The purpose of this study was to prospectively validate the MIRACLE2 score in the GLOBAL-MIRACLE registry, a multicenter, international, prospective registry of patients admitted with resuscitated out-of-hospital cardiac arrest of presumed cardiac cause.

Peripheral artery disease (PAD) and its severe form, chronic limb-threatening ischemia (CLTI), significantly impair blood flow to the lower extremities, affecting millions of adults globally. Intramuscular adipose tissue (IMAT) and fibrosis accumulation distinguish patients with CLTI from those with mild PAD, suggesting a role in CLTI pathobiology. However, the functional consequences of IMAT in CLTI remain unclear.

The arterial vasculature is the second most frequently calcified structure in the human body after the skeleton. Calcification of the aorta and aortic valves occurs in most individuals in westernized societies with advancing age, with abdominal aortic calcification generally preceding ascending thoracic aortic disease. In cardiac valves and the thoracic aorta, however, calcification often arises earlier in common disease contexts characterized by metabolic, mechanical, or inflammatory injury (eg, metabolic syndrome, chronic kidney disease, irradiation). In these settings, calcification frequently involves the arterial media as a histoanatomic feature, and is associated with accelerated neurocognitive decline and increased cardiovascular mortality, reflecting a form of precocious aging. The term arteriosclerosis was coined nearly 2 centuries ago to describe the calcium-mediated hardening of the aorta and conduit arteries observed at autopsy with aging. However, much of our understanding of the causes, characterization, and consequences of aortic calcium deposition has emerged only within the past decade. Features of disease biology, including engagement of innate immunity, senescence (inflammaging), and ectopic activation of osteogenic mechanisms, are consistently revealed. In this article, we briefly review the burgeoning literature, highlighting recent advances in clinical and discovery science with translational implications. Given the current trajectory, after 2 centuries of disease recognition, the next decade of innovation promises meaningful progress toward effective medical treatments to prevent and treat the clinical consequences of calcific aortopathy.

Sarcomere gene variants are a key cause of hypertrophic cardiomyopathy (HCM), and have been associated with worse prognosis. However, it is unclear how comorbidities influence clinical trajectories, the timing of events, and causes of death in sarcomeric and nonsarcomeric HCM.