Transcatheter aortic valve replacement (TAVR) is a transformative technology that has changed the management of patients with severe, symptomatic aortic stenosis. The use of TAVR in intermediate- to high-risk patients has been validated in several rigorously performed, randomized clinical trials. Recent studies using newer generation devices have demonstrated the noninferiority of TAVR as compared with surgical aortic valve replacement in low-risk patients, supporting the increased utilization and expansion of TAVR. The use of TAVR in low-risk patients has important implications and requires a multifaceted approach that includes a highly functional multidisciplinary heart team for careful patient selection; a need to understand and help mitigate certain key complications, such as stroke, paravalvular regurgitation, and conduction disturbances; careful data collection for continual outcome assessment and improvement; and the necessary expertize and procedural volume to maintain excellent outcomes and ensure optimal clinical care pathways.

Non-vitamin K antagonist oral anticoagulants (NOACs), or direct oral anticoagulants have not been tested in randomized trials conducted in patients with atrial fibrillation (AF), who had malignant disease. However, their use in cancer patients increases and real-life evidence for their effectiveness and safety in this vulnerable subset of patients is growing. The challenges of the use of NOACs in cancer patients with AF and the current expert opinions on this subject have been summarized in this review article.

Amaç: İskemik ardkoşullanma (PostC)’nın koruyucu etkileri yaş ve kronik kalp hastalıklarıyla ile birlikte azalır/ortadan kalkar. Benzer şekilde, aynı risk gruplarında düşük serum melatonin düzeyleri de bildirilmiştir. Bu çalışmanın amacı, iskemi-reperfüzyon (I/R) hasarında PostC'nin koruyuculuğunda melatoninin etkilerini araştırmaktır.
Metod: Sıçanlar, I/R çalışmalarından 2 ay önce pinealektomize (Px) veya sham (non-Px) ikiye ayrıldı. Sol ana koroner artere 30 dakika iskemi ve 120 dakika reperfüzyon uygulandı. PostC, iskemiden sonra 3 siklus R/I (her biri 10 s) ile indüklendi.
Bulgular: İnfarkt alanı Px sıçanlarda (54,68 ± 1,5%) kontrol grubundan (35,1 ± 2,5%) anlamlı olarak yüksek bulundu. Non-Px sıçanlarda PostC ve melatonin uygulamaları infarkt alanını anlamlı azalttı. Öte yandan, Px sıçanlarda PostC anlamlı bir etki oluşturmazken, melatonin ile birlikte uygulandığında koruma görüldü. UCP3 seviyeleri I/R ve Px ile azaldı, PostC ve melatonin ile arttı.
Sonuç: Melatoninin fizyolojik ve farmakolojik konsantrasyonlarının PostC’nin koruyuculuğunda rolü olabilir. Yaşlanma ve kalp hastalıkları gibi fizyolojik melatoninin azaldığı durumlarda koruyuculuk azalabilir ve melatonin replasmanı bu etkiyi geri getirebilir. PostC ve melatonin; UCP3, irisin ve NFkB seviyelerini etkileyerek enerji metabolizmasını ve enflamatuar mediatörleri düzenleyebilir ve mitokondriyi koruyabilir.

Objective: Protective effects of ischemic postconditioning (PostC) decrease/disappear with age and chronic heart diseases. Similarly, low serum melatonin levels have been reported in the same risk groups. The aims of this study were to investigate the effects of melatonin on the protection of PostC in ischemia–reperfusion (I/R)-induced infarct size and roles of uncoupling protein (UCP) 3, irisin, and nuclear factor kappa B (NFkB) levels.
Methods: Rats were pinealectomized (Px) or sham operated (non-Px) 2 months before the I/R studies. The left main coronary artery was occluded for 30 min followed by 120 min reperfusion. PostC was induced with three cycles of R/I (10 s each) after ischemia.
Results: The infarct size was found to be significantly higher in Px rats (54.68±1.5%) than in the control group (35.1±2.5%). PostC and melatonin administrations to non-Px rats significantly reduced the infarct size. On the other hand, PostC did not create a significant effect in Px rats, but protection was provided when PostC was co-administrated with melatonin. While significant decreases were detected in the UCP3 levels, irisin and NFkB levels increased with I/R and Px. Treatment with PostC and melatonin in non-Px groups and their co-administration in Px groups were found to return all the genes close to normal levels.
Conclusion: The physiological and pharmacological concentrations of melatonin may play a role in the protection of PostC. In cases when physiological melatonin is reduced, such as aging and heart diseases, this protection may decrease, and this effect may be restored by melatonin replacement. PostC and melatonin may regulate energy metabolism and inflammatory mediators and protect mitochondria by affecting the UCP3, irisin, and NFkB levels.

