Rapidly Failing Heart With Rare Aneurysm Ends in Transplant, Case Report Shows

A 52-year-old man whose heart ballooned from moderate enlargement to massive dilatation within a single month, forming a rare inferolateral aneurysm along the way, ultimately needed a heart transplant to survive. The case, reported in Frontiers in Cardiovascular Medicine by a team from Wuhan No. 1 Hospital and the Affiliated Tianyou Hospital of Wuhan University of Science and Technology, describes an uncommon collision of two cardiac conditions: dilated cardiomyopathy, a disease in which the heart muscle stretches and weakens, and an ischemic injury to the heart’s lateral wall caused by blocked coronary arteries. Left ventricular aneurysms, pouch-like bulges in the heart wall that move paradoxically during each heartbeat, most commonly follow transmural myocardial infarction and are only rarely described in dilated cardiomyopathy.

Seeing one arise in a patient with newly diagnosed dilated cardiomyopathy, and seeing it develop this fast, is what makes the report stand out. The story began deceptively. After an ordinary upper respiratory infection, the man developed chest tightness and shortness of breath that worsened at night and with exertion. He had smoked about twenty cigarettes a day for more than three decades and had long-standing type 2 diabetes treated with metformin, but he denied any known history of coronary disease, hypertension, or dyslipidemia. On admission his vital signs were relatively stable, with a blood pressure of 130/70 mmHg, although the electrocardiogram recorded sinus tachycardia at 131 beats per minute with intraventricular conduction delay. Laboratory tests showed elevated inflammatory markers, including a high-sensitivity C-reactive protein of 25.75 mg/L, and markedly elevated fasting glucose of 18.98 mmol/L, but his cardiac enzymes, kidney and liver function, and viral myocarditis antibodies were all within normal ranges, an early hint that a simple viral heart inflammation was not the culprit.

The first echocardiogram already told a troubling story: an enlarged left atrium, a dilated left ventricle with an end-diastolic diameter of 6.37 centimeters, and a reduced ejection fraction of 36 percent. Crucially, the damage was not uniform. The posterior wall of the ventricle at the level of the papillary muscles moved poorly and thickened abnormally during contraction. That segmental pattern, combined with poor R-wave progression on the electrocardiogram, pushed the team to perform coronary angiography on hospital day four rather than attributing the picture entirely to cardiomyopathy.

The angiogram revealed the second disease process at work. The left main and left anterior descending arteries were clean with normal TIMI 3 flow, but the left circumflex artery showed diffuse severe stenosis of roughly 80 percent distal to the origin of its first obtuse marginal branch, with sluggish TIMI 2 flow, and the ostium of that branch was narrowed by about 90 percent. The mid right coronary artery carried a moderate-to-severe lesion of approximately 70 percent. The geography of these blockages matched the echocardiographic finding of posterior wall hypokinesis almost exactly. Interventional cardiologists implanted a 3.5 by 24 millimeter drug-eluting stent from the proximal to the distal circumflex artery, achieving a satisfactory angiographic result, and the patient left the hospital on a regimen that included aspirin, clopidogrel, atorvastatin, dapagliflozin, bisoprolol, and viliximab. Sacubitril-valsartan was withheld because his blood pressure hovered around 80/60 mmHg for most of his stay.

One month later, the trajectory had turned catastrophic. Readmitted with recurrent chest tightness and dyspnea, the man had a B-type natriuretic peptide of 2,627.40 ng/L against a reference range of 0 to 100 ng/L, a marker of severe cardiac strain. The electrocardiogram now showed a complete left bundle branch block with a QRS duration of 144 milliseconds, meaning the electrical impulse was activating the ventricles in a delayed, asynchronous fashion. The repeat echocardiogram was dramatic: the left ventricle had ballooned to an end-diastolic diameter of 113 millimeters, the walls from the papillary muscles to the apex had thinned to as little as about 3 millimeters inferiorly, and the apical inferolateral wall bulged outward as a stiff, aneurysm-like segment measuring roughly 74 by 50 millimeters that moved paradoxically with each beat. Severe functional mitral regurgitation had appeared, with structurally normal leaflets, indicating that the leaking valve was a consequence of the ventricle’s distorted geometry rather than valve disease itself. Bedside ultrasound also revealed massive bilateral pleural effusions.

