Background: Autonomic dysfunction has a prognostic significance in various cardiovascular (CV) disorders, particularly atherosclerotic coronary artery disease (CAD). Previous studies are few, regarding the association of parasympathetic dysfunction with increased complications in patients with the acute coronary syndrome, a subset of CAD. We aimed to study the correlation of trends in the serum cholinesterase (sChE) levels, the marker of parasympathetic activity, with the occurrence of major adverse cardiovascular events (MACEs) in ST-segment elevation myocardial infarction (STEMI) patients. Methodology: We prospectively observed the levels of sChE in patients with STEMI on the day of admission, day 3, and day 5 along with routine biochemical profile, electrocardiogram, echocardiography, and coronary angiography. The patients were monitored during the hospital stay and were followed up at 1 month for the occurrence of any MACE. The MACE monitored was cardiac death, complete heart block, arrhythmias, and heart failure. The sChE levels are laboratory dependent and a value between 4000 and 14000 IU/L was considered normal in our laboratory. A value <4000 IU/L is noted as a low sChE level. The receiver operating characteristic curve was plotted for the cut off value of the sChE levels to predict the outcomes of patients. Results: Of the 100 STEMI patients studied, the sChE levels were persistently lower in patients who had MACE compared to those without MACE during the hospital stay and at month follow-up, which was statistically significant. A sChE <3745 IU/l on day 5 predicted an increased MACE with a sensitivity of 93.55% and specificity of 92.11%. Conclusion: A persistently low sChE levels from the day of admission can predict MACE in STEMI patients. Larger studies with prolonged follow-up are required for the causal association in the future.

Introduction: The most plausible factor for coronary artery ectasia (CAE), a subset of coronary artery disease (CAD), is extensive inflammation. High-sensitivity C-reactive protein (hs-CRP) and serum uric acid (sUA) are well known markers of inflammation. Most of the previous studies (done in the Western population and of Middle East Asia) evaluated their role individually as a marker of inflammation in CAD. We aimed to investigate the possible association of isolated CAE with inflammation as assessed by the hs-CRP and sUA levels and check whether the inflammatory hypothesis holds good in the south Asian population. Materials and Methods: Patients admitted for coronary angiography with age ≥30 years were evaluated. Patients with both CAE and CAD were excluded. A total of 60 patients were studied. Patients with isolated CAE (30) were compared with an equal number of patients with obstructive CAD (30) and their clinical profile was studied. The hs-CRP, sUA, and novel inflammatory markers such as neutrophil–lymphocyte ratio (NLR), mean platelet volume (MPV), and red cell distribution width (RDW) were compared between the groups. Results: Of the 60 patients studied, males were 56% in the isolated CAE group and 50% in the obstructive CAD group. The hs-CRP (2.39 ± 0.41 vs. 1.41 ± 0.29, P < 0.001) and sUA levels (6.46 ± 0.58 vs. 5.36 ± 0.40, P < 0.001) were significantly elevated in the isolated CAE group compared to the obstructive CAD group. Among the novel inflammatory markers, the NLR (3.98 ± 0.42 vs. 2.91 ± 0.30, P < 0.001) and RDW (12.69 ± 0.27 vs. 12.13 ± 0.48, P < 0.001) were significantly higher in the CAE group compared to obstructive CAD group, whereas the MPV did not have a statistically significant difference (9.5 ± 0.98 vs. 9.6 ± 1.08, P = 0.525). Conclusion: The inflammatory etiology of CAE was supported by an elevated hs-CRP, sUA, and other novel inflammatory markers compared to the atherosclerotic obstructive CAD group.