Thrombocytopenia after transcatheter aortic valve implantation: prognostic value and mechanisms

Abstract

Abstract Funding Acknowledgements Type of funding sources: None. Background Thrombocytopenia post transcatheter aortic valve implantation (TPPT) in its most severe manifestation is an independent predictor of mortality. However, mechanisms that favors TPPT remain unknown. Purpose To establish the prognostic value and risk factors of TPPT in a real-life population of patients treated with transcatheter aortic valve implantation (TAVI) in a tertiary hospital. Methods We analyzed retrospectively clinical, laboratory, echocardiographic and procedure-related variables from 203 consecutive patients, treated with TAVI between January 2019 and October 2021. Results This cohort had mean age of 82,3 ±5,9 years, 56% male, 83% hypertensive, 62% dyslipidemia, 35% diabetic, 20% chronic kidney disease, 22% chronic obstructive pulmonary disease, 32% coronary artery disease, 20% had previous ICP, 38% Atrial Fibrillation (AF), 18% peripheral arterial disease, 12% neurovascular disease, 23% history of cancer, 10% pacemaker carriers. 50% of TAVIs were balloon-expandable and 50% self-expandable. Mean procedure duration was 138 ±109min, size 26,6±3mm, contrast dose 233 ±88mL. During in-hospital stay 192/203 patients had TPPT. Platelets before TAVI, 187.000 (IQR 148.000-222.000) Vs a minimum post-TAVI (PlqMin) of 135.000 (IQR 105.000-164.000); P<0,05. Platelet fall (DeltaPlq) 48.000 ±38.000. We observed a Minimum Kidney clearance (ClMin) 46 ±20,75mL/min/m2, a maximum ultrasensitive Troponin-T (Tr-TusMax) 250 ±450 pg/L, a Maximum C Reactive Protein (PCRMax) 6,68 ±6,4, and a Minimum Hemoglobin (HbMin) 9,8 ±1,7 g/dL. 31/203 (15,3%) patients were exitus at the end of follow-up. We observed a non-lineal statistically significant association between TPPT quartiles and all-cause mortality (P<0,05): 21 exitus occurred in the extreme quartiles (1 and 4) while only 11 at the central ones (2 and 3). DeltaPlq was associated with PCRMax (Pearson 0,25; P<0,001), CliMin (Pearson -0,23; P0,005), HbMin (Pearson -0,27; P 0,001), AF. The only protective factor for DeltaPlq was history of previous ICP. Among exitus patients PlqMin was observed later than in survivors (3,5 vs 2,2 days; P<0,05). TPPT’s quartiles, previous ICP, time to PlqMin, HbMin, PCRMax and Tr-TusMax were the variables found to be independent associated with all-cause mortality (P<0,05). Conclusions The non-linear association between TPPT and mortality, the temporal relation between TPPT and mortality and the linear correlation between TPPT and HbMin and PCRMax suggest that late TPPT may have a mortality prognostic value through an increased risk of low Hb in the context of an increased inflammatory status. The fact that history of ICP was associated with les platelet fall suggests that revascularization, or ICP associated drug therapy, may confer protection against after TAVI mortality.