Objective: Diabetes mellitus (DM) is a risk factor for developing in-stent restenosis (ISR) following percutaneous coronary intervention (PCI). This study aimed to examine the presentation and outcomes of drug-eluting stent (DES) ISR in diabetics.
Methods: This retrospective study included consecutive patients with clinical DES-ISR, who were hospitalized between January 2013 and December 2017 and who were grouped based on the presence or absence of DM. Clinical, angiographic features and 1-year outcomes [composite of death, myocardial infarction (MI), and repeat-target lesion revascularization] were compared.
Results: Baseline characteristics of the DM group (n=109) were comparable to the non-DM group (n=82), except for the higher prevalence of hypertension and dyslipidemia in the former (60.6% vs. 46.3%, p=0.050; 74.4% vs. 57.8%, p=0.034, respectively). Clinical presentation was similar in both groups [acute coronary syndrome (ACS): 62.4% vs. 61%, p=0.843; MI: 34.9% vs. 34.1%, p=0.918). Diabetics had a higher prevalence of stent-edge restenosis (20.3% vs. 9.2%, p=0.019). The treatment strategy was similar in both groups with 52.3% in the DM group and 57.3% in the non-DM group undergoing PCI (p=0.513). One-year outcomes of the DM group were not different from those of the non-DM group (14.7% vs. 17.1%, p=0.683). Age [hazard ratio (HR), 1.05; 95% confidence interval (CI), 1.01–1.10; p=0.017], MI presentation (HR, 2.34; 95% CI, 1.14–4.80; p=0.020), and chronic kidney disease (CKD: HR, 2.82; 95% CI, 1.21–6.58; p=0.016) were predictors of poor outcomes.
Conclusion: Stent-edge restenosis is more common in diabetics. Clinical presentation and 1-year outcomes following DES-ISR are similar in diabetics and non-diabetics. Age, MI presentation, CKD, and not DM were predictors of poor outcomes following DES-ISR.

Objective: The present study aims to investigate the effect of losartan, an selective angiotensin II type 1 receptor (AT1R) blocker, on both the increase of IKs current and shortening of action potential duration (APD) induced by stretch of atrial myocytes, and to uncover the mechanism underlying the treatment of fibrillation (AF) by AT1R blockers.
Methods: Hyposmotic solution (Hypo-S) was applied in the guinea pig atrial myocytes to simulate cell stretch, then patch-clamp technique was applied to record the IKs and APD in atrial myocytes.
Results: Hypo-S increased the IKs by 105.6%, while Hypo-S+1-20 μM of losartan only increased the IKs by 70.3-75.5% (p<0.05 vs. Hypo-S). Meanwhile, Hypo-S shortened APD90 by 20.2%, while Hypo-S+1-20 μM of losartan shortened APD90 by 13.03-14.56% (p<0.05 vs. Hypo-S).
Conclusion: The above data indicate that the effect of losartan on the electrophysiological changes induced by stretch of atrial myocytes is associated with blocking of AT1 receptor, and is beneficial for the treatment of AF that is often accompanied by the expansion of atrial myocytes and the increase of effective refractory period.

Objective: Using three-dimensional speckle-tracking echocardiography (3D-STE), we aimed to evaluate left ventricular (LV) function in type 2 diabetes mellitus (T2DM) patients with non-alcoholic fatty liver disease (NAFLD).
Methods: In total, 97 T2DM patients were categorized into three groups based on hepatic ultrasonography: group A (those without NAFLD, n=30), group B (those with mild NAFLD, n=32), and group C (those with moderate-to-severe NAFLD, n=35). Our conventional echocardiographic parameters included transmitral peak early and late diastolic velocity (E and A), septal and lateral early (e’) mitral annular diastolic tissue velocities, and left atrial maximum volume index (LAVImax). LV end-diastolic and -systolic volume, LV mass index (LVMI), and LV ejection fraction were measured using real-time three-dimensional echocardiography. The 3D-STE parameters included LV global radial strain (GRS), global longitudinal strain (GLS), global area strain (GAS), and global circumferential strain (GCS).
Results: Our results showed that in group C, GCS, GRS, GLS, GAS, and septal and lateral e’ velocity decreased, whereas average E/e’ and LAVImax increased compared to groups B and A (p<0.05). Multiple linear regression analysis showed that NAFLD is independently associated with 3D-STE parameters, and glycosylated hemoglobin also has negative impacts on all LV 3D strains.
Conclusion: When combined with conventional echocardiography, 3D-STE can assess LV function effectively in T2DM patients with NAFLD. Additionally, the severity of LV dysfunction in the moderate-to-severe NAFLD group (group C) was worse than the mild and absent NAFLD groups (groups A and B).