Critical limb ischemia (CLI) is a terminal stage of peripheral arterial disease that, in the absence of intervention, may lead to lower extremity amputation or death. Endovascular interventions have become a first-line approach to the management of CLI and have advanced considerably within the past decade. This review summarizes the types of percutaneous devices and the techniques that are available for the management of CLI and the data supporting their use. These include devices that establish and maintain vessel patency, including percutaneous transluminal angioplasty, drug-coated balloons, bare metal stents, drug-eluting stents, bioresorbable vascular scaffolds, and atherectomy; devices that provide protection from embolization; and, cell-based therapies. Additionally, ongoing trials with important implications for the field are discussed.

Critical limb ischemia (CLI) is a highly morbid disease with many patients considered poor surgical candidates. The lack of treatment options for CLI has driven interest in developing molecular therapies within recent years. Through these translational medicine studies in CLI, much has been learned about the pathophysiology of the disease. Here, we present an overview of the macrovascular and microvascular changes that lead to the development of CLI, including impairment of angiogenesis, vasculogenesis, and arteriogenesis. We summarize the randomized clinical controlled trials that have used molecular therapies in CLI, and discuss the novel imaging modalities being developed to assess the efficacy of these therapies.

Background: Patients hospitalized with acute myocardial infarction (AMI) have a high mortality rate. Despite increasing recognition of the role for comfort focused care, little is known about the prevalence of comfort measures only (CMO) care among patients with AMI. The objective of this study was to investigate patient- and hospital-level patterns and predictors of CMO care among patients admitted with AMI. Methods: This retrospective cohort study used the National Cardiovascular Data Registry Chest Pain-MI Registry, which contains data on patients admitted with AMI. Data were analyzed in 6-month increments from January 2015 to June 2018. Results: Among 483 696 patients with AMI across 827 hospitals, 13 955 (2.9%) had CMO status at discharge (2.6% non–ST-segment–elevation myocardial infarction and 3.4% ST-segment–elevation myocardial infarction). There was a modest decline in CMO rates over time (3.0% to 2.8%). Independent patient characteristics associated with CMO status included male gender, White race, nonprivate insurance, frailty, and higher estimated bleeding and mortality risks. There was substantial variation in CMO rates across hospitals, with the proportion of CMO patients ranging from 0% to 17.1% and a median odds ratio of 1.59 (95% CI, 1.56–1.62). Among the 13 955 patients who were CMO by discharge, 8134 (58.3%) underwent diagnostic catheterization. This is despite significantly elevated risks predicted using precatheterization models, specifically the ACTION Registry GWTG in-hospital major bleeding and mortality risk scores. Patients who were initially managed invasively but later made CMO experienced high rates of procedural complications, including cardiogenic shock (38.3%), dialysis (10.1%), and bleeding (33.3%). Conclusions: Most patients with AMI who were CMO by discharge had aggressive initial management and became CMO following in-hospital complications of their care. Early identification of high-risk patients and appropriate transition of such patients to CMO, if aligned with their values, remain important areas for future quality programs in AMI.

Aims: Incidence of sudden cardiac death (SCD) is 1%/year in cohorts with hypertrophic cardiomyopathy (HCM), but this estimate presumes arrhythmic cause and misses occult cases dying before diagnosis. Methods and results: POST SCD (POstmortem Systematic InvesTigation of Sudden Cardiac Death) is a prospective cohort study using autopsy, clinical records, and toxicology to adjudicate arrhythmic or non-arrhythmic causes among presumed SCDs (pSCDs) meeting WHO criteria aged 0–90 years in San Francisco County. We included all incident cases 2/1/2011–3/1/2014 (n = 525) and approximately every third day 3/1/2014–9/1/2022 (n = 497) based on medical examiner call schedule. We identified HCM victims via three approaches: (i) pathology; (ii) echocardiogram [transthoracic echocardiogram (TTE)]; (iii) genetic criteria. Incidence calculations used county data and estimated HCM prevalence of 1:500 from studies of persons aged 23–35 years old. Of 1022 pSCDs [558 (54.6%) arrhythmic deaths] during the study period, 13 had HCM: 10 met pathology criteria; 2 via review of 203 TTEs (missed on initial report); 1 via genetic testing. Of these, 11 were arrhythmic deaths, yielding 1.3% burden of sudden death (pSCD) and 2% of arrhythmic death. Only 2 of 13 (15%) pSCDs with HCM had pre-mortem diagnosis. Incidence for persons with HCM 18–35 years old was 0.2% pSCDs/year and 0.1% SADs/year. pSCDs with HCM had a higher proportion of arrhythmic cause [11/13 (85%) vs. 547/1009 (54%), P = 0.03] than those without. pSCD burden due to HCM decreased with age (P = 0.003), highest among victims <35 years old, for whom HCM accounted for 7.1% of pSCD and 9.4% of arrhythmic death. Genetic testing of 317 consented pSCDs yielded pathogenic or likely pathogenic variants in 40% (2/5) and identified one additional case without clinical phenotype. Conclusion: In this 11-year countywide post-mortem study, HCM meeting pathologic, clinical, or genetic criteria was associated with autopsy-confirmed arrhythmic cause of sudden death, accounting for 2% of SADs up to age 90, highest in cases <35 years old. Since 85% of cases were undiagnosed before pSCD, the true burden of HCM-related sudden death may be substantially underestimated.