Ischaemic Cardiomyopathy from Asymptomatic Coronary Artery Disease

A 46-year-old man with hypertension and no prior cardiac history presented after five weeks of progressive exertional dyspnoea and bilateral leg oedema that extended to involve the scrotum and penis. In the week before admission, paroxysmal nocturnal dyspnoea developed. He reported palpitations but denied chest pain entirely — a pivotal detail. He consumed approximately 12 units of alcohol weekly and was a non-smoker. Hypertension was his only recognised cardiovascular risk factor, managed with ramipril and amlodipine.

On examination, heart rate was 103 bpm, oxygen saturation 96% on room air. Elevated jugular venous pressure (5 cm), bi-basal crackles, and abdominal distension with hepatomegaly and ascites pointed to advanced biventricular congestion. Initial ECG showed T-wave inversions in V4–V6, aVL, and lead I — suggesting lateral subendocardial ischaemia rather than an acute transmural event.

Chest X-ray showed cardiomegaly (CTR 0.56) with a right pleural effusion. CT pulmonary angiography excluded pulmonary embolism but demonstrated a globally enlarged heart with contrast reflux into the inferior vena cava and hepatic veins — a radiographic hallmark of severe right-sided congestion.

Figure 1

PA Chest Radiograph on Admission

Posteroanterior chest radiograph showing blunting of the right costophrenic angle (arrow) consistent with a right pleural effusion and an enlarged cardiac silhouette (CTR 0.56). In the context of this patient's presentation, cardiomegaly plus unilateral pleural effusion should immediately raise suspicion for decompensated heart failure, even in a young patient without prior cardiac history.

Figure 2

CT Pulmonary Angiogram — Cardiac Enlargement and Pleural Effusion

Soft tissue window (A) and pulmonary window (B). Panel A arrow highlights the globally enlarged, globular cardiac silhouette. Panel B arrow identifies the right pleural effusion. Contrast reflux into the inferior vena cava and hepatic veins — visible on the soft tissue window — is a CT correlate of elevated right atrial pressure and tricuspid regurgitation.

Transthoracic echocardiography was striking: severely dilated left ventricle with ejection fraction of only 16%, a moderate-sized apical thrombus, bi-atrial dilation, borderline dilated right ventricle with impaired systolic function, and moderate tricuspid regurgitation. These findings prompted therapeutic-dose low molecular weight heparin for the thrombus and initiated the differential diagnosis of ischaemic versus non-ischaemic cardiomyopathy.

Figure 3

Transthoracic Echocardiogram — Severely Dilated LV with Apical Thrombus

Four panels from the echocardiogram: A) Parasternal long axis — severely dilated LV; B) Apical four-chamber — LV apical thrombus (arrow) and dilated left atrium; C) Close-up of apical thrombus (arrow); D) Colour Doppler showing functional mitral regurgitation with eccentric jet (arrow) secondary to annular dilation. The apical thrombus in the context of severely reduced EF is a high-risk finding mandating anticoagulation and regular surveillance imaging. RV = right ventricle; RA = right atrium; Ao = aortic valve.

Aggressive diuresis with bumetanide led to progressive improvement in liver and renal function. A comprehensive heart failure regimen — bisoprolol, dapagliflozin, ivabradine, sacubitril/valsartan, and spironolactone — produced a satisfactory clinical response. Serial laboratory trending confirmed the hepatopathy was congestive rather than intrinsic.

Figure 4

Blood Investigations — Admission, Post-Treatment, and Discharge

Serial laboratory values demonstrating the parallel trajectory of ALT normalisation and clinical improvement with IV diuresis. This pattern — markedly elevated transaminases on admission, followed by rapid normalisation with decongestion — is the biochemical signature of congestive hepatopathy rather than intrinsic hepatocellular injury.

Pre-discharge cardiac MRI with basic late gadolinium enhancement confirmed the ischaemic aetiology: a severely dilated left ventricle with nonviable mid-to-apical inferior and inferoseptal transmural post-ischaemic scarring with hypokinesia, consistent with Type I silent myocardial ischaemia progressing to dilated ischaemic cardiomyopathy. Notably, no apical thrombus was identified on MRI following anticoagulation. At three-month follow-up, the ejection fraction had improved to 41% on optimal medical therapy.

Figure 5

Cardiac MRI — Late Gadolinium Enhancement Identifying Post-Ischaemic Scar

A) Inferoseptal transmural post-ischaemic scar (arrow) in the distribution of the right coronary artery. B) Apical inferior transmural scar (arrow). The transmural pattern of late gadolinium enhancement distinguishes ischaemic from non-ischaemic cardiomyopathy — non-ischaemic causes typically show midmyocardial or subepicardial enhancement. These non-viable segments would not benefit from revascularisation, informing the decision to defer angiography while optimising medical therapy.

Discussion

This case illustrates Type I silent myocardial ischaemia — coronary artery disease causing asymptomatic ischaemic events in a patient with no prior CAD history. The mechanism of pain absence remains incompletely understood but involves altered cardiac nociception, elevated endorphin levels, brief ischaemic episodes, and cytokine interference with pain pathways. Up to 80% of transient ischaemic episodes in patients with CAD may be asymptomatic, meaning the absence of angina does not exclude progressive myocardial damage. The dramatic presentation here — severe ventricular dysfunction, AKI, congestive hepatopathy with ALT over 2000 IU/L, and a left ventricular thrombus — all without a single episode of chest pain — makes this a paradigm case for the silent ischaemia concept. The markedly elevated ALT reflected congestive hepatopathy from raised hepatic venous pressure transmitted via tricuspid regurgitation and right atrial hypertension; its normalisation with diuresis confirmed this mechanism rather than intrinsic liver disease.

From a management standpoint, the trajectory of EF improvement from 16% to 41% at three months on guideline-directed medical therapy highlights the potential for reverse remodelling even in advanced ischaemic cardiomyopathy. The REVIVED trial showed modest quality-of-life and EF benefits from PCI in this population without mortality reduction, while the STICH trial demonstrated CABG benefit primarily in reducing sudden death and pump failure in selected patients. When cardiac MRI identifies predominantly non-viable scar tissue, revascularisation is unlikely to confer functional benefit — medical optimisation should precede any revascularisation decision. Clinicians evaluating young patients with new-onset heart failure and dilated cardiomyopathy should always perform cardiac MRI before concluding the aetiology is non-ischaemic: the transmural subendocardial enhancement pattern is the gold standard for distinguishing ischaemic from non-ischaemic cardiomyopathy and directly informs treatment planning.