Closed loop stimulation in left bundle branch area pacing.

INTRODUCTION: Closed Loop Stimulation (CLS) is a rate-responsive algorithm that adjusts heart rate (HR) based on changes in intracardiac impedance measured from the right ventricle lead. However, the use of CLS in conduction system pacing has not been investigated. In this retrospective study, we aimed to assess whether CLS with left bundle branch area pacing (LBBAP) can generate an appropriate distribution of HR in daily life. METHODS AND RESULTS: Our study included 24 patients with CLS pacing and chronotropic incompetence, comparing them with 19 patients receiving DDD pacing, all with LBBAP. Cumulative HR distribution charts were generated using data from a single device interrogation with a minimum follow-up period of 30 days. In DDD-CLS mode, there was a higher percentage of atrial pacing compared to DDD mode (median 58% [interquartile range 29%-83%] vs. 13% [10%-26%], p = .001), and CLS-paced beats were present across all frequency bins. The distribution of beats between the groups was similar (p = .643), resulting in comparable mean HR (72 bpm [70-77] vs. 73 bpm [65-75], p = .615). CONCLUSIONS: In the context of LBBAP, CLS effectively modulates pacing rates over a wide frequency range. This lead position does not adversely affect the rate-responsive performance of the algorithm.

Optimization of the atrioventricular delay in conduction system pacing.

INTRODUCTION: In patients receiving conduction system pacing (CSP), it is not well established how to program the sensed atrioventricular delay (sAVD), with respect to the type of capture obtained (selective, nonselective His-bundle [HB] capture or left bundle branch [LBB] capture). The aim of this study was to acutely assess the effectiveness of an electrophysiology (EP)-guided method for sAVD optimization by comparing it with the echocardiogram-guided optimization. METHODS AND RESULTS: Consecutive patients undergoing HB or LBB pacing were enrolled. The EP-guided sAVD was defined as the sAVD leading to a PR interval of 150 ms on surface electrocardiogram (ECG). In HB pacing patients, EP-guided sAVD was obtained subtracting the time from the onset of the P wave on ECG to the local atrial electrogram (EGM) recorded by the atrial lead (right atrial sensing latency, RASL) and the His-ventricular interval from 150 ms; in LBB pacing patients, subtracting RASL from 150 ms. Transmitral flow assessment by pulsed wave Doppler was used to find the echo-optimized sAVD by a modified iterative method. The discordance between the EP-guided and the echo-optimized sAVD was recorded. RESULTS: Seventy-one patients were enrolled: 12 with selective, 32 nonselective HB capture, and 27 LBB capture. Overall, the rate of concordance between the EP-guided and the echo-optimized sAVD was 71.8%, with no significant differences between the three groups. CONCLUSION: In CSP patients, an optimal sAVD can be programmed, in more than 70% of cases, considering only simple EGM intervals to obtain a physiological PR interval on surface ECG.

Left bundle branch area pacing (LBBAP) Auto Threshold algorithms Evaluation for Conduction System Pacing: The LATECS pilot Trial.

BACKGROUND: Automated threshold measurements (ATM) and output adaptation improved safety and follow-up of cardiac implantable devices (CIED) in the last years. These algorithms were validated for conventional cardiac pacing; however, they were not suitable for permanent His Pacing. Left bundle branch area pacing (LBBAP) is an emerging technique to obtain physiologic cardiac stimulation; we tried to assess if ATM could be applied to this setting. METHODS: Consecutive patients receiving ATM-capable CIED and LBBAP in our hospital were enrolled in this prospective, observational trial; they were evaluated 3 months after implant, comparing pacing thresholds manually assessed and obtained via ATM. Subsequent remote follow-up was carried on when available. RESULTS: Forty-five patients were enrolled. ATM for LBBAP lead provided consistent results in all the patients and was therefore activated; mean value of manually obtained LBBAP capture threshold was 0.66 ± 0.19 V versus ATM of 0.64 ± 0.19 V. TOST analysis showed equivalence of the two measures (p = .66). At subsequent follow-up (mean follow up 7.7 ± 3.2 months), ATM was effective in assessing pacing thresholds and no clinical adverse event was observed. CONCLUSIONS: ATM algorithms proved equivalent to manual testing in determining capture threshold and were reliably employed in patients receiving LBBAP CIED.

Early effects of left bundle branch area pacing on ventricular activation by speckle tracking echocardiography.

