Cardiac Investigations — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mrs Patricia Walsh, 58 years old. ^[1]

Presenting complaint: Three months of exertional chest pain. The pain is central, pressing, comes on after walking 300 metres on flat ground or climbing two flights of stairs, and is relieved by 2 to 3 minutes of rest. It is occasionally associated with breathlessness. She has not had pain at rest. The symptoms are progressively limiting her daily activities. ^[1]

Past history:

• Type 2 diabetes (diagnosed 12 years ago, currently on metformin and empagliflozin, HbA1c 64 mmol/mol)
• Hypertension (on perindopril and amlodipine)
• Dyslipidaemia (on rosuvastatin 20 mg, LDL 2.1 mmol/L)
• Obesity (BMI 33)
• Former smoker (ceased 5 years ago, 30 pack-year history)
• Left ventricular hypertrophy on ECG (voltage criteria with strain pattern in lateral leads) ^[1]

Current medications:

• Metformin 1000 mg twice daily
• Empagliflozin 10 mg daily
• Perindopril 5 mg daily
• Amlodipine 10 mg daily
• Rosuvastatin 20 mg nocte
• Aspirin 100 mg daily ^[1]

Examination findings (trainee elicits):

• Comfortable at rest, no distress
• Blood pressure 148/92, heart rate 82 and regular
• BMI 33
• Normal jugular venous pressure
• Apex beat displaced 1 cm lateral to the mid-clavicular line, forceful but not sustained
• Normal heart sounds, no murmurs, no gallop
• Lungs clear, no peripheral oedema
• Normal peripheral pulses, no carotid or renal bruits
• ECG: sinus rhythm, voltage criteria for LVH (S in V1 plus R in V5 over 35 mm), with strain pattern (downsloping ST depression and T wave inversion in I, aVL, V5 to V6) ^[1]

Investigations available:

• Fasting lipids: total cholesterol 4.2, LDL 2.1, HDL 0.9, triglycerides 2.6 mmol/L
• HbA1c 64 mmol/mol
• eGFR 72 mL/min/1.73m2
• NT-proBNP 180 ng/L
• Chest X-ray: normal heart size, clear lung fields
• Echocardiogram: concentric LVH (septum 14 mm, posterior wall 13 mm), preserved LV systolic function (LVEF 62 percent), grade 1 diastolic dysfunction, no significant valvular disease, LA volume index 38 mL/m2 ^[1]

Candidate's structured presentation (model)

Opening statement: ^[1]

"Mrs Walsh is a 58-year-old woman with multiple cardiovascular risk factors — type 2 diabetes of 12 years, hypertension, dyslipidaemia, obesity, and a significant smoking history — who presents with a 3-month history of exertional chest pain that has all the features of typical angina: it is central, provoked by exertion at a predictable threshold, and relieved by rest within minutes. Her pre-test probability of coronary artery disease is high — estimated at over 50 percent using the 2019 ESC clinical likelihood model. ^[1]

Her key investigation challenge is that her resting ECG shows left ventricular hypertrophy with strain pattern, which makes exercise ECG uninterpretable. Her echocardiogram confirms concentric LVH with preserved systolic function but grade 1 diastolic dysfunction, consistent with hypertensive heart disease. Her NT-proBNP is mildly elevated, consistent with her diastolic dysfunction and LVH rather than overt heart failure. ^[1]

Her main problems are:

1. Probable stable coronary artery disease presenting as typical angina, in a high-risk patient
2. Hypertensive heart disease with concentric LVH and diastolic dysfunction
3. Multiple modifiable cardiovascular risk factors — diabetes, hypertension, dyslipidaemia, obesity
4. An ECG that precludes exercise ECG as a diagnostic test ^[1]

My approach is to perform CT coronary angiography as the initial investigation to define her coronary anatomy, recognising that her LVH with strain pattern makes exercise ECG uninterpretable and that her high cardiovascular risk warrants definitive anatomical assessment. If CTCA shows obstructive disease, I will proceed to invasive coronary angiography with physiological assessment (FFR) for intermediate lesions, guided by the severity of symptoms and the anatomical findings." ^[1]

Investigation plan: ^[1]

1. CT coronary angiography — the first-line test per the 2019 ESC CCS guidelines (PMID 31504425). Provides anatomical information with a high negative predictive value. In a patient with an uninterpretable ECG, CTCA avoids the pitfalls of exercise ECG. If the pre-test probability is considered very high (over 65 percent), direct invasive angiography may be more efficient — but CTCA is reasonable to characterise the extent and distribution of disease.
2. If CTCA shows obstructive CAD — invasive coronary angiography with FFR measurement for intermediate stenoses (under 0.80 is significant), followed by PCI or CABG depending on anatomy and symptoms.
3. If CTCA shows non-obstructive CAD — consider microvascular angina (the patient has risk factors and typical symptoms), proceed to coronary flow reserve assessment by PET or invasive methods if symptoms persist. Intensify medical therapy.
4. Optimise risk factor management in all scenarios — statin titration to achieve LDL under 1.4 mmol/L, intensify blood pressure control (consider adding an ARB or beta-blocker), glycaemic optimisation, weight management, cardiac rehabilitation. ^[1]

