Coronary microvascular dysfunction (CMD) is an important cause of angina and myocardial ischemia in patients without obstructive coronary artery disease and contributes substantially to the clinical spectrum of angina with non-obstructive coronary arteries (ANOCA) and ischemia with non-obstructive coronary arteries (INOCA). These conditions represent a heterogeneous group of coronary vasomotor disorders in which structural and functional abnormalities of the coronary microcirculation, endothelial dysfunction, coronary vasospasm, and diffuse non-obstructive atherosclerosis may occur alone or in combination. This review summarizes current knowledge on the pathophysiology, diagnosis, and management of CMD in patients with ANOCA and INOCA. We discuss the distinction between ANOCA and INOCA, the principal coronary functional endotypes, and the mechanisms responsible for impaired coronary microvascular function. We also review contemporary diagnostic approaches, including non-invasive imaging and invasive coronary function testing, with emphasis on their complementary roles in identifying the underlying mechanism of ischemia. Current management strategies are presented from a mechanism-based perspective, including lifestyle modification, pharmacological therapy, endotype-guided treatment, and emerging therapeutic approaches. Improved understanding of coronary functional abnormalities has shifted clinical evaluation beyond the exclusion of obstructive coronary artery disease toward identification of the mechanism responsible for persistent symptoms and ischemia. Continued advances in disease phenotyping, coronary function testing, and targeted therapies are expected to support more individualized management and improve outcomes in this diverse patient population.

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 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.

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.