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Table 1.  

Clinical Characteristics, Baseline Hemodynamics, and Exercise Capacity of the Studied Patient Sample

Used with permission from: Sitbon O, Humbert M, Jais X, et al. Long-term response to calcium channel blockers in idiopathic pulmonary arterial hypertension. Circulation. 2005;111:3105-3111.

Table 2.  

Acute NO/Epoprostenol Responders Group (n = 70) Long-term CCB Responders Group (n = 38) CCB Failure Group (n = 32) P*
Drug tested (NO:epoprostenol) (n) 57:13 33:5 24:8 .2
Mean PAP reached during acute vasodilator testing (mm Hg) 38 ± 11 (18-65) 33 ± 8 (18-50) 46 ± 10 (18-65) < .001
Fall in mean PAP during acute vasodilator testing (mm Hg) 19 ± 7 (10-36) 21 ± 7 (10 - 36) 16 ± 6 (10 - 33) .006
Percent fall in mean PAP 33 ± 11 (20-59) 39 ± 11 (20 - 59) 26 ± 7 (20 - 49) < .001
PVR reached during acute vasodilator testing (WU) 6.6 ± 3.4 (1.1 - 17.4) 5.2 ± 2.7 (1.1 - 13.1) 8.6 ± 3.3 (1.1 - 17.4) < .001
Fall in PVR during acute vasodilator testing (WU) 5.6 ± 3.3 (1.6 - 16.7) 5.1 ± 3.1 (1.7 - 15.4) 6.2 ± 3.4 (1.6 -16.7) .16
Percent fall in PVR 45 ± 15 (24-77) 50 ± 15 (24 - 77) 40 ± 13 (26 - 75) .007

Hemodynamic Values Reached During Vasodilator Testing in Acute Responders

Values are mean ± SD (range).
*Comparison between long-term CCB responders and CCB failure groups (unpaired Student t or x 2 test, as appropriate.
CCB = calcium channel blockers; CO = cardiac output; NO = nitric oxide; PAP = pulmonary arterial pressure; PVR = pulmonary vascular resistance; WU = Wood units
Used with permission from: Sitbon O, Humbert M, Jais X, et al. Long-term response to calcium channel blockers in idiopathic pulmonary arterial hypertension. Circulation. 2005;111:3105-3111.

Table 2.  

Acute NO/Epoprostenol Responders Group (n = 70) Long-term CCB Responders Group (n = 38) CCB Failure Group (n = 32) P*
Drug tested (NO:epoprostenol) (n) 57:13 33:5 24:8 .2
Mean PAP reached during acute vasodilator testing (mm Hg) 38 ± 11 (18-65) 33 ± 8 (18-50) 46 ± 10 (18-65) < .001
Fall in mean PAP during acute vasodilator testing (mm Hg) 19 ± 7 (10-36) 21 ± 7 (10 - 36) 16 ± 6 (10 - 33) .006
Percent fall in mean PAP 33 ± 11 (20-59) 39 ± 11 (20 - 59) 26 ± 7 (20 - 49) < .001
PVR reached during acute vasodilator testing (WU) 6.6 ± 3.4 (1.1 - 17.4) 5.2 ± 2.7 (1.1 - 13.1) 8.6 ± 3.3 (1.1 - 17.4) < .001
Fall in PVR during acute vasodilator testing (WU) 5.6 ± 3.3 (1.6 - 16.7) 5.1 ± 3.1 (1.7 - 15.4) 6.2 ± 3.4 (1.6 -16.7) .16
Percent fall in PVR 45 ± 15 (24-77) 50 ± 15 (24 - 77) 40 ± 13 (26 - 75) .007

Hemodynamic Values Reached During Vasodilator Testing in Acute Responders

Values are mean ± SD (range).
*Comparison between long-term CCB responders and CCB failure groups (unpaired Student t or x 2 test, as appropriate.
CCB = calcium channel blockers; CO = cardiac output; NO = nitric oxide; PAP = pulmonary arterial pressure; PVR = pulmonary vascular resistance; WU = Wood units
Used with permission from: Sitbon O, Humbert M, Jais X, et al. Long-term response to calcium channel blockers in idiopathic pulmonary arterial hypertension. Circulation. 2005;111:3105-3111.

Table 3.  

Used with permission from: Barst RJ, Maislin G, Fishman AP. Vasodilator therapy for primary pulmonary hypertension in children. Circulation. 1999;99:1197-1208.

The Role of Calcium Channel Blockers in Pulmonary Arterial Hypertension: Early Attempts to Treat PAH With CCBs

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Early Attempts to Treat PAH With CCBs

In 1980, the first case report of successful treatment with CCBs of a patient with PAH was published.[6] The patient was treated with nifedipine, 100 mg daily. The authors reported improvement in symptoms and exercise capacity, although no significant change in hemodynamics was seen after 3 months of treatment. Three years later, Rubin and colleagues[7] reported their acute and chronic results in 9 patients with IPAH who had been treated with CCBs. They administered 10-20 mg of nifedipine acutely, and although 2 patients exhibited a significant reduction in mean pulmonary artery pressure (mPAP) of 30% each, there was no significant decrease in pressure in the group overall. There was, however, an increase in cardiac output (CO), which was associated with a significant decrease in pulmonary vascular resistance (PVR); P < .005. The effects were not specific to the pulmonary circulation, as there was also a significant reduction in systemic arterial pressure. Scintigraphic evaluation of right ventricular ejection fraction demonstrated a mean improvement of 18% in 8 of 9 patients. The authors found similar hemodynamic changes to those obtained during acute testing when they repeated hemodynamic evaluation in 6 patients after 4 to 14 months of treatment with nifedipine, up to 120 mg daily. No adverse affects were reported in this study.