The Impact of Left Ventricular Diastolic Dysfunction on Clinical Outcomes After Transcatheter Aortic Valve Replacement.

Asami, Masahiko; Lanz, Jonas; Stortecky, Stefan; Räber, Lorenz; Franzone, Anna; Heg, Dik; Hunziker, Lukas; Roost, Eva; Siontis, George CM; Valgimigli, Marco; Windecker, Stephan; Pilgrim, Thomas (2018). The Impact of Left Ventricular Diastolic Dysfunction on Clinical Outcomes After Transcatheter Aortic Valve Replacement. JACC. Cardiovascular Interventions, 11(6), pp. 593-601. Elsevier 10.1016/j.jcin.2018.01.240

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OBJECTIVES

This study sought to determine the impact of left ventricular (LV) diastolic dysfunction (LVDD) on clinical outcomes in patients undergoing transcatheter aortic valve replacement (TAVR).

BACKGROUND

LV hypertrophy in response to afterload increase promotes the development of LVDD and represents an early stage in the progression to valvular heart failure.

METHODS

In a consecutive cohort of 777 aortic stenosis patients undergoing TAVR, LVDD was categorized according to the latest guidelines. The primary endpoint was 1-year all-cause mortality.

RESULTS

There were 545 (70.1%) patients with LVDD. Ninety-eight (18.0%), 198 (36.3%), and 104 (19.1%) patients were classified as LVDD grades I, II, and III, respectively. In 145 (26.6%) patients, LVDD grade could not be determined because of only 1 or 2 discrepant variables. One-year all-cause mortality was higher in patients with LVDD grades I (16.3%; HR: 2.32; 95% CI: 1.15 to 4.66), II (17.9%; HR: 2.58; 95% CI: 1.43 to 4.67), and III (27.6%; HR: 4.21; 95% CI: 2.25 to 7.86) than in those with normal diastolic function (6.9%). The difference in clinical outcome emerged within 30 days, was driven by cardiovascular death, and maintained in a sensitivity analysis of patients with normal systolic LV function. Furthermore, LVDD grades I (HR: 2.36; 95% CI: 1.17 to 4.74), II (HR: 2.58; 95% CI: 1.42 to 4.66), and III (HR: 4.41; 95% CI: 2.37 to 8.20) were independent predictors of 1-year mortality.

CONCLUSIONS

Advancing stages of LVDD are associated with an incremental risk of all-cause mortality after TAVR, driven by cardiovascular death and taking effect as early as 30 days after the intervention.

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