It is commonly known that exercise capacity is impaired in pulmonary arterial hypertension (PAH). Thanks to a recent study, researchers were able to test a hypothesis on why this is the case, with the idea that perhaps cardiovascular reserve anomalies are in fact linked with an impaired hemodynamics response to pharmacological stress and negative outcomes in patients with PAH.
To test this new hypothesis, the study, which was first published by BMC Pulmonary Medicine 2014, included 18 PAH patients ℗ group 1 NYHA (New York Heart Association) class II/III and 10 controls, all of which underwent simultaneous right cardiac catheterization and intravascular ultrasound procedures at rest as well as during the dosing of low dose dobutamine (10 mcg/kg/min) with trendelenburg (DST). The PAH group’s Class II PAH patients presented milder symptoms of the disease that include shortness of breath and/or angina and slight limitation during ordinary activities, whereas Class III involves a marked limitation in activity during less-than-ordinary activity such as walking short distances. Class III PAH is so severe that patents with this level of the disease are only comfortable when they are at rest — any other exertion exacerbates their symptoms.
Researchers estimated cardiac output (CO), pulmonary vascular resistance (PVR) and capacitance (PC) and PA elastic modulus (EM) as part of their hypothesis. Tricuspid annular plane systeolic excursion (TAPSE), RV myocardial peak systolic velocity (Sm) and isovolumic myocardial acceleration (IVA) in PAH patients were measured concomitantly. All patients were were followed up for two years.
At the end of the study, based on the rounded mean + 2 SD of the increase in mPAP in our healthy control group during DST (2.8 + 1.8 mm Hg), PAH p were divided into two groups according to mean PA pressure (mPAP) response during DST, 1: DeltamPAP >5 mm Hg and 2: DeltamPAP <=5 mm Hg. Cardiovascular reserve was estimated as the change (delta, Delta) during DST compared with rest, including DeltamPAP with respect to DeltaCO (DeltamPAP/DeltaCO).
Results: PAH p showed significantly lower heart rate and CO increase than controls during DST, with a significant mPAP and pulse PAP increase and higher DeltamPAP/DeltaCO (p <0.05). Neither hemodynamic, IVUS and echocardiographic data were different between both PAH groups at rest.
In group 1, DST caused a higher DeltaEM, DeltamPAP/DeltaCO, DeltaPVR, and DeltaTAPSE than group 2, with a lower IVA increase and a negative DeltaSV (p <0.05). TAPSE correlated with mPAP and RVP (p <0.05) and, IVA and Sm correlated with CO (p <0.05).
DeltaEM correlated with DeltamPAP and DeltaIVA with DeltaCO (p <0.05). There were two deaths/pulmonary transplantations in group 1 and one death in group 2 during the follow-up (p >0.05).
Researchers concluded that pulmonary vascular reserve and RV systolic reserve were significantly impaired in patients with PAH. They also report that the lower recruitable cardiovascular reserve is significantly related to a worse hemodynamic response to DST and it could be linked with a poor clinical outcome. The new findings from this study will help researchers to now develop therapies in the future that can address these vascular conditions, and thus improve cardiovascular reserve in PAH patients so that more mobility and exercise can be maintained, even among more serious, Class III cases.