Authors: Mingmin Li, Xiaoyu Peng, Yun Teng, Nianjin Xie
Categories: Case Report, Left ventricular pseudoaneurysm, Myocardial infarction, Non-obstructed coronary artery disease, Case report
Source: Journal of Cardiothoracic Surgery
Authors: Mingmin Li, Xiaoyu Peng, Yun Teng, Nianjin Xie
Left ventricular pseudoaneurysm (LVP) is a rare complication, typically following a prior myocardial infarction. Clinical manifestations are diverse and non-specific, posing significant challenges for early diagnosis. Given the high risk of complete rupture, LVP is typically associated with poor prognosis, necessitating urgent surgery for survival. In the current LVP case, the patient presented with isolated chest pain, and further evaluation revealed non-obstructive coronary artery disease. To our knowledge, such cases are rare, and guidelines for LVP management—especially for chronic presentations—remain scarce.
A man in his 50s, complaining of recurrent chest pain over 8 months, was found to have a giant abnormal mass with rim calcification close to the posterior ventricle wall on chest computed tomography. Both contrast-enhanced echocardiography and cardiac magnetic resonance confirmed the diagnosis of a giant extensively calcified LVP in the inferolateral ventricle wall, as well as left ventricle enlargement and compromised systolic function. Coronary angiography revealed non-obstructed arteries. To prevent complete rupture, avoid systemic embolism, and improve cardiac function, the patient underwent successful surgical repair following a multidisciplinary team discussion and has achieved good subsequent recovery.
Our experience with successful surgical intervention in managing this unusual case of a chronic giant LVP provides compelling evidence that surgical repair should be considered a first-line treatment option for such patients.
The online version contains supplementary material available at 10.1186/s13019-025-03690-6.
Left ventricular pseudoaneurysm (LVP) is a rare but potentially fatal condition, often secondary to prior acute myocardial infarction (AMI) [1], with an estimated incidence < 0.5% in AMI patients [1]. Less frequent causes are cardiac surgery, chest trauma, or infection [2, 3]. It’s a distinct cardiac rupture variant, with ventricular wall disruption contained by adherent pericardium or scar tissue. LVP commonly develops after the posterior or lateral wall infarction [2], whereas true aneurysms typically occur in anterior AMI [4]. The clinical manifestations are variable and nonspecific, challenging early diagnosis. For suspected cases, early multimodal diagnosis combining echocardiogram, cardiac magnetic resonance (CMR) and ventricular angiography is recommended [1].
Little is known about the natural history of LVP. Given the relatively high risks of complete rupture and mortality, which are 30%−45% and 48% respectively [2, 5], a poor prognosis is presumed and urgent surgery is advised for life saving, especially for acute or large LVPs leading to clinical instablity [3, 4, 6, 7]. However, guidance for LVP management is scarce, particularly for asymptomatic or chronic cases [1, 8].
This rare case involves a chronic LVP identified by recurrent chest pain, with non-obstructive coronary artery disease on angiography and no definite myocardial infarction history. Successful surgical management in this patient suggests surgery is a safe and effective option for chronic giant LVP.
A 50-year-old man was transferred to our center due to recurrent episodes of chest pain over an 8-month period. The pain, which had no specific triggers, lasted from minutes to half an hour and radiated to the left shoulder and back, with exacerbation occurring half a month ago. No other discomforts, including fever, breathless, fatigue, edema, or syncope, were complained. Except for a history of stroke 2 years ago without residua, he mentioned no history of other diseases or traumas. The patient underwent chest computed tomography (CT) at a local hospital, which revealed a rim-calcified abnormal mass adjacent to the posterior ventricular wall. Upon admission, the patient’s vital signs were within normal blood pressure was 125/65mmHg, heart rate was 55 bpm, respiratory rate was 20/min, and body temperature was 36.5℃. On physical examination, the heart was enlarged to the left, S1 and S2 were audible and normal, with no pericardial rub, murmur, or jugular venous distension. Crackles and lower extremity edema were absent. Key laboratory results were summarized in Table 1. No obvious abnormalities in blood routine, coagulation function, liver or kidney function were detected.
