Myocardial infarction in organophosphorus poisoning: Association or just chance?

Dear Editor,

Acute organophosphate poisoning (OPP) most often suicidal occurs very commonly in Vidarbha region of central India where farmers who are debt ridden use organophosphorus compounds as insecticides. Here, we report a case of a 40-years-old farmer admitted in the medicine intensive care unit with alleged history of pesticide consumption about 2 h prior at his home. The patient was hemodynamically stable with pulse rate of 60 per minute, regular and blood pressure of 110/76 mm of Hg. On evaluation the patient was drowsy with pinpoint pupil and bilateral crackles in the chest. Fasciculation were noticed over the thighs and arms. Management was done with atropine and pralidoxime along with mechanical ventilation. On investigations, his serum cholinesterase levels were 1048 IU/L (normal levels 4000-12000 IU/L). His hemogram, blood sugar, liver function, renal functions and lipid profile were within normal limits. On 3rd day, patient's ECG changes were noticed which were suggestive of inferolateral myocardial infarction [Figure 1]. The creatine kinase levels (CK-MB) done at that time was 154 IU/L (normal levels 15-35 IU/L). In view of ECG changes and raised enzymes levels, we made a diagnosis of myocardial infarction and was thrombolysed with injection Streptokinase 1.5 million units and managed conservatively afterwards. ECG became normal. His coronary angiography was planned but due to non-affordability this was deferred.

Figure 1

ECG- ST elevation suggestive of inferolateral ischemia

Cardiac complications are rare, serious and little known in OPP which include repolarization abnormalities like ST segment elevation and T wave inversion, prolongation of the QTc interval, rhythm abnormalities such as sinus tachycardia, sinus bradycardia, extra systoles, atrial fibrillation and ventricular tachycardia.[1] Acute myocardial infarction as a result of acute OPP though have been reported but are exceptionally rare.[2] The mechanism of toxicity of organophosphorus compounds is the irreversible binding of the compounds with the serum cholinesterase enzyme and converts this enzyme into a inactive protein complex with subsequent accumulation of increased amount of acetylcholine at the neuromuscular junction leading to persistent stimulation and subsequent disruption of the nerve transmission both in peripheral and central nervous system.[3]

OPP are associated with the cardiac complications and most of them occur during the first few hours after exposure. However, in our case it was after three days. Possible mechanism of cardiac toxicity after OPP may include phase 1, a brief period of increased sympathetic tone; phase 2, a prolonged period of parasympathetic activity; and phase 3, in which Q-T prolongation followed by torsade de pointes ventricular tachycardia and then ventricular fibrillation occur.[4] This parasympathetic over activity plays a major role in the coronary artery spasm which is an important factor in pathogenesis of myocardial infarction. Also, pesticides release increased the amount of catecholamines and other vasoactive amines (histamines and neutral proteases) that penetrate the collagen matrix of plaque causing erosions and rupture which can lead to myocardial injury. These inflammatory mediators can cause coronary thrombosis, as well as spasm leading to myocardial infarction.[5] In our case this may be the pathogenesis as it happens after few days.

But the exact pathophysiology behind organophosphorus compound leading to cardiac manifestations is not clearly understood. Apart from the direct toxic effect of the organophosphorus compounds on myocardium, over activity of cholinergic or nicotinic receptors, the increase in sympathetic and/or parasympathetic activity, hypoxemia, electrolyte abnormalities and acidosis have been hypothesized to play a role in the damage caused to myocardium along with the high dose of atropine. More studies are required to prove this hypothesis.