Endocrine Abstracts

A 40 y /M with no previous CVS/family history, presented with fall. On history, he was feeling unwell, had Appetite loss × 3 months, progressive SOB, Orthopnoea, PND and palpitations. No chest pain/fever. On Examination, he had tachycardia (160) and irregular rhythm, raised JVP, SpO2 92%, B/l ankle edema, bibasal fine inspiratory crackles in chest, Hepatomegaly(3 cm) CVS :S3 gallop, mild TR, MR. ECG: sinus rhythm with freq ectopics, long QT, paroxysms of tachycardia, T wave inversion V4-V6. CXR revealed cardiomegaly and pulmonary oedema. His Troponin was <0.02 mg/l. Echo showed dilated LV with globally impaired systolic function with LVEF15% due to diffuse hypokinesia, moderate MR, TR. Coronary angiogram was normal, no vessel disease. Clinical Diagnosis of heart failure was made and pt started iv furosemide, digoxin, B blockers. But he started deteriorating and had irregular rhythm on cardiac monitor(ectopics/AF/Atachy). He also started c/o nocturnal muscular cramps and paraesthesia. Was shifted to ITU immediately. Further investigations revealed Calcium:1.03 mmol/l, Phosphate:2.77 mmol/l. Mg 0.63 mmol/l. PTH <0.5 pmol/l. Vitamin D 88 nmol/l, TSH 1.96 CRP < 3. Ultrasound neck: No parathyroid glands identified. So he was started on iv calcium gluconate, iv magnesium and 2 mg Alfacalcidolvit D3) and Adcal. Blood investigations over next few days showed improving ca, po4 and mg levels. ECG: HR improved (70), sinus rhythm, QT normal, Digoxin stopped, Patient’s sats improved with no O2 reqt. His overall Condition improved in 2 weeks and was discharged. -3 months later Patient was completely asymptomatic and Repeat Echo showed EF improved to 59% with improved global LV contractility, No MR. ECG HR 70/mt, normal QT, sinus. -Final Diagnosis was Hypocalcaemic cardiomyopathy secondary to primary hypoparathyroidism (Idiopathic/low Mg) Etiology of heart failure: cardiac myocytes contraction is directly dependent on Ca concentration in the ECF. Low ca leads to lowered cell membrane potential → increased membrane permeability → escape of cytoplasmic proteins from renal tubules. Also decreased natriuresis → result in fluid retention → heart failure. Correction of hypocalcemia promotes natriuresis. HYPOCALCEMIC CARDIOMYOPATHY is reversible Systolic/Dilated cardiomyopathy due to deterioration of the heart muscle’s contractility. Often a late manifestation of long standing hypocalcemia. May manifest with arrhythmias(AF, prolonged QT, VT) which is completely reversible on treating hypocalcaemia. Traditional therapy for heart failure, i.e. diuretics/digitalis alone not effective in resolving symptoms. Furosemide could decrease serum calcium level by increasing calcium excretion in urine leading to worsening symptoms. Alfacalcidol is MUST for treatment along with calcium supplementation in primary hypoparathyroidism.