Objective: Prediabetes comprises a heterogeneous group because of the poor concordance of its definition. The aim of our study was to evaluate the longitudinal deformation of the left ventricular (LV) myocardium at the two opposite ends of the prediabetes spectrum as defined by fasting blood sugar and glycated hemoglobin (HbA1c).
Methods: Eighty consecutive subjects in a cross-sectional single-center study with impaired fasting glucose (IFG) (100–126 mg/dL) and without significant epicardial coronary artery stenosis seen on selective coronary angiography were included in our study and were divided into two groups based on their HbA1c levels (<5.7% and 5.7%–6.4%). The longitudinal deformation of the LV myocardium was compared between the two groups using two-dimensional speckle-tracking echocardiography (2DSTE).
Results: The Student t-test, Mann–Whitney U test, or X2 test was used for data analysis, whichever was appropriate. The systolic strain (–16.1%±2.0 vs. –16.8%±2.4; p=0.214), systolic strain rate (–1.3±0.2 s–1 vs. –1.4±0.2 s–1; p=0.403), and early and late-diastolic strain rates (1.4±0.3 s–1 vs. 1.5±0.3 s–1; p=0.456 and 0.9±0.1 s–1 vs. 1.0±0.2 s–1; p=0.684, respectively) of the LV myocardium were not statistically different between the IFG subjects with and without increased HbA1c as detected using 2DSTE.
Conclusion: The longitudinal deformation of the LV myocardium as detected using 2DSTE in the subjects without significant epicardial coronary artery stenosis was not statistically significantly different between the IFG subjects with and without increased HbA1c.

Objective: Hypertension is a significant risk factor for atrial fibrillation (AF). The role of pulmonary vein (PV) remodeling in the mechanistic association between hypertension and AF is not definitive. In this study, we aimed to identify changes in the electrophysiology and histology in PVs in two-kidney, one-clip (2K1C) hypertensive rats.
Methods: Fifty male Sprague-Dawley rats were classified into the 2K1C and sham-operated groups. The systolic blood pressure was measured every 2 weeks. The left atrial diameter was measured by transthoracic echocardiography. Left superior PV (LSPV) and left atrial (LA) fibrosis was evaluated by Masson’s trichrome staining. The expression of fibrosis markers [angiotensin II (Ang II), transforming growth factor-β1 (TGF-β1), matrix metalloproteinase-2 (MMP-2), and collagen I (Col I)] and ion channels [Kir2.1, Kir2.3, Cav1.2, and Nav1.5] in LSVP was quantified by western blot. Conventional microelectrodes were used to record the action potential duration at 90% repolarization (APD90) and effective refractory period (ERP) in isolated LA.
Results: At 4 months, the 2K1C hypertensive rats developed LA dilation. Col deposition in LSPV and left atrium and expression of TGF-β1, MMP-2, and Col I in LSPV were significantly increased in 2K1C hypertensive rats. In addition, hypertension reduced the expression of Nav1.5 and Kir2.1, although there were no significant differences in APD90; ERP; and expression of Ang II, Kir2.3, and Cav1.2 between the two groups.
Conclusion: Hypertension may lead to changes in the electrophysiology and histology of rats PVs, which is characterized by significant reduction in the expression of Nav1.5 and Kir2.1 and increase in interstitial fibrosis. These observations may clarify the role of PVs in the mechanistic association between hypertension and AF.

Objective: Previous studies have demonstrated the importance of intensive optimal medical therapy (OMT) in patients with coronary artery disease (CAD). To investigate our hypothesis that patients with and without OMT achievement differed with respect to the risk of future cardiac events, we investigated the endothelial function in patients with CAD who underwent percutaneous coronary intervention (PCI) and contemporary medical therapy.
Methods: We conducted a prospective longitudinal cohort study to evaluate the endothelial function in 96 consecutive patients at 12 h after admission and 3 months at <12 h after admission and at 3 months after discharge by measuring the brachial artery dilatation after 5 min of forearm ischemia flow-mediated dilation (FMD). OMT achievement was defined as systolic blood pressure of ≤130 mm Hg, low-density lipoprotein cholesterol of ≤100 mg/dl, and hemoglobin A1c level of ≤7.0%. The primary endpoint was the incidence of composite major adverse cardiac or cerebrovascular events (MACCE) at 36 months.
Results: Forty-nine (51%) patients achieved all three risk factor targets at 3 months. Although baseline FMD values did not differ between the OMT achievement and non-achievement groups, the 3-month FMD significantly improved in the OMT achievement group (6.6±3.5 vs. 5.2±2.9, p=0.03). Patients with improved FMD at 3 months had a lower rate of 36-month MACCE than those with persistently impaired FMD. A multiple Cox hazards analysis showed that OMT was a protective predictor of MACCE (hazard ratio, 0.19; 95% confidence interval, 0.04–0.88, p=0.03).
Conclusion: This study demonstrated a significant association between the serial measurement of endothelial function with OMT and the clinical outcome in patients after PCI.

