You have to be careful about interpreting studies when thinking about an individual patient. From what you describe, this is someone how does not have a history of MI, nor does he have a myocardial infarction equivalent, i.e. DMII.
Usually the first line of therapy in a patient with hypertension, once lifestyle modifications have been attempted without success, is to start HCTZ. If someone has diabetes, you may think about starting an ACEI initially given its protective renal effects for the development of nephropathy.
A lot of you are saying that ASA should be started in this patient. Questions to think about:
What is the number needed to treat (or screen) in patients taking ASA for prophylaxis against MI?
What is the number needed to harm in patients taking ASA for prophylaxis against MI (GI bleeds for example)?
What symptoms or signs, when present, increase your confidence for starting ASA in someone who has not had an MI, does not have angina/chest pain/ecg changes/etc., and does not have DMII?
ASA is not benign.
Below is an abstract that kind of gets at what I'm saying. This patient does have hypertension so the following paper doesn't exactly get at this example, but worth thinking about.
Aspirin for the prevention of cardiovascular disease: calculating benefit and harm in the individual patient.
Loke YK, Bell A, Derry S.
Department of Clinical Pharmacology, University of Oxford, Radcliffe Infirmary, Oxford OX2 6HE.
[email protected]
AIMS: To estimate the absolute reduction in the risk of cardiovascular events and absolute increase in gastrointestinal haemorrhage associated with aspirin for individuals with different baseline risks. METHODS: Calculation of absolute treatment effects from estimates of: (i) baseline risks for cardiovascular event and gastrointestinal haemorrhage; and (ii) relative risks of these events with treatment. Baseline cardiovascular risks were derived from existing risk scores, and baseline risk of gastrointestinal haemorrhage from an observational cohort study. Changes in relative risks were obtained from clinical trial data. The effects of aspirin treatment were calculated in examples of two individuals with very different baseline risks. RESULTS: Treatment of a healthy 74-year-old man (blood pressure 144/88 mm Hg and no history of gastrointestinal disorder) would reduce his annual risk of a cardiovascular event from 2% to 1.74% (absolute risk reduction 0.26%, number needed to treat 385), but increase the gastrointestinal haemorrhage risk from 0.3% to 0.51% (absolute risk increase 0.21%, number needed to harm 476). In a 66-year-old obese man, following a transient ischaemic attack, and with a history of hospital treatment for a peptic ulcer, the annual risk of a cardiovascular event would be reduced from 5% to 4.35% (absolute risk reduction 0.65%, number needed to treat 153), but the risk of gastrointestinal haemorrhage would increase from 1.08% to 1.83% (absolute risk increase 0.75%, number needed to harm 133). CONCLUSIONS: Estimating benefit and harm by taking into account the baseline risks in each individual allows patients and doctors to judge for themselves the magnitude of the trade-offs involved in taking aspirin.