ECG Changes in Intracranial Hemorrhage

ECG Changes in Intracranial Hemorrhage

ECG changes are fairly common in intracranial hemorrhage. Giant T inversions with QT interval prolongation may be seen in intracranial hemorrhage even without associated myocardial damage [1]. ECG changes described in subarachnoid hemorrhage include QT interval prolongation, T wave abnormalities and ST segment deviations. Mechanism is thought to be due to sustained sympathetic stimulation, probably caused by dysfunction of insular cortex resulting in reversible neurogenic damage to the myocardium which could include contraction bands and subendocardial ischemia [2].

In a study involving patients with supratentorial hemorrhage, they found that ECG changes were more common in basal ganglia and thalamic bleeds rather than in lobar bleeds. But the number of persons with lobar hemorrhage in that study was only 17%. In that study commonest ECG abnormalites were QTc prolongation followed by brady/tachycardia and then ST segment deviations [3]. Cerebrovascular damage can cause cardiac arrhythmias related to disinhibition of right insular cortex with resulting increased sympathetic tone. Risk is thought to be higher with damage to right hemisphere than left hemisphere.

ECG changes resembling ST elevation myocardial infarction has also been described after traumatic intracranial hemorrhage [4]. Serial measurements of cardiac enzymes were normal in that case. According to J Willis Hurst, it is likely to be due to severe generalized epicardial injury and ischemia. He has noted that ST segment and T wave abnormalities are caused by an abrupt elevation of serum catecholamines. Excess of catecholamines can damage myocytes directly and can also lead to generalized spasm of coronary arteries and even consequent actual myocardial infarction [5].

Sometimes cardiac troponin elevation may accompany ECG changes in aneurysmal subarachnoid hemorrhage. In a study of 204 subjects, 31% had troponin elevation. It was found that cardiac injury was incrementally worse with increasing severity of aneurysmal subarachnoid hemorrhage and was associated with persistent prolongation of QTc and ventricular arrhythmias. They also noted regional wall motion abnormalities and some degree of depressed left ventricular ejection fraction [6].

References

1. Yamour BJ, Sridharan MR, Rice JF, Flowers NC. Electrocardiographic changes in cerebrovascular hemorrhage. Am Heart J. 1980 Mar;99(3):294-300. doi: 10.1016/0002-8703(80)90343-9. PMID: 7355693.
2. Popescu D, Laza C, Mergeani A, Bajenaru OA, Antochi FA. Lead electrocardiogram changes after supratentorial intracerebral hemorrhage. Maedica (Bucur). 2012 Dec;7(4):290-4. PMID: 23483874; PMCID: PMC3593278.
3. Popescu D, Laza C, Mergeani A, Bajenaru OA, Antochi FA. Lead electrocardiogram changes after supratentorial intracerebral hemorrhage. Maedica (Bucur). 2012 Dec;7(4):290-4. PMID: 23483874; PMCID: PMC3593278.
4. Bailey WB, Chaitman BR. Images in clinical medicine. Electrocardiographic changes in intracranial hemorrhage mimicking myocardial infarction. N Engl J Med. 2003 Aug 7;349(6):561. doi: 10.1056/NEJMicm020416. PMID: 12904521.
5. Hurst JW. Electrocardiographic changes in intracranial hemorrhage mimicking myocardial infarction. N Engl J Med. 2003 Nov 6;349(19):1874-5; author reply 1874-5. doi: 10.1056/NEJM200311063491922. PMID: 14602892.
6. Hravnak M, Frangiskakis JM, Crago EA, Chang Y, Tanabe M, Gorcsan J 3rd, Horowitz MB. Elevated cardiac troponin I and relationship to persistence of electrocardiographic and echocardiographic abnormalities after aneurysmal subarachnoid hemorrhage. Stroke. 2009 Nov;40(11):3478-84. doi: 10.1161/STROKEAHA.109.556753. Epub 2009 Aug 27. PMID: 19713541; PMCID: PMC3680357.