Drug therapy for prevention of cardiovascular disease – should surrogate measures be abandoned?

Abstract

-It has been suggested that the most effective method of reducing cardiovascular disease (CVD) is to define overall CVD risk and apply fixed doses of anti-hypertensive, hypolipidaemic and anti-platelet therapies, using the evidence base from clinical outcome studies. Such studies have examined large numbers of patients with a wide representation of subgroups and demonstrated equivalent benefits in all subsets. In so doing, there may be over-interpretation of the data leading to large-scale applicability of the findings to individuals who were not genuinely represented in the study populations. Most lipid-lowering studies have been unable to consider the possibility that optimal correction of dyslipidaemia would have been more effective than the use of a fixed dose of statins. Studies of angiotensinconverting enzyme (ACE) inhibitors and angiotensin receptor blockade have produced contradictory findings regarding unique non-hypotensive beneficial CVD effects, and suboptimal control of mild hypertension was a frequent finding in the study populations. Scrutiny of concomitant therapy in studies that focus on a particular issue such as LDL (low-density lipoprotein) cholesterol or blood pressure supports the notion that benefits from the agent may be attenuated by other drugs. Widespread application of fixed doses of all these agents to at-risk cases will increase the incidence of inappropriate use and side effects. Clinical experience with modulators of the renin-angiotensin system in hypertensive diabetic renal disease confirms reduced efficacy, and more frequent deterioration of renal function than observed in clinical trials. Measurement of individual biomedical CVD risk factors along with overall risk estimation should continue to be the mainstay of clinical practice. This will allow appropriate case selection for different agents, optimisation of dosage or better assessment of compliance where treatment is less efficacious, and monitoring for adverse effects of therapy. Pragmatic individualisation of care should remain the basis for treating asymptomatic CVD risk factors. KEY WORDS: anti-platelet therapy, cardiovascular disease, diabetes, dyslipidaemia, hypertension, statinsDefining and treating total cardiovascular disease (CVD) risk through assessment of several individual risk factors is more effective in reducing CVD than treating levels of single risk markers in isolation, 1 as they operate in a synergistic fashion. 2 There are conflicting approaches regarding drug therapy, as individuals can be selected on the basis of estimated risk and treated with fixed doses of therapies where there is an evidence base, or by dose titration to biomedical targets, based on individual levels of risk factors, co-morbidity and concurrent therapy. All patients with coronary heart disease (CHD) or an equivalent risk of future CVD events could potentially be treated with fixed doss of angiotensinconverting enzyme (ACE) inhibitors, β-blockers, statins and aspirin, assuming no contraindications. 1 Alternatively, risk p...

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