Coronary artery bypass grafting is a well-established, durable, and safe surgical intervention. However, coronary artery disease continues to progress after the procedure. Patients who have undergone bypass surgery present unique challenges in terms of secondary prevention resulting from the often severe and diffuse nature of their coronary disease, the complexities of their postoperative recovery, the burden of their comorbid conditions, and the importance of ensuring long-term graft patency and preventing further disease progression. New evidence and advances in secondary prevention strategies in the post-coronary bypass grafting population have emerged since the American Heart Association's 2015 scientific statement on this topic. Secondary prevention strongly correlates with improved outcomes after bypass surgery, providing the rationale and urgency for this updated scientific statement to promote evidence-based practical considerations and to improve their use.
Stroke is a leading cause of death and disability worldwide, and the recovery process is significantly influenced by a multitude of factors beyond immediate medical treatment. Social and environmental determinants of health-conditions in which people are born, grow, work, live, and age-play a crucial role in the functional outcomes of stroke survivors, and addressing these factors is essential to ensure equitable care and optimal recovery. Previous scientific statements have discussed the effects of social isolation on cardiovascular and brain health, as well as strategies to reduce racial and ethnic inequities in stroke preparedness, care, recovery, and risk factor control. In this statement, we review the effect of factors such as social and environmental determinants on stroke functional outcome primarily but also secondary stroke prevention when relevant. In addition, we provide actionable considerations for addressing them to improve stroke outcomes; strategies include the identification of upstream factors, use of impactful policies, and use of implementation science frameworks to translate evidence-based practices into real-world settings. Current gaps for future research include understanding the effect of cultural considerations on stroke recovery, recognizing the interaction of social and environmental determinants of health with each other and with biological factors in determining stroke outcomes, and finding effective ways to address these factors in different environments to achieve best outcomes for all stroke survivors.
Finite element analysis (FEA) is a powerful tool that forms the cornerstone of modeling cardiac biomechanics. However, FEA is computationally expensive for creating digital twins, which typically involves performing tens or hundreds of FEA simulations to estimate tissue parameters, limiting its clinical application. We have developed an attention-enhanced graph neural network (GNN)-based FEA emulator, HeartSimSage, to rapidly predict passive biventricular myocardial displacements from patient-specific geometries, chamber pressures, and material properties. Designed to overcome the limitations of current emulators, HeartSimSage can effectively handle diverse three-dimensional (3D) biventricular geometries, mesh topologies, fiber directions, structurally based constitutive models, and physiological boundary conditions. It also supports flexible mesh structures, allowing variable node count, ordering, and element connectivity. To optimize information propagation, we developed a neighboring connection strategy inspired by Graph Sample and Aggregate (GraphSAGE) that prioritizes local node interactions while maintaining mid-to-long-range dependencies. Additionally, we integrated Laplace-Dirichlet solutions to enhance spatial encoding and employed subset-based training to improve computational efficiency. Incorporating the attention mechanism allows HeartSimSage to adaptively weigh neighbor contributions and filter out irrelevant information flow, enhancing prediction accuracy. As a result, errors in the predicted biventricular myocardial displacements by HeartSimSage were limited to a median of 0.280 mm with an interquartile range of [0.167, 0.484] mm compared to traditional FEA, while achieving a computational speedup of approximately 13000X on a GPU and 190X on a CPU. We validated our model on a published left ventricle dataset and analyzed the model's sensitivity to hyperparameters, neighboring connection strategies, and the attention mechanism.
Structural heart disease (SHD) encompasses diseases involving the heart valves, chambers, walls, and muscles. Current diagnostic methods have limited accessibility and predictive value. This review aims to present recent advances in artificial intelligence (AI)-guided tools in the screening of SHD and valvular heart disease (VHD), and to present challenges and opportunities for their use in clinical practice. AI-guided models trained on ECGs, chest X-rays, and coronary artery calcium scans have a high accuracy in the diagnosis of SHD, heart failure, low left ventricular ejection fraction, and VHD. Some of these models can highlight the signals that influence their predictions, improving explainability. The use of AI in screening for SHD and VHD could lead to earlier diagnosis, enhanced accuracy, and better accessibility. However, outcome data on earlier diagnosis using these tools is required before broad deployment.
