Diurnal heart rate reactivity: A predictor of severity of experimental coronary and carotid atherosclerosis

Hisham S. Bassiouny*, Christopher K. Zarins, Daniel C. Lee, Christopher L. Skelly, John E. Fortunato, Seymour Glagov

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

Background: Elevated awake resting heart rate (HR) has been shown to be a major risk factor for cardiovascular disease. Since coronary ischaemic events appear to peak during transition from sleep to awake HR, we sought to determine whether the degree of diurnal HR fluctuation (dHRV) is an independent predictor of coronary and peripheral atherogenesis. In this study, we varied both baseline HR and dHRV using sino-atrial node ablation (SNA) in a primate model of diet-induced atherogenesis and determined the degree of plaque formation relative to both HR parameters. Methods: HR was recorded continuously for 6 months by an implantable intraaortic sensor/transmitter in 17 active unrestricted male cynomolgus monkeys. In nine monkeys, SNA was employed to create a wide spectrum of dHRV, and the power amplitude of dHRV was determined for the daily HRV cycle with power spectral analysis. After a 6-month diet induction period, percent coronary and carotid stenosis, intimal thickness and area were quantitated in each animal. Results: Total serum cholesterol and mean HR were no different between high (n = 10) and low (n = 7) dHRV groups (866 mg% vs. 740 mg%, P > 0.2 and 130 ± 22 and 115 ± 13, P > 0.1, respectively). Percent carotid stenosis was markedly greater in both high HR and dHRV animals ([HR], 54 ± 19 vs. 35 ± 10, P < 0.04) and ([dHRV], 54 ± 17 vs. 32 ± 10, P < 0.01). Significant increases in all measures of coronary atherogenesis were found in high dHRV animals when compared with those with low dHRV (percent stenosis: 48% ± 22 vs. 23% ± 16, P < 0.02), (lesion area: 1.2 ± 0.8 vs. 0.3 ± 0.3, P < 0.02), and (intimal thickness: 0.3 ± 0.1 vs. 0.1 ± 0.1, P < 0.01), respectively. While there was a trend towards greater coronary atherogenesis in animals with high HR, this did not reach statistical significance. Conclusion: Elevated HR and dHRV are both associated with enhanced experimental atherosclerotic plaque formation. However, a greater degree of carotid and coronary atherogenesis is observed in animals with high dHRV. These findings suggest that elevated dHRV is a stronger predictor for susceptibility to atherogenesis than elevated HR alone. Such a relationship may be attributed to the potential role of dHRV in modulating the frequency of adverse near wall haemodynamic forces, which have been shown to induce atherosclerotic plaques. Lowering of dHRV in humans by exercise or pharmacological agents may have a beneficial role in retarding atherosclerotic plaque induction, progression and complication.

Original languageEnglish (US)
Pages (from-to)331-338
Number of pages8
JournalJournal of Cardiovascular Risk
Volume9
Issue number6
DOIs
StatePublished - Dec 2002

Funding

Sponsorship: Dr Bassiouny, Dr Zarins and Dr Glagov are supported by National Institutes of Health SCOR Atherosclerosis Project Grant HL 15062. Dr Skelly is supported by Thoracic Surgery Foundation Research Fellowship #99019. Dr Fortunato is supported by the Cardiovascular Pathophysiology and Biochemistry Training Program, University of Chicago, under Grant 5T32 HL07237. No author has financial interests relevant to the research or constituting a conflict of interest.

Keywords

  • Atherosclerosis
  • Carotid artery
  • Coronary artery
  • Heart rate reactivity

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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