Population aging and changes in the chronic disease spectrum have gradually made geriatric multimorbidity a central issue confronting stroke care and geriatric medicine. Brain-heart multimorbidity is one of the most clinically representative and challenging phenotypes of geriatric multimorbidity, characterized by a deep intertwining of cerebrovascular and cardiovascular diseases across risk factors, pathological basis, acute events, long-term prognosis, and treatment strategies. Drawing on conceptual evolution and clinical phenotypes, this review classifies brain-heart multimorbidity into 3 clinical subtypes: brain-heart co-occurrence, brain-heart interaction, and brain-heart conflict. Taking atherosclerosis as the core pathological basis, this review systematically examines the pathophysiological mechanisms underlying brain-heart multimorbidity, including immune-mediated inflammation, endothelial injury, thrombosis, neuroendocrine dysregulation, and gut microbiota imbalance. On this basis, it analyzes critical gaps in China regarding epidemiological evidence, mechanistic research, clinical diagnosis and treatment models, polypharmacy management, and health service systems. This review proposes that prevention and treatment of brain-heart multimorbidity urgently need to shift from the traditional single-disease, single-system paradigm to a new framework of multiple coexisting diseases, whole-course management, and individualized decision-making. Such a framework should be anchored in multidisciplinary collaboration and integrate mechanistic research with real-world evidence to build a brain-heart multimorbidity prevention and treatment system tailored to China’s national conditions. As a microcosm of geriatric multimorbidity, this conceptual shift can provide methodological insights for moving geriatric multimorbidity from stacked single-disease management toward integrated multi-system governance, and is of great significance for reducing the burden of cardiovascular and cerebrovascular events in older adults and maintaining functional independence and quality of life.

Hypertension is a major cause of cerebral hemorrhage. Although they are widely used in preclinical studies on cerebral hemorrhage, traditional in vivo cerebrovascular imaging techniques, such as positron emission tomography and magnetic resonance imaging, often fall short in dynamically visualizing cerebral microcirculation blood flow in rodent models. This study leveraged the high spatiotemporal resolution of multimodal ultrafast sonography microscopy (MUSM) to assess cerebrovascular hemodynamics in vivo within hypertensive mice induced by Angiotensin Ⅱ (Ang Ⅱ) and Nω-nitro-L-arginine methyl ester (L-NAME). Cerebrovascular hemodynamics were quantified using variations in cerebral vascular density, diameter, velocity, tortuosity, cerebral flow pulsatility, and instant flow direction. Our findings revealed a decrease in cerebral vascular density and perfusion index after blood pressure increased, particularly in the cortex and basal ganglia regions. This study not only provides a comprehensive view of cerebral dynamics in hypertension but also introduces MUSM as a novel tool for in vivo cerebrovascular hemodynamic analysis in preclinical animal research.