Mean platelet volume and its prognostic value in acute coronary syndrome complicated by cardiogenic shock

Background: Elevated mean platelet volume (MPV) has been recently discussed as a predictorof death in patients with acute coronary syndrome (ACS), but the cut-off point of MPV inrelation to poor prognosis has not been estimated so far. The aim of this study was to evaluate MPV and its prognostic value in ACS complicated by cardiogenic shock (CS). Such an analysisin patients with the most serious and fatal complication of ACS has not been performed inpreviously published research.Methods: Fifty three patients with ACS complicated by CS (age 68.9 ± 11.4, 49% women, 92% STEMI, 55% fatal CS) and 53 age- and gender-matched patients with uncomplicated ACS as a control group (age 69.1 ± 10.6, 49% women, 92% STEMI, 0% fatal) were includedin our prospective study from 2010 to 2012. All the patients underwent successful primary percutaneous coronary intervention. MPV was determined on admission (MPV1) and in consecutive two days of hospitalization (MPV2, MPV3). The blood sample was analyzed immediately after collection in EDTA tubes using an automatic blood counter.Results: MPV1 was similar in both groups (8.91 ± 1.11 fl vs. 8.57 ± 0.74 fl, NS). Furthermore, there were no statistically significant differences in MPV value in fatal and nonfatal CS(8.90 ± 1.18 fl vs. 8.93 ± 1.05 fl, NS).Conclusions: The above results suggest that MPV cannot be considered a predictor of poorin-hospital outcome in patients with ACS complicated by cardiogenic shock

Symptomatic Young Adults with ST-Segment Elevation—Acute Coronary Syndrome or Myocarditis: The Three-Factor Diagnostic Model

Myocarditis may mimic myocardial infarction (MI) due to a similar clinical presentation, including chest pain, electrocardiography changes, and laboratory findings. The purpose of the study was to investigate the diagnostic value of clinical, laboratory, and electrocardiography characteristics of patients with acute coronary syndrome - like myocarditis and MI. We analysed 90 patients (≤45 years old) with an initial diagnosis of ST-segment elevation myocardial infarction; 40 patients (44.4%), through the use of cardiac magnetic resonance, were confirmed to have myocarditis, and 50 patients (55.6%) were diagnosed with MI. Patients with myocarditis were younger and had fewer cardiovascular risk factors than those with MI. The cutoff value distinguishing between myocarditis and MI was defined as the age of 36 years. The history of recent infections (82.5% vs. 6%) and C-reactive protein (CRP) levels on admission (Me 45.9 vs. 3.4) was more associated with myocarditis. Further, the QTc interval was inversely correlated with the echocardiographic ejection fraction in both groups but was significantly longer in patients with MI. Non-invasive diagnostics based on clinical features and laboratory findings are basic but still essential tools for differentiation between MI and myocarditis. The three-factor model including the criteria of age, abnormal CRP, and history of recent infections might become a valuable clinical indication

Fibroblast Growth Factor 23 and Cardiovascular Risk in Diabetes Patients—Cardiologists Be Aware

Numerous clinical studies have indicated that elevated FGF23 (fibroblast growth factor 23) levels may be associated with cardiovascular (CV) mortality, especially in patients with chronic kidney disease. The purpose of this study was to examine the hypothesis that FGF23 may be a potent CV risk factor among patients with long-standing type 2 diabetes mellitus (T2DM). Research was performed utilizing patients with T2DM and regular outpatient follow-up care. Baseline characteristics determined by laboratory tests were recorded. Serum FGF23 levels were detected using a sandwich enzyme-linked immunosorbent assay. All patients underwent echocardiograms and 12-lead electrocardiograms. Data records of 102 patients (males: 57%) with a median age of 69 years (interquartile range (IQR) 66.0–74.0) were analyzed. Baseline characteristics indicated that one-third (33%) of patients suffered from ischemic heart disease (IHD), and the median time elapsed since diagnosis with T2DM was 19 years (IQR 14.0–25.0). The hemoglobin A1c, estimated glomerular filtration rate, and FGF23 values were, respectively, as follows: 6.85% (IQR 6.5–7.7), 80 mL/min/1.73 m2 (IQR 70.0–94.0), and 253.0 pg/mL (IQR 218.0–531.0). The study revealed that FGF23 was elevated in all patients, regardless of IHD status. Thus, the role of FGF23 as a CV risk factor should not be overestimated among patients with T2DM and good glycemic control

Fibroblast Growth Factor 23: Potential Marker of Invisible Heart Damage in Diabetic Population

Two-dimensional speckle-tracking echocardiography (2DSTE) detects myocardial dysfunction despite a preserved left ventricular ejection fraction. Fibroblast growth factor 23 (FGF23) has become a promising biomarker of cardiovascular risk. This study aimed to determine whether FGF23 may be used as a marker of myocardial damage among patients with diabetes mellitus type 2 (T2DM) and no previous history of myocardial infarction. The study enrolled 71 patients with a median age of 70 years. Laboratory data were analyzed retrospectively. Serum FGF23 levels were determined using a sandwich enzyme-linked immunosorbent assay. All patients underwent conventional echocardiography and 2DSTE. Baseline characteristics indicated that the median time elapsed since diagnosis with T2DM was 19 years. All subjects were divided into two groups according to left ventricular diastolic function. Individuals with confirmed left ventricular diastolic dysfunction had significantly lower levels of estimated glomerular filtration rate and higher values of hemoglobin A1c. Global circumferential strain (GCS) was reduced in the majority of patients. Only an epicardial GCS correlated significantly with the FGF23 concentration in all patients. The study indicates that a cardiac strain is a reliable tool for a subtle myocardial damage assessment. It is possible that FGF23 may become an early diagnostic marker of myocardial damage in patients with T2DM