Platelet-large cell ratio and the extent of coronary artery disease: results from a large prospective study.

Even though platelet volume has been supposed to be indicator of platelet activation, contrasting results have been reported on its relationship with the extent of coronary artery disease (CAD). No data have been so far reported on Platelet-Large Cell Ratio (P-LCR). Thus, the aim of the current study was to investigate whether P-LCR is associated with CAD. We measured P-LCR in 1882 consecutive patients undergoing coronary angiography. Significant CAD was defined as stenosis >50% in at least 1 coronary vessel. We additionally measured Carotid Intima-Media Thickness (IMT) in 359 patients. The relationship between P-LCR and platelet aggregation was evaluated by PFA-100 and Multiplate. Patients with higher P-LCR were older (P = 0.038), with larger prevalence of diabetes (P < 0.0001), dilated cardiomyopathy or valvular heart disease (P = 0.004) and less often family history of CAD (P = 0.045), more often on statins (P = 0.002), and diuretics (P = 0.016). P-LCR was significantly associated with baseline glycaemia (P = 0.001) and RBC count (P < 0.001), but inversely related to platelet count (P < 0.0001). P-LCR was not associated with the prevalence of CAD (adjusted P = 0.3) or its severity. In addition, P-LCR was not related to Carotid IMT or platelet aggregation in patients with or without aspirin therapy. This study showed that P-LCR is not related to platelet aggregation, aspirin resistance, the extent of CAD and carotid IMT. Thus, P-LCR can not be considered as a marker of platelet reactivity or a risk factor for CAD.

Platelet distribution width and the extent of coronary artery disease: results from a large prospective study.

It has been postulated that large platelets may be an indicator of platelet activation, and thus be related to the extent of coronary artery disease (CAD). Platelet distribution width (PDW) directly measures the variability in platelet size. However, no data has been so far reported on this index and CAD. Thus, the aim of the current study was to investigate whether PDW is associated with the extent of CAD. We measured PDW in 1882 consecutive patients undergoing coronary angiography. Significant CAD was defined as stenosis >50% in at least one coronary vessel. We additionally measured Carotid Intima-Media Thickness (IMT) in 359 patients. Patients with higher PDW were older (p = 0.012), with higher weight (p < 0.0001) and waist (p < 0.0001), larger prevalence of diabetes (p = 0.014), dilated cardiomyopathy or valvular heart disease (p < 0.0001) and less often family history of CAD (p = 0.021), more often on statins (p = 0.005), and diuretics (p = 0.016). PDW was significantly associated with baseline glycaemia (p = 0.002) and Red Blood Cell count (p < 0.0001), but inversely related to platelet count (p < 0.0001). PDW was not associated with the prevalence of coronary artery disease (OR [95% CI] = 0.91 [0.81–1.04], p = 0.16; adjusted OR [95% CI] = 0.96 [0.82–1.12], p = 0.56). No relationship was observed between IMT and PDW as tertiles or as continuous variable (Mean IMT: r = 0.04; p = 0.46; Maximal IMT: r = 0.036, p = 0.49). This study showed that PDW is not related to the extent of CAD and carotid IMT. Thus, PDW can not be considered as a risk factor for CAD.

Evaluation of intracoronary adenosine to prevent periprocedural myonecrosis in elective percutaneous coronary intervention (from the PREVENT-ICARUS Trial).

Great interest has focused on pharmacotherapy to prevent periprocedural myocardial injury during elective percutaneous coronary intervention (PCI). The aim of the present trial was to investigate the benefits of preprocedural intracoronary administration of high-dose adenosine during elective PCI. This was a single-center, double-blind, randomized trial of patients undergoing elective PCI. The patients were randomized (1:1) by sealed envelops to intracoronary adenosine (120 µg for the right coronary artery and 180 µg for the left coronary artery) or placebo. The primary study end point was a periprocedural increase in troponin I >3 times the upper limit of normal. The secondary study end points were (1) the corrected Thrombolysis In Myocardial Infarction frame count; (2) troponin I release >10 times the upper limit of normal; (3) creatine kinase-MB mass release ≥3 times the upper limit of normal; and (4) the combined cumulative incidence of in-hospital death, periprocedural myocardial infarction, and in-hospital urgent target vessel revascularization. The safety end point was the occurrence of bradycardia and ventricular arrhythmias during study drug administration. From November 2009 to September 2010, we randomized 260 patients who were undergoing elective PCI to intracoronary adenosine (n = 130) or placebo (n = 130). A greater prevalence of calcified lesions was observed in the adenosine group (p = 0.002). In contrast, a greater prevalence of type C lesions (p = 0.091), chronic occlusions (p = 0.015), worse preprocedural Thrombolysis In Myocardial Infarction flow (p = 0.038), and more severely stenotic lesions (p = 0.005) were observed in the placebo group. No difference was found in the primary (67.7% vs 70%, p = 0.69) or secondary end points. No serious side effects were observed with adenosine. In conclusion, our randomized trial showed that preprocedural intracoronary administration of a single high-dose bolus of adenosine does not provide any benefit in terms of periprocedural myonecrosis in patients undergoing elective PCI.

