Relationship Between Endothelial Functions and Acetylsalicylic Acid Resistance in Newly Diagnosed Hypertensive Patients

Abstract

Background: We aimed to investigate the effects and dose dependency of aspirin on endothelial functions and prevalence of aspirin resistance in newly diagnosed hypertensive patients without previous drug therapy and development of cardiac complications. Hypothesis: Acetylsalicyclic acid improves endothelial function. Methods: Fifty-eight hypertensive patients and 61 healthy subjects in the control group were included in the study. Endothelial functions of the patient and control groups were evaluated with brachial artery examination. Patient and control groups were divided into 2 groups. A total of 100 mg and 300 mg of aspirin were given to the separate groups for 1 week. After 1 week, endothelial functions were reevaluated and aspirin resistance examined with a platelet function analyzer (PFA-100; Dade Behring, Marbourg, Germany). Results: Baseline flow-mediated dilatation (FMD) change percent in hypertensive patients was 9.8%, and it was significantly lower than in the control group (12%) (P < 0.001). Frequency of acetylsalicylic acid (ASA) resistance was 20% and 26% in control and hypertensive patient groups, respectively (P = not significant). ASA resistance was 28% and 24% in 100 mg and 300 mg in hypertensive patients, respectively (P = not significant). FMD change percent increased both in the control and hypertensive groups after ASA treatment from 12.4% to 13.3% and 9.8 % to 11.9 %, respectively. FMD percentage change was significantly increased in hypertensive patients irrespective of ASA resistance (P = 0.02, for ASA resistance [+]; P < 0.012, for ASA resistance [−]). Conclusions: Endothelial functions were impaired more in hypertensive patients compared to the control group. Endothelial functions were improved with all ASA doses in hypertensive patients irrespective of ASA resistance. IntroductionThe vascular endothelium regulates cardiovascular homeostasis and blood pressure (BP) through the release of nitric oxide (NO).1,2 NO is an anti-inflammatory, antithrombotic, and antiproliferative agent that limits expression of adhesion molecules and chemotactic factors on endothelium, and inhibits platelet aggregation and proliferation of smooth muscle cells.

The Relationship Between Aspirin Resistance and Carotid Imaging in Young Patients With ST-Segment Elevated Myocardial Infarction: A Cross-Sectional Study

“…There are contradictory studies on the relation of aspirin with hypertension in the literature. In 2 separate studies—in newly diagnosed patients and patients with chronic hypertension—there was no relationship between AR and hypertension, 17,18 whereas the presence of hypertension in patients with stable coronary artery was found as predictive of AR. 19 In our study, ABPM was performed in all patients, and mean/daytime/nighttime SBP and night time DBP was higher in patients with AR.…”

Can the Previous Therapeutic Control of the Main Risk Factors of Cerebrovascular Disease Influence the Acetylsalicylic Acid–Nonresponsive Status in Acute Ischemic Stroke Patients? Results from a Portuguese Prospective Cohort Study

“…34 In hypertensive patients, basal NO activity is decreased and endothelium-dependent vasodilation in response to acetylcholine is impaired in forearm circulation. 31,35,36 Sahin et al 31 have found that endothelial functions were improved in hypertensive patients after treatment with ASA. The benefit of antiplatelet therapy with ASA in patients with hypertension is well established, and it has been suggested that ASA modulates acetylcholine-induced peripheral vasodilation in patients with atherosclerosis, possibly via inhibition of 1 or more COX-dependent vasoconstrictors.…”

“…31,32 Oxidative stress and endothelial dysfunction are consistently observed in hypertensive patients; however, emerging evidence suggests that they also have a causal role in the molecular processes leading to hypertension. ASA is a potent antioxidant agent, and reduction in vascular production of superoxide in normotensive and hypertensive rats has been demonstrated previously.…”

“…The benefit of antiplatelet therapy with ASA in patients with hypertension is well established, and it has been suggested that ASA modulates acetylcholine-induced peripheral vasodilation in patients with atherosclerosis, possibly via inhibition of 1 or more COX-dependent vasoconstrictors. 31 It has been proposed that the neutralization of cytokine response to an inflammatory stimuli is indicating a novel mechanism by which aspirin can regulate endothelial function. 37 Results by Feher et al 24 showed that ASA-nonresponsive status was lower in hypertensive patients who were under ACE inhibitor and b-blocker treatment and that these drugs may exert an additive antiplatelet action when combined with ASA.…”

Will the epidemic of metabolic syndrome raise the prevalence of antiplatelet drug resistance?

“…Presence or greater severity of hypertension, visceral obesity, low high density lipoprotein cholesterol and/or high triglyceride values, insulin resistance, kidney disease, elevated CRP levels, and endothelial dysfunction amplify cardiometabolic risk in most instances. Obesity,[10] hypertension,[11] diabetes,[12] dyslipidemia, high CRP levels,[13] and other individual risk factors/biomarkers are connected with antiplatelet drug resistance. These data suggest that, although such resistance frequently occurs in patients without MetS, additional features that intensify the thrombotic, inflammatory, and hyperglycemic burdens, particularly those that thwart availability of nitric oxide through potent prooxidative mechanisms, may increase the likelihood of antiplatelet drug resistance.…”