An 85-year-old gentleman presented with chest pain and sustained ventricular tachycardia and underwent emergency Percutaneous Coronary Intervention (PCI) of his right coronary artery using drug eluting stents.

A staged PCI was planned for the Left Anterior Descending Artery (LAD) three days later. The patient was known to have atrial fibrillation for many years and we planned to occlude the Left Atrial Appendage (LAA) in the same sitting in order to avoid long-term triple therapy.

This study has been designed to investigate the role of phosphatidylinositidyl-3-kinase gamma (PI3Kγ) in Mono Cro Taline (MCT)-and nicotine-induced endothelial dysfunction in pulmonary arteries. MCT (60 mg/ kg, s.c, once in 4 weeks) and nicotine (2 mg/kg, i.p, regularly) were administered in respective groups to produce pulmonary vascular endothelium dysfunction. Vascular endothelial dysfunction was assessed in terms of attenuation of acetylcholine-induced endothelium-dependent relaxation, sodium nitroprusside-induced endothelium-independent vasorelaxation (Isolated pulmonary artery ring preparation), decrease in serum nitrate/ nitrite level, mRNA expression of eNOS (rtPCR) and increased oxidative stress (superoxide anions and TBARS level), mean arterial blood pressure and right ventricular hypertrophy. PI3Kγ inhibitor CAY10505 (0.6 mg/kg, p.o) [(5-[5-4-fluorophenyl)-2-furanyl]-2, 4-thiazolidinedione] and atorvastatin (30 mg/kg, p.o, positive control) treatment for 7 days (21st-28th day) significantly improved, mean arterial blood pressure and right ventricular hypertrophy in both nicotine and Mono Cro Taline-induced pulmonary vascular endothelial dysfunction. Therefore, it may be concluded that CAY10505, a specific inhibitor of PI3Kγ up regulates eNOS expression and nitric oxide production to improve Mono Cro Taline and nicotine-induced pulmonary vascular endothelial dysfunction.

Lymphedema, a condition which typically affects the extremities, is characterized by accumulation of protein-rich fluid in the soft tissues due to malfunction of the lymphatic system. The normal role of the lymphatic system is to passively convey and actively pump interstitial fluid back into the blood stream. Primary (congenital) lymphedema arises from poorly understood factors, while secondary lymphedema is caused by another known disease. Most often, upper extremity secondary lymphedema is the result of breast cancer, with an incidence of 15-20% among female breast-cancer patients who have undergone a mastectomy or radiation as part of therapy [1]. It has been estimated that primary lymphedema affects 1.15 out of 100,000 children in North America [2].

Lymphedema, a condition which typically affects the extremities, is characterized by accumulation of protein-rich fluid in the soft tissues due to malfunction of the lymphatic system. The normal role of the lymphatic system is to passively convey and actively pump interstitial fluid back into the blood stream. Primary (congenital) lymphedema arises from poorly understood factors, while secondary lymphedema is caused by another known disease. Most often, upper extremity secondary lymphedema is the result of breast cancer, with an incidence of 15-20% among female breast-cancer patients who have undergone a mastectomy or radiation as part of therapy [1]. It has been estimated that primary lymphedema affects 1.15 out of 100,000 children in North America [2].

Arrhythmogenic Right Ventricular Cardiomyopathy/dysplasia (ARVC) is a genetic form of cardiomyopathy affecting primarily the Right Ventricle (RV) but also may involves the Left Ventricle (LV) and may culminate in life-threatening ventricular arrhythmias, Sudden Cardiac Death (SCD) and/or heart failure. In most cases it is transmitted with an autosomal dominant pattern of inheritance, with incomplete penetrance and variable expression, but there are also some rare autosomal recessive forms as Naxos disease and Carvajal syndrome.

The term “cardiomyopathy” should be preferred to “dysplasia”, as already suggested by WHO/ International Society and Federation of Cardiology in 1996 and Maron, about classification of cardiomyopathy in 2006 [1,2].