Clinical Case 28—Hyperacute synchronous cardiocerebral infarction in a patient with new-onset atrial fibrillation a rare case of MINOCA. (21st October 2022)

• Record Type: Journal Article
• Authors: Papakonstantinou, Panteleimon E; Manousiadis, Konstantinos; Bei, Ilianna; Lentza, Malamati-Eleni; Panourgia, Maria; Tachmetzidi-Papoutsi, Dimitra; Sideris, Antonios
• Is Part Of: Cardiovascular research. Volume 118(2022)Supplement 2
• Publication Date: 2022-10-21
• Subjects: Cardiocerebral infarction -- Atrial fibrillation -- Myocardial infarction -- Stroke -- MINOCA; Cardiovascular system -- Diseases -- Periodicals; Cardiovascular system -- Periodicals; 616.1
• DOI: 10.1093/cvr/cvac157.145
• Languages: English
• ISSNs: 0008-6363

Abstract

Abstract: Introduction: Hyperacute synchronous cardiocerebral infarction (CCI) is an extremely rare condition with an incidence of 0.009%. Herein, we present a case of hyperacute synchronous CCI in an elderly patient with new-onset atrial fibrillation (AF). Case report: An 80-year-old male patient was referred to our emergency department due to acute onset left hemiparesis and dysarthria. Computed tomography (CT) of the brain showed a hyperdense M3-M4 branch of the right middle cerebral artery. The electrocardiogram (ECG) revealed new-onset AF without specific signs of acute myocardial ischemia. Subsequent ECG revealed AF with Q waves and ST elevation in leads V1-V6, II, III, and aVF, while the patient remained hemodynamically stable, without symptoms indicative of myocardial ischemia. Intravenous tissue plasminogen activator (alteplase) was administered. During the thrombolytic therapy, the patient expressed sudden severe upper back pain, while the ECG showed 'tombstone' ST elevation in leads V1-V6, II, III, and aVF. The thrombolytic therapy was immediately terminated and a CT angiography of the aorta was performed, which did not show any evidence of aortic dissection. Coronary angiography revealed no angiographically significant coronary artery stenosis. ECG evolution, echocardiography, and coronary angiography findings were consistent with myocardial infarction with non-obstructive coronary arteries (MINOCA). Discussion: There are several conditions that lead to simultaneous acute CCI. The precise pathophysiological mechanism that leads to this synchronous CCI is difficult to be identified. In our case, the presence of new-onset AF can partly explain this situation as a source of both cerebral and coronary embolism. Figure 1 A . The hyperdense M3-M4 branch of the right MCA (arrow) was shown on the non-contrast axial CT scan performed shortly after the onset of symptoms. A hyperdense vessel represents an intravascular thrombus and is the earliest sign of acute infarct on non-contrast CT. B . A non-contrast axial CT scan performed 24 hours after the onset of symptoms shows brain swelling with sulcal effacement regarding the right MCA territories (arrows). The above findings are evidence of an acute infarct. C . A non-contrast axial CT shows hypoattenuating brain tissue along with loss of grey-white matter differentiation (arrow), findings consistent with ischemic damage due to infarcts concerning branches of the right MCA. D . Axial CT angiography revealed a fusiform aneurysm of the ascending thoracic aorta measuring approximately 5 cm at the level of the pulmonary artery trunk. E . ECG: AF (∼70 bpm) without specific signs of acute myocardial ischemia. F . ECG: AF (∼70 bpm) with Q waves and ST elevation in leads V1-V6, II, III, and aVF. G . ECG: AF (∼100 bpm) with Q waves and 'tombstone' ST elevation (arrows) in leads V1-V6, II, III, and aVF. H . ECG: AF (∼100 bpm) with deep Q waves and ST elevation in leads V1-V6, II, III, and aVF. CT: computed tomography; MCA: middle cerebral artery; ECG: electrocardiogram; AF: atrial fibrillation; bpm: beats per minute.