(Circulation. 1997;95:1185-1192.)
© 1997 American Heart Association, Inc.
Articles |
the Department of Cardiology, Royal Brompton Hospital, London, United Kingdom.
Correspondence to Dr D.J. Patel, Department of Cardiology, Harefield Hospital, Harefield, Middlesex UB9 6JH, United Kingdom.
Background Transient ischemia in stable coronary disease peaks in the morning, reflecting increased myocardial oxygen demand and coronary vasomotor tone after waking. In acute coronary syndromes, however, ischemia may result from transient thrombus formation or coronary spasm at the site of a ruptured plaque. We report on the pathophysiological mechanisms underlying transient ischemia in acute coronary syndromes despite optimal therapy, on the basis of analysis of heart rate changes preceding ischemia and its circadian variation.
Methods and Results Two hundred fifty-six patients with unstable angina or nonQ-wave myocardial infarction underwent continuous ST-segment monitoring for 48 hours while receiving maximal medical therapy. All ischemic episodes were characterized by their timing, duration, association with pain, and heart rate changes before the onset of ischemia. During 10 629 hours of monitoring, 44 patients (17.2%) had 176 episodes of transient ischemia. The mean heart rate at onset of ischemia was 68±12.8 bpm, and >55% of ischemic episodes were not preceded by a significant increase in heart rate. Ischemic activity had a single nocturnal peak, with 64% of all episodes occurring between 10 PM and 8 AM, this nocturnal preponderance being evident for episodes with or without a preceding increase in heart rate. The characteristics and timing of transient ischemia were similar in unstable angina and nonQ-wave myocardial infarction, but transient ischemia was more frequent (27.3% versus 15.1%; P<.05) and prolonged (median, 20 versus 13.5 minutes; P<.01) in nonQ-wave myocardial infarction.
Conclusions In acute coronary syndromes, transient ischemia has a low threshold, occurs predominantly without an increase in myocardial oxygen demand, and is present mainly at night rather than in the morning. These findings in patients receiving maximal medical therapy suggest significant pathophysiological differences underlying transient ischemia compared with stable coronary disease.
Key Words: angina ischemia coronary disease circadian rhythm
This article has been cited by other articles:
![]() |
G. Heper and M. Bayraktaroglu The Importance of von Willebrand Factor Level and Heart Rate Changes in Acute Coronary Syndromes: A Comparison with Chronic Ischemic Conditions Angiology, May 1, 2003; 54(3): 287 - 299. [Abstract] [PDF] |
||||
![]() |
T. Jernberg, P. Abrahamsson, B. Lindahl, P. Johanson, L. Wallentin, and M. Dellborg Continuous multilead ST-monitoring identifies patients with unstable coronary artery disease who benefit from extended antithrombotic treatment Eur. Heart J., July 2, 2002; 23(14): 1093 - 1101. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. G. Goodman, A. Barr, A. Sobtchouk, M. Cohen, G. J. Fromell, L. Laperriere, C. Hill, A. Langer, and for the Canadian Efficacy and Safety of Subcutaneo Low molecular weight heparin decreases rebound ischemia in unstable angina or non-Q-wave myocardial infarction: the Canadian ESSENCE ST segment monitoring substudy J. Am. Coll. Cardiol., November 1, 2000; 36(5): 1507 - 1513. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Jernberg, B. Lindahl, and L. Wallentin ST-segment monitoring with continuous 12-lead ECG improves early risk stratification in patients with chest pain and ECG nondiagnostic of acute myocardial infarction J. Am. Coll. Cardiol., November 1, 1999; 34(5): 1413 - 1419. [Abstract] [Full Text] [PDF] |
||||
![]() |
S Viskin, M Golovner, N Malov, R Fish, I Alroy, Y Vila, S Laniado, E Kaplinsky, and A Roth Circadian variation of symptomatic paroxysmal atrial fibrillation. Data from almost 10000 episodes Eur. Heart J., October 1, 1999; 20(19): 1429 - 1434. [Abstract] [PDF] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1997 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |