Issue 121 Item 8 EASD: Low-Dose Acetylsalicylic Acid Counteracts ACE Benefits an

New research suggests Low-dose acetylsalicylic acid (ASA, Aspirin) may increase systolic blood pressure in type 1 diabetic patients, especially in those taking angiotensin-converting enzyme (ACE) inhibitors. >Dr. Lena Thorn, with the Helsinki University Hospital, Finland, presented their findings at the European Association for the Study of Diabetes (EASD) annual meeting in Budapest, Hungary.

Low-dose ASA (81 to 325 mg/day) is recommended for the prevention of cardiovascular disease (CVD) in high-risk diabetic patients, although some studies have suggested that high doses of non-steroidal anti-inflammatory drugs (NSAIDS) increase blood pressure by causing sodium retention.

With their study, the researchers investigated whether low-dose ASA increased blood pressure in diabetic patients. They also determined whether ACE inhibitors would influence this effect compared to other classes of antihypertensive drugs.

Included in the analysis were 2,021 adults with type 1 diabetes in a multicenter study of patients from 55 referral centers.

One thousand and fifty-five of the patients had a normal albumin excretion rate, 282 had microalbuminuria, 421 had proteinuria, and 263 had end-stage renal disease (ESRD). Signs of CVD were observed in 142 patients and 924 were taking antihypertensive drugs. A total of 279 of the patients were taking low-dose ASA. Ten patients taking high-dose NSAIDs were eliminated from the trial.

Compared to those not taking ASA, patients taking ASA had higher systolic blood pressure (SBP) (151 plus or minus 1 versus 134 plus or minus 1 mmHg; p<0.0001) and diastolic blood pressure (DBP) (84 plus or minus 1 versus 80 plus or minus1, p<0.0001).

Similarly, in patients without CVD and not taking antihypertensive drugs (n=37), SBP was still higher in those taking ASA (142 plus or minus 3 mmHg) compared to the 1042 participants who were not taking it (128 plus or minus 1 mmHg) (p<0.0001), although no difference was observed in DBP between the two groups.

SBP was also higher in patients taking low-dose ASA in the normoalbuminuric and macroalbuminuric groups (p<0.0001), but there was no difference in the microalbuminuric or ESRD groups.

After excluding those with ESRD, patients taking a combination of low-dose ASA and ACE inhibitors had a higher SBP (148 plus or minus 1 mmHg) compared to those taking only ACE inhibitors (141 plus or minus 1) (p<0.01), though this effect did not extend to patients taking other types of antihypertensives.

"A potentially negative effect of Aspirin should be considered when high-risk patients do not respond to antihypertensive therapy adequately," Dr. Thorn said in an interview. She emphasized, however, that the findings do not imply that physicians should stop giving Aspirin to their patients.

"Aspirin’s mechanism is not entirely clear," Dr. Thorn said, "but the effect is thought to be at least partly due to local prostaglandin inhibition in the kidneys, causing sodium and thereby fluid retention," she said.

She also noted that the same effect might hold true for patients with type 2 diabetes taking ACE inhibitors