[Hypoxic pulmonary hypertension: nifedipine therapy].
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Aged↗
Biomedical subjects
E Doria
Publications and source records attributed to E Doria.
Afterload reduction: a comparison of captopril and nifedipine in dilated cardiomyopathy.
Nifedipine and captopril are potent vasodilators and may be expected to help left ventricular failure by reducing afterload. Nifedipine (20 mg three times a day) and captopril (50 mg three times a day) were added to an optimal regimen of digitalis and diuretics in a double blind crossover trial in 18 cases of dilated cardiomyopathy. New York Heart Association functional class rating symptoms and exercise tolerance times improved on captopril but not on nifedipine. The reduction in pulmonary capillary wedge pressure and the increase of cardiac output on captopril indicated that the augmented functional capacity may have resulted in part from an improved performance of the left ventricle. Although there were comparable decreases in systemic vascular resistance and presumably in impedence to ejection by the left ventricle on both drugs, the dimensions of the ventricular cavity were found to be reduced by captopril and augmented by nifedipine, and only captopril reduced the afterload (wall stress). In addition, the force-length relation (between left ventricular end systolic stress and end systolic diameter) was shifted to the left of baseline by captopril and to the right by nifedipine, suggesting that muscle contractility was reduced by nifedipine and not by captopril. These results suggest that nifedipine and captopril have different effects on afterload and contractility and these may account for the different effects of these drugs on the performance of the heart and clinical responses.
Adult↗
Hemodynamic response to oral prenalterol in dilated decompensated cardiomyopathy as a result of cardiac and vascular effects.
The initial antifailure efficacy of beta-adrenergic agonists is generally lost during prolonged treatment. The reasons are not fully understood. In 11 patients with advanced cardiac decompensation due to dilated cardiomyopathy, prenalterol, a selective beta 1 adrenergic agonist, improved the left ventricular contractility after acute intravenous and during prolonged oral administration. However, after periods of treatment ranging from 2 to 18 weeks, blood pressure and systemic vascular resistance were raised in each patient. These changes resulted in an increase of the left ventricular afterload which was such as to overwhelm the effects of the enhanced contractility, and to extinguish the initial improvement of the cardiac function and of the clinical condition. Stimulation of the presynaptical beta-receptors facilitating norepinephrine release or of the renin secretion by this beta 1 agonist, may be the causes of the systemic vasoconstriction and of the loss of effectiveness in the long run.
Administration, Oral↗
A new formula for echo-Doppler estimation of right ventricular systolic pressure.
The Doppler formulas currently used for right ventricular systolic pressure (RVSP) evaluation include right ventricular-right atrial (RV-RA) gradient and RA pressure. The former is expressed by the velocity of the trans-tricuspid regurgitant flow; the latter is generally assumed and is different from one formula to another. In 110 patients with cardiac disease with normal or elevated pulmonary pressure, we tested a new echo-Doppler formula for the evaluation of RVSP based on the estimation of RA pressure by means of the inferior vena cava collapsibility index (IVCCI) and compared this method with two traditional formulas (methods A and B) and with cardiac catheterization values. Patients were classified into three groups on the basis of IVCCI (group 1 > 45%, group 2 between 35% and 45%, and group 3 < 35%). RVSP was evaluated by method A (RV-RA gradient + 10), method B (RV-RA gradient x 1.1 + 14), and our new method, method C, which assigns 6, 9, and 16 mmHg to RA pressure in the presence of normal (> 45%), moderately reduced (between 35% and 45%), or markedly reduced (< 35%) IVCCI, respectively. IVCCI correctly identified RA pressure in the three groups (group 1, 6.8 mmHg; group 2, 10.8 mm Hg; and group 3, 13.1 mmHg); a high correlation existed between Doppler-derived and invasively determined RV-RA gradient (r = 0.99). Method C improved noninvasive estimation of RVSP in groups 1 and 3 compared with the other methods; in group 2, Doppler estimation of RVSP by methods A and C were comparable, whereas method B significantly overestimated the actual values.(ABSTRACT TRUNCATED AT 250 WORDS)
Atrial Function, Right↗
Hypoxia-induced pulmonary hypertension: nifedipine only temporarily reduces pulmonary artery pressure and vascular tone.
Fifteen patients affected by hypoxia-induced pulmonary hypertension were studied before and during (1st and 8th week) nifedipine (180 mg/die) treatment. Nifedipine reduced pulmonary pressure (33 +/- 4 vs 26 +/- 3 mmHg, p less than 0.02) after 1 week of treatment; this pulmonary hypotensive effect was due to a reduction of pulmonary vascular tone as assessed by a reduction of Y-intercept on the pulmonary pressure/flow plot drawn from invasive recordings of pulmonary pressure/cardiac output obtained during exercise. Oxygen breathing effects on pulmonary pressure were also measured with and without nifedipine. Oxygen significantly reduced pulmonary pressure only in the absence of nifedipine regardless of the severity of pulmonary hypertension. Therefore nifedipine is not suitable for long-term treatment of hypoxia-induced pulmonary hypertension and inhibits O2 capability to reduce pulmonary pressure.
Adult↗