Elio DiSegni

Experimental ultrasonic angioplasty: Disruption of atherosclerotic plaques and thrombi in vitro and arterial recanalization in vivo

To investigate the use of high energy ultrasound as an alternative energy for angioplasty, an experimental ultrasonic angioplasty device was developed. The device was studied in two bioassay systems: an in vitro system for the disruption of atherosclerotic plaques and thrombi and an in vivo system for the recanalization of occluded canine femoral arteries. In vitro, sonication efficiently reduced the size of the plaques. Atheromatous plaques (n = 11) disrupted at a rate of 21 +/- 8 s/cm2; complicated plaques (n = 14) disrupted at a rate of 132 +/- 45 s/cm2 (p less than 0.001). Histologic examination revealed that the disruption of the plaques took place without concurrent damage to the media or adventitia. Ninety percent of the disrupted plaque debris had a diameter of less than 20 microns and was composed primarily of cholesterol monohydrate crystals. Solid thrombus (n = 5) weight was reduced from 1.6 +/- 0.2 to 0.4 +/- 0.1 g (p less than 0.0001) after 20 s of sonication. In vivo, sonication resulted in recanalization in all seven arteries tested in seven dogs. The obstruction was reduced from 93 +/- 11% to 18 +/- 7% (p less than 0.001). On histologic examination, the arterial wall injury index was found to be 1.56 +/- 0.42 in the test arteries compared with 1.37 +/- 0.47 in the control arteries (p = NS). The disruption of atherosclerotic plaques and thrombi, together with the efficient recanalization of the occluded arteries, demonstrates the potential of ultrasound angioplasty as a catheter-based technique for angioplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

The acute hemodynamic effects of intravenous verapamil in coronary artery disease. Assessment by equilibrium-gated radionuclide ventriculography.

The acute hemodynamic effects of an i.v. bolus of verapamil, 0.1 mg/kg or 0.06–0.075 mg/kg, were examined by serial radionuclide studies in 46 patients with coronary artery disease. In 20 patients with ejection fractions (EFs) > 35% (group 1A), verapamil, 0.1 mg/kg given over 1–1½ minutes, had a biphasic effect: first, a transient decrease in EF accompanied by increased left ventricular (LV) volumes and cardiac output equivalents; then, an overshoot of EF to values above control, accompanied by a decrease in peripheral vascular resistance and a drastic decrease in LV volumes, while cardiac output equivalent remained slightly elevated. In eight patients with EFs < 35% (group 1B), only the first effect on EF was noted. In 10 patients with EFs > 35% (group 2), verapamil, 0.06–0.075 mg/kg, exerted qualitatively similar but milder effects on hemodynamic function. Finally, verapamil, 0.1 mg/kg given more slowly, over 2–2½ minutes, produced no significant changes in EF or LV volumes in another eight patients (group 3). The acute effects of verapamil are thus both time-related and dose-dependent. They are also related to the baseline functional reserve of the left ventricle. This study documents that verapamil exerts a depressant effect on LV function. However, the transient nature of this depression and the quick recovery to normal or above-normal values indicate that verapamil, in the doses used in this study, is safe to use intravenously in patients with coronary artery disease.

Exercise haemodynamics may unmask the diagnosis of diastolic dysfunction among patients with pulmonary hypertension

Heart failure with preserved ejection fraction can lead to pulmonary hypertension. The aim of the present study was to evaluate the role of exercise during right heart catheterization in the unmasking of diastolic dysfunction.

The paradox of sudden slowing of idioventricular rhythm during exercise in complete heart block: Modulation of automatic focus, concealed reentry, or wedensky inhibition?

As a rule, exercise enhances the rate of discharge of idioventricular rhythms in complete atrioventricular (AV) block. The opposite effect, a sudden drop in the rate of discharge with subsequent resetting of the firing rate, was observed in an 18-year-old boy with chronic complete AV block. Two mechanisms for this paradoxical response to exercise are proposed: (1) delay in discharge of the automatic pacemaker focus by successful penetration of electrotonic potentials from nonconducted P waves across the area of block in the AV conduction system and into the pacemaker focus; and (2) discharge of the pacemaker focus by concealed reentrant extrasystoles. Wedensky inhibition is ruled out because of the resetting of the firing rate.