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Statins Decrease Aortic Stiffness in Hypertensive Patients With High Cholesterol: Presented at ISA

By Eurona Earl Tilley

KYOTO, JAPAN -- September 30, 2003 -- Long-term use of fluvastatin or simvastatin appear to decrease aortic stiffness while not affecting blood pressure levels of hypertensive patients with hyperlipidaemia.

Atsuhiro Ichihara, of Keio University School of Medicine, Keio, Japan, presented these findings here on September 29^th at the 13^th International Symposium on Atherosclerosis.

Dr. Ichihara and associates conducted a 12-month, single blind, randomised, prospective study of 85 patients with a median age of 60 years, who had hyperlipidaemia with hypertension that did not respond to antihypertensive treatments. Patients with secondary hypertension, cardiovascular disease, and peripheral arterial disease were excluded from the study.

Each participant was randomly placed in 1 of 4 antihyperlipidaemic treatment groups -- pravastatin 10 mg/day, simvastatin 5 mg/day, fluvastatin 20 mg/day, or a non-statin antihyperlipidaemic treatment control group given either clofibrate 750 mg/day or probucol 500 mg/day.

Each patient was evaluated in 3-month intervals. Fasting venous blood samples were taken in addition to ankle brachial index (ABI), heart rate, blood pressure, and pulse wave velocity (PWV) between the brachium and ankle. In hypertensive patients, assessing aortic stiffness via PWV along the aortoiliac pathway is useful in predicting cardiovascular related mortality, Dr. Ichihara explained.

At the beginning of the study, there was no considerable difference in demographics, antihypertensive medications used, blood pressure level, ankle brachial index, PWV, as well as levels of serum lipids, creatinine, and C-reactive protein. By the end of the study, serum cholesterol levels had decreased in all 4 treatment groups, while blood pressure, ankle brachial index, and serum triglyceride levels remained unaffected.

Although both the simvastatin and fluvastatin groups exhibited significantly decreased serum levels of low-density lipoproteins, there was no such change in the pravastatin or non-statin group. Serum levels of C-reactive protein were notably reduced in the 3 statin groups, but not in the non-statin group. Most significantly, while the PWV remained unchanged in the pravastatin and non-statin group, it was moderately decreased in the simvastatin group, and remarkably reduced in the fluvastatin group.

Dr. Ichihara theorized that lipophilic statins, such as fluvastatin, reduce aortic stiffness via 3 mechanisms -- decreasing serum total cholesterol levels without reducing serum high-density lipoprotein levels, providing powerful scavenging reactive oxygen species, as well as reducing serum levels of low-density lipoprotein and C-reactive protein.


[Study title: Long-Term Use of Fluvastatin Reduces Aortic Stiffness Without Affecting Blood Pressure in Hypertensive Patients With Insufficiently Controlled Blood Pressure. Abstract 1P-0071]

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