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ABSTRACT Introduction: The impact of mitral regurgitation (MR) on valve-in-valve transcatheter aortic valve implantation (VIV-TAVI) in patients with failed bioprostheses remains unclear. The purpose of this study was to assess the prognostic impact of residual moderate MR following VIV-TAVI. Methods: We retrospectively analyzed 127 patients who underwent VIV-TAVI between March 2010 and November 2021. At least moderate MR was observed in 51.2% of patients before the procedure, and MR improved in 42.1% of all patients. Patients with postoperative severe MR, previous mitral valve intervention, and patients who died before postoperative echocardiography were excluded from further analyses. The remaining 114 subjects were divided into two groups according to the degree of postprocedural MR: none-mild MR (73.7%) or moderate MR (26.3%). Propensity score matching yielded 23 pairs for final comparison. Results: No significant differences were found between groups before and after matching in early results. In the matched cohort, survival probabilities at one, three, and five years were 95.7% vs. 87.0%, 85.0% vs. 64.5%, and 85.0% vs. 29.0% in the none-mild MR group vs. moderate MR-group, respectively (log-rank P=0.035). Among survivors, patients with moderate MR had worse functional status according to New York Heart Association (NYHA) class at follow-up (P=0.006). Conclusion: MR is common in patients with failed aortic bioprostheses, and improvement in MR-status was observed in over 40% of patients following VIV-TAVI. Residual moderate MR after VIV-TAVI is not associated with worse early outcomes, however, it was associated with increased mortality at five years of follow-up and worse NYHA class among survivors.
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ABSTRACT OBJECTIVE: Atrial fibrillation and neurocognitive decline are common complications after cardiopulmonary bypass. By utilizing genomic microarrays we investigate whether gene expression is associated with postoperative atrial fibrillation and neurocognitive decline. METHODS: Twenty one cardiac surgery patients were prospectively matched and underwent neurocognitive assessments pre-operatively and four days postoperatively. The whole blood collected in the pre-cardiopulmonary bypass, 6 hours after-cardiopulmonary bypass, and on the 4th postoperative day was hybridized to Affymetrix Gene Chip U133 Plus 2.0 Microarrays. Gene expression in patients who developed postoperative atrial fibrillation and neurocognitive decline (n=6; POAF+NCD) was compared with gene expression in patients with postoperative atrial fibrillation and normal cognitive function (n=5; POAF+NORM) and patients with sinus rhythm and normal cognitive function (n=10; SR+NORM). Regulated genes were identified using JMP Genomics 4.0 with a false discovery rate of 0.05 and fold change of >1.5 or <-1.5. RESULTS: Eleven patients developed postoperative atrial fibrillation. Six of these also developed neurocognitive decline. Of the 12 patients with sinus rhythm, only 2 developed neurocognitive decline. POAF+NCD patients had unique regulation of 17 named genes preoperatively, 60 named genes six hours after cardiopulmonary bypass, and 34 named genes four days postoperatively (P<0.05) compared with normal patients. Pathway analysis demonstrated that these genes are involved in cell death, inflammation, cardiac remodeling and nervous system function. CONCLUSION: Patients who developed postoperative atrial fibrillation and neurocognitive decline after cardiopulmonary bypass may have differential genomic responses compared to normal patients and patients with only postoperative atrial fibrillation, suggesting common pathophysiology for these conditions. Further exploration of these genes may provide insight into the etiology and improvements of these morbid outcomes.