Anxiety in Patients With Arrhythmogenic Right Ventricular Cardiomyopathy and Implantable Cardioverter Defibrillators

Day, Sharlene M.

doi:10.1161/circgenetics.111.962639

Cited by 6 publications

(5 citation statements)

References 17 publications

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“…This study supports the literature that individuals who have an ICD as a primary treatment for a genetically linked heart condition, as with ARVC/D, do have unique needs (Day, 2012; Ingles et al, 2013). Not only is this population dealing with the fact that they are at risk of a lethal heart condition, but if they wish to survive a cardiac event, they must have an ICD, even if they are asymptomatic.…”

Section: Discussionsupporting

confidence: 88%

“…Having knowledgeable and consistent health care providers in rural communities to provide care to this cohort is the first step. Furthermore, as noted by others (Day, 2012) we need to consider the uniqueness of genetic conditions such as ARVC/D, and address the question of precisely what factors contribute to the psychosocial distress related to having an ICD, versus those associated with the actual disease itself. On a broader level, nurses need to be aware of prevalent genetic conditions in regions that they serve and coinciding treatments.…”

Section: Resultsmentioning

confidence: 99%

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Embodying a New Meaning of Being At Risk

Manuel

2016

Global Qualitative Nursing Research

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Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D) is a genetic condition that can cause fatal arrhythmias. The implantable cardioverter defibrillation (ICD) is a primary treatment for ARVC/D. Using a grounded theory approach, this study examines the experiences of 15 individuals living with an ICD. The ability to cope with and adjust to having an ICD is influenced by the acceptance of the ICD as something needed to survive, an understanding of the ICD’s function, existing support networks, and ones’ ability to manage everyday challenges. Coping well requires reshaping ideas about the meaning of being at risk and understanding how the ICD fits into that changing personal risk narrative. A thorough understanding of the unique needs of individuals with ARVC/D and of the specific factors contributing to the psychosocial distress related to having an ICD (vs. having the disease itself) is needed. Nurses must be prepared to provide ongoing support and education to this population.

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Section: Discussionsupporting

confidence: 88%

Section: Resultsmentioning

confidence: 99%

Embodying a New Meaning of Being At Risk

Manuel

2016

Global Qualitative Nursing Research

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“…As pointed out, similarly to what is found in patients with hypertrophic cardiomyopathy and long-QT syndrome, reaching a diagnosis of ACM imposes a psychological burden on patients and the weight of SCD and/or genetic transmission [32]. Another layer of stress is channeled by the implantation of a cardioverter defibrillator (ICD) needed for primary or secondary prevention of SCD [33].…”

Section: Discussionmentioning

confidence: 96%

Psychosocial Stress Hastens Disease Progression and Sudden Death in Mice with Arrhythmogenic Cardiomyopathy

Agrimi

Scalco

Agafonova

et al. 2020

JCM

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Physiological stressors, such as exercise, can precipitate sudden cardiac death or heart failure progression in patients with arrhythmogenic cardiomyopathy (ACM). Yet, whether and to what extent a highly prevalent and more elusive environmental factor, such as psychosocial stress (PSS), can also increase ACM disease progression is unexplored. Here, we first quantified perceived stress levels in patients with ACM and found these levels correlated with the extent of arrhythmias and cardiac dysfunction. To determine whether the observed correlation is due to causation, we inflicted PSS-via the resident-intruder (RI) paradigm—upon Desmoglein-2 mutant mice, a vigorously used mammalian model of ACM. We found that ACM mice succumbed to abnormally high in-trial, PSS mortality. Conversely, no sudden deaths occurred in wildtype (WT) counterparts. Desmoglein-2 mice that survived RI challenge manifested markedly worse cardiac dysfunction and remodeling, namely apoptosis and fibrosis. Furthermore, WT and ACM mice displayed similar behavior at baseline, but Desmoglein-2 mice exhibited heightened anxiety following RI-induced PSS. This outcome correlated with the worsening of cardiac phenotypes. Our mouse model demonstrates that in ACM-like subjects, PSS is incisive enough to deteriorate cardiac structure and function per se, i.e., in the absence of any pre-existing anxious behavior. Hence, PSS may represent a previously underappreciated risk factor in ACM disease penetrance.

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“…Forced and high-intensity exercises can trigger pathological progression in ACM, not only due to exacerbated hemodynamic load under excessive physical activity but also as a consequence of psychological stress observed in ACM mice [ 97 ], which imparts additional concerns for research outcomes. A relevant consideration in patients diagnosed with ACM is the anxiety, psychosocial adjustment, and depression that contribute to both psychological burden and disease progression [ 98 ]. Ultimately, it is key to correlate both high-intensity exercise and psychological stress to facets of ACM disease phenotype worsening.…”

Section: The Deleterious Impact Of Exercise In Acm and Its Translatio...mentioning

confidence: 99%

Arrhythmogenic Cardiomyopathy: Exercise Pitfalls, Role of Connexin-43, and Moving beyond Antiarrhythmics

Coscarella

Landim-Vieira

Pinto

et al. 2022

IJMS

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Arrhythmogenic Cardiomyopathy (ACM), a Mendelian disorder that can affect both left and right ventricles, is most often associated with pathogenic desmosomal variants that can lead to fibrofatty replacement of the myocardium, a pathological hallmark of this disease. Current therapies are aimed to prevent the worsening of disease phenotypes and sudden cardiac death (SCD). Despite the use of implantable cardioverter defibrillators (ICDs) there is no present therapy that would mitigate the loss in electrical signal and propagation by these fibrofatty barriers. Recent studies have shown the influence of forced vs. voluntary exercise in a variety of healthy and diseased mice; more specifically, that exercised mice show increased Connexin-43 (Cx43) expression levels. Fascinatingly, increased Cx43 expression ameliorated the abnormal electrical signal conduction in the myocardium of diseased mice. These findings point to a major translational pitfall in current therapeutics for ACM patients, who are advised to completely cease exercising and already demonstrate reduced Cx43 levels at the myocyte intercalated disc. Considering cardiac dysfunction in ACM arises from the loss of cardiomyocytes and electrical signal conduction abnormalities, an increase in Cx43 expression—promoted by low to moderate intensity exercise and/or gene therapy—could very well improve cardiac function in ACM patients.

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Anxiety in Patients With Arrhythmogenic Right Ventricular Cardiomyopathy and Implantable Cardioverter Defibrillators

Cited by 6 publications

References 17 publications

Embodying a New Meaning of Being At Risk

Embodying a New Meaning of Being At Risk

Psychosocial Stress Hastens Disease Progression and Sudden Death in Mice with Arrhythmogenic Cardiomyopathy

Arrhythmogenic Cardiomyopathy: Exercise Pitfalls, Role of Connexin-43, and Moving beyond Antiarrhythmics

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