PR Interval Behavior During Exercise: Implications for Physiological Pacemakers

Abstract

The relationship between heart rate response and the dynamic changes in the PR interval was assessed in 631 patients undergoing routine cardiac exercise tests for a variety of clinical indications. Patients were stratified into four subsets: nonmedicated normals (n = 437), patients on beta-antagonist agents (n = 118), those on antiarrhythmic agents alone (n = 61) and those with a clinical diagnosis of advanced (New York Heart Association [NYHA] Class III or IV) congestive heart failure. All patients were in stable sinus rhythm throughout the test. PR intervals were measured at rest, at mid-exercise and at peak exercise. Mean PR intervals shortened to a statistically significant degree in most subgroups. This effect was predominantly observed in the earlier stages of exercise. In patients with advanced heart failure, there was no statistically significant shortening of exercise PR intervals later in exercise, demonstrating a parallel with their relatively blunted heart rate response. These changes in exercise PR intervals suggest that implanted pacemaker algorithms may be constructed to maximize hemodynamic benefit in patients requiring physiological pacemakers.

Atrioventricular Interval Optimization and Exercise Tolerance

“…48 Stroke volumes appear to be particularly sensitive to multiple AV interval settings in patients with damaged myocardiums. [11][12][13]49,50 While improved cardiac function in AV sequential compared to asynchronous ventricular pacing has been previously documented, 24,25,46,[51][52][53][54] the importance of appropriate AV timing during exercise remains controversial. 10 Frielingsdorf et al 11 previously examined the effects on exercise capacity of optimizing the AV interval at rest by radionuclide ventriculography.…”

Adverse Effects of Long‐Term Right Ventricular Apical Pacing and Identification of Patients at Risk of Atrial Fibrillation and Heart Failure

“…Even though AV nodal conduction at rest is intact, the AV conduction system can change at higher rates resulting in excessive prolonged PR interval. Thus, the patient could develop AAIR PM syndrome, 46 where the atrial‐paced, ventricular sensed interval, rather than shortening as occurs with normal physiology, 47 would progressively lengthen, causing the atrium to be depolarized and contract against closed mitral and tricuspid valves. A possible AAI PM syndrome might partially explain why a minimal amount of AV synchrony in DDD mode appears beneficial in ICD recipients.…”

The effects of nicotine and cigarette smoking on cardiac electrophysiology.

“…Although most participants were on β-blockers, prevalence did not significantly differ by cotinine strata, and PR and P wave durations did not differ by βblocker use. This latter point accords with observations that β-blockers do not alter resting PR interval whereas they partially attenuate PR and RR interval shortening during exerciseinduced sympatho-excitation [297,298]. Additionally, we were unable to assess associations between other cigarette components or smoking habits (e.g., frequency) and cardiac electrophysiology.…”