Acute coronary syndromes comprise a large spectrum of clinical conditions ranging from unstable angina pectoris to acute ST-elevation myocardial infarction. Chest pain is usually the major symptom of atherosclerotic heart disease; however, it may be challenging to diagnose correctly, especially in the emergency department, because of the ambiguous way that pain is characterized by some patients. Cardiac troponins are sensitive and specific biomarkers used in the diagnosis of myocardial infarction that are released into the bloodstream when cardiac myocytes are damaged by acute ischemia or any other mechanism. They are the cornerstone for the diagnosis, risk assessment, prognosis, and determination of antithrombotic and revascularization strategies. However, troponin elevation indicates the presence, not the mechanism, of myocardial injury. There are many clinical conditions other than myocardial infarction that cause troponin elevation; thus, the physician should be aware of the wide spectrum of disease states that may result in troponin elevation and have a clear understanding of the related pathophysiology to effectively make a differential diagnosis. This review focuses on causes of troponin elevation other than acute coronary syndromes.
Greater improvement was detected for PD and GI, and for serum levels of APO-A and HDL cholesterol when using SRP+SDD compared with SRP+placebo in this study. An investigation with larger numbers of patients and a longer duration of drug treatment is needed to confirm these preliminary findings.
Background:Matrix metalloproteinases (MMPs) and Tissue Inhibitor of Matrix Metalloproteinases (TIMPs) may be associated with atherogenesis and plaque rupture. We evaluated the relationship between MMP-1, MMP-9, TIMP-1 and IL-6 levels and risk factors, presentation, extent and severity of atherosclerotic coronary artery disease (CAD). Methods:Consecutive patients who underwent coronary angiography were randomly included. The serum concentrations of MMP-1, MMP-9, TIMP-1 and IL-6 were analyzed with ELISA method in 134 patients. Participants were divided into 5 groups; stable angina pectoris (SAP; n= 34), unstable angina pectoris (USAP; n=29), non-ST elevation myocardial infarction (NSTEMI; n=16), acute ST elevation myocardial infarction (STEMI; n=25) and controls (n=30). Coronary angiographic Gensini score was calculated. Results:MMP-1 levels were higher in STEMI and NSTEMI groups compared with USAP, SAP and control groups (STEMI vs USAP p=0.005; STEMI vs SAP p=0.001; STEMI vs control p<0.001; NSTEMI vs USAP p=0.02; NSTEMI vs SAP p=0.027; NSTEMI vs control p<0.001). In STEMI group, MMP-9 levels were higher than USAP and control groups (p=0.002; p<0,001). TIMP-1 levels were not significantly different within all 5 groups. MMP-1 levels were found to be elevated in diabetic patients (p=0.020); whereas MMP-9 levels were higher in smokers (p=0.043). Higher MMP-1, MMP-9 and IL-6 levels were correlated with severe Left Anterior Descending artery (LAD) stenosis and higher angiographic Gensini Score (for severe LAD stenosis; r = 0.671, 0.363, 0.509 p<0.001; for Gensini score; r = 0.717, 0.371, 0.578 p<0.001). Conclusions:Serum levels of MMP-1, MMP-9, and IL-6 are elevated in patients with CAD; more so in acute coronary syndromes. MMP-1, MMP-9 and IL-6 are associated with more extensive and severe CAD (as represented by Gensini score).
Symphatovagal imbalance as shown by disturbed HR variability and HR turbulence parameters was demonstrated for the first time in patients with mild-to-moderate AS. This imbalance, which was shown to be correlated with echocardiographic findings of diastolic dysfunction, may lead to arrhythmic complications in this seemingly low-risk patient population.
Background. Subclinical hypothyroidism (SH) predominantly affects women. The necessity of treatment in SH is controversial. Objective. We aimed to investigate the response of diastolic dysfunction to thyroid hormone replacement therapy (THRT) in women. Methods and Results. Twenty-two female subjects with SH and 20 euthyroid female controls were enrolled. Baseline and follow-up biochemical, hormonal, and echocardiographic evaluations were performed. Repeat echocardiograms were performed three months after the achievement of a euthyroid status with THRT. Mean baseline myocardial performance index (MPI) was 0.27 ± 0.08 in the SH group, and 0.22 ± 0.06 in the control group (P = 0.03). MPI did not change significantly after THRT. Pulsed-wave Doppler findings were not different among the groups. However, tissue Doppler-derived mitral annular E' velocities were significantly lower in the SH group. A moderate but significant improvement was observed in E' velocities after THRT (13.2 ± 3.87 versus 14.53 ± 2.75, P = 0.04). We also observed left ventricular concentric remodeling in SH patients which was reversible with THRT. Conclusions. Tissue Doppler echocardiography may be a useful tool for monitoring the response of diastolic dysfunction to thyroid hormone replacement therapy in patients with SH. Our findings suggest that THRT may reverse diastolic dysfunction in women with SH.
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