ST Segment Depression Detected by Continuous Electrocardiography in Patients With Acute Ischemic Stroke or Transient Ischemic Attack

Forty percent of patients with a history of ischemic stroke or transient ischemic attack (TIA) have concomitant coronary artery disease. ST segment depression, detected by continuous electrocardiography, is associated with increased cardiac morbidity and mortality in patients with known coronary artery disease. While electrocardiographic changes have been associated with acute stroke, the etiology and significance of these changes remain unclear. In this pilot study we report the prevalence of ST segment depression and ventricular arrhythmias in patients with acute ischemic stroke or TLA monitored by continuous electrocardiography. Clinical predictors of ST segment depression and ventricular arrhythmia are also identified. Methods Consecutive patients presenting with acute ischemic stroke or TLA were enrolled within 72 hours of hospital admission and monitored by continuous electrocardiography for 48 hours. The electrocardiographic results were analyzed for periods of ST segment depression and ventricular arrhythmias. Results Of 51 patients with ischemic stroke or TIA, 15 (29%) had episodes of ST segment depression (95% confidence interval, 15% to 43%), and 18 (35%) had ventricular arrhythmias (95% confidence interval, 21% to 49%). In logistic regression analysis, increasing age (P<.02) and a left-sided neurological event (P<.01) were significant predictors of ST segment depression. Increasing numbers of atherosclerotic risk factors, a history of cardiac disease, and increasing or decreasing mean arterial pressure were not predictive of ST segment depression. Conclusions Patients with acute ischemic stroke or TIA have a 29% prevalence of ST segment depression within the first 5 days after their event. In comparison, the prevalence of ST depression is 2.5% to 8% in asymptomatic adults and 43% to 60% in patients with symptomatic coronary artery disease. The association of ST segment depression with left-sided neurological events suggests that the electrocardiographic changes are in part neurologically mediated. Further study is necessary to better define the brain-heart interaction and to determine whether ST segment depression in patients with ischemic stroke or TLA reflects underlying coronary artery disease.

[1]  S. Oppenheimer,et al.  The anatomy and physiology of cortical mechanisms of cardiac control. , 1993, Stroke.

[2]  D. Cechetto,et al.  Experimental cerebral ischemic lesions and autonomic and cardiac effects in cats and rats. , 1993, Stroke.

[3]  J. Ferguson.  Meeting highlights: 42nd Annual Scientific Sessions, American College of Cardiology, March 14 to 18, 1993. , 1993, Circulation.

[4]  J. Girvin,et al.  Cardiovascular effects of human insular cortex stimulation , 1992, Neurology.

[5]  C. McKay,et al.  Coronary Artery Disease and Cardiac Events With Asymptomatic and Symptomatic Cerebrovascular Disease , 1992, Stroke.

[6]  D. Mulcahy,et al.  Therapeutic implications of ischemia in the ambulatory setting. , 1992, Progress in cardiovascular diseases.

[7]  V. Hachinski,et al.  The cardiac consequences of stroke. , 1992, Neurologic clinics.

[8]  S. Oppenheimer,et al.  Plasma and organ catecholamine levels following stimulation of the rat insular cortex , 1992, Brain Research.

[9]  E. Cook,et al.  Long-term prognosis of myocardial ischemia detected by Holter monitoring in peripheral vascular disease. , 1990, The American journal of cardiology.

[10]  J. Keegan,et al.  Circadian variation of heart rate is affected by environment: a study of continuous electrocardiographic monitoring in members of a symphony orchestra. , 1990, British heart journal.

[11]  D. Cechetto,et al.  Cardiac chronotropic organization of the rat insular cortex , 1990, Brain Research.

[12]  Gregory P. Lee,et al.  Unilateral cerebral inactivation produces differential left/right heart rate responses , 1990, Neurology.

[13]  P. Deedwania,et al.  Silent ischemia during daily life is an independent predictor of mortality in stable angina. , 1990, Circulation.

