Ischemic cerebrovascular event (CVD) and acute myocardial infarction (AMI) are two of the leading causes of morbidity and mortality worldwide, together accounting for more than a quarter of global deaths. Both entities share risk factors, pathophysiological mechanisms and, in some cases, a close temporal relationship. Although they usually occur independently, they can rarely occur simultaneously or in a short interval of time, configuring the so-called cardio-cerebral infarction (CHF), a rare but highly serious clinical entity.CHF is defined as the concomitant or close sequential occurrence of a cerebral ischemic event and a cardiac ischemic event. Since its initial description, its epidemiology has been difficult to establish due to its low incidence and the limited evidence available, based mainly on reports and case series. Observational studies have reported variable incidences, with rates of stroke associated with AMI between 4% and 29%, and of AMI after stroke between 0.8% and 15%. Synchronous presentation is even more infrequent, with reported incidences close to 0.009% in some series, although it can reach up to 0.5–2% in recent population records.Several pathophysiological mechanisms have been proposed to explain this association, including the formation of mural thrombi after AMI, atrial fibrillation as a source of cardioembolic embolism, paradoxical embolism through a patent foramen ovale, aortic dissection, and severe hemodynamic alterations. It has also been described that lesions in the insular cortex can induce autonomic dysfunction and adverse cardiac events.From a clinical point of view, CHF represents a significant diagnostic and therapeutic challenge, as cerebral and coronary reperfusion strategies may conflict, particularly in the use of systemic thrombolysis or endovascular interventions. The absence of specific clinical guidelines and clinical trials limits decision-making, forcing an individualized approach based on clinical experience.In this context, we present the case of a patient with simultaneous cardio-cerebral infarction associated with atrial fibrillation, complicated with hemorrhagic transformation after intravenous thrombolysis, with the aim of highlighting the diagnostic, pathophysiological, and therapeutic challenges of this complex entity.

A 67-year-old male patient with a history of arterial hypertension, type 2 diabetes mellitus, recently diagnosed atrial fibrillation, ischemic heart disease with a history of anteroseptal myocardial infarction in 2024, with a coronary stent and being treated with losartan, carvedilol, metformin and NPH insulin. Previous cardiological studies performed in 2024 using a 24-hour Holter showed sinus rhythm without evidence of pathological bradyarrhythmias or significant pauses, with the presence of multiple episodes of supraventricular tachycardia such as paroxysmal atrial fibrillation and sinus tachycardia, in addition to moderate-density monomorphic ventricular extrasystoles (6.4% of total beats), including pairs and triplets, without sustained ventricular tachycardia.

He presented with a sudden onset of approximately 2 hours characterized by dysarthria, left brachial monoparesis and deviation of the left lip commissure, for which the stroke code was activated. On admission he has a NIHSS score of 5 points. The initial cranial computed tomography showed no hemorrhage or early signs of ischemia, so intravenous thrombolysis with alteplase (0.9 mg/kg) was performed, with a total dose of 87.3 mg administered, with subsequent partial clinical improvement (NIHSS 4). During the evolution, ST-segment elevation was documented in the electrocardiogram, associated with atrial fibrillation with rapid ventricular response.

On neurological examination, the patient was awake but disoriented in time and space, with moderate dysarthria and cognitive alterations characterized by acalculia, right-left confusion and digital agnosia, suggesting cortical involvement. Muscle strength was preserved (Daniels 5/5), with right brachiocrural hypoesthesia and symmetrical decreased osteotendinous reflexes.

From the syndromatic point of view, the condition is compatible with a left parietal cortical syndrome associated with contralateral sensory deficit and alterations of higher cortical functions, configuring a Gerstmann syndrome. Topographically, it is located in the territory of the left middle cerebral artery, with involvement of the dominant parietal lobe and possible extension to frontal opercular areas.

The clinical picture suggests a cerebral ischemic event of probable cardioembolic origin in the context of atrial fibrillation, associated with a concomitant coronary event, compatible with a simultaneous cardio-cerebral infarction.

