Diabetes mellitus (DM) is a pandemic disease and an important cardiovascular (CV) risk factor. The atherogenic dyslipidemia in diabetes (ADD) is characterized by high serum triglycerides, high small dense LDL levels, low HDL levels and postprandial lipemia. Insulin resistance is a primary cause for ADD. Though statins are highly effective for CVD prevention in DM but a significant residual CV risk remains even after optimal statin therapy. Fibrates, niacin and omega-3 fatty acids are used in addition to statin for treatment of ADD (specifically hypertriglyceridemia). All these drugs have some limitations and they are far from being ideal companions of statins. Many newer drugs are in pipeline for management of ADD. Dual PPAR α/γ agonists are in most advanced stage of clinical development and they have a rational approach as they control blood glucose levels (by reducing insulin resistance, a primary factor for ADD) in addition to modulating ADD. Availability of dual PPAR α/γ agnosits and other drugs for ADD management may improve CV outcomes and decrease morbidity and mortality in diabetic patients in future.

Dyslipidemia is the most common modifiable risk factor for atherosclerotic cardiovascular disease (ASCVD). There is unequivocal evidence that Low Density Lipoprotein Cholesterol (LDL-C) is the main culprit. Statins, ezetimibe, bempedoic acid and Proprotein Convertase Subtilisin/ Kexin Type 9 (PCSK9) inhibitors are used to target LDL-C. Statin is always utilized as the first line therapy and they decrease LDL-C by approximately 1 mmol/l (40 mg/dL). If the LDL goals are not achieved ezetimibe is used and this decreases LDL-C by 15-20%. Bempedoic acid can also be utilized to lower LDL-C before initiating PCSK9 inhibitors but this is not available in India as yet. PCSK9 inhibitors decrease LDL-C by 1 to 1.5 mmol/l (40-60 mg/dL) on top of all lipid lowering therapy and with this very low LDL-C level targets of < 55 or even < 40 mg/dL can be achieved in very high risk patient. After the LDL-C goal is achieved, non HDL-C is targeted if the triglycerides (TG) levels are above 200 mg/dL. Targeting HDL-C with drugs is not recommended because all trials of HDL-C elevating drugs on top of statins have been negative. The role of TG has a causal factor for ASCVD is still in the process of evolution. Icospent ethyl in REDUCE IT trial has shown reduction in ischemic cardiovascular events in patients with established CVD or diabetics with other risk factors on statins and elevated TG between 135-499 mg/dL. but the mechanism of benefit does not seem to be related to lowering of TG because the benefit was similar in subgroup of patients with TG > 150 <150 mg/dL. Inclisiran which blocks the synthesis of PCSK9 is emerging as very exciting molecule for the future. It decreases LDL-C by 50% which remains there for six months after a single injection of 300 mg.

Background Off-pump Coronary Artery Bypass Grafting (OPCAB) reduces the complications related to use of cardiopulmonary bypass. However the effects of using aortic side clamp during OPCAB is not eliminated if any graft is anastamosed to aorta. We describe here a simple technique of OPCAB using in-situ bilateral Internal Mammary Artery (IMA) as the only source of blood supply to the coronary grafts. Methods Every patient underwent preoperative assessment of bilateral subclavian artery. In our technique, one IMA was used to graft Left Anterior Descending Artery (LAD) and its branches. Other IMA was used to create a composite graft with Radial Artery (RA). This composite graft was used to revascularize the remaining coronary arteries. Results Out of 194 consecutive OPCABs performed, this technique of bilateral IMA was used in 138 patients. Conclusion The patency and efficacy of in-situ IMA graft for Coronary Artery Bypass Grafting (CABG) is well documented. Our simple technique using bilateral in situ IMA provides dual inflow and can be used in every possible coronary anatomy.

Fibrosis in myocardium [1]This predisposes the individual to heart failure [2] with preserved ejection fraction and also predisposes to ventricular arrhythmias [3] which may culminate in sudden cardiac death. AbstractThe guidelines for hypertension provide all information regarding day-to-day management of hypertension. However, there are several issues such as mortality in a controlled hypertensive, fibrosis in cardiovascular system, vascular age, and target heterogeneity in response to decrease blood pressure which also require attention as they are clinically relevant. R e v i e w A r t i c l e

Dyslipidemia is the most common modifiable risk factor for atherosclerotic cardiovascular disease (ASCVD). There is unequivocal evidence that Low Density Lipoprotein Cholesterol (LDL-C) is the main culprit. Statins, ezetimibe, bempedoic acid and Proprotein Convertase Subtilisin/ Kexin Type 9 (PCSK9) inhibitors are used to target LDL-C. Statin is always utilized as the first line therapy and they decrease LDL-C by approximately 1 mmol/l (40 mg/dL). If the LDL goals are not achieved ezetimibe is used and this decreases LDL-C by 15-20%. Bempedoic acid can also be utilized to lower LDL-C before initiating PCSK9 inhibitors but this is not available in India as yet. PCSK9 inhibitors decrease LDL-C by 1 to 1.5 mmol/l (40-60 mg/dL) on top of all lipid lowering therapy and with this very low LDL-C level targets of < 55 or even < 40 mg/dL can be achieved in very high risk patient. After the LDL-C goal is achieved, non HDL-C is targeted if the triglycerides (TG) levels are above 200 mg/dL. Targeting HDL-C with drugs is not recommended because all trials of HDL-C elevating drugs on top of statins have been negative. The role of TG has a causal factor for ASCVD is still in the process of evolution. Icospent ethyl in REDUCE IT trial has shown reduction in ischemic cardiovascular events in patients with established CVD or diabetics with other risk factors on statins and elevated TG between 135-499 mg/dL. but the mechanism of benefit does not seem to be related to lowering of TG because the benefit was similar in subgroup of patients with TG > 150 <150 mg/dL. Inclisiran which blocks the synthesis of PCSK9 is emerging as very exciting molecule for the future. It decreases LDL-C by 50% which remains there for six months after a single injection of 300 mg.