FP10 Prescribing Exercise
GP Secondary Prevention Review

Aspirin irreversibly inhibits cyclo-oxygenase-1 (COX-1), blocking thromboxane A₂ synthesis and thereby reducing platelet aggregation. In secondary prevention post-MI, aspirin reduces the risk of recurrent MI, stroke and cardiovascular death by approximately 25% (Antithrombotic Trialists' Collaboration). It is continued indefinitely following NSTEMI and PCI.

After drug-eluting stent (DES) implantation, aspirin forms one half of dual antiplatelet therapy (DAPT). The two mechanisms are complementary: aspirin blocks the COX-1 / thromboxane A₂ pathway; ticagrelor blocks the ADP / P2Y12 pathway. Both are required to prevent in-stent thrombosis — one drug alone is insufficient.

Aspirin irritates the gastric mucosa directly and also systemically by inhibiting COX-1-mediated prostaglandin production (prostaglandins protect the stomach lining). Gastro-resistant formulations delay aspirin release until the small intestine, reducing GI side effects. However, note that a PPI (e.g., omeprazole) should be co-prescribed in patients with additional GI risk factors (history of ulcer, concurrent NSAID use, Helicobacter infection). Mr Park's discharge letter should be checked for PPI prescribing.

The 300mg loading dose was given at the time of the acute event to rapidly saturate COX-1. For maintenance secondary prevention, 75mg OD gives equivalent platelet inhibition with substantially less GI toxicity. Higher doses do not confer additional cardiovascular benefit but do increase bleeding risk (CURRENT-OASIS 7 trial).

Ticagrelor is a reversible P2Y12 ADP receptor antagonist. Unlike clopidogrel (a prodrug requiring hepatic conversion), ticagrelor acts directly and has predictable platelet inhibition regardless of CYP2C19 polymorphisms. The PLATO trial demonstrated superior cardiovascular outcomes versus clopidogrel in ACS patients, including a significant reduction in cardiovascular death.

DAPT = aspirin + ticagrelor for a minimum of 12 months following PCI with drug-eluting stent. Mr Park received his DES in January 2026, so DAPT should continue until at least January 2027. The GP must not switch or stop ticagrelor without cardiology agreement.

For ACS patients (both STEMI and NSTEMI), ticagrelor is preferred over clopidogrel per NICE TA236 and ESC guidelines because of superior outcomes in the PLATO trial. Clopidogrel may be used if ticagrelor is not tolerated (e.g., intractable dyspnoea) or in patients with a high bleeding risk. The GP should not switch without cardiologist input.

Post-ACS patients require high-intensity statin therapy regardless of baseline cholesterol. Atorvastatin 80mg is a high-intensity statin (reduces LDL by ≥50%). The evidence base (PROVE IT-TIMI 22, TNT trial) shows that more intensive LDL lowering after MI reduces recurrent cardiovascular events significantly — independent of starting LDL level.

NICE NG185 recommends that for secondary prevention post-ACS, the LDL-C target is <1.4 mmol/L AND ≥50% reduction from baseline. Mr Park's LDL is currently 1.8 mmol/L — not at target. Options include checking compliance, considering ezetimibe 10mg OD as add-on therapy, or referral to lipids clinic for a PCSK9 inhibitor if targets remain unmet.

HMG-CoA reductase (the enzyme blocked by statins) is most active at night, when cholesterol synthesis peaks. Taking atorvastatin at night maximises its efficacy. Unlike some statins (e.g. simvastatin, which has a short half-life and must be taken at night), atorvastatin has a long half-life (~14 hours) and can theoretically be taken at any time — but nocte dosing remains conventional and the standard instruction on FP10.

LFTs: Baseline before starting; recheck at 3 months and 12 months. If ALT >3× ULN, reduce dose or consider alternative. Mr Park's ALT is 28 U/L — normal. Myopathy: Ask about unexplained muscle pain, tenderness or weakness at each review. If CK >5× ULN with symptoms, stop statin. Risk of myopathy increases significantly with fibrates or ciclosporin. Diabetes: Statins are associated with a small increased risk of new-onset T2DM — Mr Park already has T2DM, so this is not a new concern.

ACE inhibitors reduce angiotensin II production, leading to vasodilation, reduction in preload and afterload, and prevention of adverse cardiac remodelling. Following MI — particularly anterior MI with LAD involvement as in Mr Park — there is risk of left ventricular dilatation (remodelling) and development of heart failure. The AIRE and TRACE trials demonstrated that ramipril significantly reduces mortality, re-infarction and progression to heart failure post-MI.

NICE NG185 recommends ACE inhibitor for all patients post-MI, regardless of LV function, starting within 24h of diagnosis and up-titrating to target dose. Ramipril 10mg OD is the target maintenance dose for secondary prevention. It also benefits Mr Park's T2DM by reducing proteinuria and protecting renal function (MICRO-HOPE trial).

ACE inhibitor cough affects ~10–15% of patients (more common in women and South Asian patients) — a dry, persistent cough due to bradykinin accumulation. If this develops, switch to an ARB (candesartan or valsartan). Angioedema is rare but serious — absolute contraindication to re-challenge, switch to ARB. Hyperkalaemia — monitor K⁺ especially if combined with potassium-sparing diuretics. AKI — remind patient about sick-day rules (SADMANS): withhold during vomiting, diarrhoea, dehydration or before contrast procedures.

