Cardiac remodeling and ventricular pacing represent intertwined phenomena with profound implications for cardiovascular health and therapeutic interventions. This review explores the intricate relationship between cardiac remodeling and ventricular pacing, spanning from the molecular underpinnings to biomechanical alterations. Beginning with an examination of genetic predispositions and cellular signaling pathways, we delve into the mechanisms driving myocardial structural changes and electrical remodeling in response to pacing stimuli. Insights into the dynamic interplay between pacing strategies and adaptive or maladaptive remodeling processes are synthesized, shedding light on the clinical implications for patients with various cardiovascular pathologies. By bridging the gap between basic science discoveries and clinical translation, this review aims to provide a comprehensive understanding of cardiac remodeling in the context of ventricular pacing, paving the way for future advancements in cardiovascular care.

Gestational complications, such as preeclampsia and gestational diabetes mellitus (GDM), pose significant risks to maternal and fetal health and increase long-term cardiovascular disease risk in offspring. This review aims to synthesize current knowledge on the roles of ferroptosis and neutrophil extracellular trap formation (NETosis)—two regulated cell death pathways—in these pregnancy-related conditions. We performed a comprehensive analysis of preclinical and clinical studies that investigate the involvement of dysregulated iron metabolism, oxidative stress, inflammation, and endothelial dysfunction mediated by ferroptosis and NETosis in gestational pathologies. Evidence indicates that disturbances in maternal iron homeostasis and enhanced formation of lipid peroxides and NETs contribute to placental dysfunction and systemic inflammation, exacerbating disease severity. Therapeutic strategies targeting these pathways are emerging but require further validation. Our review also identifies key gaps in mechanistic understanding, biomarker development, and translational research needs. We conclude that modulation of ferroptosis and NETosis offers promising avenues for improving diagnosis and treatment of pregnancy complications, though carefully designed clinical studies are essential to confirm their clinical utility and safety.

Heart failure (HF) remains a prevalent, high-risk condition particularly common among the elderly population. The impairment of systolic function, secondary dysregulation of maladaptive neurohormonal systems and HF therapies lead to electrolyte disturbances. Hyponatremia is a well-studied, robust marker of adverse prognosis in HF. Serum chloride has emerged as a promising prognostic marker, accurately predicting adverse outcomes in both acute and chronic settings. Hypochloremia reflects a compound of maladaptive neurohormonal, renal and acid–base mechanisms, frequently worsened by diuretic therapy. In the context of HF, low chloride levels are independently associated with increased cardiovascular mortality, HF hospitalization and diuretic resistance. Urinary chloride (uCl⁻) has recently been shown to serve as a dynamic biomarker of HF severity, Renin–Angiotensin–Aldosterone-system (RAAS) activation, and poor outcomes, offering incremental prognostic value. Our review synthesizes the latest evidence on serum and urinary chloride disturbances in HF, framing key distinctions between acute versus persistent electrolyte disturbances. We also explore the interrelationship between chloride and sodium, the differential impact of hypochloremia in Heart Failure with Preserved Ejection Fraction (HFpEF) versus Heart Failure with Reduced Ejection Fraction (HFrEF), and clinical outcomes stratified by the temporary vs. persistent nature of chloride imbalance. We have also included visual flowcharts for classifying and managing hypochloremia based on the underlying etiology.

Cardiac amyloidosis (CA) is an increasingly recognized cause of restrictive cardiomyopathy characterized by amyloid fibril deposition in the heart, leading to severe functional impairments and poor prognosis. This review aims to provide a comprehensive overview of the pathophysiology of CA, emphasizing the mechanisms underlying functional capacity limitations and highlighting the importance of precise physiological assessment tools. We focus on objective measures such as cardiopulmonary exercise testing, field-based functional tests, and frailty evaluations that are vital for prognosis and tailoring patient care. With recent advances in disease-modifying therapies extending survival, maintaining and improving functional status through multidisciplinary rehabilitation emerges as a crucial therapeutic target. Evidence suggests that structured aerobic and resistance training can enhance exercise tolerance, strength, and quality of life in CA patients, although further research is needed to optimize rehabilitation protocols. By integrating clinical, physiological, and rehabilitative insights, this review underscores the value of a patient-centered approach aimed at preserving functional capacity and improving outcomes in this complex and systemic disease.

Background: Cardiac amyloidosis (CA) is an increasingly recognized cause of heart failure with preserved ejection fraction, resulting from myocardial deposition of misfolded amyloid fibrils derived predominantly from transthyretin (ATTR wild-type [ATTRwt] or variant [ATTRv]) or immunoglobulin light chains (AL). Despite advances in noninvasive imaging and disease-modifying therapies, delayed diagnosis remains common, and clinically actionable molecular biomarkers for early detection, phenotypic discrimination, and therapeutic monitoring are limited. MicroRNAs (miRNAs), small noncoding regulators of post-transcriptional gene expression, have emerged as key modulators of cardiovascular remodeling and systemic amyloid biology. Methods: We performed a comprehensive review of experimental, translational, and clinical studies to evaluate the role of miRNAs in transthyretin and light-chain cardiac amyloidosis, incorporating data from myocardial tissue analyses, circulating miRNA profiling, and mechanistic studies in cellular and animal models. Results: Dysregulated miRNA networks contribute to amyloid-induced cardiac injury by modulating mitochondrial energetics, oxidative stress, inflammation, fibrosis, proteostasis, and neurocardiac signaling. Specific miRNAs, including members of the miR-21, miR-29, and miR-30 families, as well as miR-150-5p and miR-339, have been associated with amyloid burden, adverse myocardial remodeling, plasma cell biology, and disease severity. Distinct circulating and tissue miRNA signatures differentiate transthyretin from light-chain cardiac amyloidosis and correlate with functional status, heart failure biomarkers, and clinical outcomes. Conclusions: MiRNAs represent promising diagnostic and prognostic biomarkers in cardiac amyloidosis and offer mechanistic insights into disease pathogenesis. Integration of miRNA profiling with multimodality imaging and emerging RNA-based therapeutics may enable earlier diagnosis and support precision management of amyloid-related heart failure.

Heart failure remains a prevalent, high-risk condition particularly common among the elderly population. Impairment of systolic function, secondary dysregulation of maladaptive neurohormonal systems and HF therapies lead to electrolyte disturbances with hyponatremia being considered a robust marker of adverse prognosis in HF. Serum chloride has emerged as a promising prognostic marker, accurately predicting adverse outcomes in acute and chronic HF. Hypochloremia reflects a compound of maladaptive neurohormonal, renal, and acid–base mechanisms, frequently worsened by diuretic therapy, and is independently associated with increased cardiovascular mortality, HF hospitalization, and diuretic resistance. uCl⁻ has recently been shown to serve as a dynamic biomarker of HF severity, RAAS activation, and poor outcomes, offering incremental prognostic value. Our review synthesizes the latest evidence on serum and urinary chloride disturbances in HF, framing key distinctions between acute versus persistent electrolyte disturbances. We also explore the interrelationship between chloride and sodium, the differential impact of hypochloremia in HFpEF versus HFrEF, and clinical outcomes stratified by the temporal vs persistent nature of chloride imbalance. We have as well included practical, visual flowcharts for classifying and managing hypochloremia based on underlying etiology.