Key result
Hypercortisolism affects 7.5% of nondiabetic nonobese hypertensive patients and is linked to early vascular damage.
Why the study?
The prevalence of hypercortisolism in hypertension and its association with cardiometabolic risk in hypertensive patients remained unknown.
Is hypercortisolism associated with increased cardiometabolic risk and carotid atherosclerosis in nondiabetic, nonobese hypertensive patients?
Cross-Sectional (n=106)
Is hypercortisolism associated with increased cardiometabolic risk and carotid atherosclerosis in nondiabetic, nonobese hypertensive patients?
Hypercortisolism is present in a notable minority of uncomplicated hypertensive patients and is strongly associated with early vascular damage such as increased carotid intima-media thickness.
May prompt targeted cortisol evaluation in select hypertensives; leaves open causal links to vascular damage.
OBJECTIVE: The prevalence of hypercortisolism in hypertension and its association with cardiometabolic risk in hypertensive patients remains unknown. This study investigates the prevalence of hypercortisolism and the relationship between cortisol secretion and cardiometabolic parameters in hypertensive patients. METHODS: In 106 nondiabetic and nonobese hypertensive patients (age 37-70 years; 53 females), cortisol levels after a 1 mg dexamethasone suppression test (F-1mgDST), carotid intima-media thickness (cIMT), blood pressure dipping pattern, carotid stenosis, fasting glucose (FG), and glycated hemoglobin were evaluated. Hypercortisolism was defined as F-1mgDST >1.8 μg/dL (50 nmol/L). RESULTS: Hypercortisolism was identified in 8 patients (7.5%). Compared with those without, patients with hypercortisolism were older (56.9 vs 63.0 years, P = .04), had higher FG (95.3 vs 103.8 mg/dL, P = .03), glycated hemoglobin (5.4% vs 5.6%, P = .001), more frequently altered blood pressure dipping pattern (22.0% vs 62.5%, P = .026), pathologic cIMT (>1 mm; 7% vs 66.7%, P = .001), and frequently required ≥2 antihypertensive drugs (14.3% vs 50.0%, P = .027). Pathologic cIMT levels were associated with F-1mgDST levels (odds ratio 14.00, 95% CI 2.70-72.48, P < .002) after adjusting for age, sex, body mass index, smoking status, and presence of impaired FG/impaired glucose tolerance. The optimal F-1mgDST cut-off for predicting increased cIMT was identified as 1.14 μg/dL (31.4 nmol/L). This F-1mgDST threshold predicted the risk of cIMT >1 mm (odds ratio 15.57, 95% CI 2.88-84.29, P = .001), after adjustment for age, sex, body mass index, smoking, and presence of impaired glucose metabolism. CONCLUSION: Hypercortisolism was detected in 7.5% of nondiabetic and nonobese hypertensive patients and was associated with early vascular damage. Hypercortisolism may worsen the cardiometabolic risk in hypertension.
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Musolino et al. (2025) conducted a cross-sectional in Hypertension (n=106). Hypercortisolism vs. No hypercortisolism was evaluated on Prevalence of hypercortisolism. Hypercortisolism was detected in 7.5% of nondiabetic and nonobese hypertensive patients and was significantly associated with early vascular damage, including pathologic carotid intima-media thickness.
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