SYNOPSIS
Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore.
“ELECTROCARDIOGRAPHIC CHANGES IN CEREBROVASCULAR ACCIDENTS ’’
Name of the candidate : Dr. Suja. P
Guide : Dr. M.G. Bandelkar
Course and Subject : M.D. Physiology
Department of Physiology,
A.J. INSTITUTE OF MEDICAL SCIENCES,
Kuntikana, Mangalore – 04
2009
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA, BANGALORE.
ANNEXURE II
PROFORMA FOR REGISTRATION OF SUBJECTS FOR DESSERTATION
1 / Name of the candidate and address (in block letters) / DR SUJA.P,JUNIOR RESIDENT,
DEPARTMENT OF PHYSIOLOGY,
A.J. INSTITUTE OF MEDICAL SCIENCES, MANGALORE.
2 / Name of the Institution / A.J. INSTITUTE OF MEDICAL SCIENCES, MANGALORE.
3 / Course of study and Subject / MD PHYSIOLOGY.
4 / Date of admission to course / 01/06/2009
5 / Title of the Topic
“ELECTROCARDIOGRAPHIC CHANGES IN CEREBROVASCULAR ACCIDENTS"
BRIEF RESUME OF THE INTENDED WORK:
6.1 Need for the study
Stroke has been reported to be the third commonest cause of death worldwide1. The authors have also reported the prevalence rate of stroke in India to be about 250-350/ 1 lakh.
Patients with cerebrovascular accidents have an increased incidence of electrocardiographic abnormalities2. These changes have been recognized since previous century and till date innumerable researchers have tried elucidating the relationship between intracranial events and corresponding changes in ECG2.
Studies have shown that stroke victims may die unexpectedly of cardiac arrest, arrhythmia or severe hypotension in the absence of any premature existing heart disease3. This is mainly due to the association of arteriosclerotic cerebral and coronary heart disease, which have common risk factors2
There are very few reports of ECG changes associated with cerebrovascular accidents from India. With this view in mind, the present study is undertaken to determine the frequency and significance of ECG changes in patients with acute ischemic stroke.
6.2Review of literature
Stroke is applied to a sudden focal neurologic syndrome, specifically the type due to cardiovascular disease. The term cerebrovascular disease designates any abnormality of the brain resulting from a pathologic process of the blood vessel. Pathologic process is given an inclusive meaning- namely , occlusion of the lumen by embolus or thrombus, rupture of a vessel, an altered permeability of the vessel wall, or increased viscosity or other change in the quality of blood flowing through the cerebral vessels4.
The WHO MONICA (World Health Organization Monitoring Trends and Determinants In Cardiovascular Disease) project was initiated in the early 1980s with the aim to study the occurrence of coronary events and stroke in a defined population over 10yrs and to analyze the relation between these factors5. Electrocardiographic abnormalities have been known to occur in the context of neurological disease for long time. The effect of brain injury on the heart was first demonstrated in experimental animals in 1930s6. Byer et al7 have described a patient with intracerebral hemorrhage whose electrocardiogram showed marked QT prolongation with large T and U waves. The relation between specific ECG alteration and intracranial events was recognized by Burch et al8 who have described a new pattern in many patients with CVA. According to the authors, the ECG changes consists of T waves of considerable amplitude, width and long QT intervals. Cropp and Manning9 have reported ECG changes showing myocardial infarction in 29 patients with subarachnoid hemorrhage. Of these, 7 patients died and autopsy on 5 confirmed the presence of ruptured cerebral aneurysm.
There is clear evidence that cardiac lesions can be produced as a result of diseases of the nervous system. The concept of visceral organ dysfunction that occurs as a result of neurological stimuli can be traced to Ivan Pavlov and his student Hans Selye10. Melville et al11 produced ECG changes and myocardial necrosis by stimulation of hypothalamus in cats. In their study, with anterior hypothalamic stimulation, parasympathetic responses occurred predominantly in the form of bradycardia, lateral hypothalamic stimulation produces tachycardia and ST segment depression. With intense bilateral and repeated stimulation, persistent irreversible changes occurred and post mortem examination revealed a stereotyped cardiac lesion characterized by intense eosinophilia with loss of cross striations and some hemorrhage. Koskelo et al12 demonstrated ECG changes in patients with subarachnoid hemorrhage.
More recently, Oppenheimer and Cechetto13 have mapped the chronotropic organizational structure in the rat insular cortex, wherein the authors reported the central role of insula in the cardiovascular function. Despite the fact that myocardial damage could definitely be produced in animals, until the mid 60s, there was little recognition that this actually occurred in human beings9. Connor14 reported focal myocytolysis in 8% of 231 autopsies, with the highest incidence seen in patients who suffered fatal intracranial hemorrhages.
Greenshoot and Reichenbach15 have reported cardiac lesions of varying degrees in patients with subarachnoid hemorrhage. The authors went on to report that, the ECG abnormalities and the cardiac pathology found in these patients could be reproduced in cats by the stimulation of mesencephalic reticular formation. Hawkins and Clower16 injected blood intracranially into mice producing myocardial lesions. They found that pretreatment with adrenalectomy, use of reserpine or atropine reduced the number of these lesions. This gave evidence for the fact that these lesions were in part caused by sympathetic over activity and in part caused by parasympathetic over activity.
