PMC:3750932 / 74751-76714
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/3750932","sourcedb":"PMC","sourceid":"3750932","source_url":"http://www.ncbi.nlm.nih.gov/pmc/3750932","text":"Calcium channel blockers\nCalcium channel blockers (CCB) are indicated in patients with a positive vasodilatation challenge test after inhaled NO. CCB are vasodilators and were initially introduced in the 1980’s as part of PAH therapy to counteract vasoconstriction that has traditionally been assumed to be a preponderant mechanism in PAH. In the 1990’s, Rich and colleagues showed in an open prospective study that high dose of calcium channel blockers (nifedipine 90 to 240 mg/day or diltiazem 360 to 900 mg/day) significantly improve prognosis in patients with an acute vasodilation response [203]. Sitbon et al. showed that only 12.6% out of the patients could be treated by CCB according to criteria's establish by Rich and co-workers [203]. Moreover, only half of them maintained actual long-term benefit defined as NYHA FC I or II at one year without the need for additional treatment [205]. In this study, a decrease in mean PAP \u003e 10 mmHg to reach a value \u003c 40 mmHg, with a stable or increased cardiac output, during acute vasodilator test was predictive of long-term response to CCB. Contrarily, CCB must be avoided in the absence of acute vasoreactivity because of the risk of significantly reduced cardiac output and systemic blood pressure [205]. The choice of CCB is based upon the patient’s heart rate; nifedipine and amlodipine were preferred in the presence of relative bradycardia and diltiazem in the presence of tachycardia. Doses of CCB used in this setting are relatively high, 120-240 mg de nifedipine, 240-270 mg for diltiazem, and up to 20 mg for amlodipine [15]. If the patient does not show a correct response (NYHA FC I or II with marked hemodynamic improvement), additional PAH specific therapy should be added. Of note, CCB is contraindicated in PVOD because of the high-risk of life threatening pulmonary edema, even in the presence of acute vasodilator response that can be observed in the same proportion as in idiopathic PAH 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