Ventricular apical wall rupture and ventricular aneurysm formation concurrent with ventricular septal dissection and rupture due to ST-segment elevation myocardial infarction: a case report.

The most common mechanical complications of acute myocardial infarction include free-wall rupture, ventricular septal rupture (VSR), papillary muscle rupture and pseudoaneurysm. It is rare for a patient to experience more than one mechanical complication simultaneously. Here, we present a case of ST-segment elevation myocardial infarction (STEMI) complicated with three mechanical complications, including ventricular apical wall rupture, ventricular aneurysm formation and ventricular septal dissection (VSD) with VSR. Cardiac auscultation revealed rhythmic S1 and S2 with a grade 3 holosystolic murmur at the left sternal border. Electrocardiogram indicated anterior ventricular STEMI. Serological tests showed a significant elevated troponin I. Bedside echocardiography revealed ventricular apical wall rupture, apical left ventricle aneurysm and VSD with VSR near the apex. This case demonstrates that several rare mechanical complications can occur simultaneously secondary to STEMI and highlights the importance of bedside echocardiography in the early diagnosis of mechanical complications.

Ignored Role of Paroxysmal Atrial Fibrillation in the Pathophysiology of Cryptogenic Stroke in Patients with Patent Foramen Ovale and Atrial Septal Aneurysm.

The association between cryptogenic stroke (CS) and patent foramen ovale (PFO) with or without atrial septal aneurysm (ASA) has been a debate for decades in terms of pathophysiologic processes and clinical courses. This issue has become more interesting and complex, because of the concerns associating the CS with so-called normal variant pathologies of interatrial septum, namely ASA and PFO. While there is an anatomical pathology in the interatrial septum, namely PFO and ASA, the embolic source of stroke is not clearly defined. Moreover, in patients with PFO and CS, the risk of recurrent stroke has also been associated with other PFOunrelated factors, such as hyperlipidemia, body mass index, diabetes mellitus, and hypertension, leading to the difficulty in understanding the pathophysiologic mechanism of CS in patients with PFO and/or ASA. Theoretically, the embolic source of cryptogenic stroke in which PFO and/or ASA has been involved can be categorized into three different anatomical locations, namely PFO tissue and/or ASA tissue itself, right or left atrial chambers, and venous vascular territory distal to the right atrium, i.e., inferior vena cava and lower extremity venous system. However, the possible role of paroxysmal atrial fibrillation associated with PFO and/or ASA as a source of cryptogenic stroke has never been mentioned clearly in the literature. This review aims to explain the association of cryptogenic stroke with PFO and/or ASA in a comprehensive manner, including anatomical, clinical, and mechanistic aspects. The potential role of paroxysmal atrial fibrillation and its contribution to clinical course have been also discussed in a hypothetical manner to elucidate the pathophysiology of CS and support further treatment modalities.

Urea nitrogen-to-albumin ratio predicts ventricular aneurysm formation in ST-segment elevation myocardial infarction.

AIMS: Left ventricular aneurysm (LVA) is an important complication of acute myocardial infarction. The aim of this study was to investigate the possible predictive value of blood urea nitrogen-to-albumin ratio (BAR) for the LVA formation in acute ST-segment elevation myocardial infarction (STEMI) patients who underwent primary percutaneous coronary intervention (PCI). METHODS AND RESULTS: A total of 1123 consecutive patients with STEMI were prospectively enrolled. The clinical and laboratory data were compared between LVA group and non-LVA group. Multivariable logistic regression analysis was performed to assess the independent risk factors of LVA formation. Predictive power of BAR and composite variable for LVA formation were assessed using receiver operating characteristic curve. LVA was detected in 162 patients (14.4%). The BAR was significantly higher in patients with LVA [0.16 (0.13-0.19) vs. 0.13 (0.10-0.17), P < 0.001]. Multivariable logistic regression analysis revealed that left ventricular ejection fraction (LVEF) [odds ratio (OR) = 0.865, P < 0.001], culprit vessel-left anterior descending artery (LAD) (OR = 4.705, P < 0.001), and BAR (OR = 2.208, P = 0.018) were all independent predictors for LVA formation. The predictive value of BAR remained significant even after cross-validation by splitting population into training set (OR = 1.957, P = 0.034) and validation set (OR = 1.982, P = 0.039). The maximal length and width of LVA were significantly increased in patients with BAR ≥ 0.15 when compared with BAR < 0.15 (3.37 ± 1.09 vs. 2.92 ± 0.93, P = 0.01, for maximal length, and 2.20 ± 0.55 vs. 1.85 ± 0.63, P = 0.001, for maximal width). The discriminant power of BAR for LVA is 0.723, which is superior to both blood urea nitrogen (C statistic = 0.586, P < 0.001) and albumin (C statistic = 0.64, P < 0.001). The combination of BAR, LVEF, and culprit vessel-LAD could significantly increase the predictive ability (C statistic = 0.874, P < 0.001, for vs. BAR). Subgroup analysis of age, sex, hypertension, diabetes, smoking, LVEF, serum albumin, multiple-vessel disease, and Gensini score had no effect on the association between BAR and risk of LVA formation (P < 0.05 for all subgroups). CONCLUSIONS: A higher BAR was an independent predictor for LVA formation in STEMI patients with primary PCI.

