Primary Aldosteronism Causing Aortic Dissection: A Case Report

Introduction

Hypertension is a common condition that poses significant health risks, including cardiovascular disease, stroke, and renal failure. Defined as a persistent elevation of blood pressure above 140/90 mmHg, hypertension is classified into primary (essential) and secondary forms. Primary aldosteronism (PA) is the most common cause of secondary hypertension, affecting approximately 5% to 10% of hypertensive adults [1]. PA typically manifests as hypertension and hypokalemia. Compared to patients with essential hypertension, those with PA have a higher risk of developing cardiovascular complications such as atrial fibrillation, stroke, and myocardial infarction [2]. Even in cases of mild hypertension, PA increases risks of cardiovascular morbidity and mortality [3,4]. Therefore, early and accurate diagnosis is critical given its high prevalence and the potential for severe cardiovascular outcomes.

Aortic dissection, particularly of the descending aorta, is a life-threatening condition characterized by a tear in the aortic intima that allows blood to enter the medial layer, creating a false lumen. This can result in severe pain, hypotension, and organ ischemia. Management typically requires surgical intervention such as thoracic endovascular aortic repair (TEVAR), which has shown efficacy in stabilizing the condition and preventing further complications [5].

Here, we report a case of primary aldosteronism complicated by descending aortic dissection, and review the relevant literature to enhance clinical awareness and provide valuable insights for effective management, and to provide references for effective management of this disease.

Case Report

A 36-year-old man was admitted with poorly controlled hypertension and gingival hyperplasia. Three years earlier, he had experienced chest and back pain, with recorded BP of 200/110 mmHg at initial presentation and CT angiography revealed a descending aortic dissection. He underwent successful TEVAR. Retrospective evaluation of CT confirmed a subtle right adrenal nodule at that time; no intervention was performed owing to the absence of hypokalemia and the nonspecific symptoms. During follow-up, his blood pressure remained elevated, peaking at 200/110 mmHg, despite treatment with valsartan, nifedipine, and carvedilol. He also developed severe gingival hyperplasia (Figure 1A).

CT angiography showed no new dissection. The patient reported intermittent fatigue without clear triggers, which was relieved by resting. Persistent hypokalemia was noted, with serum potassium at 2.32 mmol/L. Despite supplementation, levels remained low (2.45–2.92 mmol/L). Further workup showed a plasma aldosterone concentration of 150 ng/dL and an aldosterone-to-renin ratio over 200. Adrenal CT revealed a well-defined low-density mass (23×14 mm, ~9 HU) in the right adrenal gland. Contrast-enhanced CT showed a round lesion with enhancement values of 67, 61, and 40 HU in arterial, venous, and delayed phases, respectively.

Given the suspicion of PA, the patient underwent laparoscopic partial adrenalectomy. Histology confirmed adrenal cortical adenoma (Figure 1B, 1C). Postoperatively, his blood pressure improved immediately, although valsartan was required during the early recovery period for additional control. However, his blood pressure normalized completely within 8 to 10 weeks, allowing discontinuation of antihypertensive therapy. Serum potassium levels also returned to normal, and the gingival symptoms showed marked improvement.

Discussion

Primary aldosteronism (PA), a leading cause of secondary hypertension, has been increasingly recognized for its association with severe cardiovascular complications, including aortic dissection. Excess aldosterone promotes sodium retention and potassium loss, leading to hypertension and vascular damage. Compared to essential hypertension, PA presents with more severe cardiovascular risk profiles, including increased incidences of stroke, heart failure, and aortic dissection [6].

This case highlights the potential link between PA and aortic dissection. While the association between PA and cardiovascular complications is well-documented, aortic dissection remains underrecognized. Our findings support recent observations that PA can predispose patients to a wider range of cardiovascular pathology, underscoring the need for early diagnosis and intervention [7–9].

