What is the clinical evidence from this study?

Study design: Other. Population: Myocardial failure (n=14). Intervention: Rapid ventricular pacing vs. Baseline (before pacing). Primary outcome: Shortening fraction at 220 beats/min (p=<0.001).

October 1, 2002Open Access

Changes in concentrations of neuroendocrine hormones and catecholamines in dogs with myocardial failure induced by rapid ventricular pacing

Q: What are the key findings of this study?

Prolonged ventricular pacing for 9 weeks with increasing heart rates up to 220 beats/min significantly reduced shortening fraction from 35.5% to 12.2% and increased neuroendocrine hormones in dogs.

Key Result

Prolonged ventricular pacing for 9 weeks with increasing heart rates up to 220 beats/min significantly reduced shortening fraction from 35.5% to 12.2% and increased neuroendocrine hormones in dogs.

PICO

Population

Myocardial failure (n=14)

Intervention / Comparator

Rapid ventricular pacing vs Baseline (before pacing) (180, 200, and 220 beats/min)

Primary Outcome

Shortening fraction at 220 beats/min, p=<0.001

Main Result

Absolute Event Rate: 12.2% vs 35.5%

p-value: p=<0.001

Limitations

High dropout rate, with only 6 of 14 dogs completing the entire 9-week protocol due to severe clinical signs of heart failure.
Lack of a control group of dogs that did not undergo ventricular pacing.
Potential confounding effects of butorphanol sedation and varying degrees of agitation among dogs during blood collection.

Abstract

OBJECTIVE: To describe neuroendocrine responses that develop in dogs subjected to prolonged periods of ventricular pacing. ANIMALS: 14 adult male hound-type dogs. PROCEDURE: Samples were obtained and neuroendocrine responses measured before (baseline) and after 3 periods of ventricular pacing. A pacemaker was used to induce heart rates of 180, 200, and 220 beats/min (BPM). Each heart rate was maintained for 3 weeks before increasing to the next rate. Atrial natriuretic peptide, antidiuretic hormone, aldosterone, norepinephrine, epinephrine, and dopamine concentrations and plasma renin activity were measured. Severity of left ventricular compromise was estimated. RESULTS: Shortening fraction decreased significantly with increasing heart rates (mean +/- SE, 35.5 +/- 1.4, 25.0 +/- 1.4, 19.5 +/- 1.9, and 12.2 +/- 2.3 for baseline, 180 BPM, 200 BPM, and 220 BPM, respectively). Atrial natriuretic peptide concentrations increased significantly at 180 BPM (44.1 +/- 3.0 pg/mL) and 200 BPM (54.8 +/- 5.5 pg/mL), compared with baseline concentration (36.8 +/- 2.6 pg/mL). Dopamine concentration increased significantly at 200 BPM (70.4 +/- 10.4 pg/mL), compared with baseline concentration (44.2 73 pg/mL). Norepinephrine concentrations increased significantly from baseline concentration (451 +/- 46.2 pg/mL) to 678 +/- 69.8, 856 +/- 99.6, and 1,003 +/- 2676 pg/mL at 180, 200, and 220 BPM, respectively. CONCLUSIONS AND CLINICAL RELEVANCE: Dogs subjected to ventricular pacing for 9 weeks developed neuroendocrine responses similar to those that develop in humans with more chronic heart failure and, except for epinephrine concentrations, similar to those for dogs subjected to ventricular pacing for < 6 weeks.

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