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Year : 2015  |  Volume : 3  |  Issue : 1  |  Page : 18-20

Acute Myocardial Infarction Following Viper Bite: A Rare Scenario

1 Department of General Medicine, Institute of Cardiovascular Sciences, Institute of Post Graduate Medical Education and Research, Kolkata, West Bengal, India
2 Department of Cardiology, Institute of Cardiovascular Sciences, Institute of Post Graduate Medical Education and Research, Kolkata, West Bengal, India

Date of Web Publication14-Mar-2015

Correspondence Address:
Subrata Chakrabarti
Doctor Hostel, Institute of Post Graduate Medical Education and Research, Ajc Bose Road, Kolkata - 700 020, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2321-449X.153281

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Acute myocardial infarction (AMI) is a rare complication of snake bite with few reported cases in literature. The author reports a case of a 32-year-old male who developed an anterior wall AMI several hours after a Russell's viper bite. The diagnosis of myocardial infarction was confirmed by a characteristic retrosternal chest pain, typical electrocardiographic changes, and elevated Troponin I levels. The patient had no risk factors for coronary artery disease and the coronary arteries were normal on cardiac catheterization. The importance of the case report is to highlight upon the fact that physicians, especially from developing countries like India should be aware of this potentially life-threatening complication of viper bite and take immediate steps for its recognition and management.

Keywords: Acute myocardial infarction, cardiac catheterization, viper bite

How to cite this article:
Chakrabarti S, Biswas P, Patil S, Pan K. Acute Myocardial Infarction Following Viper Bite: A Rare Scenario. Heart India 2015;3:18-20

How to cite this URL:
Chakrabarti S, Biswas P, Patil S, Pan K. Acute Myocardial Infarction Following Viper Bite: A Rare Scenario. Heart India [serial online] 2015 [cited 2023 Mar 27];3:18-20. Available from: https://www.heartindia.net/text.asp?2015/3/1/18/153281

  Introduction Top

Viper bites are notorious for local and systemic complications including local tissue necrosis, hemolysis and hemorrhagic complications, nephrotoxicity, coagulation abnormalities and neurological complications. Ischemic cardiac events, arrhythmias and cardiac tamponade rarely occur after viper bites. [1],[2] The author reports a case of anterior wall ST segment elevation myocardial infarction after Russell's viper bite.

  Case report Top

A 35-year-old male, a farmer by occupation, presented to the emergency with severe swelling and pain in the left foot and gross hematuria and diminished urine output after being bitten by a snake 5 hours back. The snake (which was later killed by his relatives and brought to the emergency) was identified as a Russell's viper (based on presence of flattened, triangular, distinct head with large, single nasal scale and continuous almond-like solid spots of blackish color present in three longitudinal rows along the body starting from the head and generally becoming faint or absent on posterior side). The species was also confirmed by forensic experts. On arrival, the patient was fully conscious and alert, with no pallor or jaundice. Examination revealed fang marks with severe swelling and oozing with inflammation in the dorsum of left foot (at the site of bite). His blood pressure was 125/81 mm Hg, heart rate -92 beats per minute, regular rate and sinus rhythm; temperature 37.7°C, and respiratory rate 16 breaths per minute. Arterial oxygen saturation (SpO 2 ) was 98%. Examination of the heart, lungs, abdomen and nervous system was unremarkable. Twenty-minute whole blood clotting time was deranged. The patient was immediately administered poly-valent anti-snake venom (after proper skin tests) along with local wound care (including tetanus prophylaxis). Other supportive measures were instituted. Initial laboratory parameters revealed that blood counts, serum electrolytes, blood urea nitrogen, creatinine, liver function tests, coagulation parameters, urinalysis and fasting plasma glucose levels were within normal limits. Lactic dehydrogenase was 237 U/L (normal 225-450 U/L) and creatinine kinase (CK) was 109 U/L (normal 24-195 U/L). Chest radiograph and electrocardiograph were all within normal limits. Eight hours after admission and 2 hours after administration of AVS, he developed retrosternal crushing chest pain, faintness, and vomiting. He was a known non-smoker and he denied ever using any psychoactive drugs (including cocaine). There was no family history of dyslipidemia or premature deaths due to probable cardiac events. He was profusely sweating with regular thready pulse of 124/min, his blood pressure dropped to 67/46 mm Hg and he was tachypneic, with respiratory rate of 38/min. Sensorium was obtunded and he became drowsy and disoriented. On auscultation, bi-basal fine crepitations were noted. Arterial oxygen saturation (SpO 2 ) dropped to 88%. Examination findings suggested that the patient was in cardiogenic shock. An urgent electrocardiogram (ECG) showed a pattern of ST segment elevation antero-septal myocardial infarction [Figure 1],[Figure 2] and [Figure 3]. No arrhythmias were noted. Portable chest X-ray showed evidence of pulmonary edema. Cardiac Troponin I assay was found to be positive in high titers and CPK-MB was raised significantly. Bedside 2-dimensional transthoracic echocardiogram revealed regional wall motion abnormalities in LAD territory [Video 1]. He was immediately intubated and transferred to intensive care unit. He was started on inotropes and volume expansion. It was decided to immediately go for primary coronary intervention (PCI). However, as the patient's party did not give consent for PCI despite repeated counseling explaining its obvious necessity, after discussing the risk and benefits of thrombolysis, he was treated with bolus doses of reteplase. Post-thrombolysis, there was complete ST-segment resolution and the hemodynamics stabilized and patient's symptoms improved. Eight days later, when he was asymptomatic, the patient underwent cardiac catheterization and coronary angiography and repeat echocardiography, which were entirely normal, except for a mild anterior wall hypokinesia [Videos 2 and 3]. He was discharged in a stable condition on day 10 with advice for regular follow-up.
Figure 1: ECG showing ST segment elevation in lead V1-V4 suggestive of antero-septal AMI

