Both the demographic change toward an older population and the fast pace of urbanization have contributed to the prevalence of unhealthy lifestyles, which has increased exposure to risk factors for cardiovascular and cerebrovascular disorders (Zhang et al., 2023). Both myocardial infarction (MI), sometimes known as a heart attack, and stroke are serious cardiovascular events that occur when there is a disruption in the circulation of blood (Li et al., 2024; Matter et al., 2024). MI is a condition that affects the heart muscle, while stroke is a condition that affects the brain (Stengl et al., 2025). Both diseases have the potential to be lethal and are associated with a multitude of risk factors, with MI being a potential consequence of stroke (Saba and Libby, 2025).

Restoring coronary blood flow is crucial for preserving the lives of patients experiencing acute MI and minimizing myocardial damage (Shamsuzzaman et al., 2024). Nevertheless, myocardial reperfusion can also exacerbate the extent of MI due to the overproduction of reactive oxygen species (ROS), intracellular calcium overload, and mitochondrial impairment, collectively referred to as reperfusion injury (Saba and Libby, 2025). Consequently, when examining the pathophysiological mechanisms associated with acute myocardial ischemia, it is essential to differentiate between the ischemic and reperfusion phases, as the molecular processes that lead to myocardial injury in these two phases are markedly distinct (Fig. 1).

Acute MI is categorized as STEMI and NSTEMI. Unstable angina is classified as an acute coronary syndrome (ACS) due to its status as a potential prelude to MI (McLaren et al., 2024). Unstable angina and NSTEMI have traditionally been consolidated for management purposes, and together they are referred to as non-ST-segment elevation ACS (NSTE-ACS) (Díez-Villanueva et al., 2024). MI often results from the rupture of a susceptible atherosclerotic plaque or the degradation of the coronary artery endothelium (type 1) (Młynarska et al., 2024). A significant stenosis (i.e., ≥70% diameter) is necessary to induce angina; nevertheless, such stenoses seldom result in type 1 MI, since they often possess robust fibrotic caps that are less prone to rupture, and collateral circulation develops with time (Fathima, 2021; Martínez et al., 2022). In contrast, susceptible plaques often exhibit 30–50% stenosis, possess thin fibrous caps, and contain a higher concentration of inflammatory cells, including lipid-laden macrophages. Upon rupture, the plaque discharges its thrombogenic constituents, leading to platelet activation, the commencement of the mural thrombus formation, the coagulation cascade, and the downstream embolization of atherosclerotic debris (Severs and Robenek, 2024). This hypercoagulable condition may lead to the rupture of further susceptible fibroatheromas, resulting in multiple culprit lesions (Jansen et al., 2024). The outcome is myocyte necrosis, which is accompanied and identifiable by increased levels of cardiac biomarkers in the peripheral blood (Aydin et al., 2019; Yu and Yu, 2024). The determinants of ischemia severity include the degree of vascular blockage, length of occlusion, volume of myocardium fed, existence of collateral circulation, and the sufficiency of reperfusion post-treatment (Bokhari et al., 2025; Netala et al., 2025). During acute myocardial ischemia, the death of necrotic cells initiates a pro-inflammatory response via various mechanisms, such as the production of reactive oxygen species (ROS), activation of the complement cascade, and the release of damage-associated molecular patterns (DAMPs) (Fig. 2) (Kologrivova et al., 2024). DAMPs facilitate the death of cardiomyocytes by interacting with Toll-like receptors (TLRs), attracting leukocytes to the area of infarction, and enhancing the release of various pro-inflammatory cytokines (Jin et al., 2025; Zhang and Dhalla, 2024).

The term “cardioembolic” is often used to refer to ischemic strokes when there is a high probability that the stroke was caused by a cardiac embolism (Kato et al., 2024). It is generally accepted that important embolic sources include intracardiac thrombi that are associated with atrial fibrillation or MI. As a result of the fact that anterior MIs are the most common cause of left ventricular thrombi, prophylactic strategies that include the use of anticoagulants are primarily focused on those who have had such infarctions (Massussi et al., 2021). Despite this, the mechanisms that are related to MI and stroke are not yet fully understood. The importance of the anterior site of the infarction, and therefore a left ventricular thrombus, has recently been called into question regarding its significance as a risk factor for stroke. Furthermore, the use of thrombolytic therapy and aspirin regularly for acute MI has not resulted in a change in the prevalence of left ventricular thrombi; nevertheless, it may have affected the risk of embolism (Fonseca, 2023; Mooe et al., 1997; Th et al., 1997).

There are similarities in the etiology of coronary heart disease and some subtypes of ischemic stroke, including inflammation and the advancement of atherosclerosis (Młynarska et al., 2024; Qian et al., 2025). Furthermore, MI may be a risk factor for stroke via mechanisms such as emboli. These emboli can form either during revascularization or as a result of atrial fibrillation associated with acute MI. Additionally, emboli can occur as a consequence of blood stasis in a left ventricle that is dysfunctional (Echeverría et al., 2025). In addition, many of the risk factors that are associated with stroke and MI are the same. These risk factors include hypertension, hypercholesterolemia, dependence on tobacco products, diabetes, and advanced age. There is a possibility that the risk of both complications of illness may be reduced by modifying these risk factors in conjunction with antiplatelet medication (Buckley et al., 2024; Kamalova, 2025).