Mean platelet volume (MPV) is an indicator of platelet activation. High MPV has been recently considered as an independent risk factor for poor outcomes after ST-segment elevation myocardial infarction (STEMI). We analyzed 128 patients diagnosed with first STEMI successfully reperfused during three consecutive years. MPV was measured on admission and a cardiac magnetic resonance (CMR) exam was performed within the first week in all patients. Myocardial necrosis size was estimated by the area of late gadolinium enhancement (LGE), identifying microvascular obstruction (MVO), if present. Clinical outcomes were recorded at 1 year follow-up. High MPV was defined as a value in the third tertile (≥9.5 fl), and a low MPV, as a value in the lower two. We found a slight but significant correlation between MPV and infarct size (r = 0.287, P = 0.008). Patients with high MPV had more extensive infarcted area (percentage of necrosis by LGE: 17.6 vs. 12.5%, P = 0.021) and more presence of MVO (patients with MVO pattern: 44.4 vs. 25.3%, P = 0.027). In a multivariable analysis, hazard ratio for major adverse cardiac events was 3.35 [95% confidence interval (CI) 1.1-9.9, P = 0.03] in patients with high MPV. High MPV in patients with first STEMI is associated with higher infarct size and more presence of MVO measured by CMR.

Background Pulmonary hypertension (PH) conveys a worse prognosis in heart failure (HF), in particular when right ventricular (RV) dysfunction ensues. Cardiovascular magnetic resonance (CMR) non-invasively estimates pulmonary vascular resistance (PVR), which has shown prognostic value in HF. Importantly, RV to pulmonary artery (PA) coupling is altered early in HF, before significant rise in PV resistance occurs. The aim of this study was to assess the prognostic value of mean velocity at the pulmonary artery (mvPA), a novel non-invasive parameter determined by CMR, in HF with reduced ejection fraction (HFrEF) with and without associated PH. Methods Prospective inclusion of 238 patients admitted for new-onset HFrEF. MvPA was measured with CMR during index admission. The primary endpoint was defined as a composite of HF readmissions and all-cause mortality. Results During a median follow-up of 25 months, 91 patients presented with the primary endpoint. Optimal cut-off value of mvPA calculated by the receiver operator curve for the prediction of the primary endpoint was 9 cm/s. The primary endpoint occurred more frequently in patients with mvPA≤9 cm/s, as indicated by Kaplan-Meier survival curves; Log Rank 16.0, p <  0.001. Importantly, mvPA maintained its prognostic value regardless of RV function and also when considering mortality and HF readmissions separately. On Cox proportional hazard analysis, reduced mvPA≤9 cm/s emerged as an independent prognostic marker, together with NYHA III-IV/IV class, stage 3–4 renal failure and ischemic cardiomyopathy. Conclusions In our HFrEF cohort, mvPA emerged as an independent prognostic indicator independent of RV function, allowing identification of a higher-risk population before structural damage onset. Moreover, mvPA emerged as a surrogate marker of the RV-PA unit coupling status.

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