Arterial baroreflex impairment in patients during acute coronary occlusion

• Published in: Journal of the American College of Cardiology Vol. 32; no. 6; pp. 1641 - 1647
• Main Authors: Airaksinen, K.E.Juhani, Tahvanainen, Kari U.O, Eckberg, Dwain L, Niemelä, Matti J, Ylitalo, Antti, Huikuri, Heikki V
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 15.11.1998; Elsevier Science
• Subjects: Acute Disease; Aged; Angioplasty, Balloon, Coronary; Arteries - physiopathology; Baroreflex - physiology; Biological and medical sciences; Blood Pressure - drug effects; Blood Pressure - physiology; Cardiology. Vascular system; Catheterization; Coronary Disease - diagnosis; Coronary Disease - physiopathology; Coronary Disease - therapy; Coronary heart disease; Coronary Vessels - physiopathology; Female; Heart; Heart Rate - physiology; Humans; Male; Medical sciences; Middle Aged; Phenylephrine; Space life sciences; Systole; Vasoconstrictor Agents; BRS; TIMI; Arterial disease; Vascular disease; Human; RR interval; Heart rate; Acute; Baroreflex; Coronary artery; Cardiovascular disease; Complication; Coronary heart disease; Thrombosis; Non-programmatic
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/S0735-1097(98)00452-5

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.