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Case Report: Radiofrequency Catheter Ablation of Atrial Tachycardia due to Myocarditis Following Viper Bite

Ardashev AV, MD, PhD, ScD, Klimov VP, MD, Zhelyakov EG, MD, Shavarov AA, MD, Steklov VI, MD, PhD, Korneev NV, MD, PhD

Interventional Cardiology Center, Burdenko Head Veterans / Military Clinical Hospital, Moscow, Russia

Introduction
Toxic action of snake venoms can result in development of cardiac arrhythmias in the near future after a bite (1,2). However, such complications are reversible. In the modern literature we have not found any data on development of chronic rhythm disorders after snakebites.

Case
A healthy 20-year old male was bitten by the snake in a finger of the left hand six month prior to ablation. The snake has been identified by the description of the patient and a witness as a Viperae berae. Within four hours after a bite an increasing edema and numbness of the left hand were observed as well as a sharp dizziness. He has been admitted in a regional hospital. He was given an antibiotics, prednisolone, and preventive prophylaxis against tetanus. For the second day the status of the patient was stabilized, within the next five days subfebrile temperature has been noted. For the third day after a snake bite the patient has paid attention to occurrence of palpitation. Weakness and fatigue were observed during usual physical loading. Incessant atrial tachycardia with 126-156 beats per minute, frequent premature atrial beats (PAB) with the intermittent episodes (1-2 complexes) of sinus rhythm were registered at a routine numerous 24-hours ECG monitoring. Antiarrhythmic treatment (verapamil, propranolol, ethacyzin) was of inefficiency. Six month later on moderate left ventricles dilatation up to 57 mm, ejection fraction up to 54% are revealed during transthoracic echocardiography. The activity of inflammation and its association with infection were excluded. Taking into account an efficiency of antiarrhythmic treatment , the decision on carrying out radiofrequency ablation (RFA) of tachycardia was accepted.

Patient underwent an electrophysiological study (EPS) and RFA. Under local anesthesia four quadripolar electrode catheters were introduced percutaneously into the right and left femoral veins and positioned at the high-right atrium, His-bundle region, right ventricular apex. EPS was carried out with simultaneous use of GE Prucka CardioLab systems and Siemens RECOR. SNRT, CSNRT, sinoatrial time were of normal values. Anterograde effective refractory period of AV conduction was normal. The Wenckebach point was 140 impulses per minute. At atrium burst pacing with cycle length of 300 ms there was tachycardia induced of 100-150 beats per minute. Spontaneous PAB, including bi- and trigeminy were observed at moderate physical and emotional loading and at a top of the inspiration (Fig.2, 3). The optimum target for RF application was determined to localize towards basis of right auricle at crista terminalis region (Fig.2, 3). After RFA performed during tachycardia the warming up and subsequent interrupture of tachycardia was observed. While of the expected control period and provocative maneurors using after the procedure a recurrence of a tachycardia was not observed. Control 24-hours ECG monitoring for the fourth day after RF ablation revealed 245 PAB, but pairs and runs were not.

Figure 1. From top to bottom: I, II, III and V1 ECG leads, HRA, His (proximal, medial, distal), RVA recording channels . First and second complex are sinus beats. An incessant atrial tachycardia starts after the second complex.

Figure 2. From top to bottom: I, II, III and V1 ECG leads, His (proximal, medial, distal), RVA recording channels . Atrial allorhythmia. Second, third and sixth complexes are PAB.

Figure 3. From top to bottom: I ECG lead, mapping bipolar and unipolar channels . Activation mapping of incessant atrial tachycardia, targeting for ablation.

Discussion
An arrhythmia could be a criteria for the diagnosis of myocarditis while of chronological linkage with snakebite. Unfortunately, we have no data of immunnologic shifts and echocardiographic heart image characteristics during the acute phase period. On the one hand increase in the sizes of a left ventricular cavity and slightly decrease in ejection fraction before carrying out RFA could be a result of myocardial inflammatory reaction, but on the other hand these changes are most likely caused by remodeling of myocardium following persistent course of atrial tachycardia.

The mechanism by which snake venom poisoning leads to myocarditis is unclear. Case of myocarditis with extensive myocardial necrosis at postmortem examination was reported in two horses after injection of Viperae palaestinae venom for production of antibodies (3). Rowlands and others (4) revealed focal myocardial damages in a fatal case after snakebite by a species of the Australian elapid family. The main role in development immunnologic (allergic) reactions in a myocardium is played by products of disintegration of a cardiac myocytes. On the other hand, endothelins and hemorrhagins, including viper venoms, have coronary vasoconstrictor effects (5,6). It results in development of myocardial cells hypoxia and acidosis. Direct toxic effect of hemorrhagins and endothelins on myocardium is not excluded as well. The other possibilities might include penetration of the infectious agent in a blood and direct damage of myocardium. Sites of a non-uniform myocardial tissue depolarization create preconditions for reentrant arrhythmia to occur.

T he present case has been demonstrated a rare cause of toxic-allergic myocarditis associated with the persistent arrhythmia time course and subsequent RF ablation of persistent atrial tachycardia.

References
• Gupta OP, Mewar SH, Kalantri SP, Jain AP, Jajoo UN. Reversible atrial fibrillation following snakebite. J Assoc Physicians India. 1987; 35(7):535-6.

• Pahlajani DB, Iya V, Tahiliani R, Shah VK, Khokhani RC. Sinus node dysfunction following cobra bite. Indian Heart J. 1987; 39(1):48-9.

• Hoffman A, Levi O, Orgad U, Nyska A. Myocarditis following envenoming with Viperae palaestinae in two horses. Toxicon. 1993; 31:1623-1628.

• Rowlands JB, Mastaglia FL, Kakalus BA, Hainsworth D. Cardiac muscle damage by myotoxins: clinical and pathological aspects of a fatal case of mulga (Pseudechis australis) snakebite. Med J Australia. 1969; 1:226-230.

• Wollberg Z, Bdolah A, Kochva E. Cardiovascular effects mammalian endothelins and snake venom sarafotoxins. In: Abraham S, Amitai G, eds. Calcium channal modulators in heart and smooth muscle. Deerfield Beach, FL: VCH, Weinheim. 1990:283-299.

• Benerjee RN. Poisonous snakes of India, their venoms, symptomatology and treatment of envenomation. In: Ahuja MMS, ed. Progress in clinical medicine in India. New Delhi: Arnold Heineman. 1978 : 136-180.