Lucia Kris Dinarti

Persistent left superior vena cava in atrial septal defect sinus venosus type: diagnosis with saline contrast echocardiography—a case series

Persistent Left Superior Vena Cava (PLSVC) should be suspected if we find dilatation of coronary sinus. Sophisticated imaging is not always available in each health care provider. Transthoracic echocardiography (TTE) with agitated saline injections through the left and right antecubital veins provides a simple, and inexpensive, but effective study for a rapid bedside diagnosis of PSLVC.

Right-sided infective endocarditis in patients with uncorrected ventricular septal defect and patent ductus arteriosus: Two case reports

Uncorrected left‐to‐right shunt congenital heart defect is a predisposing factor for infective endocarditis (IE), especially right‐sided IE which has different clinical manifestations and complications from left‐sided IE. Prompt diagnosis by means of transthoracic echocardiography and timely antibiotics management for IE are encouraged to prevent multiorgan failure and fatal pulmonary embolism.

Large Atrial Septal Defect Closure in a Patient with Severe Pulmonary Arterial Hypertension

Patients with an atrial septal defect (ASD) and severe pulmonary arterial hypertension (PAH) are considered ineligible for defect closure surgery because of the risk of right ventricular decompensation and death after the operation. We report the case of a patient with large ASD and severe PAH who was able to undergo defect closure surgery successfully following long-term use of combined oral sildenafil and beraprost.

Plaque, Platelets, and Plug – The Pathogenesis of Acute Coronary Syndrome

Acute coronary syndrome is a clinical condition of partial or total obstruction of blood flow in the coronary artery due to acute thrombus formation. Culprit vessel, coronary artery segment within which the site of origin of thrombus formation lies, is occupied by eroded or ruptured atherosclerotic plaque. Direct contact between circulating blood constituent and atherosclerotic plaque content owing to loss of endothelial cell barrier orchestrates the haemostasis events, i.e. thrombus formation and coagulation activation. Evolved within years of human life span, atherosclerotic undergoes three main steps: initiation, progression and finally complication (Libby, 2002). Atherosclerotic plaque development involves cellular and molecular interactions as well as blood flow dynamic alterations in the affected area. Although these steps affect all individual, some gather the risk factors to develop progression and complication of coronary atherosclerotic lesion faster and more prominent than others. Given the dynamic nature of these steps, understanding several mechanisms engage in every step will provide insight into therapeutic approach. Here, we review the last two steps of coronary atherosclerotic plaque development, with the focus in the role of platelets, anucleated cells being the target for therapeutic advancement in atherosclerosis and acute coronary syndrome.