Dyah Wulan Anggrahini

Circulating soluble CD40 ligand mediates the interaction between neutrophils and platelets in acute coronary syndrome

Following plaque rupture, activated platelet will induce subsequent inflammatory process including neutrophil recruitment. In vitro study demonstrated an interaction between neutrophils and platelets via a mechanism involving CD40-CD40 ligand. However, whether this mechanism exists in the clinical setting remains unknown. Fifty-four patients with acute myocardial infarction (AMI) and 25 with unstable angina of pain onset of ≤24 h were enrolled consecutively. Acute myocardial infarction was diagnosed from three diagnostic criteria, i.e., anginal pain, electrocardiogram ST-T changes, and cardiac enzyme elevation. Unstable angina was diagnosed in patients without elevated cardiac enzymes. Peripheral venous blood was drawn at admission for routine blood count and soluble CD40 ligand (sCD40L) measurement. Neutrophil count was determined by an automated blood cell counter. Circulating sCD40L was measured using a standard enzyme-linked immunosorbent assay. Neutrophil count was significantly higher in AMI as compared with unstable angina (P < 0.001), whereas circulating sCD40L did not significantly differ. Despite marked elevation, no correlation was observed between neutrophil count and circulating sCD40L in AMI. Interestingly, we observed a strong and positive significant correlation between neutrophil count and circulating sCD40L level (r = 0.607, P = 0.002) in unstable angina. Circulating sCD40L is associated with neutrophil count and may mediate interaction between neutrophils and platelets in acute coronary syndrome, particularly in unstable angina.

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.

Significance of Six Minute Walking Distance in Predicting Functional Capacity Status of Patients with Pulmonary Hypertension Complicating an Atrial Septal Defect

Background: Six minute walk test (6 MWT) is a sub-maximal exercise test that measures an integrated response of all systems responsible during exercise. Pulmonary arterial hypertension (PAH) is a problem encountered by patients with atrial septal defect (ASD). Assessment of functional capacity in patients with PAH based on the WHO functional classifi cation remains a powerful predictor of survival in these patients. The World Health Organization functional classifi cation is a subjective tool because it is based on anamnesis of ordinary activity. On the contrary, 6 MWT is an objective tool to measure functional capacity of patients with pulmonary hypertension. Objective: To determine the walking distance obtained using 6 MWT as a measurement of functional capacity in ASD patients with PAH. Methods: A cross sectional study was used to determine the walking distance as a measurement of functional capacity in ASD patient with PAH. This study was a sub-study of an Atrial Septal Defect Registry done in RSUP Dr. Sardijto, Yogyakarta, since 2012. Pulmonary arterial pressure was measured using Pulmonary Arterial Systolic Pressure (PASP) obtained from echocardiography. Pulmonary hypertension was divided into three categories based on PASP, mild with PASP of less than 45 mmHg, moderate with PASP of 45-59 mmHg and severe with PASP of more than 60 mmHg. All patients did 6 MWT to measure their functional capacity. The relationship between 6 MWT distance and severity of PAH was measured using Pearson correlation analysis. Results: Forty-three patients were included in this study with 32 female patients (74%) and 11 male patients (26%) with an age range of 17-70 years old. Forty-four patients (44%) with ASD had severe PAH. The mean of 6 MWT distance was 337 m. There were signifi cant differences between mild, moderate and severe PAH in correlation with the 6 MWT distance (p= 0.001). The patients with severe PAH had only 278 m walking distance compared to those with mild PAH who had 394 m walking distance. There was a significant relationship between the 6 MWT distance and severity of PAH (p=0.01). This study showed that 6 MWT correlates negatively with the severity of PAH. We found that the higher pulmonary arterial pressure, the shorter walking distance (p=0.01, r -0,506). Conclusion: ASD defect patients with severe PAH had shorter walking distance compared to those with mild PAH. The 6 MWT is a reliable and objective measurement of functional capacity for ASD patients with PAH.

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.

582 DECOMPENSATED CARDIAC HYPERTROPHY IS RELATED TO LOWER PLASMA HIF-1α AND SVEGF LEVELS IN PATIENTS WITH HYPERTENSIVE HEART DISEASE

Background: Chronic hypertension causes cardiac pressure overload leading to increased myocardial O2-consumption. Previous animal studies showed that inhibition of HIF-1&agr; and VEGF resulted in cardiac decompensation following fibrosis and hypertrophy, due to its failure to maintain myocardial capillary density in response to hypoxia. However, it is still not clear whether this mechanism applied in human. Therefore, we sought to measure plasma HIF-1&agr; and sVEGF level among chronic hypertensive patients with structural and functional cardiac changes. Methods: Eighty hypertensive subjects participated in this study. Echocardiographic study, plasma HIF-1&agr; and sVEGF measurement were performed in hypertensive (n=30); compensated hypertrophy (n=25); decompensated hypertrophy (n=25) patients. Results: There were no significant differences in the SBP and DBP between groups, however decompensated patients were significantly older and were longer to suffer from hypertension. The LVMI was significantly higher in decompensated as compared to compensated and hypertensive group (157±5.2 and137±2.2 vs.98±2.3gr/m2 p<0.05). Furthermore, there was higher proportion of diastolic dysfunction in decompensated group compared with compensated one (44vs.96%; p<0.05); with significantly lower systolic function (64±1.2vs70±1.7%; p<0.05). Interestingly, the plasma HIF-1&agr; was significantly lower (1038.2±363vs.261±113pg/L; p<0.01) followed by decreased in sVEGF level (427.8±56.2vs.240.3±20.5pg/L; p<0.05) in decompensated group; which might explain the inadequate response to persistent hypoxia. Conclusion: Our study revealed that there was a reduction in plasma HIF-1&agr; and sVEGF level among hypertensive subjects with decompensated cardiac hypertrophy. This implies that preservation of cardiac function requires adequate response to chronic hypoxia to maintain myocardial capillary function and that strategy for anti-hypertensive therapy should be considered for that purpose. Table. No title available.