| Article Access Statistics|
| Viewed||4590 |
| Printed||127 |
| Emailed||4 |
| PDF Downloaded||24 |
| Comments ||[Add] |
| Cited by others ||1 |
Click on image for details.
|Year : 2013 | Volume
| 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
|Date of Submission||01-Nov-2012|
|Date of Decision||03-Dec-2012|
|Date of Acceptance||21-Feb-2013|
|Date of Web Publication||21-Jun-2013|
Department of Medicine, Sri Aurobindo Institute of Medical Sciences, Indore, Madhya Pradesh
Source of Support: None, Conflict of Interest: None
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.
Keywords: Cardiac toxicity, myocardial infarction, organophosphorus poisoning, pesticides
|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;59:142-4
|How to cite this URL:|
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 2021 May 8];59:142-4. Available from: https://www.jpgmonline.com/text.asp?2013/59/2/142/113843
| :: Introduction|| |
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%.  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. ,
| :: 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.
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: ECG (day 2) showing ST segment coving with T wave inversion in leads V3– V6|
Click here to view
| :: Discussion|| |
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:
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.  Other cardiac manifestations of it are sinus tachycardia, sinus bradycardia, QT prolongation, and rarely ventricular arrhythmias.
- Brief period of increased sympathetic tone
- Prolong period of parasympathetic activity
- QT prolongation followed by torsades de pointes. ,
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. , 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. 
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.  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.
| :: References|| |
|1.||Shadnia S, Esmaily H, Sasanian G, Pajoumand A, Hassanian- Moghaddam H, Abdollahi M. Pattern of acute poisoning in Tehran-Iran in 2003. Hum Exp Toxicol 2007;26:753-6. |
|2.||Karki P, Ansari JA, Bhandary S, Koirala S. Cardiac and electrocardiographical manifestations of acute organophosphate poisoning. Singapore Med J 2004;45:385-9. |
|3.||Kidiyoor Y, Nayak VC, Devi V, Bakkannavar SM, Kumar GP, Menezes RG. A rare case of myocardial infarction due to parathion poisoning. J Forensic Leg Med 2009;16:472-4. |
|4.||Ludomirsky A, Klein HO, Sarelli P, Becker B, Hoffman S, Taitelman U, Q-T prolongation and polymorphous (torsade de pointes) ventricular arrhythmias associated with Organophosphorus insecticide poisoning. Am J Cardiol 1982;49:1654-8. |
|5.||Anand S, Singh S, Nahar Saikia U, Bhalla A, Paul Sharma Y, Singh D. Cardiac abnormalities in acute organophosphate poisoning. Clin Toxicol (Phila) 2009;47:230-5. |
|6.||Kiss Z, Fazekas T. Arrhythmias in organophosphate poisonings. Acta Cardiol 1979;34:323-30. |
|7.||Yasue H, Touyama M, Shimamoto M, Kato H, Tanaka S. Role-of autonomic nervous system in the pathogenesis of Prinzmetal's variant form of angina. Circulation 1974;50:534-9. |
|8.||Horio Y, Yasue H, Rokutanda M, Nakamura N, Ogawa H, Takaoka K, et al. Effects of intracoronary injection of acetylcholine on coronary arterial diameter. Am J Cardiol 1986;57:984-9. |
|9.||Karasu-Minareci E, Gunay N, Minareci K, Sadan G, Ozbey G. What may be happen after an organophosphate exposure: Acute myocardial infarction? J Forensic Leg Med 2012;19:94-6. |
|10.||Gázquez V, Dalmau G, Gaig P, Gómez C, Navarro S, Mercé J. Kounis syndrome: Report of 5 cases. J Investig Allergol Clin Immunol 2010;20:162-5. |
[Figure 1], [Figure 2], [Figure 3]
|This article has been cited by|
||Cardiotoxicity in OPC poisoning: Time to think differential diagnosis
| ||Senthilkumaran, S., Balamurugan, N., Jayaraman, S., Thirumalaikolundusubramaniam, P. |
| ||Journal of Postgraduate Medicine. 2013; 59(4): 337 |