Mean platelet volume as a predictor of cardiovascular risk: a systematic review and meta-analysis

Abstract

Aim: To determine whether an association exists between mean platelet volume (MPV) and acute myocardial infarction (AMI) and other cardiovascular events. Platelet activity is a major culprit in atherothrombotic events. MPV, which is widely available in clinical practice, is a potentially useful biomarker of platelet activity in the setting of cardiovascular disease.

Methods and results: We performed a systematic review and meta-analysis investigating the association between MPV and AMI, all-cause mortality following myocardial infarction, and restenosis following coronary angioplasty. Results were pooled using random-effects modeling. Pooled results from 16 cross-sectional studies involving 2809 patients investigating the association of MPV and AMI indicated that MPV was significantly higher in those with AMI than those without AMI [mean difference 0.92 fL, 95% confidence interval (CI) 0.67-1.16, P < 0.001). In subgroup analyses, significant differences in MPV existed between subjects with AMI, subjects with stable coronary disease (P < 0.001), and stable controls (P < 0.001), but not vs. those with unstable angina (P = 0.24). Pooled results from three cohort studies involving 3184 patients evaluating the risk of death following AMI demonstrated that an elevated MPV increased the odds of death as compared with a normal MPV (11.5% vs. 7.1%, odds ratio 1.65, 95% CI 1.12-2.52, P = 0.012). Pooled results from five cohort studies involving 430 patients who underwent coronary angioplasty revealed that MPV was significantly higher in patients who developed restenosis than in those who did not develop restenosis (mean difference 0.98 fL, 95% CI 0.74-1.21, P < 0.001).

Conclusions: Elevated MPV is associated with AMI, mortality following myocardial infarction, and restenosis following coronary angioplasty. These data suggest that MPV is a potentially useful prognostic biomarker in patients with cardiovascular disease. Whether the relationship is causal, and whether MPV should influence practice or guide therapy, remains unknown.

Conflict of interest statement

Disclosure of Conflict of Interests

D.L. Bhatt discloses the following relationships: Research Grants - Bristol Myers Squibb, Eisai, Ethicon, Heartscape, Sanofi Aventis, The Medicines Company; Consultant/Advisory Board - Arena, Astellas, Astra Zeneca, Bayer, Bristol Myers Squibb, Cardax, Centocor, Cogentus, Daiichi-Sankyo, Eisai, Eli Lilly, Glaxo Smith Kline, Johnson & Johnson, McNeil, Medtronic, Millennium, Molecular Insights, Otsuka, Paringenix, PDL, Philips, Portola, Sanofi Aventis, Schering Plough, Scios, Takeda, The Medicines Company, Vertex. The other authors state that they have no conflict of interest.

Figures

Fig. 1

Flow chart showing results of the search strategy and reasons for exclusion. CAD, coronary artery disease; MPV, mean platelet volume; UA, unstable angina.

Fig. 2

Random-effects pooled mean difference of mean platelet volume (MPV) between acute myocardial infarction (AMI) cases and non-AMI controls.

Fig. 3

Random-effects pooled odds ratio of mean platelet volume and mortality following myocardial infarction from prospective studies. CI, confidence interval; OR, odds ratio.

Fig. 4

Random-effects pooled mean difference of mean platelet volume (MPV) between restenosis cases and no restenosis controls. AMI, acute myocardial infarction.

Fig. 5

Potential mechanisms of action of mean platelet volume in cardiovascular thrombosis. Larger platelets contain more α-granules [52], which release prothrombotic factors such as P-selectin (P-sel), serotonin (5-HT), ADP, and β-thromboglobulin (β-TG) [6,7,53,63]. Larger platelets also have increased levels of thromboxane A2 (TxA2) [6,7] and express more adhesion receptors, glycoprotein (GP) Ib and GPIIb–IIIa [49]. These factors have a variety of effects on inflammation and endothelial function, promoting cell adhesion and aggregation, and vasoconstriction, and ultimately inducing thrombosis. Platelet size may be determined by megakaryocyte ploidy, which is regulated by thrombopoietin (TPO) [30,58] and interleukin-6 (IL-6) [59].