Mean platelet volume is associated with infarct size and microvascular obstruction estimated by cardiac magnetic resonance in ST segment elevation myocardial infarction

Fabregat-Andrés, Óscar; Cubillos, Andrés; Ferrando-Beltrán, Mónica; Bochard-Villanueva, Bruno; Estornell-Erill, Jordi; Fácila, Lorenzo; Ridocci-Soriano, Francisco; Morell, Salvador

doi:10.1097/mbc.0b013e32835d9bca

Cited by 21 publications

(25 citation statements)

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“…This phenomenon, due to microvascular blockage, is typically seen after stenting with low TIMI flow (angiographic “no reflow”) and is independently associated with major adverse cardiac events 19 . The cause of microvascular obstruction is multifactorial including anatomical obstruction (clumped leukocytes or platelets 20 , perivascular edema and/or cell swelling 21 ) , reduced vasoreactivity, or frank microvascular necrosis. A combination of intrinsic and extrinsic obstruction may result from intramyocardial hemorrhage which occurs after prolonged ischemia in pigs 22 .…”

Section: Recognition Of Microvascular Disease In Humansmentioning

confidence: 99%

The Human Microcirculation

Gutterman

Chabowski

Kadlec

et al. 2016

Circulation Research

234

141

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The microcirculation is responsible for orchestrating adjustments in vascular tone to match local tissue perfusion with oxygen demand. Beyond this metabolic dilation, the microvasculature plays a critical role in modulating vascular tone by endothelial release of an unusually diverse family of compounds including nitric oxide, other reactive oxygen species, and arachidonic acid metabolites. Animal models have provided excellent insight into mechanisms of vasoregulation in health and disease. However there are unique aspects of the human microcirculation that serve as the focus of this review. The concept is put forth that vasculo-parenchymal communication is multimodal, with vascular release of nitric oxide eliciting dilation and preserving normal parenchymal function by inhibiting inflammation and proliferation. Likewise, in disease or stress, endothelial release of ROS both mediates dilation and parenchymal inflammation leading to cellular dysfunction, thrombosis, and fibrosis. Some pathways responsible for this stress-induced shift in mediator of vasodilation are proposed. This paradigm may help explain why microvascular dysfunction is such a powerful predictor of cardiovascular events, and help identify new approaches to treatment and prevention.

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Section: Recognition Of Microvascular Disease In Humansmentioning

confidence: 99%

The Human Microcirculation

Gutterman

Chabowski

Kadlec

et al. 2016

Circulation Research

234

141

View full text Add to dashboard Cite

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“…In this regard, Şarlı et al (11), reported a significant association of higher MPV with poor postinterventional myocardial blush grade, which is considered a reliable marker for microvascular patency, in patients with STEMI who underwent primary percutaneous coronary intervention. Other studies went further and confirmed the relationship between elevated MPV and a greater area of necrosis and microvascular obstruction, estimated by cardiac resonance (12).…”

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confidence: 64%

Mean platelet volume and impaired myocardial reperfusion: Risk factor or innocent bystander?

Fabregat-Andrés¹

2014

Anadolu Kardiyol Derg

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Mean platelet volume (MPV) has emerged in recent years as a potential independent risk factor for poor clinical outcomes among patients with unstable angina and ST-segment elevation myocardial infarction (STEMI) (1, 2). Since MPV is an indicator of platelet activation and correlates with agreeability, larger and hyperreactive platelets could accelerate the formation of intracoronary thrombus and therefore play an essential role in the pathophysiology of coronary artery disease. Additionally, it has been also related with culprit lesion severity in acute coronary syndromes (3) and left ventricular systolic function in STEMI patients (4).With the purpose of justifying a pathophysiological mechanism that correlates MPV with major cardiovascular complications, some studies have evaluated the association between MPV and impaired myocardial reperfusion in patients with STEMI (5, 6). Microvascular impairment after STEMI in the presence of infarct-related artery patency could be attributable to small platelet aggregates, among other factors, which could mediate the presence of microvascular injury and endothelial dysfunction in both coronary arterioles and capillaries. High MPV may correspond with an increased number of these platelet aggregates and thus explain the phenomena as slow coronary flow or no reflow of an infarct-related coronary artery (7,8). This point could be the key to explaining why MPV acts as a risk factor in these patients.In this context, Kırbaş et al. (9), published in this issue, conducted a retrospective analysis of patients with a first STEMI who underwent reperfusion therapy with thrombolysis to assess the association of MPV with ST-segment resolution, a widely used electrocardiographic variable of successful reperfusion. The study found that higher MPV on admission was associated with impaired ST-segment resolution, defined by the lack of at least 50% ST-segment resolution in the single lead with maximal ST elevation, measured 90 minutes after thrombolytic therapy. These findings could help to strengthen the evidence that correlates higher MPV with impaired reperfusion in STEMI, although some aspects of the study should be considered.Firstly, as the authors acknowledge in the limitations section, prior use of antiplatelet drugs was not reported because of the retrospective study design, which could modify the MPV values and response to thrombolysis. This is especially relevant if we take into account that MPV is a quantitative variable with a relatively narrow range of values, the regulation of which is multifactorial, and because antiplatelet agents are a significant factor in the modulation of platelet size (10).Furthermore, the absence of imaging tests for the analysis of the effects of unsuccessful reperfusion should also be considered a major limitation of the study, especially given that other studies have indeed considered this aspect. In this regard, Şarlı et al. (11), reported a significant association of higher MPV with poor postinterventional myocardial blush grade, which is conside...

