Chronic anabolic androgenic steroid usage associated with acute coronary syndrome in bodybuilder.

INTRODUCTION: It has been argued in current studies that anabolic androgenic steroids (AAS) are misused by a great number of bodybuilders and athletes. However, there is diverse and often conflicting scientific data on the cardiac and metabolic complications caused by the misuse of AAS. There may be various reasons for myocardial infarction (MI) with normal coronary arteries. However, for the majority of patients, the exact cause is still unknown. CASE REPORT: A 32 year-old male who was complaining about severe chest pain was admitted to our emergency department. He had been taking methenolone acetate 200 mg weekly for a period of three years for body building. His cardiac markers were significantly elevated and electrocardiogram (ECG) showed peaked T waves in all derivations, which did not show ST elevation or depression. Both right and left coronary artery systems were found to be completely normal as a result of the angiogram. CONCLUSION: The purpose of this study is to show that AAS induced MI can be encountered with normal coronary arteries during acute coronary syndrome.

Altered expression of micro-RNA 199a and increased levels of cardiac SIRT1 protein are associated with the occurrence of atrial fibrillation after coronary artery bypass graft surgery.

BACKGROUND: Postoperative atrial fibrillation (POAF) is a potentially life-threatening complication after coronary artery bypass graft (CABG) surgery. The expression of the cardioprotective SIRT1 protein with its antioxidant activity is increased in cardiac tissue of patients suffering from POAF. So far, information is lacking about the relationship between SIRT1 regulating micro RNAs (miRs), SIRT1 protein and the occurrence of POAF. METHODS: A total of 63 patients undergoing CABG were recruited, and biopsies were obtained from the right atrial appendage during cannulation. Postoperative, all patients were rhythm-monitored until discharge and randomized to POAF (n=20) or sinus rhythm (n=43). The expression of the micro RNAs miR-199a and miR-195 was quantified by real-time PCR. SIRT1 protein was detected by western blot analysis. RESULTS: The relative expression of miR-199a in the POAF group was significantly decreased compared to the control group (0.77±0.27 vs. 1.11±0.69, P=.022) Accordingly, SIRT 1 protein was significantly induced in tissue probes of patients with POAF (P<.001). CONCLUSION: Altered expression of the SIRT1 protein regulating miR-199a in human atrial tissue was found to be related to the occurrence of POAF, indicating its usefulness as a biomarker for cardiac surgery management.

Role of cathepsin D activation in major adverse cardiovascular events and new-onset heart failure after STEMI.

AIM: Increased serum levels of the activated aspartic lysosomal endopeptidase cathepsin D (CatD) have been found in patients with acute myocardial infarction (AMI). However, to date there have been no analyses of clinical follow-up data measuring the enzyme course and its role in the development of post-MI heart failure. This study aimed to evaluate the role of serum CatD activity in the development of heart failure in patients with ST-segment elevation acute myocardial infarction (STEMI). PATIENTS AND METHODS: Eighty-eight consecutive patients (79.5 % men, mean age 57.4 ± 10.2 years) with STEMI were included in this study. Serum CatD activity was measured directly after primary percutaneous coronary intervention (PCI), before discharge, and at the 6-month follow-up. Patients were monitored for major adverse cardiovascular events (MACE), defined as hospitalization due to cardiovascular causes, recurrent nonfatal myocardial infarction, unplanned PCI, new-onset heart failure, and cardiovascular mortality. RESULTS: Serum CatD activity was significantly higher in patients with AMI after PCI and during follow-up (FU) than that in age-matched controls (16.2 ± 7.5 and 29.8 ± 8.9 vs. 8.5 ± 4.2 RFU; p < 0.001 for each time point). At the 6-month follow-up, serum CatD activity in these patients was inversely related to new-onset cardiac dysfunction compared with patients with preserved and improved LVEF after treatment (23.1 ± 3.2 vs. 28.8 ± 7.0 and 29.7 ± 5.0 RFU respectively, p < 0.01). Patients suffering from MACE during a follow-up period of 6 months had lower serum levels of activated CatD than those without any MACE (23.8 ± 4.6 vs 29.6 ± 6.9 RFU; p < 0.001). CONCLUSIONS: Serum CatD activity as a marker of healthy endogenous phagocytosis and remodeling was impaired in patients with new-onset cardiac dysfunction, and lower levels of serum CatD were associated with MACE at the 6-month post-MI follow-up.

