The aim of the study was to investigate the pulmonary vasodilator effect of the dihydropyridine calcium channel blocker amlodipine in patients with clinically stable chronic obstructive pulmonary disease (COPD) and pulmonary hypertension (PH). Many patients with COPD develop chronic PH and this may predict mortality in this disorder. The treatment with calcium channel blockers is accepted as a therapeutic strategy for primary pulmonary hypertension. In twenty male patients (mean age 57+/-7 years) with clinically stable COPD and PH, we investigated whether amlodipine could effectively decrease pulmonary vascular resistance (PVR) and pulmonary arterial pressure (PAP) and improve right heart function. PAP was recorded by a balloon-tipped thermodilution catheter and cardiac output was determined in triplicate by thermodilution at rest and during exercise. In addition, blood gas values were determined from the capillary blood of the earlobe. All measurements were done under identical conditions before and after 18 days of chronic treatment: with 10 mg amlodipine once daily starting with 5mg in the first week. At a mean maximal achieved workload of 71.3+/-20 Watts, amlodipine achieved a significant reduction in PVR (-13.4%; p<0.01) and PAP (-12.1%; p<0.001) implying an improved right heart function assessed by a significant reduction in mean right atrial pressure (-20.6%; p<0.05). During the action of amlodipine there were no significant changes in pulmonary gas exchange and pulmonary capillary wedge pressure. Amlodipine given as a single daily oral dose of 10mg is a safe and effective pulmonary vasodilator in COPD patients with PH and leads to an improvement in right heart function.

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Background: The pump function during exercise can be disturbed not only in hypertensives with coronary artery disease (CAD), but also in those with a normal angiogram. Methods: In 10 hypertensive patients (group 1; aged 52±4 years, 1 men, 9 women) with ST segment depression during exercise and concomitant angina pectoris but normal coronary angiograms (microangiopathy) and without left ventricular hypertrophy (LVMI <110 g/m²), the left ventricular function at rest and during exercise was studied by cardiac catheterization and compared with 10 hypertensives with CAD (group 2; aged 57.6±4 years, 7 men, 3 women) and 10 hypertensives without ST segment depression (group 3; aged 51.8±5 years, 10 men) before and after intravenous administration of 1.25 mg enalaprilat. Results: The pulmonary capillary wedge pressure (PCWP) was normal at rest and pathologically increased at 60±13 W only in groups 1 and 2 (27.2±3 and 32.2±8 mm Hg, respectively), but not in group 3 (12.2±4 mm Hg; p<0.001). At the identical load level, the PCWP in patients with microangiopathy (group 1) was significantly (p<0.01) reduced after enalaprilat (–21.7%) and even normalized in 5 of 10 patients. This was accompanied by a significant (p>0.01) decrease in ST segment depression (–73.9%) and in the occurrence of angina pectoris, despite the fact that the rate–pressure product as a measure of myocardial oxygen consumption was significantly (p<0.05) increased. Also in patients with CAD enalaprilat had a significant effect on PCWP (p<0.01), ST segment depression (p<0.01), occurrence of angina pectoris (p<0.001), cardiac index (p<0.05), and stroke index (p<0.05) during exercise. In group 3 there were no significant changes in PCWP, cardiac index, and stroke index after enalaprilat either at rest or during exercise. Conclusion: The functional improvement under the action of enalaprilat suggests that the advantages of the drug may be mediated mainly through an increase in myocardial blood flow and that angiotensin II might be involved in the restricted increase in coronary blood flow during dynamic exercise in hypertensives with coronary microangiopathy.