Rare complications of infective endocarditis in marfan-like morphotype: diagnosis of multiple mitral valve aneurysms and aortic root abscess using three-dimensional transesophageal echocardiography.

Mitral valve aneurysm (MVA) is characterized by a saccular outpouching of the mitral leaflet, and it represents a rare condition typically associated with aortic valve endocarditis. Three-Dimensional Transesophageal Echocardiography (3D-TEE) serves as an effective tool for detecting the presence of MVA and its potential complications. In this report, we present a case involving a young man with striking images of bicuspid aortic valve endocarditis complicated by an aortic root abscess and multiple perforated mitral valve aneurysms, diagnosed using 3D TEE. This case suggests the uncommon coexistence of Marfan like morphotype, bicuspid aortic valve, and infective endocarditis as a triple mechanism in the occurrence of MVA. It underscores the significance of early and accurate imaging diagnosis for facilitating prompt surgical intervention.

Surgical treatment of left ventricular aneurysm in patients with prior myocardial infarction in the absence of obstructive coronary artery disease (MINOCA): a cohort study.

BACKGROUND: There is a paucity of studies examining the treatment of patients with prior myocardial infarction in the absence of obstructive coronary arteries (MINOCA) and with a concomitant left ventricular aneurysm. Our study aims to illustrate the clinical characteristics and report the mid-term surgical outcomes in this distinct entity. METHODS: Ten patients with MINOCA and left ventricular aneurysm were investigated. The MINOCA was diagnosed according to Scientific Statement from the American Heart Association. The indication for left ventricular reconstruction was as follows: clear evidence of both an aneurysmal and akinetic left ventricle with a history of myocardial infarction accompanied by heart failure symptoms, angina, or ventricular arrhythmias. Major adverse cardiovascular and cerebrovascular events (MACCE), including death, myocardial infarction, stroke was considered the primary endpoints. RESULTS: The median follow-up for the whole study population was 64.5 months. Seven MINOCA patients developed a left ventricular aneurysm within 4 years and three MINOCA patients were found to have a concomitant left aneurysm at the first admission. Before surgery, no patients were prescribed angiotensin-converting enzyme inhibitors. Statins, dual antiplatelet therapy, and ß-blockers were prescribed in 2, 5, and 5 patients, respectively. After surgery, no MACCE occurred in the follow-up. There was a significant increase in ejection fraction (EF) in the follow-up (p = 0.0009). CONCLUSIONS: Close monitoring and standard medical treatment are required before a left ventricular aneurysm occurs in MINOCA patients. Left ventricular reconstruction remains a viable option for MINOCA patients with left ventricular aneurysms and mid-term outcomes were satisfying in this distinct entity.

Echocardiography Diagnosis of Mitral Valve Aneurysm Complicated with Infective Endocarditis.

Mitral valve aneurysm (MVA) is a relatively rare but life-threatening condition that may occur as a complication of an infective endocarditis (IE) involved aortic valve. Rupture of the valve aneurysm is one of the most serious complications, which could result in severe mitral regurgitation and cause rapid hemodynamic deterioration, especially in heart failure patients. Timely diagnosis using echocardiography and appropriate treatments, such as invasive surgical repair or replacement of the valve, can effectively prevent catastrophic complications. Here, we present a 57-year-old male patient with MVA after IE and emphasize the key role of echocardiography in the early diagnosis and management of these kinds of conditions.

An isolated mid-anterolateral wall true ventricular aneurysm due to coronary artery disease.

Aneurysms following a myocardial infarction usually involve the apical wall segments. We present a case of a rare isolated mid-anterolateral wall aneurysm due to occlusion of a diagonal branch. We review the echocardiographic criteria for diagnosing a left ventricular (LV) aneurysm and discuss how to differentiate one from a more critical pseudoaneurysm. We demonstrate the utility of using ultrasound enhancing contrast and review imaging protocols for ruling out associated LV thrombus.

[Analysis of conventional echocardiographic features in apical hypertrophic cardiomyopathy patients complicated with left ventricular apical aneurysm].