Heart failure with preserved ejection fraction (HFpEF) accounts for nearly half of heart failure cases, with obesity emerging as a key pathophysiologic driver. Oxylipins are lipid signaling molecules linked to adverse HFpEF outcomes, but their relationship with obesity remains unclear. To evaluate association between obesity and arterialized and venous oxylipins in HFpEF patients. In this prospective single-center cohort study, 90 patients with HFpEF underwent transthoracic echocardiography and right heart catheterization with arterialized pulmonary capillary and venous blood sampling. Serum oxylipins were quantified via liquid chromatography-mass spectrometry. Oxylipin levels were log-transformed and standardized. Oxylipin associations with obesity (BMI ≥ 30 kg/m²) were evaluated using logistic regression, and pulmonary hypertension (PH) subgroup analyses using a one-sample proportion test. Of the 90 patients, 61 (67.8%) were obese. Obese patients were younger, more frequently female and African American, had higher prevalence of diabetes (54.1% vs. 17.2%, p < 0.001) and exhibited greater interventricular septal and posterior wall thickness. Multivariable and volcano plot analyses demonstrated inverse associations between obesity and several arterialized oxylipins, including 12,13-DiHOME (OR:0.48; p = 0.03), 19,20-DiHDoPE (OR:0.53; p = 0.03), 11,12-DiHETrE (OR:0.31, p = 0.04), 9,10-DiHOME (OR;0.42; p = 0.02), and 5(S),6(S)-DiHETE (OR:0.51; p = 0.02). In contrast, arterialized 19R-hydroxy-prostaglandin E1 was positively associated with obesity (OR:1.91, p = 0.03). Among venous oxylipins, 15(R)-PGE1 (OR:2.23; p = 0.02) and 19R-hydroxy-prostaglandin E1 (OR:1.91; p = 0.02) showed positive associations with obesity. Obese patients constituted a higher proportion of combined pre- and post-capillary PH subgroup (p = 0.003). Obesity in HFpEF is associated with reduced oxylipin diol levels, higher levels of prostaglandin E1 metabolites, and higher burden of pulmonary hypertension.
This study examined the relationships between medication adherence and demographic and clinical characteristics in American Indian adults with Type 2 diabetes who live on tribal lands and receive medication at no cost to them. From tribal electronic health record data, we constructed a cross-sectional cohort of 3042 adults with Type 2 diabetes. Tribal citizens of a federally recognized tribe were included if aged ≥ 18 years, had Type 2 diabetes, had ≥ 1 Choctaw Nation of Oklahoma healthcare encounter in 2018, and were on antihypertensive, glucose- and lipid-lowering medications in 2018. Proportion of days covered (PDC) was used to assess medication adherence with a threshold of ≥ 80%. The cohort mean age was 59.3 ± 11.6 years; the majority were male (52%), married (52%), BMI ≥ 30 (74%), and lived in a rural setting (87%). Overall, 63% of patients were adherent to their medications with a mean PDC across all medication classes of 0.81 ± 0.18. Patients aged > 55 years had a significantly higher PDC across all three medication classes compared with those aged ≤ 55 years (84% vs. 77%, p < 0.001). Also, BMI ≥ 30 (β = 0.033, p < 0.001) or having a comorbid condition (β = 0.040, p < 0.001) were each associated with higher overall PDC. Whereas insulin use (β = -0.023, p = 0.001) and rural residence (β = -0.020, p = 0.03) were associated with lower overall PDC. Additionally, patients with comorbid kidney or heart disease had a higher overall PDC compared with those without these conditions (p < 0.001). In a setting with access to no-cost medication, nearly two-thirds of our sample were considered adherent to their medications. Older adults and those with comorbid conditions or BMI ≥ 30 had higher overall adherence to medications, whereas those residing in rural areas or using insulin had lower overall medication adherence.
Hypertension is a modifiable risk factor for cardiovascular disease (CVD) and its prevalence is high in the United States and worldwide. Adequate characterization of blood pressure (BP) is essential for the diagnosis and management of hypertension. However, BP assessment can be challenging because of the unique influences across the lifespan, disease conditions, and physical environmental context. Moreover, complex uncertainties in BP assessment may contribute to underdiagnosis, undertreatment, and preventable morbidity and mortality. Recent advances in BP measurement devices have enabled comprehensive characterization of BP that could dramatically change how hypertension is managed to optimize CVD risk reduction, avoid complications of low BP, and improve hypertension control rates. To address the rapidly evolving landscape in BP assessment, the National Heart, Lung, and Blood Institute of the U.S. National Institutes of Health convened a 2-day workshop of clinicians and researchers in December 2024. The present report summarizes the topics presented and discussed during the meeting, which focused on the latest evidence on BP assessment as well as obstacles and knowledge gaps to be addressed to advance BP assessment in clinical practice and research.