BACKGROUND: Left bundle branch area pacing (LBBAP) is an emerging cardiac pacing modality that preserves fast electrical activation of the ventricles and provides very good electrical measures. Little is known on mechanical ventricular activation during this pacing modality. METHODS: We prospectively enrolled patients receiving LBBAP. Electrocardiographic and electrical parameters were evaluated at implantation, < 24 h and 3 months. Transthoracic echocardiography with strain analysis was performed at baseline and after 3 months, when ventricular mechanical activation and synchrony were analyzed by time-to-peak standard deviation (TPSD) of strain curves for both ventricles. Intraventricular left ventricular (LV) dyssynchrony was investigated by LV TPSD and interventricular dyssynchrony by left ventricle-right ventricle TPSD (LV-RV TPSD). RESULTS: We screened 58 patients with permanent pacing indication who attempted LBBAP. Procedural success was obtained in 56 patients (97%). Strain data were available in 50 patients. QRS duration was 124.1 ± 30.7 ms at baseline, while paced QRS duration was 107.7 ± 13.6 ms (p < 0.001). At 3 months after LBBAP, left ventricular ejection fraction (LVEF) increased from 52.9 ± 10.6% at baseline to 56.9 ± 8.4% (p = 0.004) and both intraventricular LV dyssynchrony and interventricular dyssynchrony significantly improved (LV TPSD reduction from 38.2 (13.6-53.9) to 15.1 (8.3-31.5), p < 0.001; LV-RV TPSD from 27.9 (10.2-41.5) to 13.9 (4.3-28.7), p = 0.001). Ameliorations with LBBAP were consistent in all subgroups, irrespective of baseline QRS duration, types of intraventricular conduction abnormalities, and LVEF. CONCLUSIONS: Echocardiographic strain analysis shows that LBBAP determines a fast and synchronous biventricular contraction with a stereotype mechanical activation, regardless of baseline QRS duration, pattern, and LV function.

The prognostic value of plasma fibrinogen concentrations of patients with ST-elevation myocardial infarction and treated by primary percutaneous coronary intervention: a cautionary message.

BACKGROUND: Fibrinogen elevation is associated with a worse prognosis in patients with acute coronary syndrome (ACS). The aim of the present study was to assess the prognostic value of increased fibrinogen concentrations in ST-elevation myocardial infarction (STEMI) patients treated with primary percutaneous coronary intervention (PCI). METHODS: A total of 428 STEMI patients treated with primary PCI were retrospectively selected (median age: 62 years; 82.5% males) from a continuous case series of 832 ACS patients. Plasma fibrinogen concentrations were measured before PCI and after 24, 48, and 72 hours. In the 4-year follow-up, one major adverse cardiovascular event (MACE) occurred in 111 patients (40%): 17 re-STEMI (7%), 64 re-PCI (22%), 22 cardiac deaths (7%), and eight non ST-elevated acute coronary syndromes (NSTEACS, 4%). RESULTS: According to the reference change value, fibrinogen concentrations increased in 25% of patients at 24 h, 64% at 48 h and 19% at 72 h. Only fibrinogen concentrations at 48 h showed a mild association with overall MACEs (p = 0.036): the risk increased, starting from a concentration of 4 g/L. However a further multivariate model did not confirm any prognostic value. No association with specific MACEs emerged. CONCLUSIONS: In contrast to NSTEACS patients, fibrinogen concentrations increased slightly in STEMI patients after primary PCI, however, they were not as prognostic as for MACEs.

Access Site Bleeding Complications with NOACs versus VKAs in Patients with Atrial Fibrillation Undergoing Cardiac Implantable Device Intervention.

There are no data on procedure-related bleeding outcome with non-vitamin K antagonist anticoagulants (NOACs) versus vitamin K antagonist anticoagulants (VKAs) in patients with atrial fibrillation (AF) undergoing cardiac implantable electronic device (CIED) intervention. Our aim was to evaluate whether NOACs have a safety benefit even in terms of fewer hemorrhagic complications at the site of CIED implant. Consecutive AF patients receiving NOACs or VKAs at the time of CIED procedure were included in this observational, retrospective, and monocentric investigation. Primary endpoint was the incidence of post-intervention pocket hematoma. A total of 311 patients were enrolled, 146 on NOACs, and 165 on VKAs. The incidence of pocket hematoma was 3.4% in the NOAC versus 13.3% in the VKA group (p = 0.002). Primary outcome-free survival at 30-days was 96.6% in patients on NOACs and 86.0% in those on VKAs (p = 0.019). Multivariate analysis, adjusted by propensity-score calculation of inverse-probability-weighting, showed a significantly lower occurrence of pocket hematoma in patients receiving NOACs versus VKAs (HR 0.35, 95% CI 0.13-0.96, p = 0.042). Such NOACs benefit was confirmed versus patients on VKAs without peri-procedural bridging with low-molecular-weight heparin (HR 0.34, 95% CI 0.11-0.99, p = 0.048). The incidence of pocket infection, surgical pocket evacuation, ischemic events, and major bleeding complications at 30 days (secondary endpoints) was similar in the two groups. In conclusion, our data suggest that, among patients with AF undergoing implantable cardiac defibrillator or pacemaker intervention, the use of NOACs versus VKAs may be associated with significant reduction of post-procedural pocket hematoma, regardless of bridging with low-molecular-weight heparin in the VKA group. These results are hypothesis generating and need to be confirmed in a specific randomized study.

