Cardiac Investigations Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Davidson is a 66-year-old man who presents with a 6-month history of exertional chest tightness. The discomfort comes on after walking approximately 150 metres on flat ground or climbing one flight of stairs, is central and pressing in quality, and is relieved by 3 to 5 minutes of rest. He has not experienced pain at rest. [1]

His past history includes hypertension, type 2 diabetes, dyslipidaemia, and a prior anterior STEMI treated with primary PCI and a drug-eluting stent to the proximal LAD 4 years ago. He also has permanent atrial fibrillation, for which he takes apixaban. [1]

His current medications are aspirin 100 mg daily, atorvastatin 80 mg, metformin 1000 mg twice daily, empagliflozin 10 mg daily, bisoprolol 5 mg daily, ramipril 5 mg daily, and apixaban 5 mg twice daily. [1]

On examination, his blood pressure is 142/84, he is in atrial fibrillation at a rate of 78, and cardiovascular examination is otherwise unremarkable. His resting ECG shows atrial fibrillation with left bundle branch block (QRS 150 ms). His echo from 6 months ago showed a left ventricular ejection fraction of 45 percent with anterior hypokinesia, mild LV dilatation, and no significant valvular disease. [1]

His main problem is recurrent angina in the setting of known ischaemic heart disease with a prior stent, likely representing in-stent restenosis, progression of disease in other vessels, or microvascular dysfunction. [1]

My approach is to risk-stratify him with functional imaging or CT coronary angiography, recognising that his LBBB makes exercise ECG uninterpretable, and then proceed to invasive coronary angiography if ischaemia is demonstrated, because he has established CAD and recurrent symptoms." [1]

Examiner probing questions and model answers

Q1: "This patient has left bundle branch block. How does that influence your choice of stress test?" [1]

"Left bundle branch block renders exercise ECG uninterpretable because the baseline ST changes associated with LBBB — which are concordant with the QRS complex — make it impossible to detect ischaemic ST change during exercise. This is a classic contraindication to exercise ECG, along with pre-excitation, digoxin effect, significant resting ST depression, LVH with strain, and paced rhythms. [1]

The options for stress testing in this patient are stress imaging or CT coronary angiography. For stress imaging, myocardial perfusion imaging (MPI) with SPECT or PET is the preferred modality in LBBB because it directly assesses perfusion rather than relying on ECG or wall motion. There is a caveat: LBBB can cause septal perfusion defects even in the absence of LAD disease, because the dyssynchronous septal contraction alters septal perfusion. This is more pronounced with exercise stress than with pharmacological vasodilator stress. For this reason, vasodilator stress (regadenoson or adenosine) is preferred over exercise in LBBB. PET with coronary flow reserve measurement is the most accurate single test in LBBB. [1]

Alternatively, CT coronary angiography can be used to define the coronary anatomy non-invasively. CTCA has a high negative predictive value and would reliably exclude obstructive CAD. However, in this patient who has known CAD with a prior stent, CTCA may be less useful because stent artefact can obscure in-stent restenosis, and his calcium burden is likely high given his risk factors. For a patient with known CAD and recurrent symptoms, I would favour invasive coronary angiography directly, guided by the clinical picture." [1]

Q2: "Would you consider CT coronary angiography as the first-line test here?" [1]

"In a patient with no known CAD and a low-to-intermediate pre-test probability, CT coronary angiography would be my first-line test per the 2019 ESC chronic coronary syndromes guidelines (PMID 31504425). The SCOT-HEART trial (PMID 30145934) showed that CTCA improved diagnostic certainty and reduced fatal and non-fatal MI by 41 percent over 5 years. [1]

However, this patient has established CAD — a prior STEMI with a stent. CTCA is less useful in patients with known CAD for two reasons: first, prior stents create beam-hardening artefacts that obscure in-stent restenosis, particularly in smaller stents (under 3 mm); second, patients with established CAD typically have heavier calcification, which degrades CTCA image quality through calcium blooming. This patient also has a high pre-test probability — the question is not whether he has CAD but where the obstructive disease is and what to do about it. [1]

For this reason, I would proceed directly to invasive coronary angiography rather than CTCA. Invasive angiography provides definitive anatomical assessment, allows FFR measurement for intermediate stenoses, and enables immediate PCI if a treatable lesion is found. The decision to proceed directly to angiography without prior functional testing is appropriate when the pre-test probability is high and the patient has established disease." [1]

