Systolic Ejection Time is an Independent Predictor of Incident Heart Failure in a Community Based Cohort Free of Heart Failure

Systolic Ejection Time is an Independent Predictor of Incident Heart Failure in a Community Based Cohort Free of Heart Failure

S84 Journal of Cardiac Failure Vol. 21 No. 8S August 2015 Cardiovascular Structure/Imaging II 185 Systolic Ejection Time is an Independent Predictor ...

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S84 Journal of Cardiac Failure Vol. 21 No. 8S August 2015

Cardiovascular Structure/Imaging II 185 Systolic Ejection Time is an Independent Predictor of Incident Heart Failure in a Community Based Cohort Free of Heart Failure Tor Biering-Sørensen1, Gabriela Querejeta Roca1, Sheila Hegde1, Amil Shah1, Brian Clagett1, Thomas H. Mosley2, Kenneth R. Butler2, Scott D. Solomon1; 1Brigham and Women’s Hospital, Boston, MA; 2University of Mississippi Medical Center, Jackson, MS Introduction: Cardiac time intervals are sensitive markers of cardiac dysfunction. The usefulness of the systolic ejection time (SET) to predict incident heart failure (HF), however, is unknown. Hypothesis: We hypothesized that SET is a strong predictor of incident HF in a community based cohort free of HF. Methods: We studied middle-aged African-Americans from the Jackson cohort of the Atherosclerosis Risk in Communities study (n52,077) who underwent echocardiography between 1993 and 1995 and were free of heart failure. SET was measured by pulsed-wave Doppler. Results: The mean age of the participants was 59 years, 37% were men, 58% had hypertension, 22% diabetes and 4% prevalent coronary heart disease (CHD). SET ranged from 194 to 778 ms (mean 341 6 35 ms)(Figure 1). During median follow-up of 16.7 years, 394 (19%) had incident HF. In unadjusted analyses, the risk of incident HF increased with decreasing SET below the mean of the population (Figure 1); HF risk was approximately 40% higher for participants with a SET below the mean vs. above the mean (Hazard Ratio (HR) 1.41 [1.16; 1.73], p50.001). Lower SET was also significantly associated with higher age, male gender, higher blood pressure (BP) and heart rate, lower fractional shortening (FS) and lower E/A-ratio (p for trend ! 0.001 for all). The SET was similarly prognostic of FS and left atrium diameter (LAD) when assessed by c-statistics (0.58 for SET, 0.57 for FS and 0.59 for LAD). SET remained an independent predictor of incident HF after adjustment for age, gender, heart rate, body mass index, hypertension, diabetes, CHD, systolic and diastolic BP and conventional measures of systolic and diastolic function (FS, LAD and E/A-ratio)(HR 1.06 [1.01; 1.11], p50.013, per 10 ms decrease). Conclusion: SET is an independent predictor of incident HF in a community based cohort and provides similar prognostic information on the risk of future HF when compared to conventional measures of systolic and diastolic function.

TRV/TVIRVOT ratio in pts undergoing evaluation for LT. Methods: We included 100 pts who underwent RHC and TTE as part of LT evaluation from 01/10 to 03/15. Median time between the two tests was 5 days. We categorized the shape of FVERVOT as no (NN), late-systolic (LSN) or mid-systolic (MSN) notching. Unpaired ttests were used to compare sample means for continuous variables and linear regression analysis to test the correlation between invasive and non-invasive PVR. Results: The mean patient age was 5768.5 years; 50% were male with diverse etiologies of ALD (35% HCV, 21% alcoholic, 10% cryptogenic, 6% NASH, 4% autoimmune, 24% other) and 79% were transplanted. The prevalence of POPH as defined by PVR$3 on RHC was 12%. Elevated systolic pulmonary artery pressure (PAPs$40mmHg) on TTE was present in 54% and mean PAP$25mmHg on RHC in 24%. The shape of the FVERVOT Doppler exhibited NN in 81%, LSN in 10% and MSN in 9%. Pts with either LSN or MSN had higher mean PAP than those with NN (2869 vs 35611mmHg, p50.007) and higher transpulmonary gradient (TPG), diastolic pulmonary gradient (DPG) and PVR; the difference between LSN and MSN was not significant. TAPSE was lower in pts with LSN or MSN compared to NN (Fig 1), and non invasively estimated PVR was higher (1.860.5 vs 1.460.5 WU, p50.003). Poor correlation was observed between noninvasive and invasive PVR (R250.10, p50.001). RVOT notching and non-invasive PVR were poor predictors of mortality. Elevated PAPs on TTE was a sensitive but not specific screening tool for PVR$3 (Sn582%, Sp548%). Conclusions: RVOT Doppler flow velocity notching reliably predicts POPH in pts with ALD.