Ultra-sensitive troponin I levels to exclude acute myocardial infarction from myocardial injury.

BACKGROUND: Third generation troponin assays should aid in the rule-out of acute myocardial infarction (AMI). The study aim was to assess the capability of admission measurement of ultra-sensitive troponin I (TnI-Ultra) to exclude AMI from other myocardial injury. METHODS: The first TnI-Ultra sample from 856 patients at presentation to the Emergency Department and subsequent admission to the Cardiac Care Unit were considered in this case series. Myoglobin was simultaneously detected in 684 patients. RESULTS: The sensitivity of the first single TnI-Ultra level was 82.5% in overall AMI, and similar in ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI), admitted, respectively at 3 and 8 h from symptoms. The diagnostic capability of a first single TnI-Ultra level was poor for both STEMI and NSTEMI to discriminate and rule-out overall AMI from myocardial injury, with an area under the receiver-operating curve of 0.65 and a negative likelihood ratio of 0.55. Adopting an optimal test threshold or adding myoglobin detection did not improve TnI-Ultra performances. CONCLUSIONS: The capability of a first single TnI-Ultra level to exclude AMI from other myocardial injury in early and late presenters is poor. Addition of myoglobin assay offered no further improvement and was not considered useful.

[Zero-fluoroscopy transcatheter ablation and CRT-D implantation: new frontiers of electroanatomical mapping systems]. / Ablazione transcatetere e contestuale impianto di CRT-D "zero-fluoroscopy": nuove frontiere del mappaggio elettroanatomico.

In cardiac resynchronization therapy (CRT) implantation procedures, contrast-induced nephropathy risk and ionizing radiation exposure can be eliminated using electroanatomical mapping system (EAMS). Under EAMS guidance, it is possible to place the left ventricular catheter in the branch of the coronary sinus that presents the latest activation. The use of EAMS allows for both arrhythmic ablation and CRT implantation to be obtained in a single, "zero fluoroscopy" procedure. Here we report two cases of successful arrhythmia ablation and CRT-D implantation with "zero fluoroscopy" in a single procedure.

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.

Acute contractile recovery extent during biventricular pacing is not associated with follow-up in patients undergoing resynchronization.

BACKGROUND: It has been reported that contractility, as assessed using dobutamine infusion, is independently associated with reverse remodeling after CRT. Controversy, however, exists about the capacity of this approach to predict a long-term clinical response. This study's purpose was to assess whether long-term CRT clinical effects can be predicted according to acute inotropic response induced by biventricular stimulation (CRT on), as compared with AAI-VVI right stimulation pacing mode (CRT off), quantified at the time of implantation. METHODS: In 98 patients (ejection fraction 29 ± 10%), acute changes in left ventricular (LV) elastance (Ees), arterial elastance (Ea), and Ees/Ea, as assessed from slope changes of the force-frequency relation obtained when the heart rate increased, and also assessed while measuring triplane LV volumes and continuous noninvasive blood pressure, were related to death or rehospitalization during a 3-year follow-up. Other covariances tested were age, gender, disease etiology, QRS duration, amount of mitral regurgitation, LV diastolic volume, ejection fraction, and the degree of asynchrony and longitudinal strain at baseline. RESULTS: There was a marked increment in the Ees slope with CRT (interaction P = 0.004), no Ea change, and modest Ees/Ea increase (interaction P < 0.05). In Cox analysis, however, neither slope changes nor baseline values of Ees, Ea, and Ees/Ea were associated with long-term follow-up. Only ventricular diastolic volume (direct relation P = 0.002) and QRS duration (inverse relation P = 0.009) predicted death/rehospitalization. CONCLUSIONS: Acute contractile recovery in CRT patients is not associated with 3 years prognosis. Instead, death or rehospitalization can be predicted from QRS duration and LV diastolic volume at baseline.

Low--molecular weight heparins and unfractionated heparins during primary coronary intervention.

