Vincent Spagnoli

Contrast-induced acute kidney injury and mortality in ST elevation myocardial infarction treated with primary percutaneous coronary intervention

Objectives Contrast-induced acute kidney injury (CI-AKI) is a common and potentially severe complication in patients with ST elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). There is no consensus on the best definition of CI-AKI to identify patients at risk of haemodialysis or death. The objective of this study was to assess the association of CI-AKI, using four definitions, on inhospital mortality, mortality or haemodialysis requirement over 1-year follow-up, in patients with STEMI treated with pPCI. Methods In this prospective, observational study, all patients with STEMI referred for pPCI were included. We identified independent variables associated with CI-AKI and mortality. Results We included 1114 consecutive patients with STEMI treated by pPCI. CI-AKI occurred in 18.3%, 12.2%, 15.6% and 10.5% of patients according to the CIN, Acute Kidney Injury Network (AKIN), Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease (RIFLE) Modification of Diet in Renal Disease (MDRD) and RIFLE Chronic Kidney Disease - Epidemiology Collaboration (CKD-EPI) definitions, respectively. The RIFLE (CKD-EPI) definition was the most discriminant definition to identify patients at higher risk of inhospital mortality (27.1% vs 4.0%; adjusted OR 2.7 (95% CI 1.4 to 5.1), p=0.003), 1-year mortality (27.4% vs 6.6%; adjusted OR 2.8 (95% CI 1.5 to 5.3), p=0.002) and haemodialysis requirement at 1-year follow-up (15.6% vs 2.7%; adjusted OR 6.7 (95% CI 3.3 to 13.6), p=0.001). Haemodynamic instability, cardiac arrest, preexisting renal failure, elderly age and a high contrast media volume were independently associated with 1-year mortality. Of interest, contrast-media volume was not correlated to increase of creatininaemia (r=0.06) or decrease in estimated glomerular filtration rate (r=0.05) after percutaneous coronary intervention in our population. Conclusions CI-AKI is a frequent and serious complication of STEMI treated by pPCI. The RIFLE definition is the most accurate definition to identify patients with CI-AKI at high risk of mortality or haemodialysis.

Extremely late drug-eluting stent thrombosis related to uncovered struts: the phantom menace

A 75-year-old man was referred to our institution for lateral ST-elevation myocardial infarction. He previously underwent a 2.5 × 18 mm sirolimus-eluting stent implantation on the first diagonal branch 9 years earlier for symptomatic stable coronary artery disease. He has been under aspirin for the past 8 years with an uneventful evolution. Thrombolysis, clopidogrel-loading …

0495 : Prediction and prognostic values of biomarkers of contrast induced acute kidney injury in ST-segment elevetaion myocardial infarction treated by primary percutaneous coronary intervention

Background and aims Contrast-induced acute kidney injury (CI-AKI) occurring during ST-segment elevated myocardial infarction (STEMI) is associated with a high morbidity and mortality. In a setting of systematic primary percutaneous coronary intervention (pPCI) in STEMI patients, we evaluate the predicting value and prognosis value in mortality of cystatin C and neutrophil gelatinase-associated lipocalin (NGAL) in the incidence of CI-AKI. Methods NGAL and cystatin-C level were measured on arrival to the cathlab prior to primary PCI in 701 STEMI patients and were correlated to the occurrence of CI-AKI according to the various existing definitions. Association between biomarkers level and the incidence of CI-AKI, MACE and allcause mortality at 1-year-follow-up were evaluated. Biomarkers were added to clinical data into a multivariate model analysis to evaluate their additive diagnosis and prognosis value. Results Incidence of AKI varied from 12.0% to 21.5% depending of the definition. When divided in tertiles, levels of plasmatic NGAL and cystatin C were associated with a stepwise increase in the incidence of AKI and the stage of renal failure. Both biomarkers significantly predicted CI-AKI with receiver operating characteristic (ROC) analysis showing an area under curve of 0.60 for cystatin C, and 0.62 for NGAL, both p MACCE and all-cause mortality at 1-year-follow-up were also higher in the higher tertile for both biomarkers (p value Conclusions In myocardial infarction, NGAL and cystatin C are correlated with the incidence and severity of AKI, and occurrence of MACCE and all cause mortality at one year. Download : Download full-size image Abstract 0495 – Figure: K-M curves for all-cause death at 1 year The author hereby declares no conflict of interest

0321: In the aera of new P2Y12 inihibitors, high platelet reactivity on aspirin in patients with ST elevation myocardial infarction remains a predictor of ischemic events

Background Despite dual antiplatelet treatment with the new P2Y12 platelet receptor antagonists (P2Y12i), major ischemic events are common following ST elevation myocardial infarction (STEMI). Objectives To assess separately resistance to aspirin (HPR-aspirin), resistance to P2Y12i (HPR-P2Y12i) and their association during the acute phase of STEMI in relation to the occurrence of ischemic events. Methods We included all consecutive patients admitted for STEMI in our center between January 2013 and December 2013. All patients received a loading dose followed by a maintenance dose of aspirin (75mg/day) and either clopidogrel, prasugrel or ticagrelor. Platelet reactivity was assessed 4±1 days and 75±15 days after admission using light transmission aggregometry (LTA) with arachidonic acid (AA) and serum Thromboxane-B2 concentration to assess HPR-aspirin and LTA-ADP and VASP index to assess HPR-P2Y12i. Major cardiac and cerebrovascular events (MACCE) were recorded during one year. Results 106 patients (61years old, 76% male, 20% with diabetes) were included. STEMI was anterior in 52% and LV ejection fraction at discharge was 51±9%. At day 4 after STEMI, HPR-aspirin measured by LTA-AA alone was found in 23% patients and was correlated with serum thromboxane inhibition, HPR-P2Y12i (VASP≥50% and LTA-ADP≥65%) was observed only in 7% and combined resistance was present in 4% of the patients. Diabetes and age were predictors of HPR-aspirin. The large use of ticagrelor (34%) and prasugrel (50%) explained the low rate of P2Y12i resistance. HPR-aspirin was persistent 75 days later in 36% patients who were resistance at day 4. At 1 year, 7.9% patients had experienced MACCE. HPR-aspirin alone and HPR for both aspirin and P2Y12i were significantly associated with MACCE. Conclusion Aspirin resistance is frequent just after STEMI and is associated with MACCE especially when associated with P2Y12i resistance.