ENTRY TAC 17-02-2026: No apparent ischemic or hemorrhagic lesions

Control Ct 18-02-2026: Intraparenchymal Hemorrhage in the Left Occipital Region

Hypodensity is Observed at the Level of the Left Parietal Region

23-02-2026: Left Parieto-Occipital Intraparenchymal Hematoma with Mild Perilesional Edema

27-02-2026: It is Observed that the Perilesional Edema has Decreased the Borders are Well Defined

ICH SCORE: 1 Estimated Mortality Of 13% In 30 Days Ecass Hemorrhagic Transformation: Ph1 (Hematoma Occupies Less Than 30% Of The Infarction Area)

Cardiocerebral infarction (CHF) is a rare but highly serious clinical entity, characterized by the simultaneous or sequential occurrence of acute myocardial infarction (AMI) and acute ischemic stroke (CVA). Although both pathologies share common risk factors such as hypertension, diabetes mellitus, and atrial fibrillation, their concomitant presentation poses significant diagnostic and therapeutic challenges. The available evidence suggests a variable, generally low incidence, with rates ranging from 0.3% to 2%, which explains the limited availability of specific evidence-based guidelines.

In the case presented, the coexistence of a cerebral ischemic event in the territory of the left middle cerebral artery and the elevation of the ST segment in the electrocardiogram suggests a synchronous CHF, probably of cardioembolic origin in the context of atrial fibrillation. This mechanism is widely recognized as one of the main contributors in this entity, since it favors the formation of intracardiac thrombi with emboligenic potential into the cerebral circulation. In addition, a history of ischemic heart disease and atherosclerotic disease reinforce the shared pathophysiological substrate.

From a therapeutic point of view, CHF poses a critical dilemma due to the need to prioritize both cerebral and coronary reperfusion strategies. Current guidelines suggest the use of intravenous thrombolysis with alteplase in stroke doses as the first line in patients within the therapeutic window, followed by evaluation for coronary intervention if necessary. However, the difference in optimal dose between AMI and stroke, as well as the increased risk of bleeding complications, limits the standardization of management. In this case, intravenous thrombolysis allowed partial neurological improvement, although the evolution may be complicated by hemorrhagic events, as described in the literature.

The prognosis of CHF is significantly worse compared to isolated events, with high mortality and complication rates. Studies have shown a higher frequency of hemorrhagic transformation, prolonged hospital stay, and worse functional recovery. This highlights the importance of an early multidisciplinary approach, which allows optimizing therapeutic decisions and improving clinical outcomes.

Finally, the absence of clinical trials and the heterogeneity in diagnostic criteria underscore the need for future research to establish clear protocols and standardized management strategies for this complex clinical entity.

Cardiocerebral infarction is a rare but highly complex clinical entity, characterized by the coexistence of a cerebral ischemic event and an acute myocardial infarction in a short period of time. Early recognition is essential, as it is associated with high morbidity and mortality and a worse prognosis compared to the isolated presentation of each pathology.

The case presented illustrates the importance of considering this entity in patients with multiple cardiovascular risk factors, especially atrial fibrillation, which is a key mechanism in the genesis of cardioembolic events. Clinical presentation may be variable and require a high index of suspicion, particularly when concomitant neurological and cardiological findings are documented.

From a therapeutic point of view, the management of cardio-cerebral infarction represents a significant challenge due to the need to balance cerebral and coronary reperfusion strategies. Intravenous thrombolysis in the therapeutic window continues to be a valid option, although it is not without risks, such as hemorrhagic transformation, which requires an individualized evaluation in each case.

Likewise, the absence of specific clinical guidelines and robust clinical trials limits the standardization of treatment, so decisions should be based on comprehensive clinical evaluation and a multidisciplinary approach involving neurology, cardiology, and critical care.

Finally, it is necessary to promote the development of prospective and multicenter studies that allow the definition of uniform diagnostic criteria and the establishment of optimal therapeutic strategies, with the aim of improving the prognosis and quality of life of patients affected by this complex entity.