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Experimental Model of Inappropriate Sinus Tachycardia: Initiation and Ablation

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Abstract

Objective: The purpose of the present study was to develop an experimental model of inappropriate sinus tachycardia (IST) by injecting a catecholamine into a fat pad containing autonomic ganglia (AG) innervating the sinus node (SN).

Methods: Initial protocols in 3 groups of pentobarbital anesthetized dogs consisted of (1) slowing the heart rate (HR) by electrical stimulation of AG in the fat pad; (2) the effect of intravenous injection of epinephrine (0.1–0.3 mg) on the HR and systolic blood pressure (BP); (3) the response of SN rate to intravenously injected isoproterenol (1 μgm/kg). These studies established a reference for the response to epinephrine injection (mean dose 0.2 ± 0.9 mg, n = 14) into the fat pad at the base of the right superior pulmonary vein (RSPV). ECG leads, right atrial and His bundle electrograms, BP and core body temperature were continuously monitored.

Results: Epinephrine, injected into the fat pad, caused a significant increase in heart rate (HR, average: 211 ± 11/min, p < 0.05 compared to control) but little change in systolic BP, 149 ± 10 mmHg, p = NS (Group I, N = 8). The tachycardia lasted >30 minutes. Ice mapping and P wave morphology showed the tachycardia origin in the SN in 6/8 and in the crista terminalis (CT) in 2. Injection of 0.4 cc of formaldehyde into the FP restored HR (159 ± 16) toward baseline (154 ± 18). In Group II (N = 6), the same regimen induced a significant increase in both HR and systolic BP (194 ± 17/min and 230 ± 24 mmHg, respectively) compared to control values (143 ± 23/min, 162 ± 24 mmHg) which lasted for > 30 minutes. Ice mapping and P wave morphology showed that the pacemaker was in the SN (1), overlying the CT (2), or atrioventricular junction (2). Formaldehyde (0.4 cc) injected into the FP restored both HR and systolic BP toward baseline values (148 ± 29/min and 152 ± 24 mmHg, p = NS) and prevented, slowing of the HR by electrical stimulation of the AG; moreover, the same dose of epinephrine injected intravenously increased HR and SBP but only for 2–5 minutes; Isoproterenol (1 μ g/kg) injected intravenously induced essentially the same increase in sinus rate after AG ablation as in the control state (194 ± 15/min vs 193 ± 23/min, p = NS).

Conclusion: Experimental IST is mainly localized in the SN or CT. Ablation of the AG terminates IST without impairing the SN response to an adrenergic challenge.

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Abbreviations

AF:

Atrial Fibrillation; AG: autonomic ganglia; ECG: electrocardiogram; HR: heart rate; IST: inappropriate sinus tachycardia; RSPV: right superior pulmonary vein; SBP: systolic blood pressure; and SN: sinus node.

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Authors and Affiliations

  1. Cardiac Arrhythmia Research Institute at the University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma

    Benjamin J. Scherlag Ph.D, William S. Yamanashi, Rohit Amin, Ralph Lazzara & Warren M. Jackman

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  1. Benjamin J. Scherlag Ph.D
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  2. William S. Yamanashi
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  3. Rohit Amin
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  4. Ralph Lazzara
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  5. Warren M. Jackman
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Correspondence to Benjamin J. Scherlag Ph.D.

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Supported by grants from the Helen and Wil Webster Arrhythmia Research Fund of the University of Oklahoma Foundation, Norman, Oklahoma and Roger and B. Ann Cole, Edmond, Oklahoma.

Helen Webster Professor of Cardiac Arrhythmias, 1200 Everett Drive, Room TUH6E103, Oklahoma City, OK 73104.

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Scherlag, B.J., Yamanashi, W.S., Amin, R. et al. Experimental Model of Inappropriate Sinus Tachycardia: Initiation and Ablation. J Interv Card Electrophysiol 13, 21–29 (2005). https://doi.org/10.1007/s10840-005-1045-z

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  • DOI: https://doi.org/10.1007/s10840-005-1045-z

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