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Stable angina – medical therapy gives us time to optimise management

The three strategies to tackle the problem of chronic stable angina remain medical therapy which includes lifestyle changes, percutaneous coronary interventions (PCI) and coronary artery bypass surgery (CABG) (1). The decision to adopt one approach above another should be evidence based with the proviso that evidence-based medicine can only be practised along with good clinical judgement. Clinical judgement must take into account the wishes of the patient, the patient’s age and general condition including comorbidities and their psychological and social circumstances. We are treating people not statistics and not their anatomy in isolation from their feelings. There is no doubt that medical therapy has progressed and improved over the last 10 years or more so that decision making based on trials performed before this period must be put into perspective. We can view medical therapy prognostically [aspirin, statin, angiotensin-converting enzyme (ACE) inhibitor and b-blocker] and as a means of symptom relief (b-blockers, calcium antagonists, potassium channel activators, nitrates and metabolic agents such as trimetazidine). All should be on the former (if tolerated and not contraindicated) and the latter used as needed. Medical therapy as well as being an alternative to PCI and CABG is also additive from the prognostic viewpoint and needs to be continued post intervention given that though the disease process may be locally symptomatic, it is a systemic condition. Vulnerable plaques may well be asymptomatic and apparently insignificant but need stabilizing to prevent subsequent rupture (2). The seven-year outcome from the RITA-2 trial of coronary angioplasty vs. medical therapy reports no difference in the risk of death or myocardial infarction (MI) between the two groups (3). It is well known, though often forgotten, that the event rate in patients with chronic stable angina is low with death and non-fatal MI rates of 1–3% per year (4). In RITA-2 73 (14.5%) of the 504 undergoing PCI died or sustained an MI compared with 63 (12.3%) of the 514 medical patients once more confirming the low yearly event rate. There were 43 deaths in each group, but only 41% were cardiac related. PCI improved angina and exercise tolerance. The trial concluded that patients suitable for PCI or medical therapy could be safely managed medically and that PCI should be recommended when symptoms were not adequately controlled. Prognostic markers of increased risk must be excluded at the onset of symptom presentation, and this can be achieved non invasively using the clinical parameters of previous MI or CABG, left ventricular hypertrophy on the baseline resting electrocardiogram (ECG), time to 1mm ST depression on the exercise ECG (4–5min), a reduced ejection fraction (<40%) and increased end diastolic and systolic dimensions on echocardiography (5). The RITA-2 trial can be criticised because of the low use of stents (44, 9%) but stents only decrease the rate of angiographic restenosis not death or MI, and we have no data on drug eluting stents except on restenosis rates and their high cost with some concerns about the potential for rare allergic reactions (6). Medical therapy was suboptimal with only 13% taking lipid-lowering therapy, and the use of ACE inhibitors and thienopyridines along with established b-blockers and aspirin in combination was not a routine practice. A symptom relief strategy using medical therapy was not standardised and metabolic agents such as trimetazidine not utilised (7). We can see therefore that medical therapy should be utilised aggressively in all stable angina patients because there is time to do so. There is time to establish prognostic risk and the need for CABG in those at increased baseline risk (1). There remains no evidence to support routine CABG in those not at risk unless symptoms are intrusive to the quality of life. Until the Clinical Outcome Utilizing Revascularization and Aggressive drug Evaluation (COURAGE) trial (intensive medical therapy vs. PCI plus intensive medical therapy) and the BARI-2D trial of medical therapy and revascularization in type 2 diabetes report, we have no mandate to perform any type of PCI unless the patient is symptomatic in spite of medical therapy (8). It goes without saying that the medical therapy should be prognostically and symptomatically optimal (9). The medical management of stable angina has improved dramatically with our better understanding of the pathophysiology of coronary disease, the importance of risk reduction which includes lifestyle changes (weight loss and increased exercise) as well as drug therapy (9) and availability of symptom relieving drug therapy. PCI and CABG are important but need to be targeted to the right patient at the right time. All patients need to be treated as the individual they are, have the options explained and the reason for each strategy made clear. We have time – medical therapy gives us the time. Graham Jackson Editor