Clinical impact of pathology-proven etiology of severely stenotic aortic valves on mid-term outcomes in patients undergoing surgical aortic valve replacement

Abstract

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.

Fig 1. Study population flow chart.

Fig 2. Gross inspections of post-inflammatory (A), congenital (B), and calcific/degenerative (C) aortic stenosis in the representative cases from our study.

A: Post-inflammatory tricuspid aortic valve on the aortic side showing severe thickening of the cusps and fusion of the commissures with nodular calcification (asterisk). B: Bicuspid aortic valve on the aortic side demonstrating marked calcification of the raphe (black arrowheads) and heavy nodular calcification and severe fibrous thickening (red arrowheads). C: Calcific/degenerative tricuspid aortic valve characterized by patchy, moderate fibrotic thickening and focal heavy calcification at the base on the aortic side of the three cusps with adjacent portions of the cusps partially translucent.

Fig 3. Kaplan-Meier event curves for mid-term outcomes following surgical AVR among the three types of aortic valve etiologies with respect to (A) all-cause death, (B) cardiac events, and (C) combined adverse events.

Follow-ups were commenced on the day of index surgical AVR. Cardiac events were defined as all-cause death, aortic valve deterioration requiring repeated AVR, and hospitalization for HF. Combined clinical events included, along with cardiac events, non-fatal stroke, new-onset ischemic heart disease requiring unplanned coronary revascularization, symptomatic bradycardia/ventricular tachycardia treated with pacemaker/implantable cardioverter defibrillator, and admission for non-fatal gastrointestinal bleeding. AVR, aortic valve replacement.

Fig 4. NYHAfc of patients with severe aortic stenosis at the first diagnosis, within 30 days prior to surgical AVR, and at 3 years after surgical AVR (A) with a comparison of the three different aortic valve etiologies (B–D).

NYHAfc, New York Heart Association functional classification; AVR, aortic valve replacement.