Background: microRNAs (miRs) have emerged as important modulators of cardiovascular development and disease. Our aim was to determine whether cardiac-related miRs such as miR-21-5p and miR-1-3p were differentially expressed in acute viral myocarditis and whether any of them was related with the extent of myocardial damage and left ventricular dysfunction. Methods: We enrolled 40 patients with acute viral myocarditis. Blood samples were taken on admission and miRs expression levels in peripheral blood mononuclear cells were quantified by real-time reverse transcription polymerase chain reaction. Results: miR-21-5p, miR-1-3p were significantly elevated in acute myocarditis. miR-21-5p levels showed a strong correlation with global longitudinal strain (r = 0.71, p < 0.01), while miR-1-3p had significant correlations with troponin I (r = 0.79, p < 0.01). Conclusions: The expression of miR-21-5p and miR-1-3p in peripheral blood is increased in acute viral myocarditis, and this increase is correlated with myocardial damage and indicative of left ventricular systolic dysfunction in these patients.

Background: Cardiac amyloidosis (CA) is a progressive disorder characterized by amyloid fibril deposition in the heart, leading to heart failure and arrhythmias. Arterial stiffness, assessed by pulse wave velocity (PWV), is recognized as an adverse consequence of amyloidosis, yet its progression and relationship with myocardial dysfunction remain inadequately explored. This study examines the progression of PWV and its potential association with the deterioration of global longitudinal strain (GLS) in CA patients over a 6-month follow-up period. Methods: This prospective study enrolled 31 patients who were diagnosed with CA, including both the immunoglobulin light chain (AL) and transthyretin (ATTR) forms. All participants underwent a full echocardiographic study and PWV measurements (carotid-femoral [c-f] and carotid-radial [c-r] PWV) at baseline and 6-month follow-up. Age- and sex-matched individuals with similar cardiovascular risk factors were included as a control group. Results: In the CA group, the left ventricular mass index (LVMI) increased significantly from 119.4 ± 52.1 to 124 ± 53.2 g/m² (p = 0.002). Both c-f and c-r PWV showed significant increases at the 6-month follow-up (p < 0.001 and p = 0.005, respectively). The GLS deteriorated significantly from −14 ± 4.4% to −12.8 ± 4.9% (p = 0.018). No significant changes were observed in the control group. A weak correlation (r = 0.3; p = 0.095) was found between increases in PWV and GLS deterioration. Conclusions: Both arterial stiffness and myocardial dysfunction worsen rapidly in CA patients. However, the weak correlation between PWV and GLS suggests that they may evolve through independent mechanisms, necessitating further research to understand their complex interplay in CA.

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.