Q3: "What if his stress test shows a large area of inducible ischaemia — does the ISCHEMIA trial change your approach?" [1]

"The ISCHEMIA trial (PMID 32227755) showed that in patients with stable coronary disease and moderate-to-severe ischaemia, an initial invasive strategy did not reduce the rate of death or myocardial infarction compared with an initial conservative strategy of optimal medical therapy, over a median follow-up of 3.3 years. The composite primary outcome was 13.3 percent in the invasive group versus 15.5 percent in the conservative group (P equals 0.34). [1]

However, several important caveats apply to this patient. First, the ISCHEMIA trial excluded patients with recent MI (within 2 months), significantly reduced ejection fraction (under 35 percent), and left main disease. This patient has a prior STEMI and an LVEF of 45 percent — he would have been borderline for inclusion. Second, the ISCHEMIA trial showed that the invasive strategy was superior for symptom control: patients with angina had more relief with revascularisation. Third, this patient has recurrent symptoms despite what appears to be adequate medical therapy (beta-blocker, ACE inhibitor, antiplatelet). [1]

My interpretation: the ISCHEMIA trial supports an initial conservative strategy for truly stable patients with moderate ischaemia and acceptable symptoms. But in a patient with recurrent limiting angina despite optimal medical therapy, revascularisation is indicated for symptom relief. I would optimise his medical therapy first — increase the beta-blocker if tolerated, add a long-acting nitrate, ensure his antianginal regimen is maximised — and if symptoms persist, proceed to angiography with intent to revascularise. The key is that revascularisation is primarily for symptom control in this patient, with prognostic benefit in high-risk anatomy." [1]

Q4: "His echocardiogram shows an ejection fraction of 45 percent with anterior hypokinesia. What does the anterior hypokinesia signify?" [1]

"The anterior hypokinesia is the residual wall motion abnormality from his prior anterior STEMI. The LAD territory (anterior wall, septum, and apex) was damaged by the infarction 4 years ago. The scarred myocardium does not contract normally, producing the regional wall motion abnormality seen on echo. [1]

The ejection fraction of 45 percent tells me that the infarct was moderate in size — the overall pump function is only mildly reduced, suggesting that a significant portion of the LV remains viable and functioning. The anterior hypokinesia represents a mixture of scarred tissue (from the infarct core) and potentially hibernating or stunned myocardium (tissue that is underperfused but still viable). [1]

If I wanted to determine whether there is viable myocardium in the anterior wall that could recover with revascularisation, I would perform a cardiac MRI with late gadolinium enhancement and low-dose dobutamine stress. The transmural extent of LGE would tell me how much scar there is: under 25 percent LGE is viable and likely to recover; over 50 percent is predominantly scar and unlikely to recover. Low-dose dobutamine stress echo or MRI can also demonstrate contractile reserve in hibernating myocardium. In practice, the anterior wall of a patient 4 years post-STEMI with a patent stent is likely to be fixed scar rather than hibernating — the time course makes chronic hibernation less likely." [1]

Q5: "How would you counsel this patient about the risks of coronary angiography?" [1]

"I would explain that coronary angiography is a well-established and generally safe procedure, but like all invasive procedures it carries risks. The main risks are: bleeding or bruising at the access site (radial or femoral artery) — this is the most common complication; contrast-related kidney injury — he has diabetes, which increases this risk, so I would ensure he is well hydrated before and after the procedure and consider holding nephrotoxic medications; a small risk of stroke (under 0.5 percent), heart attack (under 0.5 percent), or major bleeding requiring transfusion; and a very small risk of death (under 0.1 percent). [1]

I would also explain that the procedure may lead to an intervention — if a significant narrowing is found, the cardiologist may place a stent during the same procedure. Stenting carries additional risks including restenosis and stent thrombosis, which is why he would need dual antiplatelet therapy afterwards. I would discuss the fact that he is already on apixaban for atrial fibrillation, and adding dual antiplatelet therapy increases bleeding risk — this is the triple therapy dilemma, and the regimen would need careful planning with his cardiologist, typically involving a short course of triple therapy followed by de-escalation to dual therapy (an oral anticoagulant plus a single antiplatelet, usually clopidogrel). [1]

I would emphasise that the benefit of the procedure — identifying and treating the cause of his recurrent angina — outweighs the risks, and that the procedure can be both diagnostic and therapeutic." [1]

Short Case Discussion

Scenario: "Interpret this echocardiogram and cardiac MRI"