[14]  E. Cook,et al.  Correlation Between Preoperative Ischemia and Major Cardiac Events After Peripheral Vascular Surgery , 1989, The New England journal of medicine.

[15]  W. Aronow,et al.  Usefulness of silent myocardial ischemia detected by ambulatory electrocardiographic monitoring in predicting new coronary events in elderly patients. , 1988, The American journal of cardiology.

[16]  A. Andreoli,et al.  Incidence of silent myocardial ischaemia in patients with cerebral ischaemia. , 1988, European heart journal.

[17]  L. Goldman,et al.  Prognostic importance of myocardial ischemia detected by ambulatory monitoring in patients with stable coronary artery disease. , 1988, Circulation.

[18]  M. Weisfeldt,et al.  Silent ischemia on Holter monitoring predicts mortality in high-risk postinfarction patients. , 1988, JAMA.

[19]  V. Hachinski,et al.  Changes in plasma catecholamine levels after insula damage in experimental stroke , 1986, Brain Research.

[20]  V. Hachinski,et al.  Value of cardiac monitoring and echocardiography in TIA and stroke patients. , 1985, Stroke.

[21]  N. Hertzer,et al.  Coronary angiography in 506 patients with extracranial cerebrovascular disease. , 1985, Archives of internal medicine.

[22]  J. Deanfield,et al.  Analysis of ST-segment changes in normal subjects: implications for ambulatory monitoring in angina pectoris. , 1984, The American journal of cardiology.

[23]  M. Verani,et al.  Coronary artery disease in patients with cerebrovascular disease: A prospective study , 1984, Annals of neurology.

[24]  A. Quyyumi,et al.  Ambulatory electrocardiographic ST segment changes in healthy volunteers. , 1983, British heart journal.

[25]  U. de Faire,et al.  Prognosis in acute stroke with special reference to some cardiac factors. , 1983, Journal of chronic diseases.

[26]  P A Wolf,et al.  Survival and recurrence following stroke. The Framingham study. , 1982, Stroke.

[27]  S. Papson,et al.  “Model” , 1981 .

[28]  V. Hachinski,et al.  Plasma Norepinephrine in Stroke , 1981, Stroke.

[29]  A. Crowther,et al.  Controlled study of 24-hour ambulatory electrocardiographic monitoring in patients with transient neurological symptoms. , 1980, Journal of neurology, neurosurgery, and psychiatry.

[30]  D. Goldstein,et al.  The Electrocardiogram in Stroke: Relationship to Pathophysiological Type and Comparison with Prior Tracings , 1979, Stroke.

[31]  J. Dimant,et al.  Electrocardiographic Changes and Myocardial Damage in Patients with Acute Cerebrovascular Accidents , 1977, Stroke.

[32]  E. Melamed,et al.  The Effect of Acute Stroke on Cardiac Functions as Observed in an Intensive Stroke Care Unit , 1974, Stroke.

[33]  D. Reichenbach,et al.  Cardiac injury and subarachnoid hemorrhage. A clinical, pathological, and physiological correlation. , 1969, Journal of neurosurgery.

[34]  R. Connor.  Heart Damage Associated with Intracranial Lesions , 1968, British medical journal.

[35]  S. Punsar,et al.  Subendocardial Haemorrhage and E.C.G. Changes in Intracranial Bleeding , 1964, British medical journal.

[36]  G W MANNING,et al.  Electrocardiographic Changes Simulating Myocardial Ischemia and Infarction Associated with Spontaneous Intracranial Hemorrhage , 1960, Circulation.

[37]  J. E. Szakacs,et al.  L-Norepinephrine myocarditis. , 1958, American journal of clinical pathology.

[38]  B. Tomlinson,et al.  Subendocardial haemorrhages associated with intracranial lesions. , 1954, The Journal of pathology and bacteriology.

[39]  H. Levine.  Non-specificity of the electrocardiogram associated with coronary artery disease. , 1953, The American journal of medicine.