Kanokwan Bunsawat

Wild-type transthyretin amyloidosis (wtATTR) is a unique cause of heart failure typically associated with orthostatic hypotension, likely implicating baroreflex dysfunction; however, this is yet to be investigated. Using the lower-body negative pressure technique to simulate orthostatic stress, we have identified impaired peripheral vascular responsiveness, which occurred in tandem with an inability to arterial blood pressure, suggesting that diminished sympathetic vasomotor responsiveness likely contributes to baroreflex dysfunction and impaired blood pressure regulation in patients with wtATTR.

Patients with chronic kidney disease (CKD) face high cardiovascular risk from both fluid overload and heightened sympathetic nervous activity. In healthy individuals, fluid expansion suppresses sympathetic tone; however, this inverse relationship was absent in our cohort with CKD stage II–IV. Using direct intraneural recordings and validated volume measures, we found that extracellular fluid and muscle sympathetic nerve activity increased in parallel, highlighting disrupted volume-autonomic interplay and underscoring the need to better understand neurogenic contributions to fluid dysregulation in CKD.

Han CJ, et al. Clin Hypertens. 2026 ;32:e45. https://doi.org/10.5646/ch.2026.32.e45

Kim HJ, et al. Korean Circ J. 2026 Jan;56:e41. https://doi.org/10.4070/kcj.2025.0365

Ye Ji Choi, Min Jeong Cho, Kanokwan Bunsawat, Byul Kim, Hyun Jeong Kim, Sae Young Jae. KJSM 2025;43:228-37. https://doi.org/10.5763/kjsm.2025.43.4.228

Heart failure with preserved ejection fraction (HFpEF) is a complex multi-organ clinical syndrome representing ~50% of all heart failure related cases nationwide. HFpEF is more prevalent in women yet both men and women with HFpEF present with distinct clinical phenotypes and prognosis that may be attributable, in part, to sex differences in anatomical, physiological, and/or hormonal characteristics. Of particular interest is the role of sex hormones, namely estrogen, as a contributing factor to sex differences in vascular health in patients with HFpEF. This mini review provides a summary of recent evidence regarding sex differences in coronary microvascular function, peripheral vascular function, and central arterial stiffness in patients with HFpEF. Focus will also be given to potential mechanisms by which age-related loss of estrogen may alter these aspects of physiology in women with HFpEF and provide potential future directions related to implications for women‘s health in adults with HFpEF.

Hemodialysis requires functional vascular access, which serves as the conduit for blood flow between the patient and the hemodialysis machine. The arteriovenous fistula (AVF), created by surgically connecting an artery to a nearby vein in the upper extremity, is the preferred form of vascular access for maintenance hemodialysis. Newly created AVFs must undergo a maturation process, during which the fistula vein enlarges and develops sufficient lumen size and blood flow to be used effectively for dialysis. However, since the invention of AVFs 60 years ago, rates of AVF maturation failure have remained high. Currently, no proven therapies exist to promote maturation or prevent maturation failure. This review examines the current understanding of the cellular and molecular mechanisms underlying AVF maturation failure, with particular focus on the impact of the chronic kidney disease (CKD) environment on the vascular system. In CKD, patients often have elevated levels of uremic toxins, increased oxidative stress, and chronic inflammation, all of which adversely affect the function of vascular wall cells (such as endothelial cells, vascular smooth muscle cells, and fibroblasts) and circulating cells (such as platelets and immune/inflammatory cells). The goal of this review is to explore the mechanisms influencing both native and AVF vasculature in the context of CKD. In addition, we will discuss current therapies aimed at improving native vasculature in patients with CKD, as well as investigational approaches to promote AVF maturation.

Chronic kidney disease (CKD) is a progressive, multisystemic disorder that augments the risks of cardiovascular (CV) morbidity and mortality as kidney function declines. The endothelium plays a key role in modulating vascular tone, integrity, and homeostasis by producing and releasing a variety of endothelium-derived relaxing factors, including nitric oxide (NO). Endothelial dysfunction is a salient pathogenic mechanism underlying the development and progression of CKD and is characterized by reduced production of vasodilators and increased production of vasoconstrictors (e.g., endothelin-1). Factors such as the uremic milieu, inflammation, and oxidative stress are putative contributors of endothelial dysfunction and reduced NO bioavailability that ultimately impact functional and structural integrity of the vasculature. Because endothelial dysfunction is an independent predictor of CV morbidity and mortality in patients with CKD, several clinical studies have examined disease-related changes in endothelium-dependent vasodilation across the arterial tree. This review will focus on the clinical evidence regarding CKD-associated endothelial dysfunction involving both the micro- and macrovasculature, briefly discussing underlying physiological mechanisms, and summarizing available and emerging pharmacotherapies along with a brief summary of exercise training as a lifestyle intervention.