STEMI complicated with serum sodium of 113 mmol/L from syndrome of inappropriate antidiuretic hormone secretion: How worse could it be?

Abstract

Hyponatremia commonly occurs in acute coronary syndrome and has been recognized as a worse prognostic indicator in patients with ST-segment elevation myocardial infarction (STEMI). However STEMI with preexisting hyponatremia from syndrome of inappropriate antidiuretic hormone secretion (SIADH) has never been described in the literature.

We describe a case of 59-year-old woman who presented with STEMI and received emergent percutaneous coronary intervention who also had SIADH with the lowest serum sodium measurement of 113 mmol/L. Initially, she was treated with hypertonic saline to reduce central nervous system complications. Then, vasopressin receptor 2 antagonist and demeclocycline were started as well as fluid restriction and salt tablet. Her sodium level and clinical symptoms improved. Subsequently, we found cavitary right upper lung mass and a biopsy report revealed small cell lung cancer as a cause of SIADH.

Severe hyponatremia from SIADH complicated with STEMI could potentially have reduced adverse outcomes by normalizing sodium level through vasopressin receptor 2 antagonist or demeclocycline.

<Learning objective: Hyponatremia in STEMI from SIADH, prognosis, and treatment options.>

Introduction

Hyponatremia commonly occurs in acute coronary syndrome (ACS) [1] and has been recognized as a worse prognostic indicator in patients with ST-segment elevation myocardial infarction (STEMI) [2]. In addition, hyponatremia is also an independent predictor of adverse clinical outcomes in hospitalized patients due to decompensated heart failure [3]. However, STEMI with preexisting hyponatremia from syndrome of inappropriate antidiuretic hormone secretion (SIADH) has never been described in the literature. We would like to present a case of a woman with STEMI who also had SIADH with the lowest serum sodium measurement of 113 mmol/L.

Case report

A 59-year-old female who was recently diagnosed with stage 1 breast cancer with ongoing radiation therapy, also had a history of hypertension and 40-pack year smoking. Lisinopril was the only home medication. She presented to our institution with acute severe burning sensation in the epigastric area. The physical examination was remarkable only for mild epigastrium tenderness. Laboratory test revealed a troponin of 11.46 ng/mL. Electrocardiography revealed 3-mm elevation of ST-segment in V2–V5. The patient immediately underwent cardiac catheterization with drug-eluting stent placement in proximal left anterior descending artery without immediate complications. After the procedure, the patient complained of headache, nausea, and vomiting. Additionally, the initial electrolyte results revealed serum sodium of 113 mmol/L with serum osmolality of 244 mOsm/kg. Symptomatic hyponatremia was a concern and 3% NaCl intravenous infusion was initiated. Other countermeasures included cessation and withholding of all possible medications that could cause hyponatremia including lisinopril. Further laboratory results confirmed the diagnosis of SIADH (urine sodium 62 mmol/L, urine osmolality 547 mOsm/kg, serum glucose 140 mg/dL, serum thyroid stimulating hormone 0.55 μIU/mL, serum cortisol 15.8 μg/dL, plasma arginine vasopressin 1.8 pg/mL, and total cholesterol 148 mg/dL.) After her headache and nausea improved, we stopped 3% NaCl and treated the SIADH with 1 L fluid restriction and 6 g per day of salt tablet. As a consequence, her sodium level was gradually rising but still below 125 mmol/L. We decided to administer vasopressin receptor 2 antagonist and demeclocycline to better control her sodium level. Slowly, her serum sodium was trending up to 126 mmol/L. The trend of serum sodium level is shown in Fig. 1. The 2D transthoracic echocardiography showed reduced left ventricular function to 40% with apical akinesis and mural thrombus at left ventricular apex. Furthermore, her chest radiography revealed a cavitary opacity at right upper lung (Fig. 2) which was confirmed by subsequent computed tomography of the chest (Fig. 3). The lung biopsy result showed small cell lung cancer which was likely a primary cause of her SIADH. At the time magnetic resonance imaging of the brain revealed no acute intracranial finding and no evidence of intracranial metastases. The patient was discharged uneventfully with triple anti-thrombotic therapy, beta blocker, and angiotensin-converting enzyme inhibitor. Afterward, the patient developed hemoptysis. She underwent palliative radiation for hemostasis. Then she had 4 cycles of chemotherapy. The patient passed away 5 months later from brain metastasis.

Fig. 1.

The serum sodium level during hospitalization.

Fig. 2.

Chest radiography demonstrated cavitary opacity in the right upper lobe (arrow).

Fig. 3.

Computed tomography of chest with contrast revealed a 4.4 cm × 4.2 cm × 4.0 cm ill-defined area of consolidation in the right upper lobe with marked surrounding irregular spiculated densities, airspace opacity, and central cavitation. There is interlobular septal thickening of the right lung apex which may be due to lymphangitic spread of malignancy.

Discussion

Over time, more and more data suggested that hyponatremia could predict worsened short- and long-term outcomes of patients who had STEMI 2, 4. Additionally, hyponatremia patients who had ACS were more likely to have a lower ejection fraction, elevated creatinine on admission, and longer hospitalization duration [5].

Several mechanisms are known to promote the development of hyponatremia in heart failure, such as increased production and release of vasopressin from arterial underfilling [6] and upregulation of vasopressin-regulated water channel (AP2) in the collecting duct [7]. However, the mechanism of hyponatremia in ACS is not well understood. The proposed mechanism is non-osmotic release of vasopressin due to the acute development of left ventricular dysfunction; similar to the response to pain and nausea/vomiting 8, 9, 10.

Recently, Qureshi et al. [5] found that achieving hyponatremia correction in ACS demonstrated no mortality benefit from hypertonic saline and also increased readmission rates and adverse cardiac outcomes. However, hyponatremia correction achieved through vasopressin receptor 2 antagonist use was associated with a significant reduction in 30-day mortality when initial serum sodium levels lay between 115 and 125 mEq/L. This could be explained by intense neurohormonal activation including vasopressin in acute phase of myocardial infarction.

Our patient, who had severe symptomatic hyponatremia from SIADH caused by small lung cancer, was treated with hypertonic saline, vasopressin receptor 2 antagonist, and demeclocycline which were necessary to control her symptoms. Per Qureshi et al., hypertonic saline would not be the treatment of choice for achieving hyponatremia correction in ACS, but it is the treatment of choice for symptomatic hyponatremia. Hence the patient received it. We hypothesize that hyponatremia from an external cause, as SIADH from small cell lung cancer as this patient, might have the same response and outcome as the treatment in ACS-associated hyponatremia. So in this patient, hypertonic saline infusion would be less likely to reduce her short- or long-term complications from a cardiac standpoint but vasopressin receptor 2 antagonist might.

Rarely, angiotensin-converting enzyme inhibitor could cause drug-induced SIADH. However, in drug-induced hyponatremia, cessation of the offending agent usually resolves in the normalization of serum sodium. In this case, after cessation of lisinopril, her sodium was persistently low and we had a more convincing reason for SIADH. So home lisinopril was resumed when she was discharged, taking into consideration that the patient also had left ventricular dysfunction.

Conclusion

We describe an unusual case of severe hyponatremia from SIADH with STEMI. The knowledge of correcting hyponatremia in this scenario is not well established. However, we believed that successfully corrected hyponatremia through vasopressin receptor 2 antagonist or demeclocycline could potentially reduce the adverse outcomes. Additionally, the treatment of primary lung condition would be a definite method to normalize the sodium level.

Conflict of interest

All authors have no conflict of interest and no commercial or proprietary interest in any drug, device, or equipment mentioned in the submitted article.