Goldstein17 has reported the presence of very high percentage of ECG abnormalities in patients with stroke. The author reported 92% (138/150) of the study subjects to have ECG abnormalities following stroke. The most common ECG abnormalities in that were: QT prolongation (68 patients, 45%), ischemic changes (59, 35%), U waves (42, 28%), tachycardia (42, 28%), and arrhythmias (41, 27%). Patients with cerebral embolus had a significantly increased frequency of atrial fibrillation (9 patients, 47%) and patients with subarachnoid hemorrhage had an increased frequency of QT prolongation (20, 71%) and sinus arrhythmia (5, 18%). Recently a study done by Soliman et al18 has reported the ethnic distribution of ECG abnormalities in patients with ischemic stroke. The authors have reported blacks to have a higher prevalence of atrial fibrillation and a greater risk of stroke.
6.3 Objectives of the study
1. To determine the ECG changes occurring in cerebrovascular accidents.
2. To determine the differences in ECG manifestations in different types of cerebrovascular accidents viz, cerebral infarction, intracranial bleed and subarachnoid hemorrhage.
27. / Material and methods:
7.1 Source of data.
50 CT documented cases of cerebrovascular accidents admitted in the Department of Neurology, A.J. INSTITUTE OF MEDICAL SCIENCES.
7.2 Method of collection of data ( including sampling procedure, if any)
Study type: A prospective Hospital based study.
Sample and sampling technique: 50 CT documented cases of cerebrovascular accidents admitted in the Department of Neurology, A.J. INSTITUTE OF MEDICAL SCIENCES.
Inclusion criteria:
I. Age ≥ 45yrs.
II. CT documented cases of cerebrovascular accidents admitted in the Department of Neurology, A.J. INSTITUTE OF MEDICAL SCIENCES.
Exclusion criteria:
I. Patients in whom admission to the hospital was delayed for more than twenty four hours after the appearance of acute stroke.
II. Stroke due to trauma.
III. Stroke occurred in the setting of dissecting aortic aneurysm.
IV. Patient with previous documented cardiac disease.
Plan for data analysis: Collected data will be analyzed by unpaired t test or chi- square test.
7.3 Does the study require any investigations or interventions to be conducted on patients or other humans or animals? If so, please describe briefly.
Yes, ECG and CT scan
7.4 Has ethical clearance been obtained from your institution in case of 7.3
Yes
8 / References
1. Ropper AH, Brown RH. Adams and Victors Principle of Neurology. 8th edition. USA: McGraw-Hill; 2005. 660p.
2. Banerjee TK, Das SK. Epidemiology of stroke in India.Neurology Asia 2006;11:1-4
3. Dimant J, Grob D. Electrocardiographic changes and Myocardial damage in patients with Acute Cerebrovascular accidents. Stroke 1977; 8(4):448-455.
4. Lavy S, Yaar I, Melamed E, Stern S.The effect of acute stroke on cardiac functions as observed in an intensive stroke care unit. Stroke 1974;5(4):775-779.
5. Pedoe HT, Kuulasmaa K, Mahonen M, Tolonen H, Ruokokoski, Amouyel P.Contribution of trends in survival and coronary event rates to changes in coronary heart disease mortality. The Lancet 1999;353:1547-1557
6. Bozluolcay M, Ince B, Celik Y, Harmanci H, Iierigelen B, Pelin Z.Electrocardiographic findings and prognosis in ischemic stroke.Neurology India 2003;51(4):500-502.
7. Byer E, Ashman R, Toth LA. Electrocardiogram with large upright T waves and long QT intervals. Am Heart J 1947;33:796-806
8. Burch GE, Myers R, Abildskov JA. A new electrocardiographic pattern observed in cerebrovascular accidents. Circulation 1954; 9: 719-726.
9. Cropp CF, Manning GW. Electrocardiographic change simulating myocardial ischemia and infarction associated with spontaneous intracranial hemorrhage. Circulation 1960; 22: 25–38.
10. Samuels MA, The Brain-Heart connection. Circulation 2007; 116:77-84.
11. Melville KI, Blum B, Shister HE, Silver MD. Cardiac ischemic changes and arrhythmias induced by hypothalamic stimulation. Am J Cardiol. 1963; 12: 781–791.
12. Koskelo P, Punsar SO, Sipila W. Subendocardial hemorrhage and ECG changes in intracranial bleeding. BMJ. 1964; 1: 1479–1483.
13. Oppenheimer SM, Cechetto DF. Cardiac chronotropic organization of the rat insular cortex. Brain Res. 1990; 533: 66–72.
14. Connor RCR. Myocardial damage secondary to brain lesions. Am Heart J. 1969; 78: 145–148.
15. Greenshoot JH, Reichenbach DD. Cardiac injury and subarachnoid haemorrhage. J Neurosurg. 1969; 30: 521–531.
16. Hawkins WE, Clower BR. Myocardial damage after head trauma and simulated intracranial haemorrhage in mice: the role of the autonomic nervous system. Cardiovasc Res. 1971; 5: 524–529.
17. Goldstein DS. The electrocardiogram in stroke: Relationship to pathophysiological Type and Comparison with prior tracings. Stroke 1979; 10(3):253-259.
18. Elsayed Z,Soliman,Ronald J et al.Stroke 2009;40:1204-1211
9.Signature of the candidate:
10. Remarks of the guide
11.Name and Designation of
(in block letters)
11.1 Guide Dr. M.G. BANDELKAR
PROFESSOR
DEPT.OF PHYSIOLOGY
A.J. INSTITUTE OF MEDICAL SCIENCES.
MANGALORE
11.2 Signature
11.3 Head of Department: Dr. SHARAD B.KOLE
PROFESSOR & HOD
DEPT.OF PHYSIOLOGY
A.J. INSTITUTE OF MEDICAL SCIENCES.
MANGALORE
11.4 Signature
12.Remarks of the Chairman and Principal
12.2Signature
10