Key result
Intravenous tPA improves stroke deficits and resolves concurrent inferior STEMI without PCI.
Why the study?
Simultaneous acute ischemic stroke and acute myocardial infarction require urgent reperfusion, but there is no common algorithm regarding treatment doses, interventional approaches, and bleeding risk.
Case Report (n=1)
No
Answers are grounded in this paper and cite their sources.
This case report illustrates that intravenous alteplase administered at standard stroke doses for hyperacute ischemic stroke may simultaneously achieve coronary reperfusion in a patient presenting with concurrent ST-elevation acute coronary syndrome (cardiocerebral infarction).
Introduction: The simultaneous occurrence of acute ischemic stroke and acute myocardial infarction, described as “cardiocerebral infarction,” is a clinically challenging condition. Although both diseases require urgent reperfusion, there is no common algorithm regarding treatment doses, interventional approaches, and bleeding risk. This report aims to present a patient whose neurological and coronary findings regressed after IV thrombolytic therapy given for acute ischemic stroke.Case: A 66-year-old woman with a history of HTN and DM presented to another center with simultaneous onset of right arm weakness and chest pain. On presentation, right upper extremity muscle strength was 3/5 and NIHSS was 2. Brain CT showed no hemorrhage; diffusion MRI showed diffusion restriction in the bilateral frontal regions. At 2 hours from symptom onset, IV tPA was given with a diagnosis of hyperacute ischemic stroke. Afterward, right upper extremity strength rose to 4/5 and NIHSS fell to 1. The ECG obtained at the same time showed ST elevation in leads II, III, and aVF, and troponin was 30.9 initially, 724.2 on follow-up, and peaked at 1,300 nanogram/L. She was referred to our center’s coronary intensive care unit with a preliminary diagnosis of ACS. Serial ECGs showed regression of the ST elevations. Transthoracic echo showed EF 50%, basal inferior hypokinesis, grade 2 mitral and aortic regurgitation, LA 39 mm (diameter) and LVH. On coronary angiography the next day, 40% stenosis of the proximal and mid LAD, 30% stenosis of the proximal RCA, and diffuse plaques in the Cx were seen. Percutaneous coronary intervention was not required, and medical follow-up was decided. The patient was then transferred to the neurology ward. In our patient, the regression of chest pain and ST elevations together with neurological improvement after IV tPA given at the stroke dose suggests that the coronary thrombus may have been dissolved by IV tPA. However, spontaneous coronary reperfusion, coronary vasospasm, MINOCA, stress cardiomyopathy, and stroke-related neurogenic myocardial injury should also be considered in the differential diagnosis. The timing of antiplatelet therapy and invasive coronary intervention after thrombolysis should be individualized, taking the risk of intracranial hemorrhage into account (Figure 1–6).Discussion/Conclusion: In patients with acute neurological deficit accompanied by chest pain, cerebral and cardiac evaluation should be carried out together. IV tPA given for acute ischemic stroke may contribute to reperfusion in a concomitant thrombotic coronary occlusion. However, this possibility should be interpreted together with serial ECGs, cardiac biomarkers, echocardiography, and coronary angiography data.Keywords:
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Ersin et al. (2026) conducted a case report in Concurrent acute ischemic stroke and ST-elevation acute coronary syndrome (cardiocerebral infarction) (n=1). Intravenous alteplase (tPA) was evaluated on Neurological and coronary clinical and electrocardiographic regression. Intravenous tPA administered 2 hours after symptom onset improved NIHSS from 2 to 1 and resolved inferior ST-elevations and chest pain without requiring PCI.
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