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Hypocalcaemia As A Rare Reversible Cause Of Dilated Cardiomyopathy
Bilal Ahmad1, Saddam Hussain2, Jamal Shah2
1Lady Reading Hospital Peshawar, Pakistan.
Insights
Hypocalcaemia, or low calcium levels, can cause reversible dilated cardiomyopathy and heart failure. Prompt correction of calcium levels in patients with dilated cardiomyopathy is crucial for improving heart function.
Area of Science:
- Cardiology
- Endocrinology
- Internal Medicine
Background:
- Dilated cardiomyopathy involves ventricular enlargement and impaired systolic function.
- Calcium is essential for myocardial contraction; hypocalcaemia impairs this process.
- Hypocalcaemia is a rare, yet reversible, cause of heart failure with reduced ejection fraction.
Observation:
- A patient presented with symptoms of heart failure, including dyspnea and edema.
- Clinical examination revealed signs of fluid overload and a heart murmur.
- ECG showed a prolonged QT interval, and echocardiography confirmed dilated cardiomyopathy with reduced ejection fraction.
Findings:
- The patient's low calcium and parathyroid hormone (PTH) levels indicated hypocalcaemia.
- Treatment with calcium and vitamin D supplements led to improved ejection fraction.
- The patient was successfully weaned off ionotropic support after calcium correction.
Implications:
- This case highlights hypocalcaemia as a treatable cause of dilated cardiomyopathy.
- Monitoring and correcting calcium levels are vital in managing patients with heart failure.
- Early diagnosis and intervention can significantly improve cardiac outcomes in hypocalcaemic cardiomyopathy.
Abstract:
Dilated cardiomyopathy is characterized by dilation and enlargement of one or both ventricles with reduced systolic function. Calcium plays a key role in myocardial contraction. Hypocalcaemia can lead to a decrease in contraction, left ventricular systolic dysfunction, and heart failure with reduced ejection fraction (EF). Hypocalcaemia is a rare reversible cause of dilated cardiomyopathy. The author presents a case who presented with complaints of shortness of breath on exertion, orthopnoea, paroxysmal nocturnal dyspnoea, numbness and crampy muscular pains. He had a high JVP, systolic murmur on auscultation, hepatomegaly, pedal oedema and crackles on chest auscultation. His ECG showed sinus rhythm with prolonged QT interval. His echocardiography showed dilated cardiomyopathy with reduced ejection fraction, moderate mitral regurgitation and mild tricuspid regurgitation. His Calcium levels and PTH levels were both low. He was treated with ionotrophes, diuretics, vitamin D and calcium supplements, including both intravenous and oral. With the correction of calcium levels, he was weaned off the ionotrophic support and his ejection fraction improved. Calcium levels if low should be corrected in patients with dilated cardiomyopathy.
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