Several electrocardiogram (ECG) abnormalities are frequently found in patients without heart disease who experience an ischemic stroke or subarachnoid hemorrhage (SAH). However, knowledge about the ECG changes in patients with intracranial hemorrhage (ICH) is currently limited, including subdural hemorrhage and intraparenchymal hemorrhage (IPH), which are the most frequent and second most frequent ICHs, respectively (1,2). Among the most common ICH ECG abnormalities are ST segment depression, left ventricular hypertrophy, prolongation of the corrected QT interval and inversion of the T wave (3). These nonspecific ECG findings may confuse medical diagnoses and, consequently, lead to erroneous therapeutic decisions.

ECG variations are usual in supratentorial hemorrhagic stroke, predominantly in basal ganglia and thalamic localization (4,5). These changes are frequently present in patients with ventricular effraction and include mainly QTc prolongation, followed by brady/tachycardia and subsequently ST segment modification (5,6). Certain investigations substantiate the assumption that a cardiac cortical rhythm control site is possibly inside the middle cerebral artery context or in the frontal cingulate cortex (4,6). Vascular injury to this part may be followed by cardiac arrhythmias linked to a disinhibition of the right insular cortex with subsequent augmented sympathetic tone. Ischemic commitment of the right hemisphere stimulates a greater risk for cardiac arrhythmia incidence than that of the left hemisphere (4-6). Imbalances of the autonomic nervous system role are important for these disruptions of rate, rhythm and conduction. Tachycardia and pressor replies are more usual following stimulus of the right insular cortex and after experimental stimulus of the left vagus, which innervates the atrioventricular node and the cardiac transference arrangement. Bradycardia appears to be more usual following stimulation of the left insular cortex or the right vagus nerve, which innervates the sinoatrial node, or it may be a source of the Cushing outcome (4-6).

ECG fluctuations appear in 49-100% of patients after SAH (7). The most usual ECG changes after SAH and IPH include repolarization irregularities, such as QT interval extension, ST-segment and T-wave modifications (8). Atrioventricular block, atrial flutter and ventricular arrhythmia are the most usual modifications related to cardiac arrhythmias; however, the mechanisms remain to be completely elucidated (7,8).

It was reported that ECG fluctuations were existent in >90% of unselected patients with ischemic stroke and intracerebral hemorrhage, but the occurrence was inferior regarding the omission of patients with preexistent heart sickness. Those patients with subarachnoid hemorrhage, repolarization and ischemic-like ECG alterations are related to direct effects of the cerebral disorder (9).

Furthermore, the nontraumatic IPH group comprises IPH and SAH. Acute SAH is noticed on the tomography as hyperdensity (blood clot density) in the cerebrospinal fluid spaces surrounding the brain. While the main source of SAH is a disrupted aneurysm, it may additionally be caused by intracranial dissection, trauma, vasculitis, dural AVM or cervical fistulas (10).

The scientific literature has reported various ECG abnormalities, particularly in SAH (11-13), but no case reports of ECG abnormalities in patients with IPH have been published, to the best of our knowledge. The present study reported on the ECG findings and the therapeutic management of a patient with IPH who was initially diagnosed with acute myocardial infarction.

A 78-year-old male patient was transferred from a lower-complexity to a high-complexity hospital in August 2021 because imaging and hemodynamic services were unavailable in the former setting. At the lower-complexity hospital, the patient presented with weakness and decreased muscle strength in the left half of the body with 2 h of evolution, which was associated with dysarthria and deviation of the right labial commissure. The patient was admitted with elevated blood pressure (220/110 mmHg), for which 20 mg of labetalol was administered intravenously. An ECG was immediately performed, which revealed elevation of the ST segment, a situation that was managed pharmacologically as a myocardial infarction by administering 80 mg of atorvastatin and 300 mg of clopidogrel. Subsequently, the patient was transferred to a higher-complexity hospital, where it was observed that the patient neither had a history of angina or dyspnea, nor symptoms of a coronary syndrome. Fig. 1 presents ST-segment elevation in V1, V2 and V3 (acquired at the low-complexity hospital). Fig. 2 depicts ST-segment elevation in V3 and V4 (acquired at the high-complexity hospital) and Fig. 3 presents right temporal intraparenchymal hematoma with vasogenic edema and ventricular involvement (acquired at the high-complexity hospital).

