An 82-year-old woman with antineutrophil cytoplasmic antibodies-associated vasculitis and previous azathioprine-induced neutropenia presented with 5 days of right upper quadrant pain, nausea, and vomiting. Laboratory evaluation revealed leukocytosis (34.14/nL) and cholestasis (alkaline phosphatase 2,296 U/L, total bilirubin 4.3 mg/dL). Computed tomography demonstrated a 16.4 × 12.0 cm multiloculated perihepatic fluid collection. Blood cultures were negative. Hepatic candidiasis was diagnosed by culture of drained fluid, which grew Candida albicans . Treatment with fluconazole and percutaneous drainage with adjunctive fibrinolytics achieved complete resolution at 9 weeks. This case underscores the importance of considering hepatic candidiasis in immunocompromised patients with persistent or atypical liver lesions, even in the absence of candidemia or typical imaging findings.

Cardiac amyloidosis is an infiltrative cardiomyopathy caused by extracellular deposition of misfolded proteins, most commonly immunoglobulin light chains (AL) or transthyretin (ATTR), with rarer forms occurring less frequently. AL amyloidosis arises from plasma cell-derived light chains and typically follows an aggressive clinical course, whereas ATTR amyloidosis results from misfolded wild-type or variant transthyretin and progresses more indolently. Extracellular vesicles (EVs) have recently been recognized as mediators of amyloid propagation, inflammation, and myocardial remodeling, particularly at later stages of disease. Despite growing evidence, no comprehensive reviews have focused on this relationship. We conducted a structured narrative review (PubMed and Scopus, 2020–2025) following Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) guidelines to synthesize emerging data. EVs act as scaffolds for transthyretin and serum amyloid A aggregation and carry disease-specific protein and RNA cargo detectable in blood and urine. Experimental models also demonstrate EV-mediated transport of serum amyloid A under conditions of cardiac stress, representing a reactive amyloidogenic pathway rather than a common cause of human cardiac amyloidosis. Preclinical studies show regenerative and anti-fibrotic effects of stem-cell-derived EVs, and early clinical trials demonstrate the feasibility of EV-based cardiac therapy. While methodological and translational challenges persist, EVs represent promising diagnostic and therapeutic tools that could transform the precision management of cardiac amyloidosis.

Background/Objectives: Congestion drives most heart-failure (HF) hospitalizations, and several strategies now titrate therapy to a directly measured congestion signal rather than to symptoms; whether they differ by the signal measured has not been examined comparatively. Methods: We performed a systematic review and contrast-based network meta-analysis of randomized trials comparing imaging- or device-based congestion-triggered management with usual care. Thirteen chronic-phase trials formed a star network (no closed loops; rankings exploratory) of four strategies, pressure-guided (N1), lung ultrasound (N2), transthoracic lung impedance (N3), and cardiac-implantable-electronic-device (CIED) intrathoracic impedance (N5), with HF hospitalization as the primary outcome and six prespecified sensitivity analyses; four acute trials formed a gap map. Results: Only pressure-guided monitoring reduced HF hospitalization (0.72, 95% confidence interval 0.57–0.90), stable across sensitivities and matching external data. Lung ultrasound did not reduce hospitalization (0.72, 0.48–1.08) or mortality but reduced urgent visits (0.26, 0.13–0.50). The apparent CIED-impedance harm (1.12, 0.77–1.63) reflected an audible-alert trial and dissolved when early-terminated trials were excluded (0.87). Lung impedance gave the largest estimate (0.51, 0.31–0.83) but rested on one trial. No strategy tested in more than one trial reduced mortality. Conclusions: The congestion signal acted upon, and who receives the alert, track with the effect, although signal and workflow cannot be separated within trials; clinicians should match modality to the intended outcome, as these tools defer hospitalization, not death.