Introduction
Primary aldosteronism (PA) is the most common cause of secondary hypertension1 and has rarely been reported in combination with aortic dissection2. Whilst optimal investigation of PA requires discontinuation of interfering medications, this is not always possible.
Case Presentation
A 57-year-old man presented to the emergency department with chest and abdominal pain. Blood pressure was 224/130mmHg and he was hypokalaemic (potassium 2.5mmol/L). A computed tomography (CT) scan revealed a type B aortic dissection, initially managed conservatively, followed by an endovascular repair.
Whilst on metoprolol, perindopril and hydrochlorothiazide, aldosterone was 699pmol/L with suppressed renin <2.0mIU/L and ARR 349. Cortisol was mildly elevated on multiple 1mg dexamethasone suppression tests, without Cushingoid features. An adrenal CT reported bulky adrenal glands bilaterally and a right-sided 8mm arterially-enhancing nodule.
After further presentations with hypertensive crisis, antihypertensives were up-titrated to spironolactone, amlodipine, metoprolol, perindopril and hydralazine. The patient will be referred for adrenal vein sampling (AVS) on his current medications using metanephrines instead of cortisol due to cortisol co-secretion.
Discussion
This case highlights the challenges in PA workup and management where interfering medications cannot be withdrawn. There have been few reported cases aortic dissection associated with PA2. The main risk factor for aortic dissection is hypertension, mainly resistant hypertension3. PA is the most common form of secondary hypertension and is associated with greater end-organ damage compared with essential hypertension2,4.
To screen for PA, guidelines recommend washout of interfering medications5, however, if not safe, testing can be performed if renin remains suppressed despite the use of interfering agents1. Once PA is confirmed biochemically, AVS determines the laterality and subtype5. Co-secretion of aldosterone and cortisol (5-27% of cases1) can confound AVS results due to suppressed cortisol production from the contralateral gland. In this instance, it has been shown that plasma metanephrines can be successfully used instead6.