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To evaluate how nifedipine influences systolic and diastolic ventricular function, the effects of 20 mg sublingual nifedipine were studied in 13 stable COPD patients. Nifedipine induced no change in mean pulmonary arterial pressure, decreased mean arterial pressure, pulmonary and systemic vascular resistance index, and increased heart rate and cardiac index. It also caused an increase in right and left ventricular ejection fractions. The end-diastolic volume index of both ventricles remained unchanged, whereas the end-systolic volume index tended to decrease without reaching a significant level, and the right ventricular contractility increased. After nifedipine administration, right and left ventricular compliance increased. This study suggests that short-term administration of nifedipine improves the systolic function by a decrease in ventricular afterload and an increase in ventricular contractility and increases the ventricular compliance by a reflex sympathetic stimulation and an afterload reduction.

To evaluate the influence of β2 mimetics on ventricular contractility and pump function, radionuclide ventriculography and right heart catheterization were simultaneously performed in 10 patients with severe chronic obstructive pulmonary disease. After a 60 min constant infusion of 17 μg/min salbutamol, cardiac index increased by 60, heart rate by 39, and stroke volume index by 14. Mean pulmonary artery pressure remained unchanged and mean arterial pressure decreased slightly but not significantly. Right ventricular (RV) function improved as attested to by an increase of RV ejection fraction ( 8), a decrease of RV end-diastolic pressure (- 5 mm Hg), and RV end-systolic volume index (-18). Simultaneously, the pulmonary vascular resistance index decreased by 33 and RV contractility, appreciated by RV dP/dtmax, RV (dP/dtmax)/P, and RV end-systolic pressure/volume ratio, increased by 44, 77, and 27, respectively. Left ventricular (LV) function also improved. The LV ejection fraction increased by 18 and LV end-systolic volume decreased by 34. Concomitantly, the systemic vascular resistance index decreased by 40 and the LV end-systolic pressure/volume ratio increased by 50. Our results suggest that the infusion of salbutamol improves ventricular performance by a decrease of ventricular afterload and by a positive inotropic effect.

Pulmonary arterial hypertension represents an important parameter for the assessment of the severity of chronic bronchitis. The measurement of the pulmonary arterial pressure, however, requires invasive techniques of limited routine use because of costs and associated risks. The aim of this study is to evaluate whether the 81mKr right ventricular ejection fraction and parameters derived from equilibrium 99mTc red blood cells’ right ventricular curve allow a better estimation of PAP than the 99mTc RVEF. In 41 patients with severe chronic bronchitis, the linear correlation between PAP and 99mTc RVEF was —0.61 (p<0.001). None of the parameters derived from the right ventricular curve was better correlated to PAP than the 99mTc RVEF. In 16 other chronic bronchitis patients, the 81mKr RVEF correlated moderately to PAP. In conclusion, the alternative isotopic methods proposed in this work do not provide a reliable estimation of pulmonary arterial pressure in patients with chronic bronchitis.

The effects of aminophylline on pulmonary vascular tone, systemic hemodynamics, and ventricular ejection fractions reported in the literature show some discrepancies. We therefore studied in COPD patients the effects of aminophylline on hemodynamics, on ventricular ejection fractions, and on systolic and diastolic functions of each ventricle, and we measured simultaneously the blood level of the drug. The analysis of the data revealed a relationship between the blood level of aminophylline and the variations of right ventricular ejection fraction (RVEF) (r = 0.83, p = 0.005), left ventricular ejection fraction (LVEF) (r = 0.76, p = 0.017), pulmonary vascular resistance index (PVRI) (r = –0.58, p = 0.096), systemic vascular resistance index (SVRI) (r= –0.60, p = 0.08), and right ventricular peak systolic pressure/end-systolic volume index (RVPSP/ESVI) (r=0.75, p=0.02). Modifications of ejection fractions and vascular resistance indices were correlated for both ventricles (RVEF vs PVRI, r= –0.77, p=0.01; LVEF vs SVRI, r= –0.76, p=0.02). Finally, RVEF modification was also correlated to RVPSP/ESVI variation (r=0.78, p=0.01). These results suggest that even within the therapeutic range (10 to 20 mg/L), the effects of aminophylline seemed to depend on its blood level. This dose dependency could explain the contradictory data reported in the literature concerning the effects of aminophylline on pulmonary and systemic hemodynamics and on ventricular function.