Implication of plasma intermedin levels in patients who underwent first-time diagnostic coronary angiography: a single centre, cross-sectional study.

BACKGROUND: Intermedin (IMD) is involved in the prevention of atherosclerotic plaque progression, possessing cardioprotective effects from hypertrophy, fibrosis and ischemia-reperfusion injury. Elevated plasma IMD levels have been demonstrated in patients with acute coronary syndromes. No human study has examined the role of IMD in stable patients who underwent diagnostic coronary angiography with suspicion of coronary artery disease (CAD). Thus we investigated the role of IMD as a biomarker to discriminate patients with CAD and predict those with severe disease who require early and intensive therapeutic intervention before presenting with acute coronary syndrome. METHODS: Eligible two hundred and thirty-eight consecutive patients (123 males, mean age 58.4 ± 10.0 years) who underwent first-time diagnostic coronary angiography were included in this study. Plasma concentrations of IMD were measured from arterial blood samples by the enzyme-linked immunosorbent assay. Patients were divided into three groups according to the presence and degree of CAD, consisting of 48 patients with normal coronary anatomy (Group 1), 111 patients with < 50% coronary stenosis (Group 2), and 79 patients with ≥ 50% stenosis in at least one of the major coronary arteries (group 3). The severity and extent of CAD was evaluated by calculations of the vessel, Gensini, and SYNTAX scores. RESULTS: Circulating plasma IMD levels in patients with CAD were significantly higher than those in patients without CAD (157.7 ± 9.6, 134.8 ± 11.9, and 117.6 ± 7.9 pg/mL in groups 3, 2 and 1 respectively; p < 0.001). Besides, plasma IMD levels were correlated with Gensini and SYNTAX scores (rs = 0.742, and rs = 0.296, respectively; p < 0.05). The presence of ≥50% coronary artery stenosis could be predicted if a cut-off value of 147.7 pg/mL for plasma IMD was used with 88.6% sensitivity and 88.7% specificity. Moreover, a plasma IMD level of <126.6 pg/mL could discriminate a patient with normal coronary arteries from patients with angiographically proven CAD with a sensitivity and specificity of 84.7%, and 83.3% respectively. CONCLUSIONS: We demonstrated that IMD might be used as a biomarker to predict CAD and its severity in patients who underwent first time diagnostic coronary angiography.

Novel fibro-inflammation markers in assessing left atrial remodeling in non-valvular atrial fibrillation.

BACKGROUND: Structural remodeling is associated with the fibroinflammatory process in the atrial extracellular matrix. In the present study we aimed to investigate whether serum levels of new circulating remodeling markers differ in patients with atrial fibrillation (AF) compared to patients with sinus rhythm. MATERIAL AND METHODS: The study population included 52 patients diagnosed with non-valvular AF and 33 age-matched patients with sinus rhythm. Serum levels of Galectin-3, matrix metalloproteinase-9 (MMP-9), lipocalin-2 (Lcn2/NGAL), N-terminal propeptide of type III procollagen (PIIINP), Hs-Crp, and neutrophil-to-lymphocyte ratio (NLR) were measured. The left atrial volume (LAV) was calculated by echocardiographic method and LAV index was calculated. RESULTS: Galectin-3, MMP-9, and PIIINP levels were significantly higher in AF patients except NGAL levels (1166 pg/ml (1126-1204) and 1204 pg/ml (1166-1362) p=0.001, 104 (81-179) pg/ml and 404 (162-564) pg/ml p<0.0001, and 1101 (500-1960) pg/ml and 6710 (2370-9950) pg/ml p<0.0001, respectively). The NLR and Hs-CRP levels were also higher in AF (2.1 ± 1.0 and 2.7 ± 1.1 p=0.02 and 4.2 ± 1.9 mg/L and 6.0 ± 4.7 mg/L p=0.04, respectively). In correlation analyses, NLR showed a strongly significant correlation with LAVi, but Hs-CRP did not (p=0.007 r=0.247, Pearson test and p=0.808 r=0.025, Pearson test, respectively). Moreover, Galectin-3, MMP-9, and PIIINP had a strong positive correlation with LAVi (p=0.021 r=640, Spearman test and p=0.004 r=0.319 Pearson test, and p=0.004 r=0.325 Pearson test, respectively). CONCLUSIONS: Novel fibrosis and inflammation markers in AF are correlated with atrial remodeling. Several unexplained mechanisms of atrial remodeling remain, but the present study has taken the first step in elucidating the mechanisms involving fibrosis and inflammation markers.