Previous studies have shown that patients with a higher MPV have a greater risk of death due to IHD (Ischemic Heart Disease), with hazard ratios similar to those reported for obesity or smoking . In our study there was no meaningful association between myocardial perfusion defect and mean platelet volume in patients with DM, however, there was a statistically meaningful association in healthy participants. As shown, by one-unit increase of MPV, the SRS increased by an average of 0.46, which means higher MPV values may be an indicator of previous infarctions but not ischemia in healthy population. The association between increased MPV and myocardial infarction was previously reported by other investigators as well [27, 28], but was confirmed only in healthy individuals in our study.
This is in contrast to Savas Sarikaya et al. investigation. They found a statistically significant difference between MPV and myocardial perfusion defect in patients with DM as well. They claimed that higher MPV in patients with DM was associated with myocardial perfusion defects, which could be considered as an indicator of ischemia . The difference might be due to different designs as they did not include patients without DM in their study. Also, some other confounding variables might have an effect like differences in sample size and ischemia variables. However, our patients with DM were asymptomatic, which might need more time to develop complications.
Vascular complications including macrovascular (CAD, peripheral vascular disease and stroke) and microvascular (neuropathy, retinopathy and nephropathy) ones are common in DM. High blood sugar damages vascular endothelium leading to the above problems. Therefore, DM has been considered as an independent risk factor for atherosclerotic cardiovascular disorders [30–32], as CVD is considered the leading underlying reason for mortality in DM patients . On the other hand, DM causes asymptomatic CAD in some patients.
Cardiac perfusion scans have been widely used to predict coronary diseases. It might show perfusion abnormalities despite a normal coronary angiogram, which is probably due to microangiopathy and endothelial dysfunction and following subtle decreased tissue oxygenation .
Mean Platelet Volume is indicative of platelet function. It is believed that platelets with denser granules are more active in some processes such as inflammation, coagulation, thrombosis and atherosclerosis. This might lead to higher probability of coronary thrombosis and ischemia. Platelets with higher MPV contain more procoagulant membrane proteins, serotonin, beta-thromboglobulin and prothrombogenic thromboxane A2 [35–38].
In another investigation, MPV was found to be higher in patients with cardiac syndrome X and coronary artery disease compared to controls. They indicated that it verifies the role of higher MPV in subclinical atherosclerosis .
Despite the fact, many studies have shown higher MPV levels in patients with DM. Kodiatte et al. showed that significantly higher MPV levels in patients with DM compared to healthy individuals. They also indicated a strong correlation between MPV with fasting blood glucose, postprandial glucose and HbA1C levels . Semi Ozturk also found higher levels of MPV in patients with ischemic cardiomyopathy. They claimed that patients with non-viable myocardium had significantly higher levels of MPV. They recommended to consider MPV as a cheap, practical and easily measurable index which could be used in the prognosis of ischemic cardiomyopathy .
Papanas et al. assessed MPV level in a quite large number of patients. They compared MPV in 416 patients with type 2 DM and healthy individuals. They also evaluated the association between MPV and diabetic complications. They finally reported that MPV is higher in patients with type 2 DM compared to healthy ones. Despite the fact, MPV was more increased in patients with microvascular complications such as retinopathy or micro-albuminuria .
The reason why we did not find a statistically significant difference between myocardial perfusion defect and mean platelet volume in patients with DM is challenging. However, such an association in healthy controls could be due to small number of participants or a selection bias as a consecutive sampling method might not be enough precise. Moreover, our patients with DM were asymptomatic which might need more time to develop microvascular complications. There is no doubt that mean platelet volume can be measured as part of routine assessment in patients with cardiovascular disorders.
We had some limitations. First our sample size was quite small, which might be responsible for a non-significant difference in patients with DM. This could be addressed in further investigations as well. Despite the fact, the novelty of our study was its grouping and study design. We could not find any similar study to compare MPV in patients with and without DM who underwent myocardial perfusion scan.