SummaryEpidemiological 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. We enrolled 82 consecutive patients with acute coronary syndrome from whom venous blood for serum albumin measurement was drawn immediately upon hospital admission. Thirty-five patients had a low albumin level (hypoalbuminemia) and 47 had a normal albumin level (normoalbuminemia). In-hospital adverse outcomes (death, acute heart failure, cardiogenic shock, and reinfarction) were recorded during hospitalization in the intensive coronary care unit. The results of our study showed that the incidence of in-hospital adverse outcomes was 43%, with death occurring in 8 patients (10%). In-hospital adverse outcomes occurred more frequently in patients presenting with hypoalbuminemia, whereas mortality did not differ significantly. Univariate analysis showed that hypoalbuminemia was associated with a 2.8-fold greater risk of developing adverse outcomes. This risk was greater in the subgroup of NSTEACS (5.4-fold increased risk), but not in those with STEMI. Adjustment with other covariates revealed that hypoalbuminemia did not predict independently in-hospital adverse outcomes. It interacted with other predictors, especially Killip class II-IV, which was consistently an independent predictor of in-hospital adverse outcomes. (Int Heart J 2010; 51: 221-226)

IntroductionActivated 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.Material and methodsThis was a cross sectional study. The subjects were patients with acute coronary syndrome (ACS). Forty-one consecutive subjects with ACS admitted to intensive cardiovascular care unit were enrolled. The clinical spectrum of ACS comprised AMI (n = 26), both ST-elevation AMI (STEMI) and non-ST-elevation AMI (NSTEMI), and unstable angina (n = 15). Platelet microparticles were isolated from peripheral venous blood and detected with anti-CD42b-PE by the flow cytometry method. The extent of myocardial damage was determined by measuring the peak level of serial cardiac enzymes within 24 h of admission.ResultsSubjects with AMI had a significantly higher number of platelet microparticles than those with unstable angina (4855 ±4509/µl vs. 2181 ±1923/µl respectively; p = 0.036). Subjects with STEMI had the highest number of platelet microparticles, but no significant difference was detected as compared to those with NSTEMI (5775 ±5680/µl vs. 3601 ±1632/µl). The number of platelet microparticles in AMI was positively associated with the extent of myocardial damage (peak CK-MB: r = 0.408, p = 0.019 and peak GOT: r = 0.384, p = 0.026).ConclusionsThe number of platelet microparticles was increased in AMI as compared to unstable angina and associated with the extent of myocardial damage.

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 < or = 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.

Atrial septal defect (ASD) is the most frequent congenital heart disease in adulthood. Pulmonary hypertension (PH) complicating ASD compels patients seeking medical assistance because of its disabling symptom. Most adult ASD develop PH which render significant morbidity and mortality. The aim of the study is to characterize the clinical profiles of adult patients with ASD. The study design was cross sectional. The subjects were enrolled consecutively from outpatient clinics and inpatient wards. The demography, medical and imaging data were collected and recorded in case report form. Descriptive statistics was applied to characterize the subjects. Seventy-six subjects were enrolled. The majority were women (77.6 %) in the productive and child-bearing ages (63.2%). The most common symptoms were dyspneu on effort, fatigue, and palpitation. Most subjects had functional capacity of WHO class functional II (70.2 %). The mean oxygen saturation was 96.4 %. Based on the echocardiography examination, 77.6% of subjects had suffered from PH. The mean longest diameter of defects were 2.7 cm. The direction of blood flow was mostly left to right (77.6 %). Left and right ventricle function were within normal limit. Right heart catheterization showed mean left atrial pressure 11.5 mmHg, which confirmed the precapillary or arterial PH. Mean pulmonary artery pressure was 42.0 mmHg. The pulmonary artery resistance index mostly less than 4 Wood Unit/ m 2 (63.7 %), indicating the feasibility to close the defect. Whereas 24.6 % of subjects were contraindicated for closing. Pulmonary artery hypertension (PAH) was diagnosed in 77.6 % subjects, meanwhile 13.2 % had borderline PAH. In conclusion, most adult ASD patients had developed PAH, mostly young women in productive ages, mainly visited hospital due to symptom of PH, the direction of flow predominantly left to right side and mostly had reduced functional capacity. ABSTRAKDefek septum atrium (DSA) merupakan penyakit jantung bawaan yang paling sering dijumpai pada usia dewasa karena tanda dan gejalanya yang samar. Hipertensi paru (HP) merupakan komplikasi DSA yang mendorong pasien ke rumah sakit karena munculnya gejala yang berat. Hampir semua pasien DSA dewasa mengalami HP yang menyebabkan angka kesakitan dan kematian bermakna. Tujuan penelitian ini adalah untuk mengkaji karakteristik klinis pasien dengan DSA dan HP. Desain penelitian adalah potong lintang. J Med Sci, Volume 48, No. 2, 2016 April: 89-97 90Subjek diseleksi secara berurutan dari klinik rawat jalan dan rawat inap. Data demografi, medis dan pencitraan dikumpulkan dan dicatat dalam suatu blangko laporan kasus. Penelitian deskriptif dilakukan untuk menilai karakteristik subjek. Sebanyak tujuh puluh enam subjek dilibatkan dalam penelitian. Sebagian besar subjek adalah wanita (77,6%) usia muda, produktif dan subur (63,2%). Gejala paling sering adalah sesak saat aktivitas, mudah lelah, dan berdebar. Sebagian besar pasien masuk dalam kelas fungsional WHO II (70,2%). Rerata saturasi oksigen 96,4%. Berdasar hasil ekok...

Introduction. Serum endothelin-1 is increasingly released in acute myocardial infarction, by necrotic cardiomyocytes. In non-ST-elevation acute myocardial infarction (Non-STEMI), increased serum endothelin-1 on-admission may have clinical significance during acute hospitalisation events. Objective. The purpose of this study is to investigate whether increased serum endothelin-1 level predict adverse cardiac events in patients hospitalized with Non-STEMI. Methods. The design of this research was a prospective cohort study. Consecutive subjects with Non-STEMI undergoing symptom onset ≤24 hour were enrolled and observed during intensive hospitalization. Serum endothelin-1, troponin-I, and hs-C reactive protein were measured from peripheral blood taken on-admission. In-hospital adverse cardiac events were a composite of death, acute heart failure, cardiogenic shock, reinfarction, and resuscitated VT/VF. Results. We enrolled 66 subjects. The incidence of in-hospital adverse cardiac events is 13.6% (10 out of 66 subjects). Serum endothelin-1 level was significantly higher in subjects with in-hospital adverse cardiac events. Subjects with endothelin-1 level >2.59 pg/mL independently predicted adverse cardiac events in hospitalised Non-STEMI patients (adjusted odds ratio 44.43, 95% confidence interval: 1.44-1372.99, p value 0.03). The serum endothelin-1 level was correlated with serum troponin I level (correlation coefficient of 0.413, p value 0.012). Conclusion. Increased serum endothelin-1 on-admission correlated with increased troponin-I and independently predicted in-hospital adverse cardiac events in patients with Non-STEMI.