No Differences in Levels of Circulating Progenitor Endothelial Cells or Circulating Endothelial Cells Among Patients Treated With Ticagrelor Compared With Clopidogrel During Non- ST -Segment-Elevation Myocardial Infarction.

Background Ticagrelor use during acute coronary syndromes demonstrated a decrease in all-cause mortality in the PLATO (Platelet Inhibition and Patient Outcomes) trial. This effect has been attributed to a non-platelet-derived improvement in endothelial function. The aim of this study was to determine differences in the number of endothelial progenitor cells and/or circulating endothelial cells found in peripheral blood in patients treated with either ticagrelor or clopidogrel during non-ST-segment-elevation myocardial infarction. Methods and Results In this multicenter, randomized study ( NCT 02244710), patients were considered for inclusion after non-ST-segment-elevation myocardial infarction whenever they were P2Y12-inhibitor naïve. Ticagrelor and clopidogrel were allocated at a 1:1 ratio. Blood samples for determining endothelial progenitor cells and circulating endothelial cells were extracted before the antiplatelet loading dose, 48 hours after presentation of index symptoms, and 1 month after the event. A multichannel cytometer was used for optimal cell characterization. A total of 96 patients fulfilled the inclusion criteria. Circulating endothelial cell levels corrected by white blood cells were as follows at baseline, 48 hours, and 1 month: 44 (28-64), 50 (33-63), and 38 (23-62) cells/mL, respectively, for clopidogrel and 38 (29-60), 45 (32-85), and 35 (24-71) cells/mL, respectively, for ticagrelor ( P=0.6). Endothelial progenitor cell levels were 29 (15-47), 27 (15-33), and 18 (10-25) cells/mL, respectively, for clopidogrel and 20 (11-33), 22 (12-32), and 18 (11-29) cells/mL, respectively, for ticagrelor ( P=0.9). No differences in intraindividual changes were found. Conclusions Patients treated with ticagrelor during non-ST-segment-elevation myocardial infarction, in comparison to clopidogrel, showed similar levels of endothelial progenitor cells and circulating endothelial cells. These data suggest that the endothelial protective effect mediated by ticagrelor is not related to bone marrow physiology modulation. Clinical Trial Registration URL: https://www.clinicaltrials.gov . Unique identifier: NCT 02244710.

Influence of platelet reactivity and response to clopidogrel on myocardial damage following percutaneous coronary intervention in patients with non-ST-segment elevation acute coronary syndrome.

INTRODUCTION: A wide variability in the response to clopidogrel and magnitude of post-treatment platelet reactivity has been described. However, this has been demonstrated by light transmittance aggregometry, a method too laborious for daily practice. Point-of-care devices may overcome this limitation, but little is known on the predictive value of such measurements. Our objective was to determine the relationship between platelet reactivity and the incidence of myocardial damage following percutaneous coronary intervention (PCI) in patients with Non-ST-segment Elevation Acute Coronary Syndrome (NSTEACS). MATERIALS AND METHODS: This prospective study included 93 patients with NSTEACS and PCI. All patients received a loading dose of 300 mg of clopidogrel and 250 mg of aspirin. Myocardial damage was defined as any elevation above upper limit of normal or previous levels of troponin T, assessed every 6 h for at least 24 h following PCI. Platelet reactivity not related to clopidogrel (BASE reactivity), related to P2Y12 inhibition (P2Y12 reactivity) and inhibition of platelet aggregation (IPA) were assessed immediately pre-PCI with the VerifyNow device. RESULTS: Myocardial damage was detected in 60 patients (64.5%). Higher BASE reactivity was associated with myocardial damage (287.8+/-62.6 vs. 260+/-55.9 units, p=0.043) while a trend was found for P2Y12 reactivity (173.4+/-70.3 vs. 149.2+/-58.4 units, p=0.109). No relationship was detected for IPA. Multivariate logistic regression analysis confirmed that BASE reactivity (p=0.04) and P2Y12 reactivity (p=0.03) were independent predictors of myocardial damage. CONCLUSIONS: Platelet reactivity before PCI appears to be better predictor of myocardial damage than does response to clopidogrel.

Association between level of platelet inhibition after early use of abciximab and myocardial reperfusion in ST-elevation acute myocardial Infarction treated by primary percutaneous coronary intervention.

The interindividual response to antiplatelet treatment is considerable, with the magnitude of response often related to the appearance of clinical events after elective percutaneous coronary intervention (PCI). We investigated whether platelet aggregation inhibition (PAI) by early administration of abciximab would affect myocardial reperfusion outcomes observed after PCI in patients with acute ST-elevation myocardial infarction (STEMI). Consecutive patients with STEMI who were treated with PCI in our center were recruited (n = 56). Successful reperfusion was defined as a final Thrombolysis In Myocardial Infarction grade 3 flow, myocardial blush grade 2 or 3, and ST-segment resolution >50%. PAI grade was determined with the Ultegra Rapid Platelet Function Assay. Successful reperfusion criteria were observed in 34 patients (61%). There were 6 patients (11%) with a PAI value <80% and 34 (61%) with a PAI value > or =95%. Eight patients (36%) of those whose PAI was <95% had all the indicators of successful reperfusion compared with 26 patients (77%) whose PAI was > or =95% (p = 0.005). After adjusting for other variables (time from symptom onset to balloon, which was independently associated with myocardial reperfusion), the relation remained significant (p = 0.006). In conclusion, in patients with STEMI that was treated with direct PCI, higher platelet inhibition responses with early administration of abciximab were associated with better myocardial reperfusion outcomes.

Severe mitral regurgitation with right ventricular pacing, successfully treated with left ventricular pacing.

A case of severe mitral regurgitation with refractory heart failure, after atrioventricular junction ablation and pacemaker implant, was solved with left ventricular pacing. Mitral regurgitation was related to a change in segmental left ventricular motion during right ventricular pacing.

Taquicardia reentrante intranodal como inductora de fibrilación auricular / Atrioventricular nodal reentrant tachycardia as a trigger for atrial fibrillation

Presentamos el caso de un varón de 43 años con historia de palpitaciones paroxísticas de larga evolución autoyuguladas con maniobras vagales, donde la única arritmia documentada era fibrilación auricular. El estudio electrofisológico demostró la presencia de una taquicardia intranodal típica, que en segundos degeneraba en fibrilación auricular, reproduciendo la sintomatología arrítmica del paciente. Después de ablación mediante radiofrecuencia de la 'vía lenta', el paciente quedó sin taquicardia inducible y sin eventos arrítmicos posteriores durante un seguimiento de 20 meses. En pacientes seleccionados, el estudio electrofisiológico podría revelar causas curables de fibrilación auricular paroxística (AU)