Coronary artery diseases continue to be the most common causes of mortality and morbidity in the industrialized world, especially in the setting of acute myocardial infarction. Anticoagulation during primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) has traditionally been supported by anticoagulant unfractionated heparin (UFH). Recently, alternative anticoagulants such as low molecular weight heparin (LMWH) were included in the management of STEMI. The aim of the present review is to compare efficacy and safety outcomes among patients receiving low molecular weight heparins (LMWH) or unfractionated heparin (UFH) while undergoing PCI for STEMI.

New insights in the pathophysiology of acute myocardial infarction detectable by a contemporary troponin assay.

OBJECTIVES: ST-elevation and non-ST-elevation myocardial infarction (STEMI, NSTEMI) are considered two distinct pathophysiologic entities. We evaluated cardiac troponin I (cTnI) release in STEMI and NSTEMI using a "contemporary" (CV>10 to 20% at the 99th percentile concentration) cTnI assay for patients undergoing early percutaneous coronary intervention (PCI). DESIGN AND METHODS: 856 patients with suspected acute coronary syndrome consecutively admitted to the Emergency Department of the Maggiore Hospital of Novara (225 STEMI and 135 NSTEMI) were selected according to: 1) early (≤ 4 h from admission) and successful PCI; and 2) cTnI measurements at ED presentation and within 24h. The influence of the MI type on cTnI concentrations at baseline and after PCI as well as the velocity of cTnI [cTnI V=absolute increase (after log conversion of cTnI measurements)/delay between the two measurements] was studied by multiple regression analysis, adjusting for patient parameters. RESULTS: A statistically significant interaction between MI type and time from symptoms was reported on cTnI concentrations (p<0.0001): STEMI and NSTEMI differed for cTnI releases at admission and after revascularization. Higher cTnI V in STEMI was detectable in patients admitted within 6h from symptoms. Baseline cTnI concentrations were lower in patients with a history of coronary artery disease (CAD) and increased with aging (p<0.0001). In the elderly (>75 years), the cTnI V was significantly increased. CONCLUSION: STEMI and NSTEMI patients have different patterns and dynamics of cTnI release influenced by the interaction with time from symptoms, by aging and history of CAD.

Pharmacological adjuvant therapies in primary coronary interventions: bivalirudin.

The direct thrombin inhibitor bivalirudin has gained popularity in cardiovascular medicine over the past decade because, in comparison with unfractionated heparin, it guarantees a predictable dose-related degree of anticoagulation with a low immunogenic profile and, possibly, with reduced rates of major bleeding complications. In the past bivalirudin has been frequently employed in the management of patients with heparin-induced thrombocytopenia. The REPLACE-2, ACUITY and ISAR-REACT4 studies demonstrated bivalirudin non-inferiority in comparison with unfractionated heparin in terms of ischemic end-points with a reduction of the bleeding rate also in patients acute coronary syndrome without ST elevation. Finally the results of the HORIZONS-AMI study positioned this drug as a first choice anticoagulant during percutaneous coronary interventions in patients with ST-elevation myocardial infarction. In fact the bivalirudin alone regimen, compared to unfractionated heparin plus GP2b3a inhibitors, decreased in-hospital bleeding rates and short and long term mortality. Given the body of clinical evidence, bivalirudin is likely to contend to GP2b3a inhibitors the leading place among the proposed anticoagulation strategies in the setting of acute coronary syndromes. The duration of the bivalirudin infusion after PCI and the optimal oral antiplatelet regimen associated to bivalirudin are important issues to be solved in future randomized controlled studies.

Multi-marker network in ST-elevation myocardial infarction patients undergoing primary percutaneous coronary intervention: when and what to measure.

BACKGROUND: Data on the correlations between biomarkers to suggest cost-effective multi-marker (MM) panels predictive for ST-elevation myocardial infarction (STEMI) patients are lacking. We sought to explore the relationship between cardiac troponin I (cTnI), C-reactive protein (CRP), B-type natriuretic peptide (BNP), and chromogranin A (CgA) accounting for biomarkers' profiles detected within 48h from successful primary percutaneous coronary intervention (PPCI). METHODS: In 73 STEMI patients cTnI, CRP, BNP, and CgA were measured before PPCI and 6, 24, and 48h later. STATIS methods generalizing Principal Component Analysis on three-way data sets were employed to extract information about: 1) similarities between patients, 2) contribution of each time of sampling and 3) correlations between biomarkers' profiles. RESULTS: STEMI patients who underwent successful PPCI emerged to have a homogeneous profile tailored on biomarkers' evaluation within 48h. Their measurements at 24h contributed the most variability and information both to patients' and to biomarkers' profiles. BNP and cTnI were highly correlated and explained the 40.1% of the total variance, whereas CgA resulted independent and explained the 26.3% of the total variance. CONCLUSIONS: Markers' measurements at 24h after PPCI contributed most information to the definition of patients' profile. BNP and cTnI resulted interchangeable in a MM panel for reporting about the extent of necrosis.