Ramipril is available in both tablet and capsule formulations. The capsule is the most common community formulation and tends to be better tolerated. On FP10, specifying the formulation avoids dispensing errors if both forms are available in the same dose. The choice of capsule vs tablet does not affect clinical efficacy.

Beta-blockers competitively antagonise catecholamines at β1 receptors, reducing heart rate, myocardial oxygen demand, and sympathetic tone on the vulnerable post-infarct myocardium. Benefits post-MI include: reduction in sudden cardiac death (ventricular arrhythmias), prevention of LV remodelling, and in patients with HFrEF, reduction in mortality (CIBIS-II trial). NICE NG185 recommends beta-blockade for all post-MI patients, with up-titration to maximum tolerated dose.

Bisoprolol is a highly cardioselective β1 blocker with minimal β2 effects at therapeutic doses, making it safer in patients with mild asthma or COPD (though still use cautiously in asthma). In heart failure with reduced ejection fraction (HFrEF), only three beta-blockers have proven mortality benefit: bisoprolol, carvedilol, and metoprolol succinate. In Mr Park's post-MI setting, bisoprolol is the standard first-line choice in UK practice.

Mr Park's resting HR is 58 bpm today. This is at the lower acceptable limit for up-titration. In clinical practice, you might hold at 2.5mg today and recheck in 2 weeks rather than rushing to 3.75mg. Document your decision and rationale.

Never stop abruptly: Sudden discontinuation of beta-blockers in post-MI patients can precipitate rebound tachycardia, hypertension, and even re-infarction due to upregulation of beta-receptors. Always taper over 1–2 weeks. Counsel the patient explicitly. Asthma: Beta-blockers are contraindicated in asthma. Mr Park has no asthma — but confirm at each review. COPD: Bisoprolol can be used carefully in COPD — benefits generally outweigh risks in post-MI patients.

Glyceryl trinitrate (GTN) is an organic nitrate that releases nitric oxide (NO) in vascular smooth muscle, causing vasodilation — predominantly venodilation, reducing preload and myocardial oxygen demand, with some arterial dilation reducing afterload. Used acutely for episodes of angina or chest pain. Mr Park may experience angina from residual coronary disease or demand ischaemia, particularly on exertion — GTN spray for PRN use is standard post-ACS/PCI prescribing.

GTN must be given sublingually, not swallowed. If swallowed, GTN undergoes extensive first-pass hepatic metabolism and is rendered ineffective. The sublingual route delivers GTN directly into the systemic circulation via the rich oral mucosal vasculature, bypassing the liver. Onset of action by sublingual spray is 1–3 minutes. If Mr Park swallows the spray, he will receive no therapeutic benefit at all.

The instruction "spray under the tongue" must be clearly communicated verbally and in writing. This is a common patient counselling point tested in OSCEs.

GTN is absolutely contraindicated with sildenafil (Viagra), tadalafil, or other PDE5 inhibitors. The combination causes severe, potentially fatal hypotension. Ask Mr Park about PDE5 inhibitor use and document this in his notes. If he requires treatment for erectile dysfunction (common in cardiovascular patients), a specialist cardiology referral is needed to assess safety before initiating any vasodilator therapy.

Metformin remains the first-line oral glucose-lowering agent for T2DM in NICE NG28 guidelines. Its mechanisms include: reducing hepatic glucose production (primary mechanism via AMPK activation), improving peripheral insulin sensitivity, and modestly reducing intestinal glucose absorption. Crucially, metformin does not cause hypoglycaemia (unlike sulphonylureas or insulin), is weight-neutral or causes modest weight loss, and has a strong evidence base for cardiovascular protection in T2DM (UKPDS trial — 36% reduction in all-cause mortality).

In Mr Park's case, the combination of T2DM and recent MI makes metformin especially appropriate — it does not worsen cardiovascular outcomes and may confer additional benefit. It is safe with eGFR 71 (contraindicated below eGFR 30, caution below 45).

Metformin causes GI side effects (nausea, diarrhoea, abdominal discomfort) in up to 20–30% of patients, particularly at higher doses. Starting at 500mg BD and up-titrating every 4 weeks reduces GI intolerance significantly. The slow-release formulation (Metformin SR) is an alternative if standard metformin is not tolerated. Mr Park was started at 500mg BD at discharge — this is appropriate at 10 weeks.

The HbA1c at 10 weeks (62 mmol/mol) is only marginally above the 48 threshold. With ongoing dose titration and lifestyle modification, a target of below 53 mmol/mol is reasonable in this patient with cardiovascular disease. Review HbA1c in 3 months.

SADMANS is the mnemonic for medications to withhold during acute illness (dehydration, vomiting, diarrhoea, fever, reduced oral intake). The SADMANS drugs are:

Mr Park should withhold ramipril AND metformin if he becomes acutely unwell. He should be given a written sick-day rules card and this should be documented in his notes. He can restart both medications once he has recovered and is eating and drinking normally.

HbA1c every 3 months until stable, then every 6 months. eGFR and U&E annually (metformin is renally cleared — review dose if eGFR falls below 45; stop if below 30). Vitamin B12 — long-term metformin use can cause B12 deficiency due to reduced ileal absorption. Check B12 annually in patients on metformin for >4 years or if symptoms of peripheral neuropathy develop.