal effects of stationary coronary laser probes, laser thermal energy (50-150 J) was delivered to 25 coronary artery segments (diameter 1.9-4.0 mm) in a perfused cadaver heart preparation using a 1.7 mm tip probe. Adherence to the vessel wall occurred in 19 segments, endothelial charring in 8 segments, and perforation in 3 segments. Endothelial charring was seen in 8 of 13 nonperfused segments but in 0 of 12 segments perfused at 60 ml/minute (P less than 0.01). In all three perforations the vessel to probe diameter ratio was less than 1.6:1, perfusion was absent, and traction to dislodge the adherent probe was necessary. Lateral wall damage is a complication of stationary laser probes: smaller-tipped probes which are advanced rapidly at the time of energy delivery may enhance the safety margins of coronary laser thermal probe angioplasty.

An assessment of beta-adrenoceptor blockade in man by prizidilol hydrochloride.

1 Prizidilol hydrochloride (SK&F 92657) is a new compound which causes both arteriolar dilatation and beta-adrenoceptor blockade. The effect of a single oral dose on the responses of heart rate and blood pressure to isoprenaline infusion has been studied in healthy volunteers. 2 Isoprenaline heart rate dose-response curves showed parallel shifts to the right after oral prizidilol, indicating antagonism by this compound at beta-adrenoceptors in the heart. 3 Isoprenaline dose-response curves for decreases in diastolic blood pressure also showed shifts to the right after oral prizidilol, providing evidence of beta-adrenoceptor antagonism by this drug in peripheral resistance vessels. 4 The peak effect of a 40 mg dose of propranolol was greater than that of a 200 mg dose of prizidilol but both drugs caused persistent beta-adrenoceptor blockade for at least 7 h after ingestion.