To date, the association between primary aldosteronism (PA) and aortic dissection (AD) has been described only in a limited number of publications, mostly as isolated case reports. Although each case alone provides limited statistical value, collectively they highlight a recurring clinical pattern – most patients were relatively young, presented with severe or resistant hypertension, and were later found to have biochemical evidence of hyperaldosteronism. Future research should explore larger cohorts and incorporate biochemical markers to clarify the mechanistic links between aldosterone and aortic pathology [10,11].

For young patients with spontaneous hypokalemia and unilateral adrenal adenoma on CT, adrenal venous sampling may be omitted in favor of direct surgery [12]. Unilateral adrenalectomy can correct hypokalemia and hypertension in most cases. Our patient experienced full symptom resolution after surgery, supporting this strategy.

Given the critical nature of these complications, understanding the underlying mechanisms linking PA to aortic dissection is imperative for improving patient outcomes and treatment strategies. The present report explores the potential association between primary aldosteronism and aortic dissection through a detailed case analysis. By analyzing a specific case of a patient with PA who developed aortic dissection, this report seeks to elucidate the clinical features, diagnostic challenges, and treatment responses associated with this rare but severe complication. Our findings highlight the clinical implications of PA and contribute to the existing literature by providing new insights into the management of patients at risk for aortic dissection due to hormonal disorders [7].

This report presents novel insights into the relationship between primary aldosteronism (PA) and aortic dissection, addressing a significant gap in the existing literature. While previous research has established a link between PA and various cardiovascular complications, the specific association with aortic dissection remains underexplored. Our findings indicate that patients with elevated aldosterone levels are at an increased risk for developing aortic dissection, highlighting the importance of early recognition and intervention. Unlike the findings of prior studies that primarily focused on more common cardiovascular events, the present report emphasizes the necessity of considering aortic dissection as a potential complication in PA patients, aligning with recent reports that suggest a broader spectrum of complications associated with this endocrine disorder [8,9].

However, this study is not without its limitations. The primary restriction lies in the small sample size, which limits the generalizability of our findings. While our single-case analysis provides valuable insights, future studies should involve larger, multi-center cohorts to validate our results and explore the broader implications of PA in cardiovascular health. Additionally, we did not perform biomarker analyses, which could have enriched our understanding of the relationship between aldosterone levels and aortic dissection. Future research should aim to address these gaps by using longitudinal designs and incorporating biochemical assessments, thereby paving the way for more definitive conclusions regarding the long-term outcomes of PA patients and their cardiovascular risks [10,11].

Previous studies have shown that for young patients with spontaneous hypokalemia, excessive aldosterone secretion, and unilateral adrenal adenoma confirmed by adrenal CT, adrenal venous sampling (AVS) is not necessary and they can directly undergo unilateral adrenal lesion resection [12]. In most cases, this surgery can correct hypokalemia and hypertension, thereby reducing cardiovascular-related complications. Follow-up showed our patient’s postoperative clinical discomfort symptoms, hypertension, and hypokalemia were mostly cured. This also indicates that laparoscopic unilateral adrenal lesion resection is safe and effective for the treatment of primary aldosteronism.

The limitations of this study primarily include the small sample size, as it is based on a single case, which restricts the generalizability of the findings. Additionally, the absence of multi-center data validation limits the robustness of the conclusions drawn. Furthermore, the lack of biological marker assessments inhibits a deeper investigation into the underlying mechanisms linking primary hyperaldosteronism and aortic dissection. These factors underscore the necessity for more extensive studies with larger cohorts to substantiate the associations identified, as well as to explore potential biomarkers that could enhance diagnostic and therapeutic strategies.

Conclusions

This report shows the potential relationship between primary hyperaldosteronism and the occurrence of aortic dissection, shedding light on the underlying mechanisms and providing effective therapeutic approaches. The findings emphasize the importance of early recognition and intervention in managing this rare but critical complication. Larger, multi-center studies are needed to validate these results and further investigate the clinical implications of primary hyperaldosteronism in cardiovascular morbidity.