Abstract 1990: Calcium Channel Blockers Impair Right Atrial Contractility and Cardiac Output in Non-Responders with Chronic Pulmonary Hypertension
Background. The use of Calcium Channel Blockers (CCB) in patients with chronic pulmonary hypertension (CPH) is controversial. Concern exists that CCB therapy in “non-responders” may further impair cardiac function, but their effects on right heart mechanics in “responders” versus non-responders remains unknown.
Methods. In 12 dogs, right atrial (RA) and ventricular (RV) pressure and volume (conductance catheter) were simultaneously recorded after 3 months of progressive pulmonary artery banding (baseline). Diltiazem was given at 10 mg/h with the pulmonary artery constricted (CCB non-responder). Responders were then simulated by releasing the pulmonary artery band to unload the ventricle. RA and RV contractility and diastolic stiffness (slope of end-systolic and end-diastolic pressure-volume relations) were calculated and RA reservoir and conduit function were quantified as RA inflow with the tricuspid valve closed versus open, respectively.
Results. With CCB, RA contractility (p < 0.03) and cardiac output (p < 0.004) decreased in non-responders while RV pressure and contractility were unchanged (table⇓). After pulmonary artery band release, the right atrium became less distensible, causing a shift from reservoir to conduit function (p < 0.001) and the contractility in both chambers decreased (p < 0.007). RA and RV diastolic function in non-responders and responders was not affected by CCB.
Conclusions. CCB did not impact RV function in non-responders, but significantly impaired RA contractility and cardiac output. In responders, afterload fell substantially to maintain cardiac output despite a decline in the normal RA and RV hyperdynamic contractile response to CPH. Thus, clinical use of CCB in CPH should be restricted to documented responders.