Pulmonary Vascular Disease Articles

Providers who treat pulmonary vascular disease (PVD) or exertional dyspnea routinely face complex cardiopulmonary hemodynamic interactions. These articles discuss predictors of pulmonary hypertension (PH) severity, right ventricular (RV) performance, and hemodynamic response to exercise in patients with dyspnea.

Arkles and colleagues (Am J Respir Crit Care Med. 2011;183[2]:268) describe the correlation of elevated pulmonary vascular resistance and RV systolic dysfunction in patients with PH who demonstrated systolic deceleration or “notching” of the RV outflow tract Doppler flow velocity envelope on echocardiogram. “Notching” appears to represent a pathologic wave reflection in the setting of elevated pulmonary artery impedance. Those with midsystolic notch had the most severe PVD and RV dysfunction. This could have clinical implications, especially if “notching” can be easily identified by less experienced echocardiogram readers.

Groepenhoff and colleagues (Eur J Heart Fail. 2010;12[7]:716) discuss differences in the ability to increase cardiac output (CO) between patients with left heart failure (LHF) vs patients with pulmonary arterial hypertension (PAH). About 42% of both groups had impaired exercise tolerance on a maximal cardiopulmonary exercise test. The PAH group had significantly lower peak stroke volume (SV) response to exercise (-14 mL, P = 0.01) but had a larger HR response to increased CO. This finding highlights potential detrimental effects of beta-blockers in PAH.

Plehn and colleagues (Acta Cardiol. 2009;64[5]:617) evaluated patients with normal left heart performance by echocardiogram and exertional dyspnea with suspected left ventricular (LV) diastolic dysfunction (DD) as its cause. An exercise challenge performed during right-sided heart catheterization led to abnormal elevation of capillary wedge pressure in 74% of subjects. Peak CO response was reduced mainly because of impaired increase in SV. Invasive exercise hemodynamics can help unmask LVDD in patients with dyspnea.

Dr. Francisco Soto, FCCP
Chair