Biochemical Study of Blood Electrolytes, Hypokalaemia, and Hyperkalaemia in Genetic Heart Disease
DOI:
https://doi.org/10.61704/pr.592Keywords:
BMI, Body Mass Index, HD Patients, ACE, Angiotensin-Converting EnzymeAbstract
This study investigated the critical relationship between serum electrolyte homeostatic imbalances and hereditary heart disease within Wasit Governorate, Iraq. Conducted between October 2024 and June 2025 at Al-Karama Hospital and Al-Zahraa Teaching Hospital, the research evaluated peripheral blood samples from 68 patients diagnosed with hereditary cardiovascular conditions alongside a control group of healthy donors. Specifically, patients exhibited severe hyponatraemia (117.49 \pm 19.47 mmol/L versus 136.00 \pm 2.69 mmol/L), marked hypokalaemia (2.65 \pm 0.77 mmol/L versus 4.32 \pm 0.44 mmol/L), and critical hypocalcaemia (1.53 \pm 0.74 mg/dL versus 8.88 \pm 0.77 mg/dL). Sodium was identified as the primary pathogenic driver in cardiovascular deterioration for genetic heart disease. Correlation analyses demonstrated a significant negative correlation between serum sodium concentration and advancing chronological age (r = -0.258, p < 0.05), alongside a significant positive correlation between chloride levels and age (r = 0.246, p = 0.05). Conversely, variations in potassium, calcium, and magnesium displayed non-significant negative correlations with age, while Body Mass Index (BMI) demonstrated no statistically significant association with any measured electrolytes. Pathophysiologically, severe deficiencies in essential intracellular ions—particularly magnesium and potassium—were directly implicated as key contributors to disrupted trans-sarcolemmal electrical signalling and cardiac arrhythmias. From a molecular genetics perspective, maintaining rigorous systemic electrolyte homeostasis is vital to stabilise inherently vulnerable ion channels, particularly in cases involving SCN5A gene mutations which underlie Long QT Syndrome Type 3 and Brugada Syndrome. Ultimately, the study concludes that routine, proactive multi-electrolyte monitoring is a fundamental clinical imperative to mitigate life-threatening arrhythmic events and optimise long-term survival in genetic heart disease cohorts.
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Copyright (c) 2026 Zaman I. Hachim, Manar N. Hamad, Saif A. Muttaleb
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Copyright © 2025 by the authors. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND 4.0). You may not alter or transform this work in any way without permission from the authors. Non-commercial use, distribution, and copying are permitted, provided that appropriate credit is given to the authors and Al-Hadba University.