For patients with heart failure with reduced ejection fraction (HFrEF), identifying factors associated with lower uptake of guideline-directed medical therapy (GDMT) and higher rates of hospitalizations may inform strategies to improve quality of care. This study assessed the impact of psychosocial and socioeconomic factors on GDMT use and healthcare resource utilization among patients newly diagnosed with HFrEF between 01/01/2017-09/30/2021, in inpatient or outpatient settings across the U.S. Patients were identified from Optum's de-identified Clinformatics® Data Mart Database. GDMT improvement was defined as (1) initiation of ≥2 new GDMT classes among patients on ≤1 class, or (2) addition of ≥1 new GDMT class among patients already on ≥2 GDMT classes, within one month after the initial encounter with a new HFrEF diagnosis (the 'GDMT improvement period'). Adjusted logistic and negative binomial regressions were used to evaluate associations. The study included 230,664 patients newly diagnosed with HFrEF. For individual GDMTs, utilization rates increased by the end of the GDMT improvement period compared to baseline, but only 12.5% of patients met the definition of GDMT improvement. Psychosocial factors-including depression and substance abuse-were linked to lower odds of GDMT improvement and significantly higher rates of hospitalizations. In contrast, socioeconomic factors like household income and education levels were inversely associated with hospitalization rates but had weaker associations with GDMT improvement. In this US cohort of patients newly diagnosed with HFrEF, there was minimal initiation of GDMT after HFrEF diagnosis. Psychosocial factors were independently associated with lower GDMT uptake and higher risk of hospitalization.
Purinergic signaling is critical to myocardial inflammation and function. However, the underlying mechanisms are not well defined. Herein, we identified a protein kinase, homeodomain-interacting protein kinase 2 (HIPK2), as a novel regulator of purinergic signaling. Cardiomyocyte-specific HIPK2 knockout (CM-HIPK2-KO) hearts exhibited reduced expression of multiple key players of canonical purinergic signaling, including ectonucleases CD39 and CD73, and led to excessive inflammation and cardiac dysfunction. Multiple in vitro experiments with gain-of-function (adenovirus expressing HIPK2, Ad-HIPK2), and loss-of-function (Ad-sh-RNA-HIPK2) approaches were performed to establish that HIPK2-mediated regulation of purinergic signaling is a conserved mechanism in many cell types of diverse backgrounds. Mechanistically, we identified that the signaling circuit of HIPK2-ERK-CREB exerts its effects on purinergic signaling through transcriptional control on CD39 and CD73. Aberrant activation of purinergic signaling and inflammation was critical to cardiac pathologies because interventions with purinergic signaling inhibitor apyrase or NLRP3 inflammasome inhibitor CY09 largely rescued the detrimental cardiac phenotype of CM-HIPK2 KOs. Thus, herein, we identified HIPK2 as a novel regulator of purinergic signaling. Its deletion leads to excessive inflammation and cardiac dysfunction. Therefore, strategies to maintain HIPK2 are critical to sustaining cardiac health.
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Refractory unstable supraventricular tachycardia (SVT) that is unresponsive to both chemical cardioversion and electrical cardioversion is a rare phenomenon that may lead to significant morbidity and mortality. For this subcategory of patients, there are no clear recommendations in the current American Heart Association (AHA)/American College of Cardiology (ACC)/European Society of Cardiology (ESC) guidelines for their management. A 59-year-old male sought care in the emergency department due to chest pain, palpitation, shortness of breath, and pre-syncope. On evaluation, the patient had an unstable SVT as evidenced by acute heart failure on examination and an electrocardiogram demonstrating SVT. The SVT was unresponsive to both chemical (adenosine and amiodarone) and synchronized electrical cardioversion. With no other chemical cardioversion options and no clear recommended management guidelines, the patient was successfully converted with the use of 2 g intravenous magnesium sulfate. This case highlights the importance of considering unconventional therapy, such as magnesium sulphate, as a rescue agent in cases where the standard recommendations are ineffective, unavailable, or contraindicated.
