Circulation · 1998 · 651 citations · 37 references
Very‑low‑frequency RR‑interval variability is inversely related to post‑myocardial infarction survival, yet its physiological basis remains unclear. The study aimed to determine how sympathetic, parasympathetic, and renin‑angiotensin‑aldosterone system activity contribute to VLF RR‑interval variability using pharmacologic blockade in healthy subjects. Researchers recorded RR intervals and arterial pressures in 10 young adults during supine and 40° tilt positions, under controlled breathing, while administering saline, β‑adrenergic blocker atenolol, parasympathetic blocker atropine, combined blockade, and ACE inhibitor enalaprilat, and then performed FFT spectral analysis of VLF, LF, and respiratory frequency bands. Parasympathetic blockade nearly eliminated VLF RR‑interval power (−92 %) and all variability, β‑adrenergic blockade had no effect on VLF or LF power but doubled respiratory power, ACE inhibition modestly increased VLF power in supine, indicating that VLF rhythms are largely driven by parasympathetic outflow and only modestly modulated by the renin‑angiotensin‑aldosterone system.
Background —Survival of post–myocardial infarction patients is related inversely to their levels of very-low-frequency (0.003 to 0.03 Hz) RR-interval variability. The physiological basis for such oscillations is unclear. In our study, we used blocking drugs to evaluate potential contributions of sympathetic and vagal mechanisms and the renin-angiotensin-aldosterone system to very-low-frequency RR-interval variability in 10 young healthy subjects. Methods and Results —We recorded RR intervals and arterial pressures during three separate sessions, with the patient in supine and 40 degree upright tilt positions, during 20-minute frequency (0.25 Hz) and tidal volume–controlled breathing after intravenous injections: saline (control), atenolol (0.2 mg/kg, β-adrenergic blockade), atropine sulfate (0.04 mg/kg, parasympathetic blockade), atenolol and atropine (complete autonomic blockade), and enalaprilat (0.02 mg/kg, ACE blockade). We integrated fast Fourier transform RR-interval spectral power at very low (0.003 to 0.03 Hz), low (0.05 to 0.15 Hz), and respiratory (0.2 to 0.3 Hz) frequencies. β-Adrenergic blockade had no significant effect on very-low- or low-frequency RR-interval power but increased respiratory frequency power 2-fold. ACE blockade had no significant effect on low or respiratory frequency RR-interval power but modestly (≈21%) increased very-low-frequency power in the supine (but not upright tilt) position ( P <0.05). The most profound effects were exerted by parasympathetic blockade: Atropine, given alone or with atenolol, abolished nearly all RR-interval variability and decreased very-low-frequency variability by 92%. Conclusions —Although very-low-frequency heart period rhythms are influenced by the renin-angiotensin-aldosterone system, as low and respiratory frequency RR-interval rhythms, they depend primarily on the presence of parasympathetic outflow. Therefore the prognostic value of very-low-frequency heart period oscillations may derive from the fundamental importance of parasympathetic mechanisms in cardiovascular health.
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Frequency domain measures of heart period variability and mortality after myocardial infarction.
J. Thomas Bigger, Joseph L. Fleiss, R.C. Steinman et al. · Circulation · 1992 · 1.7K citations · Full text