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Medical Journal

Calcium-Channel Blockers

The recent ACCP consensus statement on medical therapy of PAH offers the following recommendation regarding the vasodilator response at catheterization: “Patients with IPAH, in the absence of right-heart failure, demonstrating a favorable acute response to vasodilator (defined as a fall in mean pulmonary artery pressure of at least 10 mm Hg to <40 mm Hg, with an increased or unchanged cardiac output), should be considered candidates for a trial of therapy with an oral calciumchannel antagonist. Level of evidence: low; benefit: substantial; grade of recommendation: B.” Dr Gaine, how does this recommendation fit into your usual practice?

Sean Gaine, MD, PhD
Director, Pulmonary Hypertension Unit
Mater Misericordiae Hospital
University College
Dublin, Ireland

This is a very useful new recommendation. In the past, before we had effective oral therapy for PAH, calcium-channel blockers were often used in an attempt to delay the need for intravenous epoprostenol therapy. Under the new evidence-based recommendations, unless patients have a true response to the vasodilator trial, calcium-channel blockers are avoided.

If someone without right ventricular failure had a mean pulmonary
artery pressure of 65 mm Hg and it decreased to 50 mm Hg (ie, did not go to 40 mm Hg or below), would you consider calcium-channel blocker therapy?

A drop in mean pulmonary artery pressure from 65 mm Hg to 50 mmHg is no longer considered a favorable response. Calcium-channel blockers rarely contribute much long-term benefit in this setting.

Do you use calcium-channel blocker therapy in patients with PAH but without any vasodilator response, for example, to control systemic hypertension?
Whenever I see systemic hypertension in a patient with PAH, I look for underlying medical conditions such as obstructive sleep apnea. When treatment is required, I prefer to use an angiotensin-receptor antagonist rather than calcium-channel blockers. The negative inotropic effect of calcium-channel blockers, as well as peripheral edema can be troublesome in PAH patients.

Do you ever add additional therapy (eg, an endothelin antagonist)
to the calcium-channel blocker in a stable patient with a good vasodilator response?

If calcium-channel blockers are demonstrated to achieve the same result as the vasodilator trial, then I generally stick with monotherapy as long as the patient is stable and asymptomatic. However, I have added either sildenafil or bosentan in patients who had a favorable response to a vasodilator trial, but who have been unable to tolerate sufficient calcium-channel blocker therapy to achieve a consistent
mean pressure below 40 mmHg.

The ACCP recommends acute vasodilator testing with a short-acting agent such as epoprostenol, adenosine, or inhaled nitric oxide. Which vasodilator do you use for acute testing and why?
I use inhaled nitric oxide. It is very safe, well tolerated, and its actions are specific to the pulmonary circulation.

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