Prevalence of pulmonary hypertension in reduced left ventricular systolic function and its influence on outcomes

Abstract

Abstract Background/Introduction Reduced left ventricular (LV) systolic function can lead to pulmonary hypertension (PHT). However, the significance of PHT complicating reduced LV systolic function remains poorly characterised. Purpose We aimed to describe the prevalence and prognostic importance of PHT in a large cohort of adults with at reduced left ventricular ejection fraction (LVEF). Methods We analysed the National Echocardiography Database of Australia (data from 2000-2019). Adults with a recorded tricuspid regurgitation (TR) peak velocity and LVEF <50% were included. Patients with moderate or greater left sided valvular pathology were excluded, as were patients with prior aortic or mitral valve replacements. These subjects (n= 23675) were then categorised according to their TR peak velocity. The relationship between PHT severity and mortality outcomes were evaluated (median follow-up of 2.9 years, interquartile range 1.0-5.4years). Results Subjects were aged 70±15years and 31.7% were female. Overall, 8801 (37.2%), 7061 (29.8%), 5676 (24.0%), and 2137 (9.0%) patients had normal (TR peak velocity <2.5m/sec), borderline (2.5-2.8m/sec), intermediate (2.9-3.4m/sec), or high risk PHT (>3.4m/sec), respectively. An echocardiographic phenotype for ‘left heart disease’ was evident with worsening PHT, showing rising E:e’ ratio and a greater proportion of right ventricular (RV) dilation and dysfunction (p<0.0001 for all). Left and right atrial sizes increased from low-intermediate risk, before plateauing at high risk PHT (p<0.0001). With increasing risk of PHT, 1- and 5-year actuarial mortality increased from 13.3% and 43.8%, to 41.5% and 81.4% respectively (p<0.0001). After adjustment for age, sex, LVEF, LV end diastolic diameter and LA volume index, the risk of mortality increased as TR peak velocity increased (adjusted hazard ratio (aHR) 1.31, 95% confidence interval 1.23-1.38 in borderline risk, to aHR2.38, 95%CI 2.21-2.56 in high risk PHT) (Figure 1). The cohort was also assessed in two groups based on LVEF severity according to guidelines. The sub-group of patients with mildly reduced LVEF (40-49%, n = 12495) showed that mortality risk increased as risk of PHT increased; (aHR 1.38, 95%CI 1.27-1.50 in borderline risk, to aHR2.82, 95%CI 2.52-3.15 in high risk PHT). Similarly, those with reduced LVEF (<40%, n = 11180) mirrored these trends (aHR 1.23, 95%CI 1.14-1.33 in borderline risk, to aHR2.07, 95%CI 1.88-2.28 in high risk PHT). There was a mortality threshold seen from TR peak velocity 2.41m/sec onwards (aHR1.18, 95%CI 1.04-1.33) (Figure 2). Conclusion(s) In this large cohort study, we demonstrate that PHT risk is common in patients with reduced LV systolic function and mortality increases as PHT becomes more severe. A threshold for higher mortality lies within the range of "borderline-intermediate" risk PHT.Adjusted Risk for All-Cause MortalityThreshold for Mortality