After 6 h, the patient was admitted to Hospital San Vicente Fundación (Rionegro, Colombia), a highly complex hospital (a hospital with the infrastructure, technology and specialists that allow it to provide the population with a health service that treats the most complex diseases), where the following vital signs were recorded: Blood pressure, 184/83 mmHg (hypertensive); heart rate, 52 beats per minute (bradycardia); respiratory rate, 22 breaths per minute tachypneic; and oxygen saturation, 97% (normal value). On physical examination, the patient was drowsy and oriented in three spheres. Muscular strength was 5/5 in the right half of the body and 4/5 in the left upper limb without alteration in sensitivity, aphasia or dysarthria. The patient denied symptoms including chest pain, angina, dyspnea, limitation in functional class, palpitations and previous cardio and neuromuscular events. Acute neurovascular syndrome was suspected, for which a simple skull tomography was performed, revealing spontaneous IPH of the right basal ganglion in the context of an acute cerebrovascular accident of hypertensive origin without any criteria for neurosurgical surgical intervention; furthermore, the patient did not require reversal of the administered antiplatelets. Fig. 4 reveals a right temporal intraparenchymal hematoma with vasogenic edema and ventricular involvement without any changes compared with the previous one. Fig. 5 suggests no akinesia or hypokinesia, but diastolic dysfunction and relaxation disorders are present.

It is important to note that the ECG changes were transient. At the time of establishing medical management for the patient's pathology (neurovascular syndrome), the ECG changes began to normalize.

The patient was hospitalized in the intensive care unit for a hypertensive brain emergency and required a vasodilator for 2 days (nitroglycerin and IV labetalol). A transthoracic ECG was performed, revealing an ejection fraction of 65% (calculated using Simpson's method) with type I diastolic dysfunction due to relaxation disorders and without signs of ischemia, intracavitary masses or thrombi (Fig. 5).

The patient subsequently required transfer to the hospitalization room where the antihypertensive management was adjusted. The patient was discharged on the ninth day after admission with left hemiparesis and without spasticity. Follow-up and outpatient rehabilitation were planned.

Several cases of ST segment deviation, inversion of the T wave and prolongation of the corrected QT interval in patients with SAH have been reported (11-14). As showcased in these previous SAH studies and the present case, clinicians still face challenges in differentiating the ECG changes of ICH or SAH from those of acute coronary syndrome. In the present study, ST-segment elevation was evidenced in a patient with IPH who was initially treated as a myocardial infarction. The most common ECG alterations after IPH include repolarization abnormalities, such as QT interval prolongation and ST-segment and T-wave changes (15), of which QT interval prolongation is the most frequent (2,3).

As observed in the present case, nontraumatic IPH results from small artery bleeding, commonly due to hypertension (15,16), and it generally occurs in patients older than 60 years of age (16). Previously, Yaghmoor et al (2) reported an IPH prevalence of 23% among all ICHs.

Contrary to what occurred in the present case, previous research reported that death in patients with IPH was more common in cases in which changes in the ST segment were not observed (2).

It has been suggested that, to decrease or predict the occurrence of unfavorable results after ICH, cardiac monitoring should be performed in addition to the ECG to detect arrhythmias during the first 2 to 3 days after hospitalization (2).

The most important aspects that must be considered to differentiate the ECG changes of ICH or SAH from those of acute coronary syndrome are the clinical manifestations. Not every patient with IPH should have an ECG. If the clinical manifestations indicate chest pain, discomfort, dyspnea and other suggestive symptoms, it is more likely that it is a coronary syndrome. In the patient described in the present study, the main reason for consultation was weakness and decreased muscle strength in the left side of the body, associated with dysarthria, as well as labial commissure deviation, suggesting a neurovascular syndrome (probable ischemic stroke or IPH).

It is important to note that, in addition to the presence of nonspecific ECG findings, clinicians should consider immediate brain computed tomography to confirm ICH.