Table 1Key laboratory resultsTest nameResultNormal rangeClinical significanceTroponin6.1pg/mL< 14pg/mLNo current myocardial injury was detectedCreatine kinase69U/L50-310U/LNo current myocardial injury was detectedN-Terminal pro-brain natriuretic peptide125.7pg/mL< 125pg/mLThe risk of acute heart failure was lowD -dimer570ng/mL, 420ng/ml 2 days after admission< 500ng/mLThe risk of acute thrombosis was lowLDL cholesterol levels2.03 mmol/L< 4.14mmol/LNo obvious hypercholesterolemia was noted
Fig. 118-lead electrocardiogram on admission, with an occasional premature ventricular contraction (arrow)
The electrocardiogram revealed sinus rhythm with first-degree atrioventricular block (PR interval 270ms), left ventricular high voltage, and occasional premature ventricular contraction (Fig. 1) Transthoracic echocardiogram (TTE) showed a large peripherally calcified sac communicating with the left ventricle via a narrow neck (Fig. 2A and B), as well as significant left ventricular enlargement with reduced ejection fraction. Contrast-enhanced echocardiography identified a giant cavity with distinct calcified borders and continuous disruption at the basal inferoposterior segment (Fig. 2C). CMR revealed thinning and dyskinesis in the basal-inferior, basal-inferolateral, mid-inferior and mid-inferolateral segments, with corresponding ventricular wall bulging. Additionally, markedly delayed enhancement of the surrounding pericardium and extensive thrombosis within the bulging cavity were noted (Fig. 3 and Video 1–4 in Supplementary material). Nevertheless, coronary angiography revealed non-obstructed arteries, with 20% to 30% stenosis of left anterior descending coronary artery and left circumflex coronary artery, 30% to 40% stenosis of right coronary artery (Video 5–7 in Supplementary material). Despite that ventricular angiography proves beneficial in diagnosing LVP, the procedure should be approached with caution due to the risk of complete rupture and embolism [1]. All the imaging fingdings were summarized in Table 2.
Table 2Imaging findingsModalityMain findingsClinical contributionTTEA large calcified sac communicating with the left ventricle via a narrow neck;left ventricular enlargement;Left Ventricular End-Diastolic Diameter 65 mm; Left ventricular ejection fraction (LVEF) 50%Initial diagnosis for LVP and evaluation for cardiac functionContrast-enhanced echocardiographyContinuous disruption at the basal inferoposterior segmentDifferential diagnosis, exclude true aneurysmCMRMarkedly delayed enhancement of the surrounding pericardium;extensive thrombosis in the bulging cavity;Left Ventricular End-Diastolic Volume 219 ml; LVEF 40%To further clarify diagnosis and evaluate cardiac functionCoronary angiographyNon-obstructed arteriesIndicate the absence of obstructive coronary artery disease
Fig. 2Long axis view showed the pseudoaneurysm (arrow). (A) and a bidirectional blood flow within the pseudoaneurysm (arrow). (B), there’s contrast flow inside the cavity (arrow), with a large filling defect, indicating massive thrombosis (C)
Fig. 3Perfusion scanning of CMR (short axis) showed thinning of the mid inferior and inferolateral segments and bulging of the corresponding ventricle wall (arrow)
Fig. 4A giant pseudoaneurysm filled with sediment-like calcification was identified directly in the inferolateral ventricle wall
A multidisciplinary consultation was held to deliberate on the optimal therapeutic approach. The case was particularly notable due to the patient’s mild coronary artery stenosis, contrasted with his large, extensively thrombosed pseudoaneurysm. Antithrombotic medications were promptly discontinued after angiography. Given the high risks of complete rupture and embolism, and detrimental effects on cardiac systolic function, consistent recommendations were made for urgent surgical repair.
