Chronic hypocalcemia reversed heart failure before later bradyarrhythmia emerged

A 74-year-old man with more than four decades of hypocalcemia recovered from severe heart failure after correction of his calcium levels, but his cardiac story did not end there. The case report found that calcium and calcitriol supplementation, combined with heart failure treatment, resolved his dyspnea, shortened his corrected QT interval and raised his left ventricular ejection fraction from 33% to 61% within a month. Eleven months after discharge, however, monitoring detected persistent atrial fibrillation with a slow ventricular response and intermittent complete atrioventricular block, requiring permanent pacemaker implantation. The authors describe the sequence as evidence that restoration of systolic function after hypocalcemic cardiomyopathy does not necessarily mean that all cardiac electrical abnormalities have resolved.

The patient presented with one month of progressively worsening exertional dyspnea, reduced urine output and edema, escalating to orthopnea the day before admission. Examination showed signs of substantial fluid overload, including distended jugular veins, crackles at both lung bases, muffled heart sounds and peripheral pitting edema. His heart rate was 105 beats per minute in a regular rhythm. He also had a 19-year history of coronary artery disease and had received a coronary stent, with subsequent secondary prevention including aspirin, clopidogrel and a statin; clopidogrel had been discontinued one year after the procedure.

Initial testing indicated acute decompensated heart failure. His N-terminal pro-B-type natriuretic peptide, or NT-proBNP, was 11,900 pg/mL, while cardiac troponin I and creatine kinase-MB were within reference ranges. His electrocardiogram showed sinus tachycardia, complete left bundle branch block and a corrected QT interval of 505 milliseconds, with a QRS duration of 136 milliseconds. Echocardiography revealed diffuse left ventricular hypokinesis, an end-diastolic diameter of 57 mm and an ejection fraction of 33%. Chest radiography showed pulmonary edema and small pleural effusions, leading to admission to a cardiac intensive care unit.

Because the patient had coronary artery disease, investigators initially considered ischemic cardiomyopathy. Repeat coronary angiography after stabilization found no progression of the earlier lesions and no new significant stenosis. Cardiac magnetic resonance imaging showed mid-wall delayed enhancement in the basal-to-mid interventricular septum, a pattern that is not typical of ischemic cardiomyopathy. Together with the angiographic findings, the imaging made acute myocardial ischemia unlikely to be the principal cause of the decompensation, directing attention toward the profound metabolic abnormalities found in laboratory testing.

Those tests revealed severe hypocalcemia, with serum calcium of 1.04 mmol/L against a reference range of 2.2–2.7 mmol/L. He also had hypomagnesemia at 0.63 mmol/L, hyperphosphatemia at 2.21 mmol/L, a parathyroid hormone level of 15.8 pg/mL and mildly reduced 25-hydroxyvitamin D at 17.9 ng/mL. Although the parathyroid hormone concentration was technically within the laboratory’s reference interval, it was inappropriately low for the degree of hypocalcemia and did not show the compensatory increase expected in response to such a disturbance. Repeatedly subnormal parathyroid hormone levels during follow-up, together with intracranial calcifications indicating longstanding calcium-phosphate dysregulation, led clinicians to identify primary hypoparathyroidism as the underlying cause.

Calcium and calcitriol replacement was accompanied by a marked biochemical and cardiac response. Calcium and phosphate values returned to their reference ranges, his dyspnea resolved and NT-proBNP declined substantially. His corrected QT interval shortened, while follow-up echocardiography showed left ventricular ejection fraction rising from 33% at admission to 61% after one month. These observations supported a diagnosis of hypocalcemic cardiomyopathy: a reversible form of heart failure associated with severe or prolonged disruption of calcium homeostasis. The improvement occurred within the context of both metabolic correction and conventional heart failure therapy, so the report does not isolate the effect of calcium replacement alone.