Objective: To explore the basic characteristics of conventional echocardiography of apical hypertrophic cardiomyopathy (ApHCM) patients complicating with left ventricular apical aneurysm (LVAA). Methods: This is a retrospective study. Patients who underwent echocardiography and cardiac magnetic resonance (CMR) and were diagnosed with ApHCM complicated with LVAA by CMR at Fuwai Hospital, Chinese Academy of Medical Sciences from August 2012 to July 2017 were enrolled. According to whether LVAA was detected by echocardiography, the enrolled patients were divided into two groups: LVAA detected by echocardiography group and LVAA not detected by echocardiography group. Clinical data of the two groups were compared to analyze the causes of missed diagnosis by echocardiography. Results: A total of 21 patients were included, of whom 67.0% (14/21) were males, aged (56.1±16.5) years. Patients with chest discomfort accounted for 81.0% (17/21), palpitation 38.1% (8/21), syncope 14.3% (3/21). ECG showed that 21 (100%) patients had ST-T changes and 18 (85.7%) had deep T-wave invertion. Echocardiography revealed ApHCM in 17 cases (81.0%) and LVAA in 7 cases (33.3%). The mean left ventricular apical aneurysm diameter was 33.0 (18.0, 37.0) mm, and left ventricular ejection fraction was (66.5±6.6) %, and left ventricular apex thickness was (21.0±6.3) mm. Left ventricular outflow tract obstruction was presented in 4 cases and middle left ventricular obstruction in 10 cases. The mean left ventricular apical aneurysm diameter of LVAA detected by echocardiography was greater than that of LVAA not detected by echocardiography (25.0 (18.0, 28.0) mm vs. 16.0 (12.3, 21.0) mm, P=0.006). Conclusions: Conventional echocardiography examination has certain limitations in the diagnosis of ApHCM. Smaller LVAA complicated with ApHCM is likely to be unrecognized by echocardiography. Clinicians should improve their understanding of this disease.

[Left Ventricular Plasty for Left Ventricular Aneurysm Following Takotsubo Cardiomyopathy].

An 82-years-old woman was admitted with sudden chest pain. Coronary angiography did not reveal any significant stenosis, but left ventriculography showed akinesis and ballooning of the apex with a hyperkinetic basal segment, suggestive of takotsubo cardiomyopathy. She suffered intractable heart failure, and laboratory data, electrocardiogram signs of ST-segment elevation and left ventricular( LV) apical dysfunction failed to show improvement. LV plasty was performed on 106th day after the onset because of aneurysmal change of the left ventricular apex myocardium, unremitting sanguineous pericardial effusion, and anemia. She had a good postoperative course and end-diastolic ventricular volume index was remarkably reduced from 144 to 55 ml/m2. She discharged home on the 38th postoperative day.

Idiopathic Left Ventricular Apical Aneurysm in a Sailor With Moderate Transient Chest Pain: A Unique Perspective on an Atypical Presentation in the Military Population.

Left ventricular (LV) apical aneurysm is a rare condition that carries a high risk of fatal cardiac rupture. Wall ruptures are an uncommon catastrophic complication after acute transmural myocardial infarction. Rarely is the rupture only contained by an adherent pericardium or hematoma creating a pseudoaneurysm. This clinical finding calls for emergent surgical intervention. If no ruptures are detectable and myocardium wall integrity is verified, the diagnosis of a true aneurysm can be made to be repaired via elective surgery. The etiological differential for a patient with an LV aneurysm in the setting of normal coronaries and in the absence of prior cardiac surgery remains broad, including traumatic, infectious, and infiltrative causes. In this case report, we demonstrate an atypical and rare presentation of an idiopathic LV apical aneurysm in a physically fit, active duty male in the U.S. Navy.

Large Left Ventricular Pseudoaneurysm Presenting as an Embolic Stroke After a "Silent" Myocardial Infarction.

A 72-year-old woman with no history of coronary artery disease presented with an acute left middle cerebral artery stroke and was found to have a large left ventricular pseudoaneurysm measuring 8.7 × 7.6 cm and 2 large left ventricular thrombi, the source of her systemic embolization. Despite initial medical management, she developed refractory New York Heart Association functional class III heart failure, uncontrolled atrial fibrillation, and further enlargement of her pseudoaneurysm to 5.5 × 10.6 × 9.2 cm. She underwent urgent aneurysmectomy. Left ventricular pseudoaneurysms are rare and most commonly occur following an acute myocardial infarction when a ventricular free-wall rupture is contained by pericardium or thrombi. Historically, left ventricular angiography displaying a lack of an overlying coronary artery was the gold standard for diagnosis. Now, noninvasive imaging such as computed tomography, magnetic resonance imaging, and echocardiogram with ultrasound-enhancing agent, are reliable diagnostic tools. They can distinguish a pseudoaneurysm from a true left ventricular aneurysm using characteristic findings such as a narrow aneurysm neck, bidirectional doppler flow between the pseudoaneurysm and the left ventricle, and abrupt changes in the cardiac wall structures. Progressive dilation, wall thinning, and dyskinesis can result in refractory heart failure, arrhythmias, and thrombi formation from venous stasis. Pseudoaneurysms have a 30% to 45% risk of rupture and can be treated with left ventricular aneurysmectomy.