Candidate presentation (model): [1]

"I am reviewing the echocardiogram and cardiac MRI for this 55-year-old woman with exertional dyspnoea. [1]

The echocardiogram shows a normal-sized left ventricle with preserved systolic function, ejection fraction 60 percent by Simpson method. The left ventricular wall thickness is increased, with concentric hypertrophy — the septum measures 15 mm and the posterior wall 14 mm. The left atrium is moderately dilated, volume index 42 mL per square metre. Tissue Doppler shows a reduced septal e-prime of 6 cm per second with an E to e-prime ratio of 16, indicating elevated left ventricular filling pressure. The right ventricle is normal in size and function. There is mild mitral regurgitation and trace tricuspid regurgitation with an estimated RV systolic pressure of 38 mmHg. There is a small pericardial effusion. [1]

In summary, the echo shows concentric left ventricular hypertrophy with preserved ejection fraction, grade 2 diastolic dysfunction, left atrial dilatation, and a small pericardial effusion. [1]

The cardiac MRI confirms the concentric LVH. The key finding is the late gadolinium enhancement pattern: there is diffuse subendocardial late gadolinium enhancement that is difficult to nullify — no normal reference myocardium can be identified for signal nulling. The native T1 mapping is markedly elevated at 1,050 milliseconds (normal under 1,020 at 1.5 Tesla), and the extracellular volume fraction is elevated at 42 percent (normal under 29 percent). These findings are consistent with cardiac amyloidosis. [1]

The clinical context — a 55-year-old with exertional dyspnoea, concentric LVH, low voltages on the surface ECG (which I would check), and raised NT-proBNP — further supports the diagnosis." [1]

Examiner: "What is your next step to confirm the diagnosis?" [1]

"The next step is to differentiate the type of amyloidosis — AL (light chain) versus ATTR (transthyretin) — because the treatment and prognosis differ fundamentally. I would perform: [1]

First, technetium-99m pyrophosphate (or DPD or HMDP) scintigraphy. In ATTR cardiac amyloidosis, grade 2 or 3 cardiac uptake (heart equal to or greater than ribs) is diagnostic in the absence of a monoclonal protein. This non-invasive approach avoids endomyocardial biopsy in most ATTR cases. [1]

Second, I would exclude AL amyloidosis with serum free light chain assay and serum and urine immunofixation. If a monoclonal protein is present, the scintigraphy result is not diagnostic and I would proceed to biopsy (bone marrow and/or cardiac). [1]

If ATTR is confirmed by scintigraphy with negative monoclonal screen, I would refer to clinical genetics for TTR sequencing to differentiate wild-type (senile) ATTR from hereditary ATTR, as this has implications for family screening. [1]

The treatment differs: ATTR amyloidosis is treated with tafamidis (a TTR stabiliser) which slows disease progression and improves survival. AL amyloidosis is treated with chemotherapy directed at the underlying plasma cell clone. This distinction is critical and is why the workup is essential before treatment." [1]

Examiner: "How would you interpret a subendocardial LGE pattern in a coronary territory versus the diffuse pattern you describe?" [1]

"The pattern of late gadolinium enhancement is the most important discriminator in cardiac MRI tissue characterisation. There are two fundamental categories: [1]

Ischaemic LGE follows a coronary territory and always starts at the subendocardium — the region most vulnerable to ischaemia because it is furthest from the epicardial coronary arteries. The LGE extends from subendocardial to transmural depending on infarct size. The location conforms to the perfusion territory of the culprit vessel: anterior or anteroseptal for the LAD, inferior for the RCA, and lateral for the circumflex. This is what you see after myocardial infarction. [1]

Non-ischaemic LGE does not follow a coronary territory and does not start at the subendocardium. The patterns are: midwall (intramural) enhancement — seen in dilated cardiomyopathy, myocarditis (septal), sarcoidosis, and Chagas disease; epicardial enhancement — seen in myocarditis (lateral epicardial), sarcoidosis, and hypersensitivity myocarditis; patchy focal enhancement at the RV insertion points — seen in hypertrophic cardiomyopathy; and diffuse subendocardial circumferential enhancement — the classic pattern of cardiac amyloidosis, where the infiltration is global. [1]

The key teaching point: if the LGE touches the subendocardium in a coronary distribution, it is ischaemic (infarction). If it spares the subendocardium or is diffuse, it is non-ischaemic. This single observation redirects the entire diagnostic pathway." [1]