Publications by authors named "Putrika Gharini"

Aim: One of the essential competencies of cardiology trainees is the ability to perform coronary angiography with good projection.

Purpose: This study is a research and development study aimed at testing the effectiveness of 3D-printing-based fluoroscopic coronary angiography simulator as a learning medium for diagnostic coronary angiogram.

Methods: Thirty-four cardiology trainees randomly were divided into two groups.

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Mastering coronary angiography requires practice. Cadavers and animals do not accurately represent the human anatomical body, and practicing with actual patients has medical safety issues. Simulation offers safe and realistic conditions for cardiology intervention training.

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Background: Assessment of health-related quality of life (HRQoL) are often measured as an important patient-reported outcome (PRO) in clinical studies. Pulmonary arterial hypertension (PAH) is a common complication of atrial septal defect (ASD). This study aimed to compare the HRQoL of PAH related uncorrected secundum ASD at pre and post therapy with oral sildenafil therapy.

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Introduction: Activated platelets generate microparticles. Increased platelet microparticles occur in acute myocardial infarction (AMI) and contribute to intracoronary thrombosis and subsequent myocardial injury. This study aimed to investigate the impact of platelet microparticles on intracoronary thrombosis by assessing the relationship between platelet microparticles and the extent of myocardial damage in AMI.

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Anomalous origination of coronary artery from the opposite sinus (ACAOS) is a rare coronary artery anomaly. Right ACAOS with interarterial course is a type of ACAOS, which conveys a high risk for myocardial ischemia or sudden death. We reported a case of right ACAOS with interarterial course in otherwise healthy young male.

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Aim: to assess whether different glomerular filtration rate (GFR) equations render different predictive value on hospital adverse events in patients hospitalised due to acute myocardial infarction.

Methods: the study design is cross-sectional. Data from consecutive patients with acute myocardial infarction were analyzed.

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Background: High blood glucose level is frequently encountered in acute coronary syndrome. We investigated the effects of high blood glucose measured on arrival on hospitalization adverse events in acute coronary syndrome. Our study patients were Javanese in ethnicity, which constitute half of population in Indonesia.

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Aim: to investigate the association between on admission circulating sCD40L level and in-hospital events among patients admitted with acute coronary syndrome.

Methods: a short prognostic study which recruited consecutively patients with acute coronary syndrome (ACS) admitted in Intensive Coronary Care Unit (ICCU).

Inclusion Criteria: between 35-70 years old, onset of chest pain 24 hours and approved informed consent.

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Epidemiological studies have demonstrated an association between low serum albumin levels and coronary heart disease and mortality. Nevertheless, the impact of a low serum albumin level during acute coronary syndrome has not yet been established. The aim of the present study was to investigate whether low serum albumin levels are associated with adverse outcomes in acute coronary syndrome.

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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.

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There is growing evidence for nitric oxide (NO.) being involved in cell signaling and pathology. Much effort has been made to elucidate and characterize the different biochemical reaction pathways of NO.

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Aims: The myocardial effect of tonically released nitric oxide (NO) in humans is still not known. We tested the hypothesis that low-dose NO exerts positive effects on left ventricular (LV) function.

Methods And Results: Twelve healthy volunteers, 26+/-4 years, were enrolled in this study.

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A reduced nitric oxide availability is a hallmark of endothelial dysfunction occurring early in atherosclerosis. Recently, we have shown that plasma nitrite mirrors acute changes in endothelial nitric oxide synthase activity in various mammals, including humans. Here, we examined the hypothesis that plasma nitrite levels are reduced in humans with endothelial dysfunction and the decrease is correlated with increasing numbers of cardiovascular risk factors (RF).

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The synthesis of nitric oxide (NO) in the circulation has been attributed exclusively to the vascular endothelium. Red blood cells (RBCs) have been demonstrated to carry a nonfunctional NO synthase (NOS) and, due to their huge hemoglobin content, have been assumed to metabolize large quantities of NO. More recently, however, RBCs have been identified to reversibly bind, transport, and release NO within the cardiovascular system.

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Many of the local UV-induced responses including erythema and edema formation, inflammation, premature aging, and immune suppression can be influenced by nitric oxide synthase (NOS)-produced NO which is known to play a pivotal role in cutaneous physiology. Besides NOS-mediated NO production, UV radiation might trigger an enzyme-independent NO formation in human skin by a mechanism comprising the decomposition of photo-reactive nitrogen oxides. Therefore, we have examined the chemical-storage forms of potential NO-generating agents, the mechanisms and kinetics of their decomposition, and their biological relevance.

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Nitrate is generally considered an inert oxidative breakdown product of nitric oxide (NO). Whereas it has been shown that limited amounts of NO are produced during the photolysis of nitrate in aqueous solution, the photochemistry of nitrate in biological matrices such as plasma is unknown. We hypothesized that thiols, which are ubiquitously present in biological systems, may significantly enhance NO-quantum yields from nitrate photolysis.

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Higher doses of inhaled NO exert effects beyond the pulmonary circulation. How such extrapulmonary effects can be reconciled with the presumed short half-life of NO in the blood is unclear. Whereas erythrocytes have been suggested to participate in NO transport, the exact role of plasma in NO delivery in humans is not clear.

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