Effects of increasing doses of intracoronary adenosine on the assessment of fractional flow reserve.

OBJECTIVES: The purpose of this study was to investigate the effects of increasing dose of intracoronary adenosine on fractional flow reserve (FFR) measurement. BACKGROUNDS: FFR is a validated method for the assessment of the severity of coronary artery stenosis. It is based on the change in the pressure gradient across the stenosis after the achievement of maximal hyperemia of the coronary microcirculation that may be obtained by either intracoronary bolus or intravenous infusion of adenosine. No study has explored so far the effects of very high doses of intracoronary adenosine on FFR. METHODS: FFR was assessed in 46 patients with 50 intermediate lesions during cardiac catheterization by pressure-recording guidewire (PrimeWire, Volcano, San Diego, California). FFR was calculated as the ratio of the distal coronary pressure to the aortic pressure at hyperemia. Increasing doses of adenosine were administrated (60, 120, 180, 360, and 720 µg) as intracoronary boluses. Exclusion criteria were: 1) allergy to adenosine; 2) baseline bradycardia (heart rate <50 beats/min); 3) hypotension (blood pressure <90 mm Hg); and 4) refusal to provide signed informed consent. RESULTS: High doses of intracoronary adenosine were well tolerated, with no major side effects. Increasing doses up to 720 µg progressively decreased FFR values and increased the percentage of patients showing an FFR <0.75. Among angiographic parameters, both percent stenosis and lesion length were independently associated with lower FFR values. CONCLUSIONS: This study shows that high doses of intracoronary adenosine (up to 720 µg) increased the sensitivity of FFR in the detection of hemodynamically relevant coronary stenoses. Furthermore, lesion length and stenosis severity were independent angiographic determinants of FFR.

Mean platelet volume and the extent of coronary artery disease: results from a large prospective study.

BACKGROUND: Platelets play a central role in the pathogenesis of coronary artery disease. Mean platelet volume (MPV) is an indicator of platelet activation, and has been demonstrated to be correlated with platelet reactivity. The aim of the current study was to investigate whether mean platelet volume is associated with the extent of coronary artery disease. METHODS: We measured MPV in 1411 consecutive patients undergoing coronary angiography. All angiograms were analyzed by two investigators blinded of clinical data. Significant coronary artery disease was defined as stenosis >50% in at least 1 coronary vessel. We additionally measured Carotid Intima-Media Thickness (IMT) in 359 patients. The relationship between MPV and platelet aggregation was evaluated by PFA-100 in 50 consecutive patients who were not taken any antiplatelet therapy, and in a cohort of patients who were on aspirin by PFA-100 (n=161) and Multiplate (n=94). RESULTS: Patients were divided into three groups according to tertiles of MPV. Patients with higher MPV were slightly older (p=0.038), with larger prevalence of diabetes (p<0.0001), hypertension (p=0.008), previous CVA (p=0.041), less often with stable angina (p=0.043) and family history of CAD (p=0.011), more often on statins (p=0.012), and diuretics (p=0.007). MPV was associated with baseline glycaemia (p<0.0001) and red blood cell count (p=0.056), but inversely related to platelet count (p<0.0001). MPV was not associated with the extent coronary artery disease (p=0.71) and carotid IMT (p=0.9). No relationship was found between MPV and platelet aggregation. CONCLUSION: This study showed that MPV is not related to platelet aggregation, the extent of coronary artery disease and carotid IMT. Thus, this parameter cannot be considered as a marker of platelet reactivity or a risk factor for coronary artery disease.