Beyond the Heart: Exploring the Systemic Effects of Cardiomyopathy

Kanon Maya^*
*Correspondence: Kanon Maya, Department of Cardiology, Oslo University Hospital, 0450 Oslo, Norway, Email:

Keywords

Cardiomyopathy • Cardiac health • Heart

Introduction

Cardiomyopathy, a heterogeneous group of diseases characterized by structural and functional abnormalities of the myocardium, poses significant challenges to patients and clinicians alike. Traditionally viewed as a disorder primarily affecting the heart, recent advancements in medical research have unveiled its far-reaching consequences on multiple organ systems beyond the cardiovascular domain. While the impact of cardiomyopathy on cardiac function remains paramount, its systemic effects are increasingly recognized as crucial determinants of patient morbidity and mortality [1].

Literature Review

One of the lesser-known consequences of cardiomyopathy lies in its profound influence on the endocrine system. Studies have demonstrated alterations in hormonal profiles among individuals with cardiomyopathy, including abnormalities in the renin-angiotensin-aldosterone system (RAAS) and dysregulation of thyroid hormones. These endocrine disturbances not only contribute to the progression of cardiac dysfunction but also exacerbate systemic complications such as metabolic syndrome and insulin resistance. Consequently, clinicians managing patients with cardiomyopathy must remain vigilant for signs of endocrine dysfunction and adopt targeted interventions to mitigate its impact on overall health [2].

Discussion

The intricate interplay between the cardiovascular and renal systems underscores the bidirectional relationship between cardiomyopathy and renal function. Chronic heart failure, a common sequelae of advanced cardiomyopathy, precipitates renal impairment through mechanisms such as reduced cardiac output, neurohormonal activation and renal hypoperfusion. Conversely, renal dysfunction exacerbates cardiac dysfunction by promoting fluid retention, electrolyte imbalance and systemic inflammation. This vicious cycle of cardiorenal interaction underscores the importance of holistic management strategies that address both cardiac and renal comorbidities in patients with cardiomyopathy [3].

Emerging evidence suggests a link between cardiomyopathy and neurological complications, encompassing cognitive impairment, cerebrovascular events and peripheral neuropathy. Chronic hypoperfusion resulting from impaired cardiac function predisposes individuals with cardiomyopathy to cerebral microvascular dysfunction and white matter lesions, thereby increasing the risk of stroke and vascular dementia. Furthermore, neurohormonal dysregulation and systemic inflammation associated with cardiomyopathy may contribute to the development of peripheral neuropathy, manifesting as sensory deficits and motor dysfunction. These neurological sequelae underscore the need for comprehensive neurological assessment and tailored interventions in the management of cardiomyopathy [4]. Cardiomyopathy transcends its traditional classification as a cardiac disorder, exerting profound systemic effects that extend beyond the confines of the heart. Endocrine dysfunction, renal impairment and neurological complications represent key manifestations of this multisystemic disorder, underscoring the importance of a holistic approach to its management. By recognizing and addressing these systemic repercussions, clinicians can optimize patient outcomes and enhance quality of life for individuals living with cardiomyopathy. Moving forward, further research is warranted to elucidate the intricate pathophysiological mechanisms underlying the systemic effects of cardiomyopathy, paving the way for more effective therapeutic strategies and improved patient care [5].

While cardiomyopathy primarily affects the heart, its repercussions extend to the pulmonary system, contributing to a spectrum of respiratory complications. Pulmonary congestion secondary to left ventricular dysfunction is a hallmark feature of heart failure associated with cardiomyopathy, leading to symptoms such as dyspnea, orthopnea and paroxysmal nocturnal dyspnea. Chronic pulmonary congestion may culminate in the development of pulmonary hypertension, further exacerbating right ventricular strain and precipitating right-sided heart failure. Moreover, cardiogenic pulmonary edema, resulting from increased hydrostatic pressure within pulmonary capillaries, poses a significant threat to respiratory function and necessitates prompt intervention to prevent respiratory failure [6].

Conclusion

The musculoskeletal system is intricately linked to cardiac function, with cardiomyopathy exerting notable effects on muscle mass, strength and integrity. Skeletal muscle wasting, a common consequence of chronic heart failure, is exacerbated in individuals with cardiomyopathy due to reduced exercise tolerance and physical deconditioning. Moreover, cardiomyopathyassociated muscle weakness and fatigue contribute to functional impairment and diminished quality of life. Importantly, the musculoskeletal complications of cardiomyopathy underscore the importance of exercise-based rehabilitation programs and targeted interventions aimed at preserving muscle function and mobility in affected individuals.

Acknowledgement

None.

Conflict of Interest

None.

References

1. Marian, Ali J. and Eugene Braunwald. “Hypertrophic cardiomyopathy: Genetics, pathogenesis, clinical manifestations, diagnosis and therapy.”Circ Res121 (2017): 749-770.

   Google Scholar, Crossref, Indexed at

2. Hershberger, Ray E., Michael M. Givertz, Carolyn Y. Ho and Daniel P. Judge, et al. “Genetic evaluation of cardiomyopathy-a heart failure society of america practice guideline.”J Card Fail24 (2018): 281-302.

   Google Scholar, Crossref, Indexed at

3. Zhen, Zhen, Lu Gao, Qin Wang and Xi Chen, et al. “Angiotensinogen M235T polymorphism and susceptibility to hypertrophic cardiomyopathy in Asian population: A meta analysis.”J Renin Angiotensin Aldosterone Syst21 (2020): 1470320320978100.

   Google Scholar, Crossref, Indexed at

4. Alfares, Ahmed A., Melissa A. Kelly, Gregory McDermott and Birgit H. Funke, et al. “Results of clinical genetic testing of 2,912 probands with hypertrophic cardiomyopathy: expanded panels offer limited additional sensitivity.”Genet Med17 (2015): 880-888.

   Google Scholar, Crossref, Indexed at

5. Maron, Barry J., Martin S. Maron and Christopher Semsarian. “Double or compound sarcomere mutations in hypertrophic cardiomyopathy: A potential link to sudden death in the absence of conventional risk factors.”Heart rhythm9 (2012): 57-63.

   Google Scholar, Crossref, Indexed at

6. Ingles, Jodie, Tanya Sarina, Laura Yeates and Lauren Hunt, et al. “Clinical predictors of genetic testing outcomes in hypertrophic cardiomyopathy.”Genet Med15 (2013): 972-977.

   Google Scholar, Crossref, Indexed at