Takayasu arteritis is a chronic large-vessel vasculitis that predominantly affects young women and may lead to severe vascular complications. This case series is noteworthy because it describes Takayasu arteritis revealed by severe cardiovascular and neurovascular complications, including ischemic stroke and advanced heart failure, in young women without traditional cardiovascular risk factors. We report three cases of Takayasu arteritis observed at Ibn Rochd University Hospital in Casablanca in 2024. The median age was 38 years. Two patients presented with ischemic stroke, while one presented with advanced heart failure. Clinical examination revealed upper limb claudication, dyspnea on exertion, decreased or absent radial pulses, carotid bruits, and significant blood pressure asymmetry between upper limbs. Laboratory investigations showed an inflammatory syndrome with elevated C-reactive protein and erythrocyte sedimentation rate, as well as inflammatory anemia. The diagnosis was confirmed by multimodal non-invasive vascular imaging, including Doppler ultrasound, computed tomography (CT) angiography, magnetic resonance (MR) angiography, and positron emission tomography (PET) scan, fulfilling the 2022 American College of Rheumatology classification criteria. All patients received high-dose corticosteroid therapy (1 mg/kg/day) followed by progressive tapering. Standard treatment for heart failure was initiated when indicated, and anticoagulation or antiplatelet therapy was prescribed according to the presence of embolic events. Clinical and biological improvement was observed in all patients, with partial neurological recovery and a significant reduction of inflammatory markers. Takayasu arteritis may present with highly polymorphic clinical presentations, including severe cardiovascular and neurovascular complications as initial manifestations in young women without traditional risk factors. Early recognition through multimodal non-invasive vascular imaging is essential to establish the diagnosis promptly and initiate appropriate treatment, thereby reducing the risk of irreversible complications.
Antibiotics play a crucial role in managing odontogenic infections, but inappropriate prescribing within dental practice still contributes to growing antimicrobial resistance. This review describes current U.S. recommendations from the Centers for Disease Control and Prevention (CDC), the American Dental Association (ADA), the American Heart Association (AHA) and the American Academy of Pediatric Dentistry (AAPD). Research supports using narrow-spectrum antibiotics for short treatment periods, while prophylactic use is now mainly reserved for patients with certain cardiac or immunocompromising conditions. Ongoing over prescription is often linked to uncertainty in diagnosis, patient pressure and limited stewardship systems. Thus, the need for more practical strategies like expanding education, clinical decision tools and interprofessional collaboration to strengthen antibiotic stewardship.
Sodium-glucose cotransporter 2 inhibitors have demonstrated substantial cardiovascular and renal benefits in adults, including reduced heart failure events across diabetic and nondiabetic populations. However, pediatric cardiac data remain limited, and real-world use is increasing in specialized centers despite the absence of standardized pediatric protocols. We synthesized a literature review, which was conducted using multiple databases, covering records available through January 2026, to include studies reporting cardiovascular outcomes in children with heart failure receiving dapagliflozin. Given the heterogeneity in study designs and endpoints, findings were synthesized qualitatively without conducting a meta-analysis. Six key studies were identified: 1 open-label pilot randomized trial, 1 prospective cohort, 3 retrospective cohorts, and 1 case series, encompassing heterogeneous etiologies, including dilated cardiomyopathy, myocarditis-related cardiomyopathy, congenital heart disease/Fontan physiology, and post-transplant graft dysfunction. Across observational cohorts, dapagliflozin was associated with modest improvements in ventricular function and frequent improvement in New York Heart Association/Ross functional class. Natriuretic peptide responses were variable, with reductions that were inconsistent. The pilot randomized trial did not demonstrate significant between-group differences in composite clinical outcomes or key cardiac measures over a 6-month period. Reported adverse events were predominantly genitourinary infections and transient renal events, with few discontinuations and no consistent signal of ketoacidosis, severe hypoglycemia, or clinically significant hypotension. Available data suggest a potential signal for modest improvement in cardiac function and clinical status, alongside an overall reassuring short-term safety profile. Multicenter prospective studies with standardized endpoints are needed to define efficacy, optimal patient selection, and long-term safety in pediatric cardiac care.