Objective: Failure to select the optimal left ventricular (LV) segment for lead implantation is one of the most important causes of unresponsiveness to the cardiac resynchronization therapy (CRT). In our study, we aimed to investigate the echocardiographic and clinical benefits of LV lead implantation guided by an intraoperative 12-lead surface electrocardiogram (ECG) in patients with multiple target veins.
Methods: We included 80 [42 (62.5%) male] heart failure patients who successfully underwent CRT defibrillator (CRT-D) implantation. Patients were divided into two groups. In group 1, LV lead was positioned at the site with the shortest biventricular-paced (BiV-paced) QRS duration (QRSd), as intraprocedurally measured using surface ECG. In group 2 (control), we included patients who underwent the standard unguided CRT. ECG, echocardiogram, and functional status were evaluated before and 6 months after CRT implantation in all patients.
Results: In group 1, BiV-paced QRSd measurements were successfully performed in 112 of 120 coronary sinus branches during CRT and an LV lead was successfully placed at the optimal site in all patients. Compared with group 2, group 1 had a significantly higher rate (85% vs. 50%, p=0.02) of response (>15% reduction in LV end-systolic volume) to CRT as well as a shorter QRSd (p<0.001) and a greater QRS shortening (∆QRS) associated with CRT compared with baseline (p<0.001). The mean New York Heart Association functional class was significantly improved in both groups, and no significant differences were found in clinical response to CRT (85% vs. 70%, p=0.181).
Conclusion: Surface ECG can be used to guide LV lead placement in patients with multiple target veins for improving response to CRT. Thus, it is a safe, feasible, and economic approach for CRT-D implantation.

Objective: Although differentially expressed circRNAs have been proposed to be closely associated with epithelial-mesenchymal transition (EMT), the roles of circRNAs remain unclear in endothelial-to-mesenchymal transition (EndMT), which is a subcategory of EMT. Herein, we characterized the expression and potential function of circRNAs during TGF-β1-induced EndMT in rat coronary artery endothelial cells (CAEC).
Methods: High-throughput RNA sequencing was performed for unbiasedly profiling the expression of circRNAs. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) biological pathway analysis were performed using online forecasting databases. Real-time quantitative polymerase chain reaction (RT-qPCR) was used for confirming the circRNA expression obtained from the sequencing data.
Results: Among the candidated circRNAs, 102 circRNAs were differentially expressed, among which 66 circRNAs and 36 circRNAs were up-regulated and down-regulated, respectively, in TGF-β1-treated rat CAEC. GO analysis findings revealed that numerous differentially expressed circRNAs were closely associated with the biological process. KEGG signaling pathway analysis suggested that the abnormal expression of circRNAs had been implicated in regulating the dynamics endothelial cell junctions. Furthermore, we also found that three EndMT-related circRNAs, chr5: 90817794|90827570, chr8: 71336875|71337745, and chr6: 22033342|22038870, were significantly up-regulated in TGF-β1-treated rat CAEC.
Conclusion: The findings of this study reveal a comprehensive expression and potential functions of differentially expressed circRNAs during TGF-β1-induced EndMT. These findings provide mechanistic insights into the role of circRNAs in EndMT-related cardiovascular diseases (CVDs).

Objective: Infective endocarditis is usually caused by Streptococcus sanguinis and characterized by inflammatory responses in the endocardium. This study aimed to investigate if the new compound (3R)-5,6,7-trihydroxy-3-isopropyl-3-methylisochroman-1-one (TIM) isolated from Alpinia katsumadai Hayata could provide protection against lipoteichoic acid (LTA)-induced cell damage in embryonic rat heart cells (H9c2).
Methods: LTA-induced cell damage was established in H9c2, and the protective effects of TIM against the cell damage were examined at different concentrations (0.1–2.5 μM). The inflammatory response and oxidative stress in H9c2 cells were also measured.
Results: Treatment with TIM (0.1–2.5 μM) significantly decreased LTA-induced toxicity in H9c2 cells, which was indicated by increase in cell viability, elevation in the mitochondrial membrane potential, decrease in the release of cytochrome-c and DNA damage, inhibition of caspase-3/9 activities, and change in apoptosis-related protein expression in LTA-treated H9c2 cells. TIM treatment also significantly attenuated the redox imbalance in H9c2 cells by decreasing malondialdehyde and intracellular reactive oxygen species levels as well as by enhancing superoxide dismutase activities and glutathione levels by increasing nuclear factor (erythroid-derived 2)-like 2 protein expression. Moreover, TIM treatment decreased interleukin 1 β, interleukin 12, and tumor necrosis factor α levels by inhibiting nuclear factor kappa B protein expression.
Conclusion: Our data indicated that TIM protected H9c2 cells against LTA-induced toxicity, at least partially through inhibiting the inflammatory response and oxidative stress, providing scientific rational to develop TIM to treat infective endocarditis.

