Remote patient monitoring (RPM) for hypertension combines home blood pressure (BP) monitoring with electronic transmission of BP readings and clinical support. RPM has the potential to improve BP control and reduce hypertension disparities, but because it depends on devices, connectivity, digital literacy, and sustained engagement, it may also worsen inequities if not intentionally designed. This review examines barriers to equitable RPM implementation and strategies to address them. RPM can improve hypertension control and extend care beyond traditional clinical settings, but its effect on health equity depends on program design. Equity should be treated as a core design principle. Future research should evaluate differential reach, engagement, effectiveness, and sustainability across populations and identify payment models that support equitable implementation at scale. Barriers to equitable RPM implementation occur at patient, clinician, health system, and policy levels. Key challenges include limited access to technology, language barriers, out-of-pocket costs, inadequate cuff sizing, unmet social needs, clinician workload, referral bias, infrastructure limitations, reimbursement variability, and the digital divide. Emerging evidence suggests that equity-focused strategies can improve reach and engagement, including provision of cellular-enabled devices, reduced patient costs, culturally and linguistically tailored support, team-based care, registry-based outreach, and routine monitoring of enrollment and outcomes across demographic groups. High-resource, low-resource, and hybrid RPM models each offer distinct advantages and tradeoffs in balancing scalability, sustainability, and equity.
This review examines determinants across structural, institutional, interpersonal, and individual domains that contribute to hypertensive disorders of pregnancy (HDPs) in American Indian and Alaska Native (AI/AN) populations and their long-term cardiovascular consequences. It suggests paths forward for equitable research and clinical practice. AI/AN women have the highest HDP prevalence among all racial and ethnic groups at 9.1
To evaluate the crosstalk between the liver, heart, and kidneys in metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH), highlighting the distinct regulatory roles of non-traditional hepatokines, and to assess shared therapeutic targets and molecular mechanisms driving cardiorenal complications in MASLD patients. Emerging evidence highlights that hepatic lipid accumulation drives cardiac damage, which manifests as adverse remodeling, diastolic dysfunction, and coronary microvascular dysfunction. These abnormalities are mediated primarily by systemic lipotoxicity, inflammation of epicardial adipose tissue, and a pro-thrombotic environment. Mechanistically, altered hepatokine signaling mediates systemic cross-talk. Specifically, the downregulation of cardioprotective and renoprotective brain-derived neurotrophic factor (BDNF) and the dual metabolic roles of nerve growth factor (NGF), fibroblast growth factor (FGF) 19, and FGF21 accelerate the progression of both heart failure and chronic kidney disease (CKD). Concurrently, metabolic therapies such as glucagon-like peptide-1 (GLP-1) receptor agonists, sodium-glucose cotransporter-2 (SGLT2) inhibitors, and peroxisome proliferator-activated receptor (PPAR) agonists demonstrate significant efficacy in ameliorating steatosis, inflammation, and overall metabolic outcomes. MASLD acts as a systemic driver of multi-organ dysfunction within the cardio-renal-hepatic axis. Profiling specific hepatokine signatures offers a promising frontier for identifying novel therapeutic targets and biomarkers of disease acceleration. Furthermore, while current metabolic therapies show remarkable potential, rigorous clinical testing remains critical to definitively determine whether their cardiovascular and renal benefits stem from direct tissue-specific protective mechanisms or secondary metabolic improvements.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a systemic cardiometabolic disease. This review summarizes recent advances in epidemiology, pathophysiology, biomarkers, and treatment relevant to cardiovascular risk assessment and management. Fibrosis stage is the strongest independent predictor of cardiovascular outcomes in MASLD, conferring up to a 2.5-fold increase in events beyond traditional risk factors. Noninvasive tools, including Fibrosis-4 (FIB-4) and liver stiffness measurement, also predict cardiovascular mortality. Semaglutide and resmetirom offer dual hepatic and cardiometabolic benefits. MASLD affects 38
