Sarcopenia is the loss of muscle strength, mass, and function, which is often exacerbated by chronic comorbidities including cardiovascular diseases, chronic kidney disease, and cancer. Sarcopenia is associated with faster progression of cardiovascular diseases and higher risk of mortality, falls, and reduced quality of life, particularly among older adults. Although the pathophysiologic mechanisms are complex, the broad underlying cause of sarcopenia includes an imbalance between anabolic and catabolic muscle homeostasis with or without neuronal degeneration. The intrinsic molecular mechanisms of aging, chronic illness, malnutrition, and immobility are associated with the development of sarcopenia. Screening and testing for sarcopenia may be particularly important among those with chronic disease states. Early recognition of sarcopenia is important because it can provide an opportunity for interventions to reverse or delay the progression of muscle disorder, which may ultimately impact cardiovascular outcomes. Relying on body mass index is not useful for screening because many patients will have sarcopenic obesity, a particularly important phenotype among older cardiac patients. In this review, we aimed to: (1) provide a definition of sarcopenia within the context of muscle wasting disorders; (2) summarize the associations between sarcopenia and different cardiovascular diseases; (3) highlight an approach for a diagnostic evaluation; (4) discuss management strategies for sarcopenia; and (5) outline key gaps in knowledge with implications for the future of the field.

The incidence of frailty and cardiovascular disease (CVD) increases as the population ages. There is a bidirectional relationship between frailty and CVD, and both conditions share several risk factors and underlying biological mechanisms. Frailty has been established as an independent prognostic marker in patients with CVD. Moreover, its presence significantly influences both primary and secondary prevention strategies for adults with CVD while also posing a barrier to the inclusion of these patients in pivotal clinical trials and advanced cardiac interventions. This review discusses the current knowledge base on the relationship between frailty and CVD, how managing CVD risk factors can modify frailty, the influence of frailty on CVD management, and future directions for frailty detection and modification in patients with CVD.

The population worldwide is getting older as a result of advances in public health, medicine, and technology. Older individuals are living longer with a higher prevalence of subclinical and clinical cardiovascular disease (CVD). In 2010, the American Heart Association introduced a list of key prevention targets, known as “Life’s Simple 7” to increase CVD-free survival, longevity, and quality of life. In 2022, sleep health was added to expand the recommendations to “Life’s Essential 8” (eat better, be more active, stop smoking, get adequate sleep, manage weight, manage cholesterol, manage blood pressure, and manage diabetes). These prevention targets are intended to apply regardless of chronologic age. During this same time, the understanding of aging biology and goals of care for older adults further enhanced the relevance of prevention across the range of functions. From a biological perspective, aging is a complex cellular process characterized by genomic instability, telomere attrition, loss of proteostasis, inflammation, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. These aging hallmarks are triggered by and enhanced by traditional CVD risk factors leading to geriatric syndromes (eg, frailty, sarcopenia, functional limitation, and cognitive impairment) which complicate efforts toward prevention. Therefore, we review Life’s Essential 8 through the lens of aging biology, geroscience, and geriatric precepts to guide clinicians taking care of older adults.

Older adults with cardiovascular disease (CVD) contend with deficits across multiple domains of health due to age-related physiological changes and the impact of CVD. Multimorbidity, polypharmacy, cognitive changes, and diminished functional capacity, along with changes in the social environment, result in complexity that makes provision of CVD care to older adults challenging. In this review, we first describe the history of geriatric cardiology, an orientation that acknowledges the unique needs of older adults with CVD. Then, we introduce 5 essential principles for meeting the needs of older adults with CVD: 1) recognize and consider the potential impact of multicomplexity; 2) evaluate and integrate constructs of cognition into decision-making; 3) evaluate and integrate physical function into decision-making; 4) incorporate social environmental factors into management decisions; and 5) elicit patient priorities and health goals and align with care plan. Finally, we review future steps to maximize care provision to this growing population.

Importance: Immersion pulmonary edema (IPE) is a rare but important complication associated with surface swimming and underwater diving. It tends to reoccur and can be fatal. It is not very well known to clinicians involved in the care of individuals participating in aquatic activities. We performed a systematic review of immersion pulmonary edema to describe the condition and provide guidelines for its management. Evidence Review: We searched PubMed to identify case reports and studies using the MeSH terms ‘‘immersion’’, ‘‘pulmonary edema’’, ‘‘cold-induced’’, ‘‘exercise’’, “hemodynamics”, “water immersion’’, “cardiovascular response”, alone and in combinations. We identified 121 relevant articles including 54 case reports. We reviewed in detail 24 studies and all 54 case reports. Findings: The incidence of IPE is estimated to be around 1.1% to 1.8%. The risk factors for IPE include age >50 years, female sex, overhydration before exercise, tight wetsuits, cold water exposure and physically trained individuals such as endurance athletes. Individuals with pre-existing heart disease are at increased risk, however, IPE is seen even in healthy individuals. Symptoms such as cough, sputum production, hemoptysis and shortness of breath can occur immediately after immersion. Combination of water immersion, cold exposure and exercise lead to an increase in pulmonary capillary pressures and eventual pulmonary capillary stress failure that leads to the flooding of alveolar spaces and edema. Conclusion and Relevance: Clinicians should be aware of IPE to avoid overestimating the severity of coronary or valvular conditions sometimes coincidentally present in IPE victims. Management is usually supportive. Functional and clinical recovery usually happens spontaneously within 24 hours to two days, with or without diuretic therapy and a beta-adrenergic agonist. IPE can be recurrent and fatal, hence subjects with a history of IPE should undergo extensive cardiopulmonary investigation and should avoid cold water and physically demanding swimming events or avoid immersion activities.

Cocaine is associated with a wide array of complications through a number of different mechanisms. Although the majority of cocaine-related morbidity has been attributed to complications in arterial vasculature, the deleterious impact of venous complications appears to be largely unrepresented in current literature as well as clinical practice despite emerging evidence of the high prevalence and annual incidence of deep vein thrombosis (DVT) in illicit drug users. Our case report illustrates an uncharacteristic presentation of cocaine-related widespread thrombotic cascade involving both arterial and venous circulations causing significant morbidity. The complex pathophysiology of widespread prothrombotic state caused by cocaine includes endothelial damage promoting the increase of fibrinogen and Von Willebrand factor to platelet aggregation and clot formation. It is important to identify the impact cocaine-induced venous thrombosis can mount, especially in the form of potentially fatal complications like pulmonary embolism. Although recent studies have focused on increased incidence and prevalence of venous thrombosis in the setting of cocaine abuse, ours is the first case of a documented pulmonary embolism caused by cocaine-related venous thrombosis. Further studies are needed to identify patients at higher risk for this complication like rare thrombotic disorders.