Cardiology · 2024
Electrocardiographic Strain and Relationship with Left Ventricular Remodelling and Clinical Outcomes in Patients with Aortic Stenosis Undergoing Transcatheter Aortic Valve Implantation.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Wasim Daanyaal, Mohamed Ali Abukar, Bleie Øyvind, Løland Kjetil H, Rajani Ronak, Rotevatn Svein, Saeed Sahrai
Аннотация
INTRODUCTION: Left ventricular (LV) remodelling and fibrosis are known to occur in patients with aortic stenosis (AS) and are linked to post-intervention outcomes. These myocardial changes may be detected upon the routine 12-lead electrocardiogram (ECG) by the presence of a LV strain pattern (LVS-ECG). Although LVS-ECG has been related to excessive cardiovascular morbidity and mortality in multiple patient populations, there is currently a dearth of data upon its impact in patients undergoing transcatheter aortic valve implantation (TAVI). The aim of the current study was to investigate the prevalence, predictors, and prognostic value of LVS-ECG.
METHODS: Between 2012 and 2019, 640 consecutive patients underwent TAVI at Haukeland University Hospital, Bergen. Of these, 600 patients with severe AS were included in the TAVI-NOR study. Patients with known bundle branch block (n = 85) or permanent pacing (n = 25) were excluded, leaving 490 patients (mean age 81 ± 6 years, 52% females) eligible for the analyses. LVS-ECG was defined as down-sloping, convex ST-segment depression with asymmetric T-wave inversion in V5 or V6.
RESULTS: LVS-ECG was present in 25.7% patients. Higher levels of NT-proBNP (OR 1.96; 95% CI: 1.08-3.55, p = 0.028), left ventricular ejection fraction (LVEF) <50% (OR 3.14; 95% CI: 1.61-6.13, p = 0.001), increase in LV mass index per SD (32 g/m2) (OR 1.37; 95 CI: 1.06-1.76, p = 0.014), and the presence of LV hypertrophy on ECG (OR 3.23; 95% CI: 1.97-5.32, p < 0.001) were independent predictors of LVS-ECG in the multivariable-adjusted analysis. Although all-cause mortality was significantly higher in patients with LVS-ECG compared to those without (54.8% vs. 44.2%, p = 0.041), the presence of LVS-ECG did not predict all-cause mortality during a mean follow-up of 64 ± 24 months (HR 1.05; 95% CI: 0.79-1.39, p = 0.742). Patients with LVEF <50% and concomitant LVS-ECG had a worse prognosis than those with LVEF >50% and no LVS-ECG (p < 0.001).
CONCLUSIONS: LVS-ECG may represent a simple marker of structural and functional LV remodelling that signals a propensity to excess mortality during long-term follow-up after TAVI, as it is strongly associated with other prognosticators such as reduced LVEF and increased levels of NT-proBNP.
METHODS: Between 2012 and 2019, 640 consecutive patients underwent TAVI at Haukeland University Hospital, Bergen. Of these, 600 patients with severe AS were included in the TAVI-NOR study. Patients with known bundle branch block (n = 85) or permanent pacing (n = 25) were excluded, leaving 490 patients (mean age 81 ± 6 years, 52% females) eligible for the analyses. LVS-ECG was defined as down-sloping, convex ST-segment depression with asymmetric T-wave inversion in V5 or V6.
RESULTS: LVS-ECG was present in 25.7% patients. Higher levels of NT-proBNP (OR 1.96; 95% CI: 1.08-3.55, p = 0.028), left ventricular ejection fraction (LVEF) <50% (OR 3.14; 95% CI: 1.61-6.13, p = 0.001), increase in LV mass index per SD (32 g/m2) (OR 1.37; 95 CI: 1.06-1.76, p = 0.014), and the presence of LV hypertrophy on ECG (OR 3.23; 95% CI: 1.97-5.32, p < 0.001) were independent predictors of LVS-ECG in the multivariable-adjusted analysis. Although all-cause mortality was significantly higher in patients with LVS-ECG compared to those without (54.8% vs. 44.2%, p = 0.041), the presence of LVS-ECG did not predict all-cause mortality during a mean follow-up of 64 ± 24 months (HR 1.05; 95% CI: 0.79-1.39, p = 0.742). Patients with LVEF <50% and concomitant LVS-ECG had a worse prognosis than those with LVEF >50% and no LVS-ECG (p < 0.001).
CONCLUSIONS: LVS-ECG may represent a simple marker of structural and functional LV remodelling that signals a propensity to excess mortality during long-term follow-up after TAVI, as it is strongly associated with other prognosticators such as reduced LVEF and increased levels of NT-proBNP.