CLINICAL STUDIES
Arterial baroreflex impairment in patients during acute coronary occlusion
K. E. Juhani Airaksinen, MD*,
Kari U. O. Tahvanainen, MSc ,
Dwain L. Eckberg, MD ,
Matti J. Niemelä, MD*,
Antti Ylitalo, MD* and
Heikki V. Huikuri, MD, FACC*
* Cardiovascular Laboratory, Department of Medicine, University of Oulu, Oulu, Finland
Department of Clinical Physiology, University of Tampere, Tampere, Finland
Departments of Medicine and Physiology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center and Medical College of Virginia at Virginia Commonwealth University, Richmond, Virginia, USA
Manuscript received March 26, 1998;
revised manuscript received July 7, 1998,
accepted July 24, 1998.
Address for correspondence: Dr. K.E.J. Airaksinen, Division of Cardiology, Department of Medicine, University of Oulu, Kajaanintie 50, FIN-90220 Oulu, Finland
kari.airaksinen{at}oulu.fi
Objectives. We tested whether acute coronary occlusion interferes with arterial baroreceptor control of heart rate in humans.
Background. Subnormal baroreflex sensitivity (BRS) is an important risk indicator for sudden death. Animal research indicates that both chronic myocardial infarction and acute coronary occlusion impair baroreflex modulation of heart rate.
Methods. We measured RR interval prolongation after phenylephrine-induced systolic pressure increases before and during 2-min coronary occlusions in 47 patients (27 men) undergoing clinically indicated single-vessel coronary angioplasty for stenoses in the proximal or midportion of the vessel causing >50% reduction in the arterial diameter, with normal antegrade flow (33 anterior descending, 10 circumflex, 4 right coronary artery). A control group of 11 patients treated for chronic total occlusion of a coronary artery was assessed to evaluate nonspecific changes in baroreflex function during a 2-min balloon inflation in the occluded artery.
Results. The BRS decreased from 5.2 ± 3.8 (mean ± SD) to 4.1 ± 3.5 ms·mm Hg–1 (p = 0.01) during the coronary occlusion in the 28 patients with preserved arterial baroreceptor control of heart rate—that is, adequate blood pressure responses and correlation coefficients of the slopes both in baseline and during coronary occlusion. The same phenylephrine dose increased systolic pressure less during than before coronary artery occlusion (21 ± 21 versus 36 ± 16 mm Hg, p < 0.0001), and in 6 patients it failed to prevent systolic pressure reduction during occlusion. Correlation coefficients of the baroreflex regressions decreased from 0.81 ± 0.27 to 0.47 ± 0.44 (p < 0.0001) during coronary artery occlusion in the 41 patients with adequate systolic pressure rises in both phenylephrine tests, and the association between RR intervals and rising systolic pressures was lost in 13 patients during coronary occlusion. Balloon inflation in a chronic total occlusion of a coronary artery did not cause significant changes in BRS (from 5.3 ± 4.0 to 5.2 ± 3.7 ms·mm Hg–1), correlation coefficient of the slope or phenylephrine-induced pressure rise.
Conclusions. Our study shows that abrupt coronary occlusion impairs baroreflex modulation of vagal and sympathetic nervous outflow in humans.
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Abbreviations and Acronyms
| | BRS | = baroreflex sensitivity | | TIMI | = thrombolysis myocardial infarction |
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