Intraoperative transesophageal echocardiography revealed moderate mitral regurgitation due to partial posterior chordae tendinae rupture and anterior leaflet tethering. An on-pump cardiac surgery comprising an aneurysmectomy, closure of the left ventricle defect with a bovine pericardial patch, and a prosthetic mitral valve replacement was performed. The patient’s bypass time and cross clamp time were 352 min and 213 min, respectively. Intraoperatively, a giant pseudoaneurysm filled with sediment-like calcification, measuring 70 × 80 mm, was identified in the inferolateral ventricle wall (Fig. 4). The pathological examination of the excised pseudoaneurysm tissue disclosed abundant hyperplastic collagen fibers, sparse myocardial tissue, multifocal calcifications, and superficially adherent surface thrombi.
The patient recovered well from surgery. TTE conducted prior to discharge indicated that the left ventricle had reverted to a normal size, albeit with a mildly reduced ejection fraction. The patient’s hospital stay was 25 days, with 5 days in intensive care unit preoperatively and 4 days postoperatively.
The case was followed up continuously. Currently, the patient reports no significant chest pain or dyspnea during daily activities. Postoperative TTE at 6 months, 1 year, and 1.5 years showed normalized left ventricle size with mild decline in cardiac function (LVEF 42%−43%).
Herein, we presented a middle-aged man with a giant extensively calcified pseudoaneurysm, suffering from recurrent chest pain. Cardiac examination and imaging techniques have both confirmed the presence of left ventricle enlargment with reduced ejection fraction. Notably, this patient’s LVP was not caused by typical transmural myocardial infarction, a unique feature. Based on electrocardiogram, echocardiography, CMR, and coronary angiography, a silent antecedent myocardial infarction in the absence of obstructive coronary artery disease (MINOCA) is highly suspeceted as the underlying cause. Surgery directly confirmed inferolateral wall rupture and a calcified pseudoaneurysm.
To our knowledge, similar cases are extremely rare. Naseerullah FS et al. reported a similar case of an elderly woman with nonobstructive coronary artery disease, a history of embolic stroke, no antecedent myocardial infarction, who was hospitalized for intermittent chest pain and diagnosed with LVP, ultimately undergoing surgical repair [9]. Unlike our case, her LVP was apical and had no thrombus due to pre-admission anticoagulation. The insights gleaned from our case have broaden our understanding of chronic giant LVPs management.
Firstly, despite the risk of sudden cardiac death, patients affected with LVP could be hemodynamically stable. The most common symptoms are chest pain, dyspnea, and congestive heart failure [2], less frequent are systemic embolization and symptomatic arrhythmia. Occasional nonspecific discomforts include shoulder, back, or arm pain, hemoptysis, and altered mental status. Yet, asymptomatic LVPs exist, with a reported incidence of 12%−48% across case series [2, 10].
In this case, the patient initially presented with recurrent chest pain, which was not significantly relieved by anti-anginal drugs including nitrates and nicorandil after admission. In other words, the chest pain was atypical. Coronary angiography excluded residual significant lesions; instead, it was more likely due to adjacent tissue compression and stimulation by the expanding pseudoaneurysm, as reported in the literature [11, 12].
Another important finding is extensive thrombosis in the false cavity, raising concern about systemic embolism. The patient had a stroke 2 years pre-admission, with local secondary hospital outpatient cranial CT and magnetic resonance imaging showing acute right cerebral peduncle infarction. No ambulatory electrocardiogram or echocardiography (with or without bubble test) was performed then, precluding confirmation of systemic embolism. The patient has since been on regular aspirin and statins. From a monistic perspective, embolism is strongly suspected as the etiology underlying the patient’s prior stroke.
