Left Ventricular Rupture Research Articles

Diagnosis of Postinfarction Pseudoaneurysm of the Left Ventricular Free Wall after Coronary Stenting: Case Report

The article is dedicated to topical issues of diagnosis and surgical treatment of postinfarction left ventricular (LV) myocardial rupture. Postinfarction LV rupture is one of the most life-threatening complications of acute myocardial infarction (AMI). Given the low prevalence, this complication almost always leads to a fatal outcome. At the same time, a large proportion of patients (over 60%) die before the diagnosis is verified, suddenly, without specific clinical precursors.
 The aim. To draw the attention of doctors to the problem of diagnosis and surgical treatment of LV myocardial rupture as a complication of AMI.
 The article describes a clinical case of diagnosis of pseudoaneurysm of the LV free wall after coronary stenting. The peculiarity of this case was absence of a typical pain syndrome, electrocardiographic and echocardiographic signs, suggesting the presenceof such a mechanical complication of AMI. Special attention is paid to the analysis of factors enabling to assess the risk of developing this complication in patients with AMI. The given clinical case demonstrates the importance of early hospitalization and myocardial revascularization by stenting in order to prevent mechanical complications of AMI. Timely diagnosis and urgent surgical treatment of LV myocardial ruptures can reduce mortality due to mechanical complications of AMI.
 Conclusions. Timely hospitalization and revascularization of the myocardium in AMI patients reduce the risk of LV rupture in the affected area. The use of echocardiography makesit possible to detect severe complications of AMI with sufficient sensitivity. The only effective treatment method forLV rupture is urgent surgical intervention. Postinfarction myocardial rupture repair is a difficult task considering the initial severity of the patient’s clinical condition, the significant volume and technical complexity of the surgical intervention.

Subsequent cardiac surgery after transcatheter aortic valve implantation: Indications and outcomes.

Aim of this study was to report on indications and clinical outcomes of patients who underwent subsequent open-cardiac surgery after transcatheter aortic valve implantation TAVI. Between 01/2011 and 12/2020 our centre performed 4043 TAVI procedures. Twenty-seven patients (including patients in whom TAVI was performed in other centres) underwent subsequent open-heart surgery via cardiopulmonary bypass. Demographic, intraprocedural data, indications for, and outcomes after surgery were evaluated. Indications for cardiac surgery (aged 79 [IQR 76-84]; 59.3% male) were endocarditis (n = 11; 40.7%), annular rupture, severe paravalvular leak and severe stenosis in three (11.1%) patients, respectively as well as in one patient each (3.7%) severe tricuspid valve regurgitation, valve thrombosis, valve malposition, valve migration, ostial right coronary artery obstruction, left ventricular rupture and type A aortic dissection. The interval between the index TAVI procedure to open surgery was 3 months (IQR 0-26 months). Eight patients underwent emergent surgical conversions. Immediate procedural and procedural mortality was 25.9% and 40.7%, respectively and all-cause mortality was 51.9% (11/12 died for cardiovascular reasons). No disabling stroke was observed postoperatively. New permanent pacemaker implantation was required in threepatients (11.1%). Subsequent open-cardiac surgery after TAVI is rare, but may urgently become necessary due to TAVI related complications or progressing other cardiac pathologies. Despite a substantial early attrition rate clinical outcome is acceptable and a relevant number of these high-risk patients can be discharged even after emergency conversions. The option of subsequent surgical conversion remains.

Abstract 10604: Critical Role of Cardiac Imaging of Mechanical Complication in ST Elevation Myocardial Infarction: Left Ventricular Free Wall Rupture Diagnosed With CTA and Echocardiography

