Less invasive fractional flow reserve measurement from 3-dimensional quantitative coronary angiography and classic fluid dynamic equations.

AIMS: The aim of this study was to develop a simplified model of FFR calculation (FFRsim) derived from three-dimensional (3D) coronary angiographic data and classic fluid dynamic equations without using finite element analysis. METHODS AND RESULTS: Intracoronary pressure measurements were performed by pressure wire sensors. The lumens of the interrogated vessel segments were reconstructed in 3D. The coronary artery volumetric flow was calculated based on the velocity of the contrast material. Pressure gradients were computed by classic fluid dynamic equations. The diagnostic power of the simplified computation of the FFR (FFRsim) was assessed by comparing the results with standard invasive FFR measurements (FFRmeas) in 68 vessels with a single stenosis. We found a strong correlation between the FFRsim and the FFRmeas (r=0.86, p<0.0001). The sensitivity and specificity for predicting the abnormal FFR of ≤0.80 (indicating haemodynamically significant stenosis) were 90% and 100%, respectively. The area under the curve (AUC) was 0.96. To achieve 100% negative and positive predictive values we defined the FFRsim >0.88 and the FFRsim ≤0.8 ranges. In our patient population, these ranges were found in 69% of the cases. CONCLUSIONS: According to our simplified model, the invasive FFR measurement can be omitted without misclassification in pre-specified ranges of the calculated FFRsim.

Eptifibatide-induced thrombocytopenia leading to acute stent thrombosis.

A 71-year old female patient with inferior ST-elevation myocardial infarction underwent primary percutaneous coronary intervention (PCI) within 3 h of symptom onset. She was preloaded with 300 mg aspirin and 600 mg clopidogrel before PCI. Coronary angiogram showed occlusion of the right coronary artery. During PCI, eptifibatide was initiated due to the large thrombus burden. Few hours after the procedure, on eptifibatide infusion, a severe drop in platelet count was observed (from 210,000/µl to 35,000/µl) and the infusion was discontinued. One hour later, still under eptifibatide effect and with severe thrombocytopenia, acute stent thrombosis developed. Lack of prior heparin exposure, quick onset of thrombocytopenia made heparin induced thrombocytopenia improbable that was later excluded by specific immunoassay. However, platelet function testing suggested that eptifibatide induced thrombocytopenia was mediated by activating autoantibodies since platelet reactivity was paradoxically very high at the time of stent thrombosis but decreased radically with eptifibatide washout. The patient was successfully managed without further complications on the basis of platelet function data obtained in the subsequent days. This rare subtype of thrombocytopenia highlights that not only platelet count but also platelet function should be closely monitored in case of severe thrombocytopenia to better balance bleeding and thrombosis.