Shah, Syed Asfand Yar

Cardio-oncology has emerged as a critical discipline in modern medicine due to the growing population of cancer survivors and the increasing recognition of cardiovascular disease as a major cause of morbidity and mortality in this population. While there have been significant advances in chemotherapy such as advances in chemotherapy, targeted therapies, immunotherapies, and radiation therapy, these treatments are linked to a wide range of cardiovascular toxicities such as myocarditis, arrhythmias, and progressive fibrotic remodeling. These toxicities tend to be caused by interrelated and multifactorial cellular processes including endothelial damage, immunological dysregulation and mitochondrial dysfunction. Therefore, early diagnosis of subclinical harm using multimodal surveillance strategies integrating clinical risk assessment, specialized clinical imaging, and circulating biomarkers has replaced reactive care of overt cardiotoxicity in modern cardio-oncology. Echocardiographic techniques such as longitudinal strain, with the help of biomarker-guided surveillance of natriuretic peptides and cardiac troponins, have made the early detection of cardiac dysfunction more effective. However, the current prediction risk models are still constrained and limited by their dependence on static clinical variables and their partial integration of biological mechanisms. This review examines the current methods for risk stratification and surveillance throughout the cancer care continuum, including baseline assessment, monitoring during active therapy, and long-term survivorship surveillance. Future approaches for tailored cardiovascular care are also highlighted, including new advances in precision cardio-oncology such as multi-omics profiling, molecular biomarkers, artificial intelligence, and mechanism-guided preventative strategies. Therefore, advancing biologically informed and risk-adapted monitoring frameworks may enhance early diagnosis, maximize cardioprotective measures, and lower long-term cardiovascular consequences.

Cardiovascular–Kidney–Metabolic (CKM) syndrome symbolizes a single pathophysiologic entity including obesity, type 2 diabetes, chronic kidney disease, and cardiovascular disease. These conditions altogether accelerate adverse outcomes when they coexist. Recent evidence has shown that the function of glucagon-like peptide-1 receptor agonists (GLP-1RA) and sodium–glucose cotransporter-2 inhibitors (SGLT2i) alleviate stress on multiple organs. SGLT2i has been demonstrated to benefit heart failure, hemodynamic regulation, and renal protection while GLP-1RA on the other hand has been shown to demonstrate a strong impact on glycemic management, weight loss, and atherosclerotic cardiovascular disease. This review will aim to understand and evaluate the mechanistic rationalization, clinical evidence, and the potential therapeutic treatment of SGLT2 inhibitors and GLP-1 receptor agonists to treat individuals who have CKM syndrome. This analysis also assesses whether combination therapy can be a synergistic approach that may benefit patients but is still underutilized because of the lack of clear guidelines, the associated costs, and disparities in accessibility. Therefore, in this review, we will be discussing the combination therapy’s additive and synergistic effects, current recommendations and clinical evidence, and mechanistic insights of these GLT2 inhibitors and GLP-1 receptor agonists in CKM syndrome patients. Overall, early and combination usage of GLP-1RA and SGLT2i may be essential to demonstrating a significant shift in modern cardiometabolic therapy toward patient-centered care.