Further insights into cardiovascular outcomes in diabetic and non-diabetic states: inhibition of sodium-glucose co-transports Cardiovascular diseases are the leading cause of morbidity and mortality in the world. Diabetes increase heart disease related to death by two- to four-fold. SGLT2 inhibitors are new antidiabetic agents. The growing evidence of cardiovascular benefit of SGLT2 inhibitors independent of their effects on glycemic control is especially intriguing. Several clinical trials have shown that sotagliflozin (SGLT1-1/2 inhibitor) decreases body weight and reduces blood pressure in adults with T2D. A phase 3 study designed to evaluate cardiovascular outcomes of sotagliflozin is currently ongoing. Many pre-clinical studies were conducted to investigate the potential mechanisms involved in cardiovascular benefits of SGLT1 or SGLT2 inhibition with or without diabetes. Although multiple mechanisms have been proposed, there are still not enough data to fully support the mechanisms of actions. This review aims to discuss the potential mechanisms involved in cardiovascular benefits of SGLT1 and SGLT2 inhibition in both diabetic and non-diabetic states.

Cardioprotective diabetes drugs: what cardiologists need to know In patients with diabetes, where cardiovascular morbidity is highly prevalent, recent cardiovascular outcomes trials have identified therapies in the modern glucagon-like peptide 1 receptor agonist (GLP-1RA) and sodium-glucose cotransporter 2 inhibitor (SGLT2i) classes that significantly reduce cardiovascular events. A number of drugs in both classes have demonstrated reductions in the risk of the composite outcome of major adverse cardiovascular events (myocardial infarction, stroke, and cardiovascular death). In addition, SGLT2i drugs have a substantial impact on hospitalization for heart failure. Because GLP-1RA and SGLT2i are effective in reducing cardiovascular events, independent of their effects on blood glucose, cardiologists should be familiar with how to use them. This review outlines the evidence of cardiovascular benefit for current GLP-1RA and SGLT2i drugs, practical information for prescribing them, and putative mechanisms, so that these therapies can be incorporated along with antihypertensives, statins, and antiplatelet therapies into the routine care of patients.

Estimation of apolipoprotein A in early onset ST-segment elevation myocardial infarction Aims The role of apolipoprotein A in early onset ST-segment elevation myocardial infarction is not clear. This study sought to assess the apolipoprotein A in cohort of patients diagnosed with early onset acute ST-segment elevation myocardial infarction and to corelate it with major traditional cardiovascular risk factors. Methods A total of 50 such patients and 40 age and sex-matched healthy controls, both aged less than 50 years with their baseline demographic, clinical characteristics and cardiovascular risk factors were studied. Apolipoprotein A was estimated for all enrollees. Results The mean age of cases was 43.37 ± 5.85 years. The levels of apolipoprotein A among cases were not significantly lower compared to controls (P = 0.52). They were lower among the male, current smokers and the dyslipidemia (P’s < 0.05). Considering the apolipoprotein A as the dependent factor, the early onset ST-segment elevation myocardial infarction was associated significantly with the male and the dyslipidemia in linear regression (P < 0.001 and 0.030), respectively. Conclusion Lower levels of apolipoprotein A are significantly related to conventional risk factors in early onset ST-segment elevation myocardial infarction. This apolipoprotein A that particularly develops in young patients with clustering of traditional cardiovascular risk factors should be targeted. Further studies are warranted to determine the diagnostic and prognostic indicators of this apolipoprotein in ST-segment elevation myocardial infarction.

The comparison of the relationships about the presence of branch retinal vein occlusion and endothelial functions between diabetic and non-diabetic patients Objectives The aim of this study was to investigate the endothelial functions in both patients with diabetics and non-diabetics with branch retinal vein occlusion by using pulse wave analysis and flow-mediated dilatation methods. Patients and methods This cross-sectional study included a total of 136 participants (47 diabetic patients with branch retinal vein occlusion, 43 non-diabetic patients with branch retinal vein occlusion, and 46 otherwise healthy subjects). Evaluation of endothelial functions was performed by flow-mediated dilatation and pulse wave analysis methods. Stiffness index, reflection index (RI), and pulse propagation time were calculated. Results The mean stiffness index and RI were significantly higher in the diabetic branch retinal vein occlusion group compared with the non-diabetic branch retinal vein occlusion and the healthy controls (for stiffness index: 11.5 ± 2.8 vs. 10.1 ± 2.5 and 8.3 ± 2.0, P < 0.001; and for RI: 75.1 ± 11.7 vs. 65.4 ± 8.4 and 60.2 ± 18.8, P < 0.001, respectively), whereas the pulse propagation time was significantly lower in the diabetic group (156.4 ± 32.3 vs. 174.4 ± 46.5 and 205.0 ± 58.5, P < 0.001, respectively). There was a significant negative correlation between visual acuity and stiffness index (r = −0.512, P < 0.001). Besides, there was also a significant positive correlation between visual acuity and pulse propagation time (r = 0.398, P < 0.001). Conclusion This study demonstrated that the stiffness index and RI values were higher in patients with branch retinal vein occlusion compared to the healthy subjects.

Left ventricular mass index and subendocardial myocardial function in children with chronic kidney disease, a transmural strain and three-dimensional echocardiographic study Introduction Left ventricular hypertrophy (LVH) is the commonest myocardial response to chronic kidney disease (CKD); this response has been regarded detrimental as it impairs the blood flow to the deepest layers of the myocardium causing progressive myocardial dysfunction. The aim of these series is to assess the determinants of LVH in CKD patients and its impact on subendocardial function in such patients. Methods This study has been conducted on 40 CKD patients (Group 1) and 40 age-matched controls, both groups were assessed by transmural echocardiography to determine the subepicardial and subendocardial global longitudinal strain (GLS) as an expression of the systolic function of each of those layers. LVH was assessed by calculation of left ventricle mass index (LVMI). Both groups underwent ambulatory blood pressure monitoring. Group 1 was assessed as regards lipid profile and insulin resistance by homeostasis model assessment of insulin resistance (HOMA-IR). Results HOMA-IR proved to be a more important determinant of LV hypertrophy than SBP and DBP with a P of 0.01. Moreover subendocardial GLS was negatively correlated with LVMI with r = 0.69 and P < 0.01 denoting the negative effect. LVH plays on subendocardial function probably by impairing myocardial perfusion. Conclusion This study points toward the importance of insulin resistance in aggravation of myocardial remodeling in CKD patients; more studies are warranted to examine the role of insulin Sensitizers in reversing such remodeling and restoring subendocardial function in such important systemic disorder.

Ventricular fibrillation associated with Graves' disease and amiodarone induced thyrotoxicosis This case involves a 55-year-old male patient with systolic heart failure and refractory atrial fibrillation due to thyrotoxicosis, who was electrically cardioverted but then developed torsade de pointes and ventricular fibrillation. Rate control was unsuccessful with digoxin, cardizem, labetalol, esmolol and amiodorone. Patient was externally cardioverted after which ECGs showed prolonged QT with frequent premature ventricular contractions. ECGs also showed ‘R-on-T' phenomenon leading to torsades and ventricular fibrillation. Atrial overdrive pacing was used to terminate the dangerous arrhythmia and the patient returned to sinus rhythm. Interestingly, he was found to have new onset thyrotoxicosis and started on methimazole.