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Acute and long term effect of nifedipine on pulmonary hypertension secondary to chronic obstructive airways disease.

Johnson Dc, R C Joshi, R Mehta, Cunnington Ar

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Abstract

To determine whether Nifedipine reduces pulmonary artery pressure and pulmonary vascular resistance in patients with hypoxic pulmonary hypertension, we have studied ten clinically stable patients with chronic obstructive airways disease following acute administration of sublingual Nifedipine 20 mg and also after three months long term treatment with Nifedipine tablets 20mg bd. In the acute study, Nifedipine significantly raised mean pulmonary artery pressure from 30.32 +/- 13.07 mm Hg to 34.15 +/- 14.33 mm Hg (p less than 0.001) and pulmonary wedge pressure from 6.15 +/- 5.09 mm Hg to 7.6 +/- 3.39 mm Hg (p less than 0.1). There was a significant fall in mean systematic artery pressure from 99.06 +/- 12.05 mm Hg to 89.47 +/- 10.04 mm Hg (p less than 0.005) and a rise in heart rate from 79 +/- 9.7 beats/minute to 85.45 +/- 13.46 beats/minute (p less than 0.5). There was a significant change in cardiac index from 2.96 +/- 0.76 l/min/m2 to 3.2 +/- 0.51 l/min/m2 p(less than 0.1). There was no statistically significant change in pulmonary vascular resistance from 5.06 +/- 3.45 mm Hg/l/min to 4.92 +/- 3.10 mm Hg/l/min. In the long term study, no statistically significant differences over the base line values were found in measurements of mean pulmonary artery and pulmonary wedge pressures, mean systemic artery pressure, cardiac index and PO2. There was a greater fall in pulmonary vascular resistance in comparison with the acute study. The pulmonary vascular resistance fell from 5.06 +/- 3.45 mm Hg/l/min to 4.24 +/- 2.31 mm Hg/l/min but did not achieve statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

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What this paper is about

To determine whether Nifedipine reduces pulmonary artery pressure and pulmonary vascular resistance in patients with hypoxic pulmonary hypertension, we have studied ten clinically stable patients with chronic obstructive airways disease following acute administration of sublingual Nifedipine 20 mg and also after three months long term treatment with Nifedipine tablets 20mg bd. In the acute study, Nifedipine significantly raised mean pulmonary artery pressure from 30.32 +/- 13.07 mm Hg to 34.15 +/- 14.33 mm Hg (p less than 0.001) and pulmonary wedge pressure from 6.15 +/- 5.09 mm Hg to 7.6 +/- 3.39 mm Hg (p less than 0.1). There was a significant fall in mean systematic artery pressure from 99.06 +/- 12.05 mm Hg to 89.47 +/- 10.04 mm Hg (p less than 0.005) and a rise in heart rate from 79 +/- 9.7 beats/minute to 85.45 +/- 13.46 beats/minute (p less than 0.5). There was a significant change in cardiac index from 2.96 +/- 0.76 l/min/m2 to 3.2 +/- 0.51 l/min/m2 p(less than 0.1). There was no statistically significant change in pulmonary vascular resistance from 5.06 +/- 3.45 mm Hg/l/min to 4.92 +/- 3.10 mm Hg/l/min. In the long term study, no statistically significant differences over the base line values were found in measurements of mean pulmonary artery and pulmonary wedge pressures, mean systemic artery pressure, cardiac index and PO2. There was a greater fall in pulmonary vascular resistance in comparison with the acute study. The pulmonary vascular resistance fell from 5.06 +/- 3.45 mm Hg/l/min to 4.24 +/- 2.31 mm Hg/l/min but did not achieve statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

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Available abstract

To determine whether Nifedipine reduces pulmonary artery pressure and pulmonary vascular resistance in patients with hypoxic pulmonary hypertension, we have studied ten clinically stable patients with chronic obstructive airways disease following acute administration of sublingual Nifedipine 20 mg and also after three months long term treatment with Nifedipine tablets 20mg bd. In the acute study, Nifedipine significantly raised mean pulmonary artery pressure from 30.32 +/- 13.07 mm Hg to 34.15 +/- 14.33 mm Hg (p less than 0.001) and pulmonary wedge pressure from 6.15 +/- 5.09 mm Hg to 7.6 +/- 3.39 mm Hg (p less than 0.1). There was a significant fall in mean systematic artery pressure from 99.06 +/- 12.05 mm Hg to 89.47 +/- 10.04 mm Hg (p less than 0.005) and a rise in heart rate from 79 +/- 9.7 beats/minute to 85.45 +/- 13.46 beats/minute (p less than 0.5). There was a significant change in cardiac index from 2.96 +/- 0.76 l/min/m2 to 3.2 +/- 0.51 l/min/m2 p(less than 0.1). There was no statistically significant change in pulmonary vascular resistance from 5.06 +/- 3.45 mm Hg/l/min to 4.92 +/- 3.10 mm Hg/l/min. In the long term study, no statistically significant differences over the base line values were found in measurements of mean pulmonary artery and pulmonary wedge pressures, mean systemic artery pressure, cardiac index and PO2. There was a greater fall in pulmonary vascular resistance in comparison with the acute study. The pulmonary vascular resistance fell from 5.06 +/- 3.45 mm Hg/l/min to 4.24 +/- 2.31 mm Hg/l/min but did not achieve statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

Key concepts: Nifedipine, Medicine, Pulmonary wedge pressure, Vascular resistance, Pulmonary artery, Pulmonary hypertension, Cardiac index, Cardiology

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Acute and long term effect of nifedipine on pulmonary hypertension secondary to chronic obstructive airways disease. — Research Paper | ScholarLens