Showing papers by "Angelo Branzi published in 1995"

Role of pharmacologic tests in the treatment of primary pulmonary hypertension

Abstract: Primary pulmonary hypertension (PPH) is a rare disease of unknown etiology characterized by a constant progression toward right ventricular failure and death. Vasoconstriction is 1 of the pathophysiologic factors responsible for the increase of pulmonary vascular resistance (PVR) and pulmonary artery pressure (PAP) in patients with PPH. Thus vasodilator treatment is considered 1 of the logical approaches to medical therapy of such a condition. Acute drug challenge with a short-acting, titratable vasodilator during heart catheterization is recommended to select patients who are most likely to respond to long-term treatment. Accurate methodologic guidelines need to be followed to minimize the spontaneous variability of PAP and pulmonary arteriolar resistance. Pathophysiologic interpretation of pharmacologic trials requires analysis of the 2 components of the right ventricular hydraulic load, i.e., resistance and compliance of the pulmonary vascular bed. Reduction of the calculated PVR may be considered as a demonstration of pulmonary vasodilation only if PVR is assessed using the critical opening pressure or if it is associated with a simultaneous reduction of PAP. Only those patients in whom a reduction of PVR of > or = 20% is associated with a decrease in PAP of > or = 20% should be considered as "responders" to the acute tests. In clinical studies only 20-30% of the patients are short-term responders. The most intensively studied short-acting drug for short-term challenge is prostacyclin, but other agents such as acetylcholine, adenosine, and nitric oxide have been utilized. Prostacyclin has been shown to predict pulmonary vasodilator response to the administration of long-acting vasodilators, such as calcium channel antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)

Limitation of myocardial infarct size by nicorandil after sustained ischemia in pigs.

Abstract: Nicorandil is a compound with hybrid properties of nitrates and adenosine triphosphate (ATP)-sensitive potassium channel (K ATP ) opening. The effects of nicorandil and isosorbide dinitrate (ISDN) were investigated in a model of 60-min coronary occlusion/180-min reperfusion in open chest pigs. Three groups of 10 pigs were randomly assessed to receive saline or equihypotensive doses of nicorandil or ISDN. Drug infusion was started at 30 min of ischemia and continued throughout reperfusion. Area at risk (AAR) and infarcted area (IA) were assessed by monastral blue dye-triphenyltetrazolium dual staining technique and calculated by planimetry. Myeloperoxidase concentration (MPO) in the nonischemic area and in the IA was assessed as an index of presence of neutrophils. Measurements of reduced glutathione (GSH), oxidized glutathione (GSSG), lipofuscine, and malondialdehyde were performed on coronary vein blood as indexes of oxidative stress. IA, as a percentage of AAR, was 78 ± 10% after saline, 61 ± 12% after N (p < 0.05 vs. saline), and 69 ± 14% after ISDN (not significant vs. saline). Cardiac output and left ventricular dP/dt were depressed during coronary occlusion in all groups and their recovery during reperfusion was earlier in the nicorandil group. In the saline group, MPO was increased in the IA compared to the nonischemic area (78 ± 63 vs. 21 ± 21 μg/mg prot, p = 0.02). In the ISDN group and in the nicorandil group, the increase of MPO concentration in the IA compared to the nonischemic area was not statistically significant (44 ± 27 vs. 25 ± 20 μg/mg prot, p = 0.09 and 43 ± 39 vs. 34 ± 51 μg/mg prot, p = 0.47, respectively). No differences were observed on the indexes of oxidative stress among groups. Thus, nicorandil, administered after a prolonged period of coronary occlusion, reduced IA and improved the recovery of hemodynamics during the course of reperfusion compared to saline and ISDN. Nicorandil and ISDN tended to reduce neutrophils infiltration in IA. The mechanism of the protective effect of nicorandil is elusive and may be related to a direct activation of myocardial K ATP channels and/or to the antineutrophil activity.

Adjustment of pulmonary capillary wedge pressure for wave delay increases the accuracy of mitral valve area measurement.

Abstract: Pulmonary capillary wedge pressure, currently accepted as an approximation of left atrial pressure, leads to underestimation of mitral valve area calculated with the Gorlin formula. Wave delay has been pointed out as a major source of the underestimation. The aim of this study was to increase the accuracy of pulmonary artery wedge pressure-based measurements through a correction for time delay. Electrocardiogram, pulmonary capillary wedge, left atrial and left ventricular pressures were recorded simultaneously at high paper speed in 18 patients with mitral stenosis who underwent transseptal left atrial catheterization prior to mitral valvulotomy. Heart rate and wedge pressure wave delay were closely correlated (r = 0.78, p 0.95) with measurements obtained using left atrial pressure; plotting the standard deviation against the mean, the correction of capillary wedge pressure significantly (p < 0.001) increased the accuracy of area measurement. In conclusion, pulmonary wedge pressure, properly obtained and adjusted for time delay, allows a more reliable measurement of the mitral area.