Why the study?
The association between aortic stenosis etiology and mid-term clinical outcomes after surgical aortic valve replacement had not been fully investigated.
Does pathology-proven etiology of severe aortic stenosis impact mid-term clinical outcomes after surgical aortic valve replacement?
Cohort (n=201)
Does pathology-proven etiology of severe aortic stenosis impact mid-term clinical outcomes after surgical aortic valve replacement?
Hazard Ratio: 5.69
p-value: p=0.002
Pathology-proven etiology of severe aortic stenosis, particularly calcific/degenerative, is independently associated with worse mid-term clinical outcomes after surgical aortic valve replacement compared to post-inflammatory etiology.
Etiology should not yet guide post-AVR decisions; leaves open whether pathology-proven subtypes warrant tailored surveillance in prospective studies.
BACKGROUND: The use of transcatheter or surgical aortic valve replacement (AVR) for severe aortic stenosis (AS) has considerably increased in recent years. However, the association between AS etiology and mid-term clinical outcomes after surgical AVR has not been fully investigated. METHODS AND RESULTS: We retrospectively included 201 patients (mean age, 75 years; 43%, men) who underwent surgical AVR for severe native AS (aortic valve area ≤1.0 cm2 on preoperative transthoracic echocardiography examination). The following valve etiologies were postoperatively identified on pathological examination: post-inflammatory (n = 28), congenital (n = 35), and calcific/degenerative (n = 138). The median follow-up interval was 4.1 years following surgical AVR. Of the 201 patients, 27% were asymptomatic, 40% had a history of heart failure, and 11% underwent previous heart surgery. The cumulative incidence of cardiac events (all-cause death, aortic valve deterioration requiring repeated AVR, and hospitalization for heart failure) and combined adverse events, which included non-fatal stroke, unplanned coronary revascularization, pacemaker implantation, and gastrointestinal bleeding along with cardiac events, was significantly higher in the calcific/degenerative group (p = 0.02 and p = 0.02, respectively). In multivariate analysis adjusted for age, sex, renal function, heart failure, atrial fibrillation, concomitant surgical procedures, and EuroSCORE II, AS etiology was independently associated with an increased risk of combined adverse events (congenital vs. post-inflammatory: hazard ratio [HR], 4.13; p = 0.02 and calcific/degenerative vs. post-inflammatory: HR, 5.69; p = 0.002). CONCLUSIONS: Pathology-proven AS etiology could aid in predicting the mid-term outcomes after surgical AVR, supporting the importance of accurate identification of severe AS etiology with or without postoperative pathological examination.
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Miura et al. (2020) conducted a cohort in Severe native aortic stenosis (n=201). Calcific/degenerative aortic stenosis etiology vs. Post-inflammatory aortic stenosis etiology was evaluated on Combined adverse events (cardiac events, non-fatal stroke, unplanned coronary revascularization, pacemaker implantation, and gastrointestinal bleeding) (HR 5.69, p=0.002).
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