The mechanism is consistent with the central role of calcium in cardiac excitation and contraction. Prolonged hypocalcemia can extend ventricular action-potential duration, contributing to QT prolongation, while also impairing myocardial contractility. The case is notable because the patient’s hypocalcemia had persisted for more than 40 years before the acute decompensation. Complete left bundle branch block may also have contributed to mechanical dyssynchrony and worsened heart failure in the setting of severe hypocalcemia. A review of prior reports cited by the authors found that rhythm disturbances associated with hypocalcemic cardiomyopathy were usually documented while hypocalcemia was active and often improved after correction, leaving the longer-term electrical course poorly characterized.

Recovery of the ejection fraction therefore did not provide a complete answer about myocardial recovery. The report notes that other patients with hypocalcemic cardiomyopathy have had persistent late gadolinium enhancement on follow-up cardiac magnetic resonance imaging despite symptomatic improvement and higher ejection fractions, suggesting residual fibrosis. In this patient, the septal enhancement likewise indicated that structural abnormalities persisted even as pump function improved. Because his calcium and phosphate levels were controlled throughout endocrinology follow-up, the later rhythm disorder could not simply be attributed to a continuing, readily reversible electrolyte disturbance at the time it was detected.

Approximately nine months after discharge, paroxysmal atrial fibrillation was documented. The patient had a CHA₂DS₂-VASc score of 6 and a HAS-BLED score of 2, and anticoagulation with rivaroxaban 15 mg once daily was started. No pharmacological or electrical cardioversion was performed, and the atrial fibrillation later became persistent. Importantly, he had not received beta-blockers, amiodarone, digoxin or another rate-slowing drug before the bradyarrhythmia developed, making medication-induced slowing less likely. This timeline distinguishes the reported conduction events from a simple effect of rate-control treatment in atrial fibrillation.

At 11 months after discharge, repeated Holter monitoring showed persistent atrial fibrillation with a mean ventricular rate of 54 beats per minute and a nadir of 31 beats per minute. Daytime rates below 40 beats per minute were recorded, along with a longest R–R interval of 2.25 seconds. The monitor also captured intermittent third-degree atrioventricular block during atrial fibrillation, accompanied by a regular, slow ventricular escape rhythm. The patient reported no fatigue, dizziness, presyncope or syncope. Following clinical evaluation, permanent pacemaker implantation was recommended; a dual-chamber device was initially programmed in DDD mode and later changed to VVI as persistent atrial fibrillation remained confirmed. Evaluation for reversible metabolic causes found no abnormalities in calcium, magnesium, potassium or thyroid function that could explain the bradyarrhythmia.

The authors caution that the late conduction disorder cannot be assigned a single cause. Severe or prolonged hypocalcemia can affect sinoatrial automaticity and atrioventricular nodal conduction, both of which depend on calcium currents, and may increase myocardial susceptibility to arrhythmias. Yet the patient also had advanced age, established coronary artery disease and MRI evidence of myocardial fibrosis. Those factors may have contributed to atrial electrical remodeling and abnormal conduction, making a multifactorial explanation more appropriate than claiming that hypocalcemia directly caused the later events. The case’s central lesson is observational rather than causal: in a patient whose contractile function recovered after biochemical correction, persistent or emerging electrical abnormalities remained clinically relevant. The authors therefore support periodic rhythm assessment during long-term follow-up and individualized calcium and calcitriol therapy that maintains biochemical control while limiting risks such as nephrolithiasis and ectopic calcification.

Subject of Research: Long-term cardiac outcomes after recovery from hypocalcemic cardiomyopathy in an older man with primary hypoparathyroidism

Article Title: Reversible heart failure and subsequent bradyarrhythmia during long-term follow-up in a patient with chronic hypocalcemia: a case report

Article References: Li, R., Deng, X., Li, Z., & Sun, L. (2026). Reversible heart failure and subsequent bradyarrhythmia during long-term follow-up in a patient with chronic hypocalcemia: a case report. Frontiers in Cardiovascular Medicine, 13, Article 1908024. https://doi.org/10.3389/fcvm.2026.1908024

Image Credits: AI Generated

DOI: 10.3389/fcvm.2026.1908024

Keywords: hypocalcemia, hypoparathyroidism, hypocalcemic cardiomyopathy, heart failure, bradyarrhythmia, atrioventricular block, atrial fibrillation, pacemaker, QT prolongation, cardiac electrophysiology, Reversible, heart