Myocardial Ischemia/Infarction: Biomarker Implications

In yet another outstanding set of poster presentations, several studies were presented under the topic of biomarker implications in myocardial ischemia/infarction at the 59^th Annual Scientific Sessions of the American College of Cardiology. Those that stood out are reviewed here.

The Relationship Between Glomerular Filtration Rate, Plasma Asymmetric Dimethylarginine (ADMA) Level and Development of Coronary Collateral Circulation

Researchers: Çelik M, Iyisoy A, Celik T, et al.

Purpose: To elucidate in renal failure patients the pathophysiological pathways that may cause poor coronary collateral development (CCD), as it is not yet know what factors are responsible for CCD and there are a limited number of studies that have looked at the relationship between the effect of low GFR and relatively high plasma ADMA level on coronary collateral development.

Results: The researchers concluded that their results show CCD to be poor “in patients with GFR < 60 ml/min presumably because of the adverse effect of decreased L-Arginine/ADMA ratio, relatively increased plasma ADMA level, on endothelial cells and angiogenesis.”

Candesartan Suppresses Increase in Secreted Frizzled Related Protein 2 and Fibrosis During Healing after Reperfused Myocardial Infarction in the Rat Model

Researchers: Jugdutt B, Palaniyappan A, Idikio H

Purpose: To test the hypothesis that “decreased fibrosis by the AT₁R blocker candesartan (CN) during healing after [reperfused myocardial infarction (RMI)] might involve decrease in [secreted-frizzled-related-protein-2 (sFRP-2)],” because the “mechanismof fibrosis during healing after [RMI] remains unclear;” sFRP-2 “has been suggested to induce protection during acute MI in rats via inhibition of Wnt signaling;” recent “evidence in sFRP-2 null mice suggests that sFRP-2 can act independently of Wnt, activate Tolloid-like metalloproteinases and enhance collagen deposition and fibrosis after MI;” angiotensin II (AngII), “acting through AngII type 1 receptors (AT₁Rs), has been suggested to regulate post-MI fibrosis and remodeling;” and “AT₁R antagonists can therefore limit post-MI fibrosis and remodeling.”

Results: During the healing process after an RMI, the limitation of fibrosis and remodeling might be caused by candesartan-induced suppression of sFRP-2 in the infarct/border zones.

High HDL Cholesterol Levels and Markers of Inflammation and Metabolic Health in Patients Hospitalized with Acute Myocardial Infarction

Researchers: Kosiborod M, Spertus J, Jones P, et al.

Purpose: To explore the association between levels of HDL and markers of glucose metabolism and inflammation, because, although patients with myocardial infarction (MI) have a high likelihood of harboring dysfunctional HDL, the “relationship between very high HDL and markers of inflammation and vascular health in MI” patients remains unknown.

Results: Very high HDL in MI patients is related to lower inflammatory levels and atherogenic markers. In this population, no evidence was found of worse BG metabolism. Thus, Kosiborod and colleagues suggest that the “relationship between HDL and pt outcomes should be prospectively investigated.”