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Updated: Oct 28, 2026

Technique and Patient Selection Criteria of Right Anterior Mini-Thoracotomy for Minimal Access Aortic Valve Replacement
Published on: March 26, 2018
Minimally Invasive Aortic Valve Replacement and Perioperative Stroke Risk: A Propensity-Matched Analysis
Adam Ryszard Kowalówka1,2, Julia Wojtczak2, Maria Zwinczak2
1Department of Cardiac Surgery, Upper-Silesian Heart Center, 40-635 Katowice, Poland.
Abstract:
Background/Objectives: Stroke is a devastating complication after aortic valve replacement (AVR). Whether minimally invasive AVR (miniAVR) reduces perioperative stroke risk versus conventional sternotomy remains uncertain. Methods: This single-center retrospective cohort study used propensity score matching (PSM) in 1741 consecutive patients undergoing isolated AVR (2014-2025). After exclusions, 1:1 PSM using 10 covariates created 155 matched pairs with excellent balance (all standardized mean differences < 0.20). The primary endpoint was in-hospital stroke or transient ischemic attack (TIA); secondary endpoints were 30-day and 5-year mortality and major complications. Firth penalized logistic regression identified independent predictors of stroke/TIA. Results: Stroke/TIA occurred in 0/155 (0.0%) miniAVR versus 7/155 (4.5%) conventional patients (p = 0.015); the rule-of-three upper 95% limit for miniAVR was ~1.9%. Thirty-day mortality was similar (0.6% vs. 2.6%; p = 0.371). Five-year survival favored miniAVR (94.6% vs. 87.2%; log-rank p = 0.047). miniAVR was independently associated with lower stroke/TIA odds (odds ratio [OR] 0.052; 95% confidence interval [CI] 0.003-0.832; p = 0.037); longer cardiopulmonary bypass time was associated with higher odds (OR 1.014/minute; 95% CI 1.001-1.028; p = 0.032). Conclusions: miniAVR was associated with zero observed perioperative strokes and higher 5-year survival; however, this survival comparison is limited by short median follow-up in the miniAVR group (1.9 years). Given the small number of events and the single-center design, these findings should not be interpreted as proof of a causal neuroprotective effect. Multicenter validation with longer, balanced follow-up is required.