A few studies have elaborated on anticoagulation in this context [2, 13]. For conservatively treated LVPs, the reported 1-year ischaemic stroke incidence was 10%, rising to 32.5% at 4 years [14]. These figures support considering anticoagulation to prevent systemic embolism, despite theoretical risks of complete rupture and bleeding. A similar case described by Naseerullah FS et al. illustrated this clinical a patient with embolic stroke was found to have a large mobile left ventricular thrombus during diagnosis, and following standardized anticoagulation therapy, repeat TTE demonstrated complete thrombus resolution but newly identified LVP [9]. In the absence of sufficient evidence to support or refute the use of anticoagulation, clinicians should therefore make decisions tailored to the individual patient’s condition [9, 13].
In the specific context of this case, current consensus on MINOCA notes controversial use of antiplatelet agents except for plaque disruption-related cases [15]. Given the probable embolic etiology of the patient’s stroke and planned surgery, pre-operative anticoagulation rather than antiplatelet therapy was reasonable. However, concern about complete rupture outweighed the benefit of thromboembolism prevention, anticoagulant treatment was ultimately withheld.
A final crucial point is that surgical indications and optimal timing for asymptomatic or stable chronic LVP remain undefined. Generally, LVP is classified by time from AMI onset as acute (within 2 weeks), subacute (from 2 weeks to 3 months) and chronic (beyond 3 months) [1, 16]. This classification helps predict patient outcomes and guide treatment decisions. For clinicians, key factors in surgical decision-making are the risk of fatal rupture associated with conservative treatment and surgical mortality [1, 14].
The long-term mortality rate for patients with medically treated LVP reached as high as 60%, as indicated by a small Mayo Clinic cohort study [10]. Notably, none of the deaths were due to cardiac rupture, consistent with findings in another small cohort of conservatively treated LVPs [14]. A review of 290 LVP cases showed that the mortality of medically treated patients was 48% within first week [2]. However, those surviving the early days had a median survival of 156 weeks.
Generally, the risk of complete rupture is associated with timing from AMI onset and pseudoaneurysm morphological features. Large LVPs or those developing within 3 months post-AMI are considered high rupture risk; in contrast, small chronic LVPs (< 3 cm) with heavily fibrotic edges have low rupture risk [1, 3]. Furthermore, the coexistence of impaired cardiac function or systemic embolism indicates a poor prognosis [1, 14]. Whether the optimal medical therapy that’s proven effective in heart failure patients exerts the same effect in heart failure complicated with large LVP remains uncertain.
The surgical mortality varied in different case series, ranging from 7% to 35.7% [10, 17, 18], and increasing further when accompanied by mitral valve replacement [2]. Limited studies suggest a correlation between surgical timing and surgical mortality risk. One study of 45 patients undergoing surgery for myocardial infarction-induced LVP showed that acute-phase surgery was associated with significantly higher in-hospital mortality than non-acute-phase surgery (15.6% vs. 61.5%, p = 0.0066) [16]. Since the first successful percutaneous closure of LVP reported in 2004, percutaneous approaches for anatomically suitable LVP patients has emerged as a feasible and safe alternative to sugical repair [19].
In this chronic LVP case, surgical risk is significantly lower than in the acute phase. Its anatomical features—large aneurysm, marked calcification, and proximity to basal segments—make traditional surgery preferable to percutaneous closure as the optimal treatment. These features also influence surgical techniques [20]. Chronic LVPs typically have calcified and fibrous edges, allowing direct neck closure with pledgeted sutures. Given its large cavity and basal location, a bovine pericardial patch was utilized to restore normal left ventricle geometry and avoid excessive traction of the subvalvular apparatus [20, 21]. In concomitant mitral valve replacement, internal LVP repair via the left atrium is preferred for better exposure of the sub-valvular apparatus [1, 22].
Thanks to advancements in surgical techniques and the introduction of percutaneous closure for selected patients at high surgical risk [19, 23], the operative mortality for LVP has significantly decreased in nowadays [6, 20]. Based on the limited reports available on chronic LVPs, together with our experience in this case, it’s reasonable to recommend surgical intervention for patients presenting with congestive heart failure, embolization, or in instances of large LVPs, or if there’s evidence of LVP expansion [1, 9, 17].
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