The American Heart Association (AHA) recently formalized cardiovascular-kidney-metabolic (CKM) syndrome to characterize the systemic interplay among cardiovascular failure, chronic kidney disease (CKD), and metabolic disturbances. Despite evolving clinical management, identifying a unifying cellular driver of this multi-organ deterioration remains a critical priority. This review explores the hypothesis that mitochondrial dysfunction serves as the fundamental pathological nexus of CKM syndrome, driving the progression from early-stage metabolic risk to end-stage organ failure. We synthesize evidence demonstrating how nutrient overload and lipotoxicity precipitate a vicious cycle of bioenergetic failure. In the cardiovascular system, ATP deficiency and impaired mitophagy lead to the structural remodeling observed in both heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF). In the kidney, the high mitochondrial density of proximal tubules renders them uniquely susceptible to oxidative stress and mitochondrial DNA (mtDNA) leakage, which subsequently triggers systemic inflammation. Furthermore, we analyze how established therapies-including sodium-glucose co-transporter 2 (SGLT2) inhibitors, Glucagon-like peptide-1 (GLP-1) receptor agonists, and non-steroidal mineralocorticoid receptor antagonists (MRAs)-exert organ-protective effects via mitochondrial mechanisms, promoting metabolic efficiency, reducing reactive oxygen species generation, stabilizing mitochondrial integrity, and promoting mitochondrial quality control processes. Finally, we review emerging mitochondrial-targeted strategies, such as mitoquinol, elamipretide and NAD+ boosters, which aim to restore the SIRT1-PGC-1 α signaling axis. Mitochondria function as the central engines of the CKM axis. A shift toward a mitocentric clinical model may enable earlier intervention and more precise targeting of the mechanisms driving organ crosstalk. Future success depends on multidisciplinary collaboration and the validation of mitochondrial biomarkers to advance precision medicine in CKM syndrome.
Objective The use of anticoagulant and antiplatelet medication has traditionally been cited as a contraindication for acute ischemic stroke treatments. However, the 2026 American Heart Association (AHA)/American Stroke Association (ASA) Guidelines have updated these standards, designating tenecteplase (TNK) as a preferred thrombolytic agent and identifying the benefit-to-risk ratio for thrombolysis in patients with recent anticoagulant exposure as uncertain. Conversely, mechanical thrombectomy is increasingly utilized regardless of antithrombotic status. This study examines the difference in post-intervention intracranial hemorrhage (ICH) and modified Rankin score (mRS) between patients receiving comprehensive stroke treatment who were taking these medications versus patients who were not on antithrombotic pharmacotherapy. Methods This study was a retrospective chart review. Inclusion criteria consisted of adult patients who were evaluated in the emergency department for stroke and received either thrombolysis (tissue plasminogen activator (tPA) or TNK) or procedural neurointervention between March 2018 and May 2020. Data collected included patient demographics, pre-stroke antiplatelet use, anticoagulant use, post-intervention mRS, and incidence of ICH. ICH and mRS outcomes were compared between patients based on their antithrombotic use for each of the neurointervention groups. Results A total of 251 patients met the inclusion criteria. Patients taking antiplatelets who received both thrombolysis and thrombectomy had significantly higher mRS scores compared to patients not taking these agents. Patients taking antiplatelets who received thrombolysis alone tended to have higher mRS but failed to reach significance. Patients taking only anticoagulants showed no difference in mRS for any intervention. Patients taking both anticoagulants and antiplatelets had a higher mRS than those not taking either medication. Crucially, there were no significant differences in the rate of ICH after any intervention regardless of medication usage. There was also no difference in any outcomes between patients on single versus dual antiplatelets. Conclusion Our results suggest that patients on antiplatelet and anticoagulant medication may be able to safely receive procedural neurointervention and thrombolysis for acute ischemic stroke without an increased risk of ICH. While functional outcomes (mRS) were higher in medicated groups, these results likely reflect underlying comorbidities rather than procedural complications. These hypothesis-generating findings align with the evolving 2026 clinical landscape and underscore the need for prospective studies to resolve current clinical uncertainties regarding antithrombotic status and reperfusion therapy.
The 2026 American College of Cardiology/American Heart Association/Multisociety Dyslipidemia Guideline marks a defining moment for lipidology with the reinstatement of low-density lipoprotein cholesterol (LDL‑C) and non-high-density lipoprotein cholesterol treatment goals and a decisive endorsement of combination lipid‑lowering therapy. Although statins remain foundational, statin monotherapy often fails to achieve sufficient LDL‑C lowering, particularly in high-risk patients or patients with statin intolerance or refusal. These realities elevate nonstatin therapies from secondary considerations to core components of evidence‑based care. This commentary reviews the expanded role of currently available nonstatin agents across all guideline‑defined treatment groups. New outcomes data further strengthen the rationale for greater LDL‑C reduction in high‑risk primary prevention populations and reinforce the "lower is better" principle central to lipidology. Finally, we explore the rapidly evolving pipeline of next‑generation LDL‑C-lowering therapies, including long‑acting injectables and oral proprotein convertase subtilisin/kexin type 9 inhibitors, that promise to further individualize care and address longstanding barriers to adherence and goal attainment. These advances underscore a new lipid‑lowering paradigm that includes combination therapy to achieve and sustain optimal LDL‑C levels and meaningfully reduce atherosclerotic cardiovascular disease risk.
