ABC | Volume 113, Nº2, August 2019

Original Article Kul et al PSW and type 2 DM Arq Bras Cardiol. 2019; 113(2):207-215 Methods Study population Patients with Type 2 DM who were referred to the Cardiology and Endocrinology clinic of the Trabzon Kanuni Education and Research Hospital were enrolled by the study. A total of 129 patients were included in this study consecutively. Patients were divided into two groups according to the presence of PSW on Doppler echocardiography. There were 90 patients (38 male, mean age 57.77 ± 10.91 years) in the PSW- positive group and 39 patients (13 male; mean age: 55.31 ± 11.29 years) in the PSW-negative group. Demographic characteristics, biochemical parameters, and echocardiographic characteristics of the patients were compared between the groups. The following subjects were excluded: those with a history of hypertrophic obstructive cardiomyopathy, angina pectoris, recent myocardial infarction, coronary artery bypass surgery, peripheral arterial disease, cardiac failure, moderate to severe valvular heart disease, valvular operation, history of stroke and transient ischemic attack, atrial fibrillation, chronic renal failure, chronic liver diseases, hematological disorders, malignancy, thromboembolic disorders, congenital heart disease, congestive heart failure, and acute bacterial endocarditis. The study was approved by the local ethics committee, and all patients provided informed consent. Cardiovascular risk factor assessment History of arterial HT, DM, hyperlipidemia (HL), and smoking, as well as a family history of coronary artery disease (CAD), were recorded for all patients. Type 2 DM was diagnosed on the basis of a history of treated DM and/or had a fasting blood glucose level equal to or greater than 126 mg/dl. HL was considered to exist when fasting total cholesterol level was ≥ 200 mg/dl, fasting low-density lipoprotein level ≥ 160 mg/dl, fasting triglyceride (TG) level ≥ 200 mg/dl, or using medication for HL. HT was said to be present in the case of a history of treated or untreated HT or when a mean systolic blood pressure of ≥ 140 mmHg and/or a mean diastolic blood pressure of ≥ 90 mmHg were obtained by averaging two blood pressure readings taken from each arm. The family history of CAD included a history of CAD or sudden cardiac death in first-degree male relative younger than 55 years or a first-degree female relative younger than 65 years. Echocardiography All subjects underwent a transthoracic echocardiographic examination using the Philips Epic 7 system (Philips Epic 7 UltrasoundAS) unit with a 2.5MHz FPAprobe. The conventional M-mode, B-mode, and Doppler parameters were done in compliance with the American Society of Echocardiography guidelines. 18 All echocardiographic examinations were performed by an experienced echocardiographer who was unaware of the patients’ clinical and demographic data. Quantification of LV end-diastolic and end-systolic diameters and posterior and septal wall thicknesses were carried out. The Devereux equation was used to derive LV mass (LVM): LVM=0.8× [1.04 (LVEDD+ IVST+PWT) 3 –(LVEDD 3 )] +0.6, where LVEDD denotes LV end-diastolic diameter, IVST denotes intraventricular septal wall thickness, and PWT denotes posterior wall thickness. The LVM index was calculated by the formula: LVM/body surface area. Body surface area (BSA) was calculated using the ‘BSA (m 2 ) = 0.007184 x Height (cm) 0.725 x Weight (kg) 0.425 ‘ formula. LV hypertrophy was considered positive if LVM index was above 115 g/m 2 for men and above 95 g/m 2 for women. 19 LVOT’s portion just proximal to the aortic valve was interrogated with pulsed wave Doppler in the apical five-chamber window in order to check the presence of a PSW just before the LVOT flow. PSW peak velocity was quantified whenever a quantifiable PSW signal was present Figure 1. Tissue Doppler evaluation of the left ventricle was performed from the apical four-chamber view with a frame rate of greater than 80/s. All quantifications were performed on frozen images obtained from three to five cardiac cycles. Mitral annular velocities were quantified with the sample volume being placed at the junction of the mitral valve annulus and the septal myocardial wall. Time elapsed between the end of A’ wave and the beginning of the E’ wave and between the beginning of and the end of the S wave was defined as (a) and ejection time (ET), respectively, in tissue Doppler recordings done from the apical four-chamber. MPI was calculated using the ‘MPI = (IVCT + IVRT)/ET= [(a) − (ET)]/(ET)’ formula 20,21 (Figure 2). There existed intraobserver and interobserver variability of 3% to 5% for conventional Doppler and TDI‑derived variables (PSWvelocity, Em, Am, and MPI). 0.5 and over MPI level was defined as subclinical LVD. Statistical analyses The minimum number of subjects required in each group was determined to be 32 in order to find a significant difference between the two groups. Type I Error = 0.05, Test Power 0.80. All statistical analyses were performed using SPSS (Statistical Package for Social Sciences) for Windows 19 (SPSS Inc. Chicago, IL, USA) software package. The continuous variables were reported as mean±SD or median (interquartile range) while the categorical variables were reported as frequency and percentage. Kolmogorov Smirnov test was used to test the distribution of the quantitative variables. Independent samples t-test was used to make inter-group comparisons for normally distributed quantitative data and Mann Whitney-U test for non-normally distributed data between. Qualitative variables were compared were with the Chi-square test. Univariate analysis was performed to assess the relations between the abnormal MPI and clinical and echocardiographic variables. Pearson correlation analysis was carried out to investigate the association between PSW peak velocity and mitral A and septal A' velocities. Spearman correlation analysis was carried out to investigate the association between PSW peak velocity and Em to Am ratio and septal E’ to A’ ratio. The confidence interval was set at 95 % and statistical significance was set at p < 0.05. Results Clinical and demographic characteristics of the patients are shown in Table 1. Age, sex, HT, current smoking, dyslipidemia, and family history for CAD were similar in the PSW-positive and negative groups. There was no difference between the 208