Journal of Postgraduate Medicine
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Year : 2013  |  Volume : 59  |  Issue : 2  |  Page : 142-144  

Acute myocardial infarction: Can it be a complication of acute organophosphorus compound poisoning?

P Joshi, P Manoria, D Joseph, Z Gandhi 
 Department of Medicine, Sri Aurobindo Institute of Medical Sciences, Indore, Madhya Pradesh, India

Correspondence Address:
P Joshi
Department of Medicine, Sri Aurobindo Institute of Medical Sciences, Indore, Madhya Pradesh


Organophosphorus compounds are used as pesticides and represent a common cause of poisoning in developing countries including India due to their widespread availability and use. Toxicity due to these agents can affect many organs including heart. Here, we report a case of acute organophosphorus poisoning (parathion), followed by acute myocardial infarction; documented by clinical features, electrocardiographic changes, and elevated cardiac enzymes. Myocardial infarction has been rarely reported with organophosphorus compounds exposure, thus awareness of this complication can reduce morbidity and mortality.

How to cite this article:
Joshi P, Manoria P, Joseph D, Gandhi Z. Acute myocardial infarction: Can it be a complication of acute organophosphorus compound poisoning?.J Postgrad Med 2013;59:142-144

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Joshi P, Manoria P, Joseph D, Gandhi Z. Acute myocardial infarction: Can it be a complication of acute organophosphorus compound poisoning?. J Postgrad Med [serial online] 2013 [cited 2023 Mar 22 ];59:142-144
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Organophosphorus compounds are acetyl cholinesterase inhibitors used as pesticides and represent a common cause of poisoning and a major health problem in India. They are widely used, easily available and are common causes of acute poisonings. Although it can result from occupational exposure or accidental ingestion, most cases are with suicidal intent. Mortality despite therapy ranges from 2-30%. [1] Cardiac complications accompanying this poisoning can be serious and fatal. These include cardiac arrhythmias, electrocardiographic abnormalities, conduction defects, as well as myocardial infarction, a rarely reported complication of acute pesticide poisoning. [2],[3]

 Case Report

A 40-year-old man was brought to the emergency department after two and half hours of parathion (organophosphorus compound) ingestion with suicidal intent (quantity unknown). He was a chronic smoker (10 cigarettes/day) for the past decade. On admission, he was drowsy with bilateral pin point pupils. There was sinus bradycardia (pulse rate 58/min) with a blood pressure of 110/80 mm Hg. Frothing at the mouth and fasciculations were present. ECG at presentation showed sinus bradycardia [Figure 1]. He was treated with intravenous atropine and pralidoxime in dose of 2gm bolus followed by 500mg/hr infusion. Gastric aspirate was positive for parathion. The patient's laboratory findings demonstrated normal hemoglobin (14 gm/dl), leucocytosis (20.4 per mm 3 ), normoglycemia (RBS: 100 mg/dl), and normal serum electrolytes. Serum cholinesterase level could not be measured due to lack of facilities.{Figure 1}

On second day of admission, patient suddenly went into respiratory distress and hypotension and was put on mechanical ventilation. Chest auscultation revealed fine basal crepts that were present bilaterally. ECG done at that time showed ST segment coving with T-wave inversion in leads V3-V6 [Figure 2]. Two-dimensional Echo showed hypokinesia of the anteroseptal wall and apex with LVEF 40%. X-ray chest was done which suggested presence of acute left ventricular failure. Biochemical cardiac marker Trop I was positive (3 ng/ml) and he was treated with antiplatelets, nitrates, statins, low-molecular-weight heparin (enoxaparin 60 mg twice a day) and inotropic support. Patient improved after 48 h and was weaned off from ventilator. Subsequent ECG showed resolution of the ST and T changes and patient was discharged in stable condition after ninth day of admission [Figure 3].{Figure 2}{Figure 3}


A pesticide is usually defined as a chemical substance, biological agent, antimicrobial, or disinfectant used against pests, including insects, plant pathogens, weeds, molluscs, birds, fish, nematodes (roundworms), and microbes that compete with humans for food, destroy property, and have a propensity for spreading disease. In India, the use of pesticides began in 1948 with the introduction of DDT for the control of malaria and benzene hexachloride (BHC) for locusts. Production of these substances in India started in 1952. The increase in pesticide use for agriculture has paralleled the increase in quality and quantity of food products over the years. At the same time, there has been an increase in the use of these products for deliberate self-harm (DSH). At times, pesticides have been accidentally consumed and on rare occasions have even been used for homicidal purposes. Cardiac abnormalities have been rarely reported in pesticides poisoning that too in organophosphorus poisoning. Mechanism of cardio toxicity by these compounds is still completely unknown although there are few mechanisms postulated according to which there are three phases of cardio toxicity:

Brief period of increased sympathetic toneProlong period of parasympathetic activityQT prolongation followed by torsades de pointes. [4],[5] Other possible mechanisms include sympathetic/parasympathetic overactivity, hypoxemia, acidosis, dyselectrolemia, and direct cardio toxicity. The current case can be an unusual presentation of acute myocardial infarction due to organophosphorus poisoning. In one study, out of 168 cases of organophosphorus poisoning only 5 have features of myocardial infarction. [6] Other cardiac manifestations of it are sinus tachycardia, sinus bradycardia, QT prolongation, and rarely ventricular arrhythmias.

Yasue et al. in 1974 has postulated that parasympathetic over activity plays a major role in coronary artery spasm and later Horio et al. induced coronary artery spasm in healthy adults after intracoronary injection of acetyl choline. [7],[8] Coronary vasospasm is an important factor in the pathogenesis of myocardial infarction. Also, increased release of catecholamines and other vasoactive amines (histamines and neutral proteases) by pesticides that penetrate the collagen matrix of plaque there by producing erosions and rupture which can lead to myocardial injury. [9]

Kounis syndrome is a phenomenon, which manifests as unstable vasospastic or nonvasospastic angina and even myocardial infarction, triggered by release of inflammatory mediators like histamines, neutral proteases, arachidonic acid products, platelets activating factors, and various cytokines and chemokines. [10] There are three variants: Type I, which includes patients with normal coronary artery without predisposing risk factors in which inflammatory mediators induce coronary spasm, type II in which there is rupture of a preexisting atheromatous plaque by inflammatory mediators, and type III variant includes patients with coronary thrombosis (including stent thrombosis) in whom aspirated thrombus specimens stained with hematoxylin-eosin and Giemsa demonstrate the presence of eosinophils and mast cells, respectively. Our case is probably a case of Type II Kounis syndrome.

Cardiac complications after organophosphorus poisoning are usually not appreciated by many clinicians. It usually occurs within first few hours of exposure and depends on the amount of poison intake and the time after which treatment is started.

In conclusion, organophosphorus poisoning can be associated with severe cardiac complications within few hours of exposure including myocardial infarction. Dyselectrolemia and hypoxemia may be the predisposing factors. Thus, along with initial supportive treatment, intensive cardiac monitoring should also be done which may reduce the mortality in these cases.


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