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Background: Ascending aortic aneurysms are one of the primary causes of mortality. However, not much is known about the etiologies of aortic aneurysm. Recently, in hypertensive (HT) patients, blood pressure variability (BPV) has been recommended as a remarkable risk factor for adverse cardiovascular outcomes. This study aimed to explore the association between short-term BPV and ascending aortic dilatation (AAD). Methods: In this study, a total of 53 HT patients with AAD (aortic size index [ASI] ≥21 mm/m2) and 126 HT patients with a normal ascending aortic diameter (ASI 12.95 had a sensitivity of 61% and a specificity of 59% (area under the curve, 0.659; 95% CI, 0.562–0.756; P= .01); moreover, daytime SD of SBP > 16.4 had sensitivity of 62% and specificity of 61% (AUC, 0.687; 95% CI, 0.591–0.782; P

Cardiovascular diseases are the leading cause of mortality worldwide. In recent years, the relationship between carbonic anhydrase inhibitors and atherosclerosis has attracted attention. In this study, we aimed to determine the in vitro effects of 35 frequently used cardiac drugs on human carbonic anhydrase I (hCA I) and II (hCA II). The inhibitory effects of the drugs on hCA I and hCA II were determined with both the hydratase and esterase methods. The most potent inhibitors observed were propafenone (hCA I: 2.8 µM and hCA II: 3.02 µM) and captopril (hCA I: 1.58 µM and hCA II: 6.25 µM). Isosorbide mononitrate, propranolol, furosemide, and atorvastatin were also potent inhibitors. The inhibitor constant, Ki, value from the Lineweaver–Burk plot for propafenone was 2.38 µM for hCA I and 2.97 µM for hCA II. The tested cardiac drugs showed potent in vitro inhibition of the hCA I and II isozymes. Especially, in patients with atherosclerotic heart disease, these drugs may be preferred primarily due to the beneficial effects of carbonic anhydrase inhibition on atherosclerosis.