A 27-year-old man with a past medical history notable for a motor vehicle accident (MVA) 5 months prior presented with worsening exertional dyspnoea and lower extremity oedema that was slowly progressive since his MVA. He denied any preceding viral illness, sick contacts, or travel. Initial laboratory evaluation was notable for evidence of hepatic injury (aspartate aminotransferase 632 IU/L and alanine transferase 248 IU/L), normal troponin I levels (0.04 ng/mL), and an elevated B-type natriuretic peptide level at 1787 pg/mL. A transthoracic echocardiogram (TTE) showed normal left ventricle (LV) chamber size (LV end-diastolic diameter 5.6 cm) and severely decreased LV systolic function with an estimated ejection fraction of <20% and evidence of an apical thrombus. He was given intravenous diuretics with improvement in symptoms. Given concern for low-output heart failure, he was transferred to our institution for further workup and management. On admission, the patient confirmed the above history, noting that, at the time of his MVA, he suffered significant chest wall trauma having struck the steering wheel during the accident, with ongoing chest discomfort he attributed to musculoskeletal pain. He did not seek further evaluation after the accident and his pain eventually resolved. In the following months, he noted worsening exertional dyspnoea, orthopnoea, intermittent chest tightness, and intermittent episodes of paroxysmal nocturnal dyspnoea. His admission vital signs showed tachycardia to 109 b.p.m. and a blood pressure of 98/60 mm Hg. Physical exam was notable for jugular venous distension, abdominal distension with ascites, and pitting oedema of the bilateral lower extremities. A 12-lead electrocardiogram (ECG) demonstrated sinus tachycardia with low voltage, premature ventricular contractions, and a prior anterolateral infarct pattern (). His past medical history was notable for prior MVA and prior alcohol, tobacco, and marijuana use, all discontinued following his MVA. The differential diagnosis included autoimmune or viral myocarditis, inherited or idiopathic cardiomyopathy, and stress cardiomyopathy amongst other diagnoses. Ischaemic cardiomyopathy was initially felt to be less likely based on the patient’s age, though the presence of an anterolateral infarct pattern on ECG and an LV apical thrombus increased suspicion for a prior ischaemic insult. A TTE was obtained and re-demonstrated severe biventricular systolic dysfunction in addition to an apical aneurysm vs. pseudo-aneurysm with evidence of thrombus (see, ). A subsequent cardiac magnetic resonance imaging scan confirmed severe biventricular systolic dysfunction with full-thickness late-gadolinium enhancement involving all apical LV segments, with apical aneurysm formation in addition to an associated layering thrombus ( and ). Left coronary angiography revealed a subtotal occlusion of the mid-LAD with thrombosis in myocardial infarction 2 antegrade flow (see, ), which was also filled via right-to-left collaterals from the right coronary artery. Right heart catheterization showed a mean right atrial pressure of 16 mm Hg, pulmonary arterial pressure of 54/31 mm Hg with a mean of 42 mm Hg, and pulmonary capillary wedge pressure of 29 mm Hg. Cardiac output was severely reduced with a cardiac index of 1.3 L/min/m2 by Fick and 1.27 L/min/m2 by thermodilution. The patient was diagnosed with acute low-output heart failure with reduced ejection fraction in the setting of a severe cardiomyopathy, thought to be due to an unrecognized traumatic coronary injury (sustained during prior MVA) and subsequent adverse LV remodelling. The patient’s volume status was managed with intravenous diuretics. He was unable to consistently tolerate low-dose renin–angiotensin–aldosterone system blockade or beta-blockade given his baseline hypotension and low cardiac output. He was able to tolerate dapagliflozin and low-dose spironolactone, which he continued on discharge. Milrinone was eventually initiated to augment cardiac output, and a central line was placed for the continuation of therapy at home while the patient underwent further workup and consideration of advanced heart failure therapies. His LV apical thrombus was managed with continuous anticoagulation, and he was discharged on warfarin. The patient’s subsequent course was complicated by recurrent heart failure exacerbations with readmission to the cardiac intensive care unit, subsequent Coronavirus Disease 2019 (COVID-19) infection, and delirium. He was repeatedly evaluated by the multi-disciplinary heart team for consideration of advanced heart failure therapies. Severe RV dysfunction precluded LV assist device placement. The patient had developed significant and progressive debility and severe malnutrition despite inotropes in addition to aggressive nutritional and other supportive care. There were also concerns regarding his social support and recent substance use. As such, he was not deemed to be a heart transplant candidate. He was discharged home with oral diuretics, dapagliflozin, and low-dose spironolactone as tolerated with close follow-up for labs, possible medication titration, and further management of advanced heart failure. He was evaluated for a second opinion at another major transplant referral centre and was not deemed to be a candidate for advanced therapies. He was unfortunately readmitted with acutely decompensated heart failure, this time complicated by recurrent ascites requiring paracenteses, mesenteric ischaemia, encephalopathy, continued dysphagia/malnutrition, and renal dysfunction. At the time of this manuscript, he had been discharged with home hospice.