Cardiovascular Prevention and Rehabilitation — Written Clinical Reasoning

Model answer — Part A: the 48-year-old with LDL 5.2 and a family history

Frame the problem first. This is a primary-prevention consultation with two independent risk amplifiers: a markedly elevated LDL and a first-degree relative with premature coronary disease. The task is to calculate absolute risk, exclude secondary and inherited dyslipidaemia, and treat the total risk — not just the cholesterol [1].

Assessment. Calculate 5-year absolute CVD risk with the AusCVDRisk calculator using non-fasting lipids, blood pressure, smoking, diabetes status, renal function and albuminuria; his untreated LDL of 5.2 mmol/L with premature paternal MI pushes him toward the high-risk category and also triggers formal familial hypercholesterolaemia assessment [1]. Screen for secondary causes: TSH, HbA1c, renal and liver function, urinary protein, alcohol and medications. Examine for tendon xanthomata and corneal arcus, and apply the Dutch Lipid Clinic Network criteria — premature paternal MI scores, and LDL above 5.0 mmol/L scores further points; score 3–5 is possible FH and warrants family screening regardless [2].

Management. Lifestyle for everyone: Mediterranean dietary pattern (PREDIMED-grade evidence), 150 minutes of weekly moderate exercise, weight and alcohol review, and structured smoking avoidance advice [1]. Given his risk profile, commence a statin — moderate-to-high intensity depending on the calculated category — aiming for at least a 50% LDL reduction in line with the CTT dose-response, rechecking lipids and liver enzymes at 6–8 weeks and titrating rather than abandoning [3]. Address his blood pressure against his risk category, not an isolated threshold [1].

Close the loop. If FH is confirmed or probable, explain the inheritance, arrange cascade screening of first-degree relatives (including his siblings and children at the appropriate age), and plan long-term follow-up — the EAS consensus identifies cascade screening as the most cost-effective case-finding in preventive cardiology [2].

Model answer — Part B: post-NSTEMI secondary prevention with muscle aches

Hold the bundle. Her instinct to stop everything is the teachable moment: each component of the post-ACS bundle carries independent event-reduction evidence. Aspirin plus her P2Y12 inhibitor (guideline-defined duration), a high-intensity statin, a beta-blocker (Freemantle: ~23% mortality reduction post-MI), an ACE inhibitor (SAVE: 19% mortality reduction with LV dysfunction), and a cardiac rehabilitation referral — which itself reduces cardiovascular mortality by about 26% [8] [7] [6].

The statin problem gets a protocol, not a capitulation. Characterise the symptoms (symmetrical proximal ache, temporal relationship to the drug), check CK, TSH, vitamin D, renal function and interacting drugs. If CK is modestly elevated and she is systemically well: stop the statin for 2–4 weeks, then rechallenge at a lower dose or with an alternative agent once asymptomatic. SAMSON showed most statin-attributed symptoms are reproduced by placebo — share that evidence with her explicitly, because showing patients their own nocebo data helped half of them restart therapy [5].

Preserve LDL lowering by other means. If she remains genuinely intolerant after two or three structured attempts: ezetimibe 10 mg daily on the IMPROVE-IT evidence, alternate-day rosuvastatin exploiting its long half-life, and bempedoic acid as a further option — while being explicit that some statin, even low-dose, is usually better than none [4] [5].

Finish like a physician. Confirm the rehabilitation referral happened before discharge and enrolment at follow-up; screen for post-MI depression; support smoking cessation with pharmacotherapy if she smokes — cessation is the single intervention with randomised long-term mortality evidence; and set an LDL target (below 1.4 mmol/L and at least a 50% fall) with a 6–8 week recheck, so the conversation returns to numbers she can see improving [6] [9] [3].