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Figure 2: ECG showing no ST segment elevation in lead V5, V6

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Figure 3: ECG showing no ST segment elevation in lead I, II, III, aVR, aVL, aVF

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  Discussion Top

Cardiac manifestations are common with snake bites especially viper bites, yet significant myocardial damage is very rare. A study conducted in Nigeria involving 108 snake bite patients found that more than 60% patients had hemodynamic and electrocardiographic abnormalities, but significant cardiac enzyme elevation occurred in only one patient. [2] In another study involving 51 snake bite patients by Lalloo et al, ECG abnormalities in the form of T-wave inversion, sinus bradycardia, or rarely atrioventricular block were observed commonly but while only 2 patients had elevated plasma cardiac troponin T. [3] The exact mechanism by which envenomation leads to myocardial infarction is unclear, but various postulatory mechanisms are forwarded. It is likely that the cause of myocardial infarction following viper bite may involve more than one mechanism.

Hypercoagulability with consumption coagulopathy has been suggested in most cases as evidence of thrombosis in coronary, cerebral and pulmonary vasculature has been observed following viper bites in humans. [4],[5] The absence of arterial occlusion in angiography in the index patient 10 days after the infarction does not rule out the possibility of thrombosis that may have resolved.

The direct cardiotoxic effect of snake venom can result in myocarditis and extensive myocardial necrosis. It has been proved in horses injected with Viper palaestinae venom. [6],[7],[8] Hypovolemic shock because of bleeding due to hemorrhagins or toxic vasculitis has also been considered. [9] Hypovolemic shock and toxic myocarditis are unlikely in this patient as these lead to more diffuse and extensive myocardial damage, and they take some time (>24 hours) to develop. In the index patient, the ST segment elevations were limited to the distribution of LAD and developed within hours. In addition, toxic myocarditis is unlikely due to lack of associated arrhythmias or conduction defects in ECG and lack of cardiac dilatation in repeat chest X-ray and echocardiography.

Coronary spasms due to endothelins or sarafotoxins can lead to AMI. Presence of normal coronary arteries in post-myocardial infarction coronary angiograms of the patients in most cases reportedly suggested coronary artery spasm as a candidate cause of myocardial ischemia as in this case. [10],[11] However, as urgent coronary angiography was not possible, there was no way to pinpoint whether coronary thrombosis or vasospasm was responsible for the AMI or both contributed independently to this complication. As this patient was a non-smoker and also normotensive and non-diabetic with no family history of dyslipidemias or adverse cardiac events, pre-existing coronary stenosis was considered unlikely. It is widely accepted that coronary spasm without prior stenosis usually leads to small infarctions unlike the extensive antero-septal AMI as in the index case. [12] Moreover, hypercoagulability is incriminated more often as cause of vascular complications over and above vasospasm in a case of vasculotoxic snake bite. As noted earlier, the absence of arterial occlusion in angiography in the index patient 10 days after the infarction does not rule out the possibility of thrombosis that may have resolved. Consequently, in the index patient, the AMI was attributed primarily to newly developed thrombosis in LAD vascular bed and it was decided to proceed to urgent thrombolysis (consent for the ideal treatment i.e., PCI being not available) although the possibility of vasospasm as a second contributing factor could not be nullified at the first place.

Hyperviscosity secondary to hypovolemia-induced hemoconcentration and anaphylactic shock have also been considered to be contributory alongside thrombosis. [13] Their role in most cases including the index one is debatable.

