Hypertrophic cardiomyopathy in a patient with secondary hypoparathyroidism: A case report

Betancur, Juan Felipe; Adams, Christina D.; Restrepo-Giraldo, Lina; Arévalo-Novoa, Joel; Ramírez, Beatriz; Llano, Juan Felipe; López, Gustavo A. Yepes

doi:10.1016/j.radcr.2022.08.092

Cited by 2 publications

(9 citation statements)

References 16 publications

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“…DCM, hypertrophic cardiomyopathy, arrhythmia, and congestive heart failure are among the most common cardiac involvements that hypoparathyroidism can cause. 17,18 The precise cardiac involvement in hypoparathyroidism is influenced by hypocalcemia, which can result in decreased myocardial tension, expansion of the cardiac cavity, and arrhythmia. 11,18 Acute, temporary, DCM with low EF and widespread LV hypokinesia is known as hypo-calcemic cardiomyopathy.…”

Section: Diagnosismentioning

confidence: 99%

“…17,18 The precise cardiac involvement in hypoparathyroidism is influenced by hypocalcemia, which can result in decreased myocardial tension, expansion of the cardiac cavity, and arrhythmia. 11,18 Acute, temporary, DCM with low EF and widespread LV hypokinesia is known as hypo-calcemic cardiomyopathy. It is linked to calcifications in the brain.…”

Section: Diagnosismentioning

confidence: 99%

“…It is linked to calcifications in the brain. 18 Prolonged hypoparathyroidism can result in LV dysfunction and arrhythmia. 19 LV systolic dysfunction caused by hypoparathyroidism can result in a reversible DCM.…”

Section: Diagnosismentioning

confidence: 99%

“…11 Moreover, a rare condition known as chronic hypoparathyroidism-associated cardiomyopathy may result in decreased myocardial tension, expansion of the ventricular cavity, arrhythmia, and congestive heart failure. 18 The clinical and laboratory findings are used to make the diagnosis of hypoparathyroidism. Muscle cramps, paresthesia, seizures, and neuropsychiatric complications are among the usual symptoms of hypoparathyroidism, though the clinical presentation may differ widely.…”

Section: Diagnosismentioning

confidence: 99%

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Dilated cardiomyopathy in patients with hypoparathyroidism: A narrative review

Abdolmaleki,

Ohadi,

Maleki

2024

Health Science Reports

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BackgroundHypoparathyroidism is a rare endocrine disorder characterized by low blood calcium levels, elevated phosphorus levels, and insufficient parathyroid hormone production. It can lead to dilated cardiomyopathy (DCM), a cardiac condition characterized by enlarged ventricles and reduced heart function. This review aims to explore the relationship between hypoparathyroidism and DCM, the impact of calcium on cardiac function, and the potential for DCM reversal with calcium supplementation.MethodsA comprehensive literature search was conducted using PubMed, Google Scholar, and relevant keywords and Mesh terms. Case reports evaluating dilated cardiomyopathy in patients with Hypoparathyroidism were included in the study. Additionally, references cited in each study were carefully examined to identify relevant reports. The cases included in the review were analyzed, and common cardiac manifestations, diagnostic approaches, and management were identified.ResultsDCM in hypoparathyroidism presents with symptoms of heart failure, reduced ejection fraction, and impaired left ventricular function. Laboratory tests show low serum calcium levels and elevated phosphate levels. Prompt diagnosis and treatment with calcium and vitamin D supplementation can lead to improvements in cardiac function.ConclusionHypoparathyroidism‐induced DCM is reversible with timely calcium and vitamin D supplementation. Patient compliance with prescribed medications and supplements is crucial to prevent and manage cardiac complications. Regular follow‐up check‐ups and monitoring of calcium levels can aid in early detection and improve patient outcomes. Educating patients about the importance of treatment adherence can significantly reduce the risk of developing DCM and other cardiac symptoms associated with hypoparathyroidism. Routine follow‐up of DCM among patients with endocrine disorders is recommended.

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Section: Diagnosismentioning

confidence: 99%

Section: Diagnosismentioning

confidence: 99%

Section: Diagnosismentioning

confidence: 99%

Section: Diagnosismentioning

confidence: 99%

See 2 more Smart Citations

Dilated cardiomyopathy in patients with hypoparathyroidism: A narrative review

Abdolmaleki,

Ohadi,

Maleki

2024

Health Science Reports

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“…Patients with hypertrophic cardiomyopathy (HCM) have increased risk of sudden cardiac death and arrhythmias, and further investigations of novel risk factors are needed 62 . A recent case study reported a patient with HCM presenting with secondary hypoparathyroidism, which the authors associated with the effects of hyperphosphatemia and elevated levels of calcium phosphate product and FGF23 63 . Further clinical and epidemiological investigations of dysregulated serum Pi as a novel risk factor associated with HCM are warranted, including population studies of dietary phosphate exposure, animal models, and in vitro and in vivo experiments that illuminate the effects of myocardial Pi in arrhythmia and sudden cardiac arrest.…”

Section: Pi and End‐product Inhibition Of Ca2+ Uptakementioning

confidence: 99%

Phosphate toxicity and SERCA2a dysfunction in sudden cardiac arrest

Brown

2023

The FASEB Journal

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Almost half of the people who die from sudden cardiac arrest have no detectable heart disease. Among children and young adults, the cause of approximately one-third of deaths from sudden cardiac arrest remains unexplained after thorough examination. Sudden cardiac arrest and related sudden cardiac death are attributed to dysfunctional cardiac ion-channels. The present perspective paper proposes a pathophysiological mechanism by which phosphate toxicity from cellular accumulation of dysregulated inorganic phosphate interferes with normal calcium handling in the heart, leading to sudden cardiac arrest. During cardiac muscle relaxation following contraction, SERCA2a pumps actively transport calcium ions into the sarcoplasmic reticulum, powered by ATP hydrolysis that produces ADP and inorganic phosphate end products. Reviewed evidence supports the proposal that end-product inhibition of SERCA2a occurs as increasing levels of inorganic phosphate drive up phosphate toxicity and bring cardiac function to a sudden and unexpected halt. The paper concludes that end-product inhibition from ATP hydrolysis is the mediating factor in the association of sudden cardiac arrest with phosphate toxicity. However, current technology lacks the ability to directly measure this pathophysiological mechanism in active myocardium, and further research is needed to confirm phosphate toxicity as a risk factor in individuals with sudden cardiac arrest. Moreover, phosphate toxicity may be reduced through modification of dietary phosphate intake, with potential for employing low-phosphate dietary interventions to reduce the risk of sudden cardiac arrest.

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Hypertrophic cardiomyopathy in a patient with secondary hypoparathyroidism: A case report

Cited by 2 publications

References 16 publications

Dilated cardiomyopathy in patients with hypoparathyroidism: A narrative review

Dilated cardiomyopathy in patients with hypoparathyroidism: A narrative review

Phosphate toxicity and SERCA2a dysfunction in sudden cardiac arrest

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