Jain, Vidyut

Abstract Background The non-invasive calculation of right ventricular hemodynamics such as the pulmonary artery capacitance (PAC) has proven to be feasible and easy to perform. The simplified pulmonary embolism severity index (sPESI) and pulmonary vascular resistance (PVR) are other prognostic tools that have been used in the past. Purpose To evaluate if baseline PAC can outperform PVR and sPESI to predict all-cause short-term mortality in patients with acute pulmonary embolism (PE). Methods 373 patients with acute PE and a transthoracic echocardiogram performed within one day of diagnosis from March 2013 through June 2020 were followed prospectively. PAC was calculated as: Left ventricular stroke volume/ (Pulmonary artery systolic pressure – Pulmonary artery diastolic pressure). PVR was calculated as: Tricuspid regurgitant velocity / Right ventricular outflow tract velocity time integral x 10 + 0.16. The sPESI was used to evaluate prognosis by categorizing patients into low and high-risk categories. Multiple logistic regression analyses and receiver-operating characteristic curves were used to evaluate the ability of PAC, PVR, and sPESI to predict all-cause mortality up to six months. The Youden index was used to determine the cut-off value with the highest sensitivity and specificity. Kaplan–Meier curves were performed to determine event-free survival rate, differences between groups were assessed using the Wilcoxon Test. Results Mean age was 64±15 years (58% male, 28% cancer). PAC was associated with mortality at thirty days (p 0.0003), three months (p 0.003), and six months (p 0.011) (Table). PVR was associated with mortality at thirty days, three months, and six months (p 0.045, 0.012, and 0.031 respectively). The sPESI score ≥1 (high risk) was associated with all-cause mortality at three months and six months (p 0.0136 and <0.0001 respectively). PAC was the strongest predictor of all-cause mortality with an AUC of 0.95 (CI 0.82- 0.99) at thirty days, 0.84 (CI 0.65–0.99) at three months, and 0.77 (CI 0.57–0.96) for six months. Corresponding Kaplan-Meier survival curve of PAC and thirty days all-cause mortality is presented in the Figure. PVR had an AUC of 0.75 (CI 0.48–0.95) at thirty days, 0.79 (CI 0.58–0.94) at three months, and 0.72 (CI 0.50–0.90) at six months. The sPESI had an AUC of 0.62 (CI 0.54–0.66) at three months and 0.64 (CI 0.59–0.67) at six months. Conclusion In patients with acute PE, PAC outperforms sPESI and PVR as a predictor of short-term all-cause mortality at thirty days, three months, and six months. These three variables should be explored head to head prospectively for their utility to predict short term all-cause mortality. Funding Acknowledgement Type of funding sources: None.

Abstract Background Exercise intolerance is the cardinal manifestation of heart failure (HF), yet its underlying mechanism(s) remain poorly understood. Measures of ventricular function such as ejection fraction often have no relationship with exercise capacity in HF. 2D-STE has proved to be more reliable method to evaluate myocardial mechanical function. Our hypothesis is Resistance exercise training (Resist-HFpEF) will improve exercise tolerance and exertional symptoms in patients with HFpEF. Purpose The study aims to evaluate myocardial mechanical function by strain imaging during resistance exercise training in Heart Failure patients with Preserved Ejection Fraction (HFpEF) Methods This is a single centre prospective pilot study. 24 HFpEF patients were enrolled and their baseline comorbidities were recorded. Baseline 2D-STE imaging was performed at rest and during exercise (Visit 1). Patients were then randomized to either a novel resistance exercise training program for 36 sessions (3 sessions per week for 12 weeks) or a standard of care control group. 2D STE imaging was then repeated at follow-up (Visit 2). Peak Global Longitudinal strain (GLS), systolic strain rate (SSR), early diastolic strain rate (SRe) were measured offline. Results Mean age of the Rehab cohort was 68.57±10.52 years and the control cohort was 68.1±6.47 years. 23 study subjects were male (96%). 17% of the study subjects were hypertensive, 63% were diabetic, 42% had NYHA I, 46% had NYHA II and 13% had NYHA III of heart failure. The mean LV ejection fraction in the control and Rehab group after the training program at rest was 61.88±2.26% & 54.74±2.07% (p-value 0.04) and during exercise was 59.90±2.05% and 53.13±2.05% (p-value 0.04). The peak GLS was −18.80±4.29% and −17.7±2.21% in controls during rest and exercise at Visit 1 (p-value 0.27) while the rehab cohort had −18.71±4.7% and −20.82±2.4% respectively (p-value 0.0268). The peak GLS was −17.40±3.05% and −17.96±2.65% in controls during rest and exercise at Visit 2 (p-value 0.3430) while rehab cohort had −17.97±6.21% and −16.57±3.82% respectively (p-value 0.67). (Figure 1a and 1b shows GLS, SRS, SRe at Baseline and after exercise program respectively) Conclusion This pilot study suggest systolic and diastolic reserve can be measured reliably during low grade exercise. These results could reflect improvement in clinical status and exercise tolerance. Figure 1. Comparison of peak GLS, SSR, SRe amongst HFpEF patients at rest and during exercise before and after the rehab training program. Funding Acknowledgement Type of funding source: None

