Early Significant Thrombocytopenia After Tavi in a Patient With a Mechanical Mitral Valve: When a Procedural Pattern Mimics Hit

Background Thrombocytopenia is common after transcatheter aortic valve implantation (TAVI) and is often a self–limited procedural phenomenon. In patients requiring peri–procedural heparin bridging, the early platelet drop may raise concern for heparin–induced thrombocytopenia (HIT) and prompt potentially hazardous changes in anticoagulation. Case presentation A 73–year–old man with permanent atrial fibrillation and a mechanical mitral valve on vitamin K antagonist (VKA) underwent transfemoral TAVI for symptomatic severe paradoxical low–flow/low–gradient aortic stenosis. Unfractionated heparin (UFH) bridging was started 4 days before TAVI. The procedure was uncomplicated. Platelets declined from 177x10^3/µL (pre–TAVI) to 113x10^3/µL on day 0, 106x10^3/µL on day +1, with a nadir of 75x10^3/µL on day +3 (−58%), then recovered to 114x10^3/µL by day +7. Haemoglobin decreased from 12.0 to 9.5 g/dL without overt bleeding; vascular access ultrasound excluded haematoma, pseudoaneurysm and arteriovenous fistula. Fibrinogen remained within the normal range (about 230–400 mg/dL). Clinical probability for immune HIT was low (4Ts ≤3) and an anti–PF4/polyanion immunoassay was negative. Given the very high thrombotic risk, UFH was continued as bridging while VKA was restarted, then UFH was stopped after reaching the therapeutic INR. Post–procedural echocardiography confirmed a normally functioning transcatheter valve without significant leak. Conclusions An early, marked platelet fall after TAVI—especially with day 0–3 nadir and rapid recovery—may represent a procedural “pseudo–HIT” pattern rather than immune HIT. Integrating timing, pre–test probability and anti–PF4 testing can avoid unnecessary heparin discontinuation or unsafe anticoagulation interruptions in patients with mechanical valves.