0053 : Naproxen as an alternative to aspirin for platelet inhibition in patients with cardiovascular disease requiring nonsteroidal anti-inflammatory drug?

Background Concomitant prescription of non-steroidal anti-inflammatory drugs (NSAIDs) and low dose aspirin is not recommended due to competitive interaction with cyclooxygenase-1 and higher risk of gastrotoxicity. Objectives To assess the efficacy of naproxen over time as antiplatelet agent. Methods We included 14 healthy volunteers. We first evaluated naproxen effiacy by performing aggregation tests: light transmission aggregometry with arachidonic acid (LTA-AA), platelet function analyzer-100 with epinephrine cartridge (PFA-EPI) and serum thromboxane B2 (TXB2) measurement at baseline (T0), 2 hours (T2), 12 hours (T12), 24 hours (T24) and 48 hours (T48) after receiving one single dose of naproxen 550mg and then at T24 and T48 after a twice daily dose of naproxen 550mg for three days. We then compared the peak of efficacy two hours after naproxen with ibuprofen 400mg and aspirin 75mg and tested the switch back from NSAIDs to aspirin. Results Platelet aggregation (LTA-AA) after one dose of naproxen was inhibited at T2 and T12 and 50% of volunteers recovered at T24 and 93% at T48. Similar results were found with serum TXB2 concentration and PFA-EPI and multiple doses of naproxen. After naproxen at T2, maximal aggregation intensity (MAI) was 4% [1%-16%], PFA EPI 260s [88s-300s], TXB2 inhibition 98% [89-99%]. After aspirin, MAI was 5% [0%-69%], PFA-EPI was 214s [103s-300s] and TXB2 inhibition 98% [91%-98%]. After ibuprofen, MAI was 2% [1%-4%], PFA EPI 211s [111s-300s] and TXB2 inhibition 94% [92-94%]. After a 48h interruption of NSAIDs with a verified recovery of platelet aggregation, aspirin did not inhibit platelet aggregation for 83% and 50% of subjects who took naproxen and ibuprofen. Conclusion Naproxen has a stable biological antiplatelet effect similar to aspirin. However, after naproxen or ibuprofen, aspirin was unable to inhibit platelet aggregation. These results suggest than NSAIDs could block the action of aspirin on platelets for several days. The author hereby declares no conflict of interest

Correlation between burst of thrombin and microvacular obstruction (no reflow) during ST Elevation Myocardial Infarction treated by primary percutaneous coronary Intervention

Background: The thrombotic burden at the acute phase of STEMI is a consequence of platelet and coagulation activation. Objective: To evaluate the generation of thrombin during acute phase of STEMI. In order to study the consequence, thrombin generation was correlated with other markers of coagulation activation, markers of cellular activation, microvascular injury and infarct size. Methods: Thirty six STEMI patients admitted for primary Percutaneous Coronary Intervention (PCI) were enrolled. Blood samples were collected before angioplasty, at the end of angioplasty and 2, 6, 12 and 24 hours after angioplasty. Plasma thrombin antithrombin complexes and d-dimers were evaluated by ELISA methods, fibrinogen by clothing test. Platelets and endothelial microparticles were determined by flow cytometry analysis. Microvascular obstruction was assessed by the myocardial blush grade. Myocardium at risk was determined on angiography and infarct size was assessed by area under the curve of plasma troponin and CK-MB. Results: A burst of thrombin occurred during PCI in 69% of patients and was associated with increased fibrinogen, d-dimer, circulating platelets and endothelials microparticles, when compared with patient without burst (p<0.05). Prolonged ischemic time and significant myocardium at risk were correlated with a higher level of thrombin generation (p<0.05). Thrombin generation was correlated with alteration of myocardial blush (p<0.05) and higher troponin I and CK levels (p<0.05). Conclusion: This study showed a burst of thrombin at the time of primary PCI during STEMI in two third of patients. When present, this burst was associated with more cellular, myocardial and micro-vascular damage.

004 Contrast induced nephropathy after primary PCI for STEMI: Usefulness of a new definition

including age, sex and time delays to admission. Interestingly, dyslipidemia and history of MI was less frequent in PE group. Plasma CRP levels on admission were markedly higher in PE patients. Prior chronic treatments were less frequent in PE group, in particular for aspirin (11 vs 19%, p=0.027), ACE inhibitor (10 vs 18%, p=0.014) and statin (15 vs 23%, p=0.054). Acute treatments were similar, except for BetaBlocker that were more used in patients without PE. Patients with PE were more likely to suffer from STEMI and altered LVEF. Hospital complications such as death, or heart failure (12 vs 7%, p=0.016, 47 vs 28%, p=0.001), and mechanical complications including atrial fibrillation, wall rupture, apical thrombus and mitral regurgitation (respectively, 20 vs 9%, p<0.001, 7 vs 0.5%, p<0.01, 8 vs 0.7%, p<0.01, and 8 vs 3%, p=0.03) were more frequent in PE group.