Figure 1. Hemodynamic differences in patients with no Notching (NN), late-Systolic notching (LSN) and mid systolic notching in FVEKVOT

187 Association of 4-Tiered Classification of Left Ventricular Hypertrophy With Adverse Cardiovascular Outcomes in the General Population Sonia Garg1, James de Lemos1, Colby Ayers1, Michel Khouri2, Ambarish Pandey1, Jarett D. Berry1, Ronald M. Peshock1, Mark H. Drazner1; 1UT Southwestern, Dallas, TX; 2Duke University, Durham, NC Figure 1.

186 Right Ventricular Outflow Tract Doppler Envelope Notching Predicts Pulmonary Vascular Resistance in Patients with Advanced Liver Disease Marcella Manicardi1,2, Jana Svetlichnaya1, Van Selby1, Munir Janmohamed1, Francis Yao1, John Roberts1, Teresa De Marco1; 1University of California, San Francisco, CA; 2Azienda Ospedaliero-Universitaria Policlinico di Modena, Modena, Italy Introduction: Portopulmonary hypertension (POPH) affects 6% of liver transplant (LT) candidates and is associated with poor outcomes. Screening for POPH with a transthoracic echocardiogram (TTE) is the standard of care, but diagnosis requires right heart catheterization (RHC) which carries risks in pts with advanced liver disease (ALD). Systolic deceleration or “notching” of the right ventricular outflow tract Doppler flow velocity envelope (FVERVOT) correlates with high pulmonary vascular resistance (PVR) in mixed pulmonary hypertension (PH) but has not been validated in pts with ALD. The ratio of peak tricuspid regurgitant velocity (TRV, m/s) and time-velocity integral of the RVOT (TVIRVOT) per the formula PVR5TRV/TVIRVOT x 10 has been shown to reliably estimate PVR. Hypothesis: We investigated whether PVR can be predicted by the shape of FVERVOT or estimated by the

Background: We previously proposed a 4-tiered classification of left ventricular hypertrophy (LVH) where eccentric LVH is subdivided into “indeterminate hypertrophy” and “dilated hypertrophy” and concentric LVH into “thick hypertrophy” and “both thick and dilated hypertrophy,” based on the presence of increased left ventricular end-diastolic volume. Whether these subgroups are associated with cardiovascular (CV) outcomes in a general population is unknown. Methods: Participants from the Dallas Heart study who underwent cardiac magnetic resonance imaging and did not have LV dysfunction or history of heart failure (HF) (n 5 2,458) were followed for a median of 9 years for the primary outcome of HF or cardiovascular (CV) death. Results: In the cohort, 70% had no LVH, 404 (16%) had indeterminate hypertrophy, 30 (1%) had dilated hypertrophy, 289 (12%) had thick hypertrophy, and 7 (0.2%) had both thick and dilated hypertrophy. The cumulative incidence of HF or CV death was 2% with no LVH, 1.7% with indeterminate, 16.7% with dilated, 11.1% with thick, and 42.9% with both thick and dilated hypertrophy (log rank p! 0.0001). Compared with participants without LVH, those with dilated (HR 7.3, 95% CI 2.8-18.8), thick (HR 2.4, 95% CI 1.4-4.0), and both thick and dilated (HR 5.8, 95% CI 1.7-19.5) hypertrophy remained at increased risk for HF or CV death after multivariable adjustment, whereas the group with indeterminate hypertrophy was not (HR 0.9, 95% CI 0.4-2.2). Conclusion: In the general population, the 4-tiered classification system for LVH stratified LVH into subgroups with differential risk of adverse CV outcomes.