Strain and Exercise-Induced Pulmonary Hypertension

Patients who increase mean pulmonary artery (PA) pressure (mPAP) during exercise have decreased survival and are often misdiagnosed,(1 )but diagnosis of exercise-induced pulmonary hypertension (EIPH) remains difficult because of lack of consensus. Invasive hemodynamics have shown that mPAP of 30 mm Hg is the upper limit of normal at exercise when cardiac output (CO) is below 10 L/min. 3 mm Hg/L/min is the upper limit of mPAP/CO.(2) Accordingly, exercise pulmonary vascular resistance defined as mPAP/CO with exercise has emerged as a tool for understanding EIPH.(3 )Transthoracic echocardiographic (TTE) longitudinal strain is a noninvasive modality assessing early changes in myocardial function. Right atrial and ventricular function have prognostic value in pulmonary hypertension.4 In asymptomatic degenerative mitral regurgitation, left atrial strain on exercise TTE predicts EIPH.5 However, the value of strain in EIPH based on catheter-based mPAP/CO slope >3 has not been established. Our goal was to assess the relation between left and right atrial and ventricular strain and hemodynamics on exercise right-sided cardiac catheterization (RHC). Imaging/American Society of Echocardiography/Industry Task Force. TTE and hemodynamics were compared between mPAP/CO slope3. Parameters were described as mean +/- SD using Student's t test. p Values were adjusted using false discovery rate correction. p <0.05 were statistically significant. Analyses were conducted using R v.4.0.3 (The R Foundation for Statistical Comput- ing, Vienna, Austria).