Radial approach for percutaneous coronary intervention.

The transradial approach for percutaneous coronary intervention (both diagnostic and therapeutic procedures) has gained progressive acceptance in the last years. Transradial access has been shown, also, to have several advantages over transfemoral approach; the radial artery is easily compressible, thus bleeding is controllable and hemorrhagic complications are significantly reduced. Furthermore, periprocedural bleeding and vascular complications after percutaneous coronary intervention are associated with worse clinical outcomes and increased short and long - mortality. With increasing experience and availability of dedicated equipment this technique is now being increasingly used for complex catheter intervention. The main purpose of this review is to highlight the benefits, complications and problems with transradial approach compared with conventional transfemoral approach.

Inside ST-elevation myocardial infarction by monitoring concentrations of cardiovascular risk biomarkers in blood.

BACKGROUND: No information is available on the optimal sampling time to catch the highest increase for biomarkers whose elevation after ST-elevation myocardial infarction (STEMI) is prognostic for adverse events. This study aimed to investigate release kinetics and peak times of cardiac troponin I (cTnI), C-reactive protein (CRP), B-type natriuretic peptide (BNP), chromogranin A (CgA) and cystatin C (CyC) in STEMI patients undergoing primary percutaneous coronary intervention (PPCI). METHODS: Blood concentrations of cTnI, CRP, BNP, CgA and CyC were measured before and 6 h, 24 h, and 48 h after PPCI in 84 STEMI patients. The averaged trajectory of marker kinetics was estimated by multivariable regression models adjusted for patient characteristics and orthogonal polynomials were used to describe related releases. RESULTS: From the estimated kinetics cTnI peaked at 10 h from symptoms, BNP at 28 h and CRP within 30 h. CyC concentrations did not change, whereas CgA concentrations increased from 6 to 48 h after PPCI. The amount of BNP release was found to be affected by the interaction between gender and age: females<75 years had BNP concentrations fourfold higher than males. CONCLUSIONS: According to different release kinetics a single blood sampling for measuring all biomarkers is not recommended.

Apical-sparing Tako-tsubo: a case report.

We present a case of "apical-sparing Tako-Tsubo" syndrome in a postmenopausal woman with normal coronary arteries. Atypical variants of Tako-Tsubo like syndrome have been recently reported. Our patient showed a suggestive noncoronary-distributed dyskinetic area, in a clinical setting of typical chest pain, recent stressful events, troponin elevation and normal coronary angiogram; wall motion normalized within two days.

Use of endothelial progenitor capture cell stent during percutaneous treatment of coronary bifurcations: a prospective angiographic registry.

BACKGROUND: The treatment of bifurcation lesions remains a challenge with poor immediate results and higher restenosis rate than in nonbifurcated lesions. Drug-eluting stents improve the outcome after coronary stenting, but are associated with a small but statistically significant increase in late and very late stent thrombosis. Thus, aim of the present study was to evaluate the angiographic and clinical results of a new type of stent (coated with murine monoclonal antihuman CD34 antibodies designed to attract circulating endothelial progenitor cells to rapidly establish a functional endothelial layer and promote healing stent implantation) in a cohort of consecutive patients with coronary bifurcation lesions. METHODS AND RESULTS: Between December 2007 and July 2008, a total of 43 consecutive patients were enrolled and 47 consecutive bifurcation lesions were treated with endothelial progenitor capture cell stents. The angiographic end points binary restenosis rate inside the stent (within 5 mm of the stent edges or in the segments treated with balloon angioplasty) was 5% (2.1% in the main branch and 10.5% in the side branch). No stent thrombosis was observed. Clinical follow-up was completed in all patients at mean time of 34.5 days after percutaneous coronary interventions by clinical evaluation and 12.3 months with a telephone contact. Angina at rest was present in 3 patients (7.9%). No in-hospital, 30-days, or 12-months major adverse cardiac events (death, myocardial infarction, and repeat revascularization coronary artery bypass graft or percutaneous coronary angioplasty) were reported. CONCLUSIONS: The use of endothelial progenitor capture cell in the setting of coronary bifurcation appears to be feasible and safe with no incidence of late stent thrombosis and a very low rate of repeated revascularization.

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.