Po-699-07 Risk of Sudden Cardiac Death in Patients Undergoing Cancer Treatment

Sherazi, Syed Tufail Hussain; Patel, Arpan; Hsu, Kimberly; Schleede, Susan; Watts, Arthur S.; McNitt, Scott; Aktaş, Mehmet K.; Goldenberg, Ilan

doi:10.1016/j.hrthm.2022.03.1025

Cited by 1 publication

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“…17 Additionally, tumor lysis syndrome during cancer treatment releases large amounts of Pi from tumors, which is associated with arrythmia and in-hospital mortality, 18 and sudden cardiac death increases during cancer treatment. 19 Cases of cardiac arrest following acute hyperphosphatemia have also been reported in accidental infusion with potassium phosphate 20 and administration of sodium phosphate. 21 "Hyperphosphatemia or even serum phosphate levels within the 'normal laboratory range' are highly associated with increased cardiovascular disease risk and mortality in the general population," including distinct mechanisms for vascular calcification, hypertension, myocardial fibrosis, cardiac valvular calcification, atherosclerosis, and left ventricular hypertrophy.…”

Section: Inorganic Phosphatementioning

confidence: 99%

“…Metabolic derangement in cancer patients increases risk of cardiac arrest with low survival rate, 16 which may be mediated by phosphate toxicity associated with overgrowth of cancer cells 17 . Additionally, tumor lysis syndrome during cancer treatment releases large amounts of Pi from tumors, which is associated with arrythmia and in‐hospital mortality, 18 and sudden cardiac death increases during cancer treatment 19 . Cases of cardiac arrest following acute hyperphosphatemia have also been reported in accidental infusion with potassium phosphate 20 and administration of sodium phosphate 21 .…”

Section: Cardiac Arrest and Inorganic Phosphatementioning

confidence: 99%

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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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