Despite intensified heart failure therapy, the patient progressed to end-stage failure and was transferred to Wuhan Union Hospital, where he underwent heart transplantation. The explanted heart confirmed what the imaging had suggested: marked left ventricular dilatation and a large aneurysmal segment at the inferolateral apex. Histopathology of tissue adjacent to the aneurysm showed features consistent with myocardial infarction accompanied by chronic inflammatory cell infiltration, with residual muscle cells showing blurred striations and enlarged, hyperchromatic nuclei. Examination of the sampled circumflex artery segment demonstrated atherosclerotic stenosis. Together, the pathology anchored the diagnosis: an ischemic infarct in the circumflex territory superimposed on an underlying dilated cardiomyopathy, not myocarditis, which the authors judged unlikely given the normal cardiac enzymes, cytokines, and viral antibodies during the initial admission. The authors argue that the aneurysm’s unusual location and its speed of formation are best explained by an interaction between the two diseases.

Ventricular aneurysms most commonly complicate transmural infarcts of the anterior wall supplied by the left anterior descending artery, and aneurysms described in idiopathic dilated cardiomyopathy have often involved posterior basal regions. This patient’s bulge sat in the inferolateral apex, squarely in circumflex territory, consistent with his angiographic lesions and his pathology. The team also noted that established predictors of post-infarction aneurysm formation, including a urea nitrogen-to-albumin ratio of at least 0.15, an ejection fraction below 50 percent, and a culprit vessel in the left anterior descending artery, applied in part: his ratio was 0.17 and his ejection fraction was markedly reduced, placing him in a high-risk category, although his culprit vessel was the circumflex.

The proposed amplifier was dyssynchrony. In dilated cardiomyopathy, regional fibrosis, intraventricular conduction disturbance, and mechanical dyssynchrony can make different parts of the ventricle contract at different times and with different forces, creating heterogeneity in contraction and regional wall stress. Prior work has suggested that wall stress may be higher in basal than in apical segments in this disease. In this patient, the left bundle branch block-like conduction delay would have delayed contraction of the lateral wall precisely where the infarct had thinned the myocardium, concentrating mechanical stress on a weakened segment and, in the authors’ view, accelerating aneurysm development. They also reason that the underlying cardiomyopathy came first: five days of symptoms are too short for a circumflex lesion alone to produce the marked left atrial and ventricular enlargement seen on admission, and the right-dominant coronary circulation makes a circumflex lesion an improbable cause of the complete left bundle branch block observed at readmission.

The clinical lesson the authors draw is one of vigilance rather than a new treatment rule. In patients with dilated cardiomyopathy, especially when symptoms are non-specific, coexisting ischemic injury can be overlooked, and new regional wall motion abnormalities, conduction changes, or rapid structural deterioration should prompt early ischemic assessment and, when warranted, repeat evaluation. In this case the patient and his family declined a recommended repeat angiography during the second admission, so the intermediate coronary anatomy was never directly imaged. As a single-case report, the findings cannot establish how often this overlap occurs or how reliably dyssynchrony accelerates aneurysm formation, and the authors acknowledge that the absence of comparative baseline data makes it difficult to fully disentangle the two disease processes.

Even so, the case illustrates how a stented artery, a stretched ventricle, and a delayed electrical impulse can combine to remodel a heart in weeks, and how recognizing that combination may shape decisions about revascularization, advanced heart failure therapy, and timely referral for transplantation.

Subject of Research: Heart transplantation for rapidly progressive dilated cardiomyopathy complicated by an inferolateral left ventricular aneurysm linked to ischemic injury

Article Title: Heart transplantation for rapidly progressive dilated cardiomyopathy complicated by an inferolateral left ventricular aneurysm: a case report

Article References: Yu, Z., Yang, L., Xu, Y., Li, Z., Wang, L., & He, L. (2026). Heart transplantation for rapidly progressive dilated cardiomyopathy complicated by an inferolateral left ventricular aneurysm: a case report. Frontiers in Cardiovascular Medicine, 13, Article 1789290. https://doi.org/10.3389/fcvm.2026.1789290

Image Credits: AI Generated

DOI: 10.3389/fcvm.2026.1789290

Keywords: dilated cardiomyopathy, left ventricular aneurysm, heart transplantation, myocardial infarction, coronary artery disease, mitral regurgitation, left bundle branch block, echocardiography, coronary angiography, heart failure, dyssynchrony, case report