Examiner discussion questions

Q: "Why not just send her for invasive coronary angiography directly, given her high risk?" ^[1]

"That is a reasonable alternative and many cardiologists would do exactly that. The decision between CTCA and direct invasive angiography depends on the estimated pre-test probability and the local availability and expertise. The 2019 ESC CCS guidelines recommend CTCA for low-to-intermediate pre-test probability (approximately 15 to 50 percent) and allow either functional imaging or invasive angiography for higher probability. This patient's probability is high — she has typical angina plus diabetes and multiple risk factors — so direct invasive angiography is entirely defensible. ^[1]

My reasoning for CTCA first is that it is non-invasive, lower risk, and provides excellent anatomical information that can guide the decision about whether and how to proceed invasively. If CTCA shows three-vessel disease or left main involvement, I would refer for CABG. If it shows single-vessel proximal LAD disease, I would refer for PCI. If it shows non-obstructive disease, I avoid an unnecessary invasive procedure. The downside is that if CTCA shows significant disease, she needs a second procedure (invasive angiography), but the additional information from CTCA often justifies this. In a centre where CTCA is readily available and of high quality, this is a pragmatic approach. ^[1]

However, if I were more confident that she had obstructive disease — for example, if her symptoms were crescendo or she had dynamic ECG changes — I would go straight to invasive angiography." ^[1]

Q: "Her echocardiogram shows grade 1 diastolic dysfunction. What does this mean and does it change your management?" ^[1]

"Grade 1 diastolic dysfunction on echocardiography represents impaired myocardial relaxation without elevated filling pressure. The characteristic findings are an E to A ratio under 0.8 with an E velocity under 50 centimetres per second and a normal E to e-prime ratio under 8. This is the mildest form of diastolic dysfunction and is very common in patients with hypertension and left ventricular hypertrophy — exactly this patient's picture. ^[1]

Grade 1 diastolic dysfunction does not meet the criteria for heart failure with preserved ejection fraction (HFpEF), which requires symptoms and signs of heart failure plus evidence of elevated filling pressure (such as an E to e-prime ratio over 14, enlarged left atrium, elevated NT-proBNP, or more advanced diastolic dysfunction grades). Her NT-proBNP is only mildly elevated and her left atrium is borderline — this is not overt HFpEF. ^[1]

It does not change my investigation pathway for the chest pain, but it does reinforce the importance of aggressive blood pressure control to prevent progression of the diastolic dysfunction and hypertensive remodelling. I would ensure her blood pressure is well controlled (under 130 over 80) and consider an ARB or ACE inhibitor as the foundation, which she is already on. The SGLT2 inhibitor she is taking (empagliflozin) is beneficial for both her diabetes and her cardiovascular risk, and recent evidence supports SGLT2 inhibitors in heart failure with preserved ejection fraction as well." ^[1]

Q: "The ISCHEMIA trial showed that an invasive strategy does not reduce death or MI compared with medical therapy for stable patients. How does this influence your recommendation?" ^[1]

"The ISCHEMIA trial (PMID 32227755) is an important evidence benchmark, but I would apply it cautiously to this patient. The trial randomised patients with stable coronary disease and moderate-to-severe ischaemia to an initial invasive strategy versus an initial conservative strategy. It showed no significant difference in the composite primary outcome of cardiovascular death, MI, hospitalisation for unstable angina, heart failure, or resuscitated cardiac arrest. ^[1]

Key considerations for this patient: first, the ISCHEMIA trial excluded patients with recent MI, severely reduced ejection fraction, and left main disease — these high-risk patients were not studied. Second, the trial showed clear benefit of the invasive strategy for symptom relief: patients with angina had more symptom improvement with revascularisation. Third, this patient has limiting symptoms that are affecting her quality of life and daily activities. ^[1]

My interpretation: the ISCHEMIA trial does not mean we should never revascularise stable patients. It means that for truly stable patients with acceptable symptoms on optimal medical therapy, an initial conservative approach is a safe and evidence-based strategy. But in a patient with recurrent limiting angina — like Mrs Walsh — the trial's findings support an attempt to optimise medical therapy first (maximise antianginal medications: beta-blocker, calcium channel blocker, nitrates), and if symptoms persist, proceed to angiography and revascularisation for symptom control. The revascularisation is primarily for symptom relief in her case, not necessarily for prognostic benefit. I would be honest with the patient about this — the procedure is to improve her symptoms, and the long-term outcome is driven by optimal medical therapy and risk factor modification." ^[1]

Q: "She is already on aspirin. Should she be on dual antiplatelet therapy?" ^[1]

"No. Dual antiplatelet therapy (aspirin plus a P2Y12 inhibitor such as clopidogrel) is indicated after acute coronary syndrome or after coronary stenting — it is not indicated for primary prevention or for stable angina without prior intervention or ACS. She is currently on aspirin for primary prevention given her high cardiovascular risk, which is appropriate. If she undergoes PCI and stenting, she would then require dual antiplatelet therapy for the duration determined by the stent type and clinical context — typically 6 to 12 months for a drug-eluting stent in stable disease, though recent trials support shorter durations (1 to 3 months) followed by aspirin alone or a P2Y12 inhibitor alone. Until then, single antiplatelet therapy is correct." ^[1]