Incidence and mechanisms of bioprosthetic dysfunction after transcatheter implantation of a mechanically-expandable heart valve.

BACKGROUND: The mechanically-expandable transcatheter valve is no longer commercially available, yet clinical and echocardiographic surveillance is imperative for thousands of patients who received transcatheter aortic valve implantation (TAVI) with this platform. AIMS: We aimed to determine the incidence and mechanism of bioprosthetic valve dysfunction (BVD) following TAVI with mechanically-expandable valves. METHODS: From 2013 to 2020, all 234 patients who underwent TAVI with the LOTUS valve were included. BVD was categorised as (i) structural valve deterioration (SVD), (ii) non-structural valve dysfunction (NSVD), (iii) clinical valve thrombosis and (iv) endocarditis, according to the Valve Academic Research Consortium-3 criteria. RESULTS: The mean age was 79±7 years, 60% were male, and the mean Society of Thoracic Surgeons score was 4.2±2.9%. The technical success rate was 94% and the 30-day device success rate was 78%. All-cause mortality at 1 year was 15%; median follow-up duration was 36 (IQR 18-60) months during which 47% of patients died. One hundred and three patients had ≥1 type of BVD (44%), which predominantly consisted of NSVD (39%, mostly because of ≥moderate patient-prosthesis mismatch). BVD during follow-up included endocarditis (3.4%), clinical valve thrombosis (3.4%) and SVD (1.3%). Both endocarditis and clinically apparent valve thrombosis occurred early and late after TAVI and resulted in valve-related deaths in 38% and 13% of patients, respectively. Overall, ≥moderate haemodynamic valve deterioration occurred in 5.5% and bioprosthetic failure in 7.3%, leading to valve-related deaths in 36% of cases. CONCLUSIONS: BVD represents a relevant health issue after TAVI with a mechanically-expandable valve. Serious but reversible causes of BVD include endocarditis and clinically apparent valve thrombosis, both carrying a time-independent hazard post-TAVI.

Cardiac Catheterizations in Patients With Acute Coronary Syndrome and Prior Coronary Bypass Surgery: Impact of Native vs Graft vs Absent Culprit Lesions on Clinical Outcomes and Treatment Strategy.

BACKGROUND: In patients with prior coronary artery bypass graft surgery (CABG), acute coronary syndrome (ACS) is not uncommon. This study investigated treatment strategy and compared clinical outcomes for native, graft and absent culprit lesions. METHODS: Single-center retrospective cohort study. From July 2010 to July 2019, 642 consecutive ACS patients with prior CABG were screened for eligibility. The primary endpoint was major adverse cardiovascular events (MACE) at 1 year, a composite of all-cause mortality, myocardial infarction, stroke and ischemia-driven revascularization. RESULTS: A total of 549 patients were included, with 215 (39.2 %) having native culprits, 256 (46.6 %) graft culprits and 78 (14.2 %) no clear culprits. Patients with native culprits were treated with native PCI in 94.0 %, re-CABG in 0.9 % and optimal medical therapy (OMT) in 5.1 %. Patients with graft culprits were treated with native PCI in 14.1 %, graft PCI in 81.2 %, re-CABG in 0.8 % and OMT in 3.9 %. All patients without a clear culprit received OMT. The cumulative incidence of 1-year MACE was 24.7 % for native vs 26.2 % for graft vs 21.8 % for absent culprits. Kaplan-Meier curves did not differ significantly. In patients with graft culprit, no significant difference in 1-year MACE was observed between native PCI and graft PCI (30.6 % vs 25.5 %, p = 0.36). CONCLUSIONS: This retrospective study shows that in ACS patients with prior CABG, MACE occurred frequently and was comparable for native, graft and absent culprits. Native PCI as treatment strategy for patients with a graft culprit was relatively common, with no significant difference in MACE as compared to graft PCI.