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02/2012; 5(2):245. · 1.07 Impact Factor
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ABSTRACT: The purpose of this study was to investigate the effects of increasing dose of intracoronary adenosine on fractional flow reserve (FFR) measurement.
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.
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.
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.
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.
10/2011; 4(10):1079-84. · 1.07 Impact Factor
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Giuseppe De Luca,
Matteo Santagostino,
Gioel Gabrio Secco,
Ettore Cassetti, Livio Giuliani,
Lorenzo Coppo,
Alon Schaffer,
Angelica Fundaliotis,
Sergio Iorio,
Luca Venegoni,
Giorgio Bellomo,
Paolo Marino
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ABSTRACT: 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.
Journal of Thrombosis and Thrombolysis 11/2010; 30(4):426-33. · 1.48 Impact Factor
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Giuseppe De Luca,
Matteo Santagostino,
Gioel Gabrio Secco,
Ettore Cassetti, Livio Giuliani,
Elena Franchi,
Lorenzo Coppo,
Sergio Iorio,
Luca Venegoni,
Elisa Rondano,
Gabriele Dell'Era,
Claudia Rizzo,
Patrizia Pergolini,
Francesco Monaco,
Giorgio Bellomo,
Paolo Marino
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ABSTRACT: 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.
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).
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.
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.
Atherosclerosis 03/2009; 206(1):292-7. · 3.79 Impact Factor
