Atropine Sulfate

A myocardial bridge (MB) is a condition where a segment of an epicardial coronary artery passes through the myocardial muscle. While traditionally regarded as benign, MBs have been associated with various cardiovascular conditions. Therefore, assessing their hemodynamic impact is crucial for informed treatment decisions. Intracoronary functional assessments, such as fractional flow reserve (FFR) and instantaneous wave-free ratio (iFR), have proven useful, especially under inotropic stimulation. However, their invasive nature limits their widespread clinical application. The Quantitative Flow Ratio (QFR) has emerged as a minimally invasive alternative for functional evaluation of MBs, though data on its use are still limited. This study aims to compare the diagnostic efficacy of FFR, iFR, and QFR for evaluating MBs both at rest and under stress conditions. Patients with confirmed MB on the LAD and typical angina (or abnormal noninvasive tests indicating myocardial ischemia) were included. According to a prespecified protocol, all patients underwent functional intracoronary evaluation with FFR and iFR at rest and after dobutamine and atropine intravenous infusion. QFR was also calculated for all cases both at rest and during dobutamine infusion. FFR values ≤0.80, iFR values ≤0.89 and QFR values ≤0.84 were considered indicative of significant myocardial ischemia. A total of 21 patients were included. Median FFR remained unchanged from rest (0.85) to stress (0.85), with only 1 patient showing a positive stress-FFR. In contrast, median iFR significantly decreased from 0.91 to 0.79 (p <0.001), with stress-iFR ≤0.89 in 18 patients. Resting QFR did not indicate significant hemodynamic impact of the MB (median 0.90), but under inotropic stimulation, ischemia was detected in 18 patients (median 0.79, p <0.001). QFR and iFR were concordant during stress in 19 patients, showing a significant positive correlation (Spearman's ρ = 0.702, p = 0.037) and comparable sensitivity (0.86). QFR, computed during inotropic infusion, shows high sensitivity for detecting MB-related ischemia, comparable to stress-iFR and superior to stress-FFR. The correlation between stress-induced iFR and QFR suggests QFR as a reliable, minimally invasive alternative for functional lesion-specific evaluation in MB patients. Larger studies are necessary to confirm these preliminary findings and standardize QFR use in dynamic coronary stenosis assessments.

Organophosphates (OPs) exert their toxic effects by inhibiting acetylcholinesterase in both central (CNS) and peripheral nervous systems (PNS), resulting in accumulation of acetylcholine and overstimulation of cholinergic synapses. Seizures associated with OP poisoning typically occur in the context of overt systemic cholinergic manifestations. We report a patient with OP poisoning who developed status epilepticus without developing peripheral cholinergic features.

A 40-year-old Sri Lankan man presented six hours after deliberate ingestion of 50 mL of profenofos (500 g/L emulsifiable concentrate). His past medical history was unremarkable. There was no history of substance misuse. On admission, he was conscious, haemodynamically stable, and did not have signs of cholinergic excess. Thirty-six hours post-ingestion, he developed generalized tonic-clonic seizures, which were refractory to intravenous (IV) midazolam boluses and IV levetiracetam. He was intubated and mechanically ventilated. Continuous electroencephalographic monitoring confirmed termination of seizure activity with an intravenous midazolam infusion. Atropine was administered empirically for possible central cholinergic toxicity. The patient made a full neurological recovery and was successfully extubated 72 h after ingestion. The patient remained asymptomatic in a six month follow up.

This case illustrates an uncommon presentation of OP poisoning: delayed-onset status epilepticus in the absence of peripheral cholinergic features. The high lipophilicity of profenofos may facilitate preferential accumulation in the CNS, leading to a predominantly central cholinergic syndrome. This underscores the importance of recognising atypical neurotoxic presentations of OP poisoning and the potential need for CNS-directed therapy even in the absence of classic peripheral signs.