Not-high before-treatment platelet reactivity in patients with STEMI: prevalence, clinical characteristics, response to therapy and outcomes.

Platelet reactivity (PR) has been indicated as a pathophysiological key element for ST-Elevation Myocardial Infarction (STEMI) development. Patients with not-high before-treatment platelet reactivity (NHPR) have been poorly studied so far. The aim of this study is to investigate the prevalence, clinical characteristics, response to therapy and outcomes of baseline prior to treatment NHPR among patients with STEMI undergoing primary PCI.We analyzed the data from 358 STEMI patients with assessment of PR by VerifyNow before P2Y12 inhibitor loading dose (LD). Blood samples were obtained at baseline, and after 1 hour, 2 hours, 4-6 hours and 8-12 hours after LD. High platelet reactivity (HPR) was defined as Platelet Reactivity Unit values ≥208, while patients with values <208 at baseline were defined as having NHPR.Overall, 20% patients had NHPR. Age and male gender both resulted independent predictors of NHPR, even after propensity score adjustment. The percentage of inhibition of PR after ticagrelor or prasugrel LD was similar between HPR and NHPR patients at each time point. However, patients with HPR showed worse in-hospital clinical outcomes, and the composite adverse outcome endpoint of death, reinfarction, stroke, acute kidney injury or heart failure was significantly higher (10.0% vs 1.4%; p = .017) as compared with the NHPR group.In conclusion, a significant proportion of patients presenting with STEMI has a baseline NHPR that is associated with better in-hospital outcomes as compared with patients with HPR. Further studies are needed to better elucidate the potential therapeutic implications of NHPR in terms of secondary prevention.

Platelet inhibition with orodispersible ticagrelor in acute coronary syndromes according to morphine use: the TASTER study final results.

AIM: To date, it is still unknown whether orodispersible tablet (ODT) ticagrelor might represent a suitable way to reach a proper antiaggregation in acute coronary syndrome (ACS) patients receiving morphine. Aim of the present study was to evaluate platelet inhibition with 180 mg ticagrelor loading dose (LD) administered as ODT compared with standard coated tablet ticagrelor formulation in ACS patients undergoing percutaneous coronary intervention (PCI) according to morphine use. METHODS AND RESULTS: One-hundred and 30 patients presenting with STEMI or very high-risk NSTE-ACS were randomly assigned to receive ODT or standard ticagrelor LD. Potential morphine-ticagrelor interaction was assessed by stratified randomization according to morphine use. Platelet reactivity was evaluated by Platelet Reactivity Units (PRU) VerifyNow™ 1, 2, 4, and 6 h after ticagrelor LD. The primary endpoint was residual platelet reactivity 1 h after LD across the two ticagrelor formulation and according to morphine use. Safety endpoints were major bleedings and other in-hospital ticagrelor administration-related adverse events. One hour after LD, PRU median value was higher in morphine-treated patients (N = 32) as compared with patients not receiving morphine (N = 98; PRU = 187 [70-217]) vs. 73 [7-187]; P = 0.012). In patients with morphine, 1-h PRU values were similar between study groups (192 [114-236] vs. 173 [16-215] in ODT and standard tablet ticagrelor, respectively). Similarly, in patients without morphine, 1-h PRU values were not significantly different between study groups (69 [8-152] vs. 110 [6-193] in ODT and standard tablet ticagrelor, respectively). Platelet reactivity appeared similar in the 2 study arms at 2, 4, and 6 h after LD. No significant difference was observed among patients with or without morphine regarding in-hospital adverse events or drug side-effects, even if a reinfarction due to acute stent thrombosis was observed in a patient treated with morphine. CONCLUSIONS: There was no difference between ODT and standard ticagrelor tablets in terms of post-LD residual platelet reactivity, percentage of platelet inhibition or safety regardless to morphine use.

Balloon Angioplasty of the Radial Artery to Solve a Challenging Radial Sheath Insertion.

The inability to advance the dedicated wire of the transradial sheath in a radial artery with a good pulsatile blood flow is a very rare event. In this case, the advancement of a high-performance 0.014 inch coronary wire is the only option to gain the vessel. Then, if the transradial sheath is stuck in the proximal radial artery wall, balloon angioplasty of the radial artery may allow successful reinsertion of the transradial sheath. This technique allows the preservation of radial artery access, avoiding a shift to an alternative arterial approach.

Impact of glucose-6-phosphate dehydrogenase deficiency on the severity of coronary atherosclerosis in patients with acute coronary syndromes.

AIMS: The impact of glucose-6-phosphate dehydrogenase (G6PD) deficiency on coronary atherosclerosis has not been clearly investigated so far. We aimed to assess the effects of G6PD deficiency on the extent and complexity of coronary atherosclerosis in a large unselected cohort of consecutive patients with acute coronary syndromes (ACS). METHODS: We studied 623 consecutive patients presenting with ACS and undergoing coronary angiography and percutaneous coronary intervention (PCI). G6PD activity was quantitatively measured in all individuals using a biochemical assay based on the G6PD/6GPD ratio in erythrocytes. Individuals were defined as deficient when the ratio was less than 0.80. The severity and complexity of coronary atherosclerosis were assessed by SYNTAX score at baseline angiography. RESULTS: Fifty-six patients (9%) showed G6PD deficiency. Severe (i.e. enzymatic activity < 0.10) G6PD deficiency was detected in 33 (5.3%) individuals, mainly of male sex (n = 32). Overall, the cardiovascular risk profile was similar between patients with G6PD deficiency and controls. Patients with G6PD deficiency showed similar severity and complexity of coronary atherosclerosis as compared to control patients; accordingly, the SYNTAX score (15 vs. 14.5, P = 0.90, respectively, in G6PD-deficent patients and controls), and all its components were similar between deficient individuals and controls. The only independent predictor of a SYNTAX score of more than 22 was patients' age (odds ratio 1.035, 95% confidence interval 1.018-1.051; P < 0.001). CONCLUSION: G6PD deficiency does not impact on the extent and complexity of coronary atherosclerosis assessed by coronary angiography in patents presenting with ACS.