ABC | Volume 113, Nº2, August 2019

Original Article Kul et al PSW and type 2 DM Arq Bras Cardiol. 2019; 113(2):207-215 Similar to Akyuz et al., 23 we showed a correlation between PSW velocity and age. Unlike they, however, we failed to show any correlation between PSW velocity and LVM. As of 2015, DM affects a total of 30.3 million Americans or 9.4% of the US population. Of these individuals, 7.2 million had clinically silent DM. Moreover, 1.5 million Americans yearly are added to the diabetic population in the US. 24 Diabetes is characterized by an increased risk of cardiovascular complications, mainly in the form of CAD, as the main source of morbidity and mortality among affected persons. 25 Simone et al. 26 recently reported that the risk of heart failure is heightened among type 2 diabetics and that this effect still occurs even persons do not sustain myocardial infarction or suffer HT. 26 Hence, the term diabetic cardiomyopathy has been recommended by medical communities, referring to the dysfunctional ventricle in the absence of CAD and HT. 27 Hyperglycemia is the source of advanced glycosylation end products (AGE). The latter are proteins with longer half-lives that have altered functional properties after being exposed to sugars and becoming glycated. 28 When in excess, AGE formation may alter myocardial proteins structure and lead to stiff myocardium. The latter is a direct consequence of AGEs forming crosslinks between collagen molecules, which limits their degradation and leads to their accumulation in myocardial tissue, with resulting myocardial stiffness and reduced myocardial relaxation. 29 Diabetics suffer altered myocardial function largely due to hypertrophied ventricles, metabolic abnormalities, extracellular matrix remodelling, fibrosis, vascular changes, insulin resistance, oxidative stress and apoptosis. 30,31 Hyperglycemia may also promote myocyte apoptosis necrosis, 32 resulting in net myocardial cell loss, 33 reduced ventricular contractility, and systolic dysfunction. In combination, these phenomena cause reduced LV systolic and diastolic function among diabetics. We usedMPI to detect subclinical LVD. MPI is a noninvasive tool reflecting both systolic and diastolic ventricular functions, which is easy-to-perform. 34 Its use may predict future LV impairment and development of clinical heart failure long before they become clinically apparent. 35 It has been conclusively reported that MPI independent of blood pressure, heart rate, valvular regurgitation, ventricular geometry, preload, and afterload in patients who are lying flat. 36,37 It is important for the clinician to determine subclinical LVD before apparent LVD occurs. For this purpose, we used MPI to identify subclinical LVD in type 2 DM. We demonstrated that MPI was significantly greater in PSW positive type 2 DM patients. This means that subclinical LVD is higher in the PSW positive group in type 2 DM. In addition, we found a correlation with PSW velocity and MPI in type 2 DM in this study. According to our study results, the presence of PSW on Doppler echocardiography and increased PSW velocity may be related to subclinical LVD in type 2 DM patients. We did not aim to investigate the causal relationship between PSW and subclinical LVD in our study, but this relationship can be explained by several theories. Figure 2 – Myocardial performance index calculation. ET: ejection time; IVCT: isovolumetric contraction time; IVRT: isovolumetric relaxation time; A - time spent between closure and reopening of tricuspid valve. MPI = (IVCT+IVRT)/ET = ((A)-(ET))/(ET). MPI: myocardial performance index. 210