Abstract

The treatment of primary hypertension has been one of the major success stories of clinical medicine over the last 50 years. However, there is still room for further improvement because it is now appreciated that optimally treated hypertensives still have considerable residual cardiovascular (CV) risk. A recent article showed that even after correcting for systolic blood pressure (BP), a treated hypertensive patient has a 50% increased risk of any CV event.1 Intriguingly this is not the case for lipid-lowering therapy, which is able to negate all of the increased risk caused by hyperlipidemia. When the total CV risk in treated hypertension was broken down further, the increased risk of coronary disease was 46%, for stroke it was 75%, and for CV death it was 62%. Numerous other studies have found the same increased residual CV risk in treated hypertensives.2–7 A 65-year-old man was diagnosed with primary hypertension 15 years ago at the age of 50 years. There were no noteworthy features about this man and his family history was unremarkable. He was an ex-smoker (only 4 years) with a body mass index of 24, who ingested 10 U of alcohol per week. His hypertension was well controlled on a combination of lisinopril (20 mg) and amlodipine (5 mg). His office BPs were 130/78 mm Hg. His home BPs, recorded by himself, averaged 116/78 mm Hg. His lipid profile was normal but he was commenced on a statin 3 years ago (atorvastatin 10 mg) in view of the earlier ASCOT/LLA (Anglo Scandinavian Cardiac Outcomes Trial/Lipid Lowering Arm) study results. Despite the above, he was admitted to hospital with an anterior ST-segment–elevation myocardial infarction (STEMI), which was appropriately treated with angioplasty and all other routine therapy, including the addition in the long term of aspirin, a β-blocker, and an increase …

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