Objective: Heart failure (HF) is a clinical syndrome resulting from structural or functional damages. Although clinical trials have shown that the plasma renin–angiotensin system (RAS) activation decreases HF functional status and increases hospitalization for HF patients, the effect of intrarenal RAS activity is still unknown. In this study, we investigated the relationship between the New York Heart Association (NYHA) class, duration, and number of hospitalizations in the previous year and urinary angiotensinogen (UAGT) in patients with HF with reduced ejection fraction (HFrEF).
Methods: This study included 85 patients who had an ejection fraction of <40% and were receiving optimal medical treatment. Among these, 22 were excluded from the study for various reasons. Demographically and biochemically, the remaining 63 patients were compared according to the NYHA functional classes and re-hospitalization status.
Results: When the groups were compared in terms of N-terminal pro–B-type natriuretic peptide (NT-proBNP), UAGT, and high-sensitivity C-reactive protein (Hs-CRP), it was found that these parameters were significantly higher in patients who were hospitalized more than two times in the previous year [p<0.001; p=0.007; p<0.001, respectively]. There was a significant correlation between number of hospitalizations and NT-proBNP (r=0.507, p<0.001), Hs-CRP (r=0.511, p<0.001), hemoglobin (r=0.419, p=0.001), serum sodium (r=0.26, p=0.04), and systolic blood pressure (r=0.283, p=0.02). When the independence of multiple correlations was assessed using multiple linear regression analysis, NT-proBNP, Hs-CRP, and hemoglobin levels were independent predictors of re-hospitalization, but this was not the same for UAGT.
Conclusion: Although UAGT levels are high in patients with poor NYHA functional class and repeated hospitalizations, this marker is not valuable for predicting repeated hospitalization in patients with HFrEF.

Objective: Cisplatin (CDDP) has been known to be an effective antineoplastic drug; however, it has a cardiotoxic effect. Curcumin (CMN) and beta-carotene (BC) have been suggested to protect biological systems against CDDP-induced damage. The current study was conducted to evaluate the possible protective roles of CMN and BC on CDDP-induced cardiotoxicity in rat cardiac tissues.
Methods: A total of 49 adult female Wistar albino rats were equally divided into seven groups as follows: control (no medication), sesame oil (1 mg/kg), CDDP (single dose injection two times as once a week, 5 mg/kg/week), BC (100 mg/kg), CDDP+BC (pretreated BC for 30 min before CDDP injection), CMN (200 mg/kg), and CDDP+CMN (pretreated CMN for 30 min before CDDP injection). These treatments were applied intraperitoneally for CDDP and with gavage for CMN and BC. The oxidative/antioxidant indicators, inflammatory cytokines, and histopathological alterations were examined.
Results: These alterations included a marked increase in malondialdehyde (MDA) level, significant decrease in catalase (CAT) and superoxide dismutase (SOD) activities, and significant elevation of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, interleukin (IL)-6 in the CDDP group compared with the other groups. Histopathologically, CDDP-induced severe myocardial degenerative changes were observed. However, the CDDP-induced disturbances in the above-mentioned parameters significantly improved by treatment with BC and particularly CMN.
Conclusion: This study indicated that CDDP treatment markedly caused cardiotoxicity; however, treatment with CMN or BC ameliorated this cardiotoxicity in rats. Furthermore, these findings revealed that treatment with CMN has a higher cardioprotective effect than that with BC against CDDP-induced cardiotoxicity in rat cardiac tissues.

In this paper, we reviewed the atrial fibrillation screening strategies in a stepwise manner and discussed the uncertainties in the assessment of the need for anticoagulation in light of the recently published European Heart Rhythm Association consensus document. We reviewed not only the methods and tools but also the role of health care professionals and patient organizations in addition to cost-effectiveness issues.