Takatsubo (stress) cardiomyopathy, which classically develops after severe emotional or physical stress in patients without classical risk factors of cardiovascular disease is a rare condition but a close mimicker of heart attack and its possibility in the index case was initially considered (Russell's viper bite can lead to both significant emotional and physical stress and the patient had no classical risk factors for atherosclerosis). But it is commonly reported among elderly post-menopausal females with age >50 years. [14] The index patient was a 35-year-old male. In ECG, deep T wave inversions and ST depressions are often commoner than ST elevations and cardiac enzymes and biomarkers are positive in small titers. The index patient had strong elevation in both CPK-MB and Troponin assay titers and no T wave inversions were noted within the first 48 hrs. Echocardiography in Takatsubo cardiomyopathy classically demonstrates localized apical hypokinesia with basal hypercontraction and not extensive involvement like regional wall motion abnormalities in entire LAD territory as in the index case. Moreover, a repeat echo after 1-2 weeks usually reveals complete resolution of wall hypokinesia but repeat echo in the index case on the 8 th day showed persistent anterior wall hypokinesia. [14],[15] Although, an urgent left ventriculography showing systolic ballooning of the apex and hypercontraction of the basal segment is probably the best investigation to diagnose or rule out this entity, unfortunately the performance of the said test was not possible in our institution. [14],[16] Still with the help of appropriate tests at our disposal, Takatsubo cardiomyopathy was safely ruled out.

  References Top

Phillips RE, Theakston RD, Warrell DA, Galigedara Y, Abeysekera DT, Dissanayaka P, et al. Paralysis, rhabdomyolysis and haemolysis caused by bites of Russell′s viper (Vipera russelli pulchella) in Sri Lanka: Failure of Indian (Haffkine) antivenom. Q J Med 1988;68:691-715.  Back to cited text no. 1
Karaye KM, Mijinyawa MS, Yakasai AM, Kwaghe V, Joseph GA, Iliyasu G, et al. Cardiac and hemodynamic features following snakebite in Nigeria. Int J Cardiol 2012;156:326-8.  Back to cited text no. 2
Lalloo DG, Trevett AJ, Nwokolo N, Laurenson IF, Naraqi S, Kevau I, et al. Electrocardiographic abnormalities in patients bitten by taipans (Oxyuranus scutellatus canni) and other elapid snakes in Papua New Guinea. Trans R Soc Trop Med Hyg 1997;91:53-6.  Back to cited text no. 3
Upadhyaya AC, Murthy GL, Sahay RK, Srinivasan VR, Shantaram V. Snake bite presenting as acute myocardial infarction, ischaemic cerebrovascular accident, acute renal failure and disseminated intravascular coagulopathy. J Assoc Physicians India 2000;48:1109-10.  Back to cited text no. 4
Hung DZ, Wu ML, Deng JF, Yang DY, Lin-Shiau SY. Multiple thrombotic occlusions of vessels after Russell′s viper envenoming. Pharmacol Toxicol 2002;91:106-10.  Back to cited text no. 5
Aravanis C, Ioannidis PJ, Ktenas J. Acute myocardial infarction and cerebrovascular accident in a young girl after a viper bite. Br Heart J 1982;47:500-3.  Back to cited text no. 6
Blondheim DS, Plich M, Borman M, Khair G, Tzvig L, Ezri J, et al. Acute myocardial infarction complicating viper bite. Am J Cardiol 1996;78:492-3.  Back to cited text no. 7
Hoffman A, Levi O, Orgad U, Nyska A. Myocarditis following envenoming with Viperae palaestinae in two horses. Toxicon 1993;31:1623-8.  Back to cited text no. 8
Copley AL, Banerjee S, Devi A. Studies of snake venoms on blood coagulation. Thromb Res 1973;2:487-508.  Back to cited text no. 9
Tony JC, Bhat R. Acute myocardial infarction following snakebite. Trop Doct 1995;25:137.  Back to cited text no. 10
Maheshwari M, Mittal SR. Acute myocardial infarction complicating snake bite. J Assoc Physicians India 2004;52:63-4.  Back to cited text no. 11
Stern S, Bayes de Luna A. Coronary artery spasm: A 2009 update. Circulation 2009;119:2531-4.  Back to cited text no. 12
Dissanayake P, Sellahewa KH. Acute myocardial infarction in a patient with Russell′s viper bite. Ceylon Med J 1996;41:67-8.  Back to cited text no. 13
Virani SS, Khan AN, Mendoza CE, Ferreira AC, de Marchena E. Takotsubo cardiomyopathy, or broken-heart syndrome. Tex Heart Inst J 2007;34:76-9.  Back to cited text no. 14
Zeb M, Sambu N, Scott P, Curzen N. Takotsubo cardiomyopathy: A diagnostic challenge. Postgrad Med J 2011;87:51-9.  Back to cited text no. 15
Gianni M, Dentali F, Grandi AM, Sumner G, Hiralal R, Lonn E. Apical ballooning syndrome or takotsubo cardiomyopathy: A systematic review. Eur Heart J 2006;27:1523-9.  Back to cited text no. 16


  [Figure 1], [Figure 2], [Figure 3]

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