Irsad Andi Arso

Diagnostic Performance Addition of Abnormal P Wave Dispersion on Moderate Risk Duke Treadmill Score Criteria in Detecting Severe Stenosis of Coronary Arteries in Stable Angina Pectoris Patients

Background: Moderate risk Duke treadmill score (DTS) in threadmill test (TMT), needs additional diagnostic tool to increase its sensitivity of detecting severe coronary artery stenosis in patients with stable angina pectoris. A P wave dispersion (PWD) during TMT currently has a significant relationship with DTS value and can increase the sensitivity in identifying an ischemia. This study aimed to investigate whether the addition of PWD in moderate risk DTS can improve the prediction of the severity of coronary artery stenosis in patients with stable angina pectoris. Methods: This study is a diagnostic test with cross-sectional design. The subjects were patients who had undergone TMT and coronary angiography at the Dr. Sardjito General Hospital Yogyakarta. The outcomes were sensitivity and specifi city of abnormal PWD in moderate risk DTS patients for predicting the severe stenosis in those with stable angina pectoris as compared with moderate risk DTS and normal PWD. Results: The additional of PWD at moderate risk DTS on 64 subjects had a sensitivity of 86.7%, a specifi city of 44.1%, a positive predictive value of 57.8%, a negative predictive value of 79.0%, a positive likelihood ratio of 1.6, a negative likelihood ratio of 0.3 and a prevalence of 46.9%, with a prediction accuracy of 64.1%. Conclusion: The additional of abnormal PWD in moderate risk DTS had a sensitivity of 86.7% and a specificity of 44.1% for severe coronary artery stenosis in patients with angina pectoris. Keywords: P wave dispersion, moderate risk Duke treadmill score, severe coronary stenosis.

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.