Nuclear lamins organize the structural and regulatory architecture of the nucleus, integrating nuclear mechanics, chromatin organization, and genome regulation. During cardiac development, lamin composition undergoes a coordinated transition that parallels the shift from proliferative embryonic cardiomyocytes to mechanically active postnatal cells. Recent findings reveal that B-type lamins support early nuclear plasticity and proliferative capacity, whereas Lamin A/C stabilizes nuclear architecture and transcriptional programs in mature cardiomyocytes. Beyond their structural roles, lamins participate in multiple layers of nuclear regulation, including lamina-associated chromatin organization, nucleo-cytoskeletal mechanotransduction, nucleocytoplasmic transport, and regulation of mitotic progression and cell-cycle exit. Through these interconnected functions, the nuclear lamina coordinates cardiomyocyte proliferation, maturation, and mechanical stress adaptation during heart development. Mutations in lamin genes cause a diverse group of disorders collectively known as laminopathies, many of which prominently affect the cardiovascular system. In this review, we first examine how B-type and A-type lamins are developmentally deployed to regulate cardiomyocyte proliferation and maturation in the heart. We then discuss the mechanistic pathways through which lamins organize nuclear architecture, chromatin dynamics, and nucleo-cytoskeletal signaling to coordinate cardiac cellular function. Finally, we consider how disruption of these lamin-dependent regulatory networks contributes to cardiomyopathy, cardiovascular aging, and the loss of regenerative capacity in the adult mammalian heart.
Cardiac sarcoidosis (CS) is an increasingly recognized inflammatory cardiomyopathy that can present with ventricular arrhythmias and progressive heart failure (HF). Despite advances in various imaging modalities, notable regional differences persist in how CS is suspected, diagnosed, and managed. In Japan, where CS has long been a clinical priority and advanced imaging is widely accessible, screening and diagnostic pathways are often applied earlier in the disease course. In contrast, in many North American and Western settings, CS is frequently identified after presentation with advanced cardiomyopathy or arrhythmic complications. The most profound divergence lies in the diagnostic framework. The Japanese Circulation Society (JCS) guidelines emphasize early recognition of clinically diagnosed forms for cardiac involvement in patients with known systemic sarcoidosis without the requirement of invasive endomyocardial biopsy. The JCS guidelines also formally recognize "clinically isolated CS" as a clinically defined entity confined to the heart. In contrast, the US criteria prioritize specificity, requiring histological proof from any organ for a definitive diagnosis. This divergence propagates downstream discrepancies in risk stratification and therapeutic strategies. In this review, we discuss the original research underpinning these frameworks, and the need for international harmonized research efforts to better define this entity and inform future diagnostic and management strategies.
Cardiovascular-kidney-metabolic syndrome (CKMS) is a recently launched by American Heart Association to express the importance of interplay among metabolic risk factors, chronic kidney disease, and the cardiovascular system which has profound impacts on morbidity and mortality. The common pathologic processes that impact cardiovascular, kidney and metabolic disorders include but not limited to unhealthy lifestyle (e.g. sedentary life, smoking, lack of exercise, poor nutrition), chronic inflammation, oxidative stress, and endocrine alterations. These risk factors were also implicated as risk factors for sarcopenia development. Indeed, previous studies have shown that the individual components of CKMS were associated with sarcopenia. These studies rarely examined the relationship between CKMS in constellation with sarcopenia until recently but latest studies have consistently showed associated with CKMS as a whole with sarcopenia. In this narrative review, we summarized the latest and specific studies (n: 44855) regarding the relationship between sarcopenia with CKMS. Additionally, we underlined the common pathogenic mechanisms and potential biomarkers for CKMS, and sarcopenia. We discussed non-pharmacological and pharmacological approaches for management of CKMS and sarcopenia We also highlighted potential clinical applications and knowledge gaps to be investigated in future studies.