Role of CCBs in Pulmonary Arterial Hypertension

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

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.

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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.

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Page 3 of 9

Use of High-Dose CCBs in the Treatment of PAH

References

Table 1.

Table 2.

Table 2.

Table 3.

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

Early Attempts to Treat PAH With CCBs

Table of Contents

Table 1.

Table 2.

Table 2.

Table 3.

References

Faculty and Disclosures

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

Early Attempts to Treat PAH With CCBs

Table of Contents