Key result
Cushing's syndrome was associated with significantly higher AASI and sAASI compared to matched controls in both normotensive (p=0.048 and p=0.013) and hypertensive (p=0.004 and p=0.046) groups.
Why the study?
Does Cushing's syndrome increase arterial stiffness compared to matched controls?
Case-Control (n=48)
Does Cushing's syndrome increase arterial stiffness compared to matched controls?
p-value: p=0.048 for AASI and p=0.013 for sAASI (normotensive); p=0.004 for AASI and p=0.046 for sAASI (hypertensive)
Cushing's syndrome is associated with increased arterial stiffness independent of blood pressure elevation, which may represent an additional cardiovascular risk factor.
May indicate excess CV risk beyond BP in Cushing's; hypothesis-generating for prospective validation.
Long-standing exposure to endogenous cortisol excess is associated with high cardiovascular risk. The aim of our study was to investigate arterial stiffness, which has been recognized as an independent predictor of adverse cardiovascular outcome, in a group of patients with Cushing's syndrome. Twenty-four patients with Cushing's syndrome (3 males, mean age 49±13 years; 20 pituitary-dependent Cushing's disease and 4 adrenal adenoma) underwent 24-h ambulatory blood pressure monitoring (ABPM) and evaluation of cardiovascular risk factors. The Ambulatory Arterial Stiffness Index (AASI) and symmetric AASI (sAASI) were derived from ABPM tracings. Cushing patients were divided into 8 normotensive (NOR-CUSH) and 16 hypertensive (HYP-CUSH) patients, and were compared with 8 normotensive (NOR-CTR) and 16 hypertensive (HYP-CTR) control subjects, matched for demographic characteristics, 24-h ABPM and cardiometabolic risk factors. The AASI and sAASI indexes were significantly higher in Cushing patients than in controls, either in the normotensive (p=0.048 for AASI and p=0.013 for sAASI) or in the hypertensive (p=0.004 for AASI and p=0.046 for sAASI) group. No difference in metabolic parameters was observed between NOR-CUSH and NOR-CTR or between HYP-CUSH and HYP-CTR groups. AASI and sAASI were both correlated with urinary cortisol in patients with endogenous hypercortisolism (Spearman's rho=0.40, p=0.05, and 0.61, p=0.003, respectively), while no correlation was found in controls. Both AASI and sAASI are increased in Cushing syndrome, independent of BP elevation, and may represent an additional cardiovascular risk factor in this disease. The role of excess cortisol in arterial stiffness has to be further clarified.
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Battocchio et al. (2017) conducted a case-control in Cushing's syndrome (n=48). Cushing's syndrome (endogenous cortisol excess) vs. Matched control subjects (normotensive and hypertensive) was evaluated on Ambulatory Arterial Stiffness Index (AASI) and symmetric AASI (sAASI) (p=p=0.048 for AASI and p=0.013 for sAASI (normotensive); p=0.004 for AASI and p=0.046 for sAASI (hypertensive)). Cushing's syndrome was associated with significantly higher AASI and sAASI compared to matched controls in both normotensive (p=0.048 and p=0.013) and hypertensive (p=0.004 and p=0.046) groups.
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