Introduction: Hyponatremia is a common electrolyte disorder observed in heart failure (HF) patients making it difficult to treat with diruetics. Additionally, HF remains one of the costliest diagnoses in the United States with an estimated cost of around $31 billion for Medicare recipients. Finding an effective and inexpensive treatment becomes imperative to offset these staggering rates.
Objective:The objective of this pilot study was to determine the safety of using acetazolamide in healthy individuals and to confirm that its properties would be that of an aquaretic rather than a diuretic. Methods: Baseline serum samples for electrolyte levels and kidney function were obtained. Subjects were then administered 250mg of acetazolamide orally every day for 5 days. On the final day of medication administration, each subject once again repeated the same laboratory tests.Results: Twelve healthy subjects participated. No significant change in urine sodium, urine osmolality, and serum sodium was observed at the completion of the study period.Conclusions: Acetazolamide has been classified as a diuretic, but our study indicates that it may actually act more like an aquaretic. We showed a mild trended increase yet no significant change in serum sodium levels in healthy individuals after five days. Hence, future studies in hypervolemic hyponatremic HF patients may elucidate this medications ability to improve the sodium levels, fluid status and mortality rates cost effectively in this population.
According to the Centers for Disease Control and Prevention statistics, about 6.2 million adults in the United States have heart failure. Guideline-Directed Medical Therapy (GDMT) involving the use of renin-angiotensin-aldosterone system inhibitors with or without a neprilysin inhibitor, β-blockers, mineralocorticoid-receptor-antagonists, and sodium-glucose cotransporter-2 inhibitors serve as the backbone for heart failure with reduced ejection fraction (HFrEF) therapy. However, in patients with refractory hypotension, the initiation of GDMT may not be possible. We present four cases where the use of midodrine, an alpha adrenergic agonist, serves as bridge therapy for the initiation or continuation of GDMT with marked clinical improvement. These cases illustrate how exacerbations of HFrEF may be ameliorated with outpatient midodrine titration among patients with baseline, persistent hypotension such that GDMT may be better tolerated.
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