The missing mineral: Rare cause of reversible cardiomyopathy

Vigneshvarprashanth Umapathy1, Praneetha A1, Ivan A Jones2

1Resident Internal Medicine, Kauvery Hospital, Tennur, Trichy, Tamil Nadu, India

2Consultant Physician, Kauvery Hospital, Tennur, Trichy, Tamil Nadu, India

Background

Cardiomyopathies encompass a diverse group of disorders characterized by structural and functional changes in the heart muscle, which can lead to progressive heart failure, often associated with substantial morbidity and mortality.1 These conditions can be classified as primary or secondary, depending on whether the heart disease is the primary pathological process or a result of other systemic conditions. Cardiomyopathies are typically associated with long-term complications, including arrhythmias, impaired cardiac output, and eventual heart failure, which may necessitate advanced therapeutic interventions such as heart transplantation in severe cases. While many forms of cardiomyopathy are progressive and often irreversible, there are instances where the underlying cause can be addressed, leading to full or partial recovery of heart function.

Case Presentation

A 40-year-old gentleman status post total thyroidectomy for papillary carcinoma thyroid presented with bilateral leg cramps for 1 month, dyspnea and orthopnea for 15 days.  Trousseau sign was positive, ECG (Fig. 1) showed QT prolongation, and chest x-ray (Fig. 2A) showed features of acute pulmonary edema. Echocardiography (Fig. 2B) showed dilated cardiomyopathy, severe LVSD (EF: 25%) and diastolic dysfunction.  There was no evidence of acute coronary syndrome or sepsis. Severe hypocalcemia (ionized calcium: 0.56 mmol/L), hypoparathyroidism (intact PTH: 6.27 pg/ml) along with vitamin-D deficiency were noted. He was managed with diuretics (given initially), intravenous calcium gluconate, oral calcium, vitamin-D and thyroxine supplements. 3 months following discharge, his echocardiography showed normal LV function and calcium and PTH levels normalized.

Fig. (1): Electrocardiography showing T inversion in precordial leads and QTc prolongation

Fig. 2: (A) Chest X-ray showing features of acute pulmonary edema; (B) Echocardiography showing features of dilated cardiomyopathy

Discussion

Fig. 3 (flowchart) illustrates the important reversible causes of cardiomyopathy.2,3 Our patient is a rare case of hypocalcemia leading to dilated cardiomyopathy causing heart failure. Calcium plays a vital role in cardiac automatism and excitation-contraction coupling, with low serum levels associated with myocardial contractility compromise.4 Hypocalcemia is a rare and potentially reversible cause of cardiomyopathy, with very few cases4-8 reported in the literature. It is a form of dilated cardiomyopathy.

Recently, several cases of DCM secondary to hypocalcemia have been reported. Overall, these cases carry a good prognosis, with the systolic function returning back to normal within few months.9 In some cases, patients may initially present with heart failure, and diuretic therapy, particularly with loop diuretics, may be initiated before serum calcium levels are assessed. This can inadvertently lower calcium levels, potentially exacerbating the symptoms. Heart failure due to hypocalcemia is often resistant to diuretic therapy, but responds to calcium replacement rapidly leading to normalization of serum calcium levels,9 as in our case.

Fig. (3): Flowchart illustrating the important reversible causes of cardiomyopathy2,3

Conclusion

Hypocalcemia-induced cardiomyopathy represents a rare but important cause of reversible cardiac dysfunction. Prompt recognition and correction of calcium deficiency can lead to significant improvement or even full recovery of cardiac function, underscoring the importance of considering electrolyte imbalances in the differential diagnosis of cardiomyopathy.

References

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