Abstract Background The left ventricle (LV) in obese patients undergoes different patterns of remodeling in order to normalize wall stress. However, little is known about how LV volume indices, LV global longitudinal strain and right ventricular free wall strain (GLS) vary according to the pattern of LV remodeling. Aim To define the echocardiographic reference values of LV volumes and biventricular GLS across the different LV remodeling patterns in obese patients with a preserved ejection fraction. Methods 2393 adult obese patients (1428 females, 965 males) with a normal ejection fraction who underwent echocardiography from January 2008 to December 2018 were selected. They were categorized according to 4 cardiac remodeling groups defined by LV mass index (102g/m2 in males, 88g/m2 in females) and relative ventricular wall thickness (0.42): normal geometry (NG), eccentric hypertrophy (EH), concentric remodeling (CR) and concentric hypertrophy (CH). Obese subjects were further categorized by BMI class (30–35, 35–40, >40 kg/m2). Obese subjects were gender matched to controls with a normal BMI (18.5–25 kg/m2) and normal cardiac geometry. Mean ± SD, One-way Anova and Tukey- Kramer HSD were applied. P<0.05 is considered significant. Results The mean age of controls and obese patients' were 50±16 and 57±13.6 years respectively (P<0.0001). LV GLS for controls compared to obese subjects with NG, EH, CR and CH was −21.1±2 vs. −20.2±1.9, −19.6±2.8, −18.5±2.9, −17.5±3.4 respectively (p<0.0001 for all), and for RV GLS it was −27.9±4 vs −26.7±3.9, −25.1±5, −23.5±5.5, −24.1±5.2 respectively (p<0.01 for all, except for NG where p=0.2). The distribution of LV indices according to cardiac remodeling subtypes is shown in the figure. Indexed end diastolic and end systolic volumes were smaller in NG, CH and CR compared to controls (p<0.001 for each respectively). LV GLS and ejection fraction were higher in females, while indexed LV volumes were higher in males within each remodeling category (P<0.0001). No significant difference in LV GLS or indexed LV volume was seen across BMI categories within each remodeling pattern (P>0.05). Obese subjects with CH had the highest incidence of the cardiovascular risk factors hyperlipidemia, hypertension and history of myocardial infarction or stroke, compared to those with other remodeling patterns (p<0.0001 for each, vs. NG, EH and CR). Conclusion To our knowledge, this is the largest study to define LV volumes and left and right ventricular GLS according to LV remodeling pattern and BMI category. The Lowest GLS was noted in CH. Ejection fraction was similar across the LV remodeling patterns. There were no differences in GLS and LV indexed volumes across BMI categories within each remodeling group. These results can be applied as a reference values for the obese population with a normal LV ejection fraction. Funding Acknowledgement Type of funding source: None