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“…Higher MPV correlates with the reperfusion failure in STEMI [8,9]. Higher MPV level may be associated with an impaired microvascular perfusion, even in successfully reperfused patients [10,11]. Fabregat-Andrés et al [11] showed the association of high MPV level with larger infarct size in STEMI by using a cardiac MRI, which is a very sensitive tool for the myocardial infarct assessment.…”

Section: Discussionmentioning

confidence: 99%

“…Higher MPV level may be associated with an impaired microvascular perfusion, even in successfully reperfused patients [10,11]. Fabregat-Andrés et al [11] showed the association of high MPV level with larger infarct size in STEMI by using a cardiac MRI, which is a very sensitive tool for the myocardial infarct assessment. Another study found a significant correlation between the degree of systolic depression and MPV in STEMI patients [12,13].…”

Section: Discussionmentioning

confidence: 99%

Association of mean platelet volume with presence of non-viable myocardium in ischaemic cardiomyopathy

Öztürk

Gurbuz

Efe³

et al. 2017

Kardiol Pol

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A b s t r a c tBackground: Parameters derived from complete blood count, such as mean platelet volume (MPV), neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR), have recently been proposed as measures of inflammation in addition to C-reactive protein (CRP), a classical inflammatory marker. Significant association of these parameters with atherosclerosis and complications have increasingly been reported. Aim:The aim of the study is to evaluate the relationship between these parameters and the presence of myocardial viability assessed with positron emission tomography (PET) in patients with ischaemic cardiomyopathy (ICM).Methods: A total of 122 ICM patients who had undergone PET were enrolled in this study. The patients were dichotomised depending on the presence of transmural scar. Group 1 consisted of 21 patients who had transmural scar tissue only, who were accepted as the group having non-viable myocardium. Group 2 consisted of 101 patients who had hibernation and/or non-transmural scar, who were accepted as the group having viable myocardium. Haematological parameters within 30 days of PET imaging were retrospectively analysed.Results: There were no significant differences between the two groups regarding values of white blood cell, neutrophil, lymphocyte, platelet, haemoglobin, red cell distribution width, CRP, PLR, and NLR. Patients with non-viable myocardium have significantly higher levels of MPV (p = 0.002). In multiple logistic regression analysis, MPV (odds ratio [OR] = 0.373, 95% confidence interval [CI] 0.20-0.69, p = 0.002), was identified as an independent predictor of non-viable myocardium. In receiver-operator characteristic (ROC) analysis, a cut-point of 8.19 identified patients with non-viable myocardium (area under curve: 0.72, 95% CI 0.60-0.84). An MPV value greater than 8.19 demonstrated a sensitivity of 76% and a specificity of 55%. Conclusions:The present study showed that MPV is an inexpensive, clinical, and routinely measurable parameter that is associated with the presence of viable myocardium in ICM.

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Mean platelet volume is associated with infarct size and microvascular obstruction estimated by cardiac magnetic resonance in ST segment elevation myocardial infarction

Cited by 21 publications

References 20 publications

The Human Microcirculation

The Human Microcirculation

Mean platelet volume and impaired myocardial reperfusion: Risk factor or innocent bystander?

Association of mean platelet volume with presence of non-viable myocardium in ischaemic cardiomyopathy

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