Case Presentation: An 81-year-old male with a thymoma (treated with surgery including partial pericardiectomy 25 years prior) presented to his local ER with chest pain radiating to his back. Vital signs were stable. EKG showed ST elevations in the lateral leads with Q waves. Troponin was positive. Diagnosis included STEMI as well as possible aortic dissection. CT angiography (CTA) did not show dissection; however, contrast extravasation and left ventricular (LV) free wall rupture was noted. Patient was not given thrombolysis and transferred for tertiary care. On arrival, the patient was pain free, hemodynamically stable, and an echo was obtained. Color Doppler and echo contrast confirmed a LV outpouching along the lateral wall with a “narrow neck” consistent with a pseudoaneurysm (PsA, figure 1). CT surgery declined an emergent operation due to the high risk of mortality with early operative intervention and recommended initial conservative management. After 48 hours, a repeat CTA showed increased size of the PsA (figure 2). The patient chose to be managed medically and eventually passed away 8 days after presentation. Discussion: This patient had a contained LV rupture as a STEMI complication. The CTA showed LV rupture and thrombolysis was avoided. Echo confirmed the diagnosis. This case highlights 1) the utility of imaging in in the diagnosis of LV rupture as it is usually limited by early mortality, and 2) its role in differentiating PsA from true aneurysm, which is characterized by a contained wall rupture while true aneurysms develop due to a weakened, but intact, wall.

Abstract 15267: LV Aneurysm Rupture - Dreaded Complication in an LVAD Patient

Introduction: Left ventricular (LV) aneurysm rupture is a highly fatal mechanical complication, usually seen following a myocardial infarction. We describe a unique case of a patient with a left ventricular assist device (LVAD) who presented with cardiac arrest due to an LV aneurysm rupture. Case: A 57-year-old male with history of ischemic cardiomyopathy status post HeartMate3 (HM3) LVAD presented as an out of hospital cardiac arrest. Following resuscitation, Computed Tomography Angiography (CTA) of the chest showed a large long-standing aneurysm along the inferior wall of the LV measuring 2.9 x 3.3 x 3.5 cm with rupture dissecting the pericardium and extending to cause hemo-peritoneum (Figure1), not amenable to intervention. He had presented earlier in the month with anemia that stabilized with transfusion. Abdominal imaging at the time showed a contained bleed with unknown source. He had likely suffered a progressive bleed from the rupture leading to his cardiac arrest. Decision Making: Pseudoaneurysm has been reported as a rare complication with earlier generation LVADs, but to our knowledge, this is the first reported case of an aneurysm formation with rupture with an HM3 LVAD. Conclusions: With the advent of advanced mechanical support devices, there is a heightened need for awareness and cognizance of diagnosing such mechanical complications in this patient population. An early diagnosis requires a high clinical index of suspicion and a multi-disciplinary approach. Multimodality imaging including CT scan can assist with this diagnosis.

The Moment of Left Ventricular Free-wall Rupture.

The Moment of Left Ventricular Free-wall Rupture.

Post-mortem CT: A Useful Tool to Confirm a Case of Suspected Sudden Cardiac Death

Sudden cardiac death (SCD) is defined as the unexpected death of an individual, not due to any extracardiac cause, occurring within one hour of symptom onset or within 24 hours of last being seen in good health if the death is unwitnessed. Forensic pathologists routinely encounter several SCD cases in their practice. The presentation of such cases can be of two types; firstly, with typical signs and symptoms suggestive of cardiac pathology, and secondly, devoid of any presentation history. This history helps forensic pathologists look for relevant findings during the autopsy examination. The authors intend to explore the feasibility of using advanced radiological techniques like post-mortem CT (PMCT) in determining the cause of death through a minimally invasive approach. In the present case, a 65-year-old male was found unresponsive at his residence on the morning of his death. He had a history of dull chest pain for the past two days, which had resolved after he self-prescribed a few medications. The presenting complaint of chest pain had started the intervening night prior to his death. The deceased was a known case of hypertension and was not compliant with treatment, as stated by the relatives. He was declared as brought dead by the treating emergency medicine physician at the Fortis Flt. Lt. Rajan Dhall Hospital and the body was sent by the authorities to the mortuary of the Department of Forensic Medicine, AIIMS, New Delhi for autopsy examination since an autopsy should be conducted by a government hospital or institute by law. PMCT depicted an alternate hyperdense and hypodense region circumferentially surrounding the heart, indicating hemopericardium. It was followed by