The focus of this review is to summarize findings on biomarkers of myocardial fibrosis (PICP and PIIINP), profibrotic mediators (TGF-beta1), extracellular matrix remodeling (MMP-9), myocardial stretch (BNP and NTpro-BNP), inflammation (interleukins, C-reactive protein and sCD40L), and myocardial necrosis (high-sensitivity troponin T), biomarkers, that can be used in clinical practice to stratify patients at risk for POAF.
However, serum folate and vitamin B<sub>12</sub> levels were not associated with the risk of stroke, coronary artery disease, or myocardial infarction or the development of peripheral arterial disease after adjustment for age, sex, smoking status, alcohol consumption, physical activity, body mass index, serum creatinine, and high-sensitivity C-reactive protein levels and a history of diabetes, hypertension, or dyslipidemia.
Background Beyond the controlled setting of trials, scarce information exists on the burden, predictors, and outcomes associated with elevated hs CRP (high-sensitivity C-reactive protein) in "real-world" patients with myocardial infarction ( MI ).
In a multivariate logistic regression analysis, body mass index, low‑density lipoprotein cholesterol, aspartate aminotransferase, high‑sensitivity C‑reactive protein, and palmitoleic and eicosadienoic acids were independently associated with MI.
Body mass index (BMI), waist circumference values, the average values of systolic (SBP) and diastolic (DBP) blood pressures and heart rate, total serum cholesterol levels, serum HDL (high-density lipoprotein) cholesterol levels, serum LDL (low-density lipoprotein) cholesterol levels, serum triglycerides levels, serum lipoprotein A levels, serum CRP (C-reactive protein) levels, plasma homocysteine levels, serum uric acid levels, individual and relative risks of having a heart attack or stroke over the next ten years were compared between groups (50 GH, 102 PE, 34 FGR and 90 normal pregnancies) and correlated with the severity of the disease with regard to clinical signs (25 PE without severe features, 77 PE with severe features), and delivery date (36 early PE, 66 late PE).
Factors associated with in-hospital MI (OR [95% CI]) were increasing blood glucose (1.80 [1.17-2.77] per 10 mmol/L), total leucocyte count (1.25 [1.01-1.54] per 10 × 10<sup>9</sup> /L) and CRP (1.05 [1.02-1.08] per 10 mg/L increase).
We examined 2184 consecutive patients with previous MI and CRP data at baseline in the Chronic Heart Failure Registry and Analysis in the Tohoku district-2 (CHART-2) Study.
Conclusions Baseline CRP concentrations might be associated with the benefits of LDL-C lowering on myocardial infarction, but no other outcomes, whereas the achieved and magnitude of reduction in CRP did not seem to have an important association.
At the end of the 5-year follow- up, compared with subjects without MS, hazard ratios and 95% confidence intervals for the different risks in subjects with MS were 1.86 (1.02-3.29) for myocardial infarction (MI), 1.39 (1.01-2.05) for stroke, 1.52 (1.02- 2.37) for CVD death, and 1.13 (0.62-2.58) for total death, after adjusting for age, gender, smoking, drinking, physical activity, uric acid, high-sensitivity C-reactive protein, dietary factors and carotid atherosclerosis status.
Higher endostatin was associated with a higher incidence of MI independently of established cardiovascular risk factors (OR 1.19, 95% CI 1.03-1.37, p = .02), but this association was abolished after additional adjustment for C-reactive protein.
In multivariate logistic regression analyses, ST elevation MI (P<0.001), performed coronary angiography (P<0.001) and larger changes in troponin levels (P=0.023) independently made the physicians agree significantly more often, while they disagreed more often with symptoms of dyspnoea (P<0.001), higher systolic blood pressure (P=0.001) and higher C reactive protein levels on admission (P=0.016).
We calculated hazard ratios (HRs) of MI and IS according to categories of CRP (<1, 1-3, and >3 mg/L) and plaque status (no plaque and TPA below and above median) in Cox proportional hazard models with time-varying covariates.
The Canakinumab Antiinflammatory Thrombosis Outcome Study (CANTOS) has shown that interleukin (IL)-1β blockade reduces the incidence of cardiovascular events in patients with previous myocardial infarction and C-reactive protein levels >2 mg/L.
Women with a combination of elevated CRP and values in the upper quartile of TNFR1 or TNFR2 had a 5-fold higher risk of myocardial infarction versus those with normal CRP and values in the lower three quartiles of TNFR1 or TNFR2.
Cox proportional hazards models were developed incorporating age, sex, systolic blood pressure, total and high-density lipoprotein cholesterol, smoking, diabetes mellitus, hypertension treatment, family history of myocardial infarction, high-sensitivity C-reactive protein, and CAC scores (Astro-CHARM model [Astronaut Cardiovascular Health and Risk Modification]) as dependent variables and ASCVD (nonfatal/fatal myocardial infarction or stroke) as the outcome.
The following HDL-related measures were determined upon admission (D1) and on the fifth day (D5) after MI: C-reactive protein, CETP and PLTP activity, HDL composition, efflux of cholesterol from J774 macrophages to HDL, and transfer of unesterified and esterified cholesterol, triglycerides and phospholipids from a donor nanoemulsion to HDL.
The association of CRP level above 40 mg/L at day 2 and the observation of a second peak of troponin were associated to 95% of MVO in ST-segment elevation MI patients.
The direction of effect of all 24 risk factors (including various apolipoproteins, hemoglobin A1<sub>c</sub>, high-sensitivity C-reactive protein, N-terminal pro-brain natriuretic peptide, and tissue plasminogen activator antigen) was concordant for coronary heart disease (CHD, defined as myocardial infarction and CHD death) and ischemic stroke; however, associations were generally stronger with CHD.
Multilocus analysis additionally suggested the influence of carriage of the CRP and ENOS genes variants at the development of subsequent adverse events after MI.
When additionally adjusting for total-, LDL- and HDL-cholesterol, triglycerides and C-reactive protein, acyl-alkyl-phosphatidylcholine C36:3 and diacyl-phosphatidylcholines C38:3 and C40:4 remained associated with risk of MI.