Key result
In dogs with rapid pacing-induced heart failure, the arrhythmogenic threshold dose of exogenous norepinephrine required to induce ventricular tachycardia was significantly increased (P<0.01).
Why the study?
Does rapid pacing-induced heart failure decrease sensitivity to the arrhythmogenic effects of catecholamines in dogs?
Does rapid pacing-induced heart failure decrease sensitivity to the arrhythmogenic effects of catecholamines in dogs?
In a canine model of pacing-induced heart failure, the failing heart demonstrated decreased sensitivity to the arrhythmogenic effects of catecholamines.
Answers are grounded in this paper and cite their sources.
Supports blunted norepinephrine arrhythmogenicity in pacing-induced canine HF; leaves open translation to human disease.
Increased circulating catecholamines are considered to be arrhythmogenic in heart failure. It is unclear whether increased circulating catecholamines contribute directly to ventricular arrhythmias or are only markers of the severity of heart failure. The present study determined the sensitivity of the failing heart to the arrhythmogenic effect of exogenous norepinephrine in a rapid pacing-induced model of heart failure in dogs (240 beats for 4 wk, n = 14). A similarly operated, non-paced group served as controls (n = 9). Cardiac sensitivity to the arrhythmogenic effect of catecholamines was determined by measuring the minimal dose of exogenous norepinephrine that induced ventricular tachycardia (arrhythmogenic threshold dose, ATD). ATD significantly increased after development of heart failure in heart-failure group (1.62 +/- 0.32 microgram/kg at baseline vs. 16.65 +/- 3.48 micrograms/kg at restudy, P < 0.01), whereas no significant change was noted in the control group (1.08 +/- 0.36 microgram/kg at baseline vs. 2.53 +/- 0.36 micrograms/kg at restudy, P > 0.10). Action potential duration was unchanged by superfusion with 10(-7) M isoproterenol in both ventricular muscles (230.2 +/- 6.1 vs. 229.7 +/- 5.3 ms, P = NS) and Purkinje fibers (273.2 +/- 6.5 vs. 283.8 +/- 4.2 ms, P = NS) from the failing hearts, although isoproterenol induced a shortening in the control group (204.8 +/- 0.9 vs. 181.3 +/- 1.6 ms in ventricular muscles, P < 0.01; 313.8 +/- 6.5 vs. 279.5 +/- 5.7 ms in Purkinje fibers, P < 0.01). We conclude that the failing heart has a decreased sensitivity to the arrhythmogenic effect of catecholamines.
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Li et al. (1993) studied Heart failure (n=23). Exogenous norepinephrine vs. Non-paced control group was evaluated on Arrhythmogenic threshold dose (ATD) of exogenous norepinephrine that induced ventricular tachycardia (p=<0.01). In dogs with rapid pacing-induced heart failure, the arrhythmogenic threshold dose of exogenous norepinephrine required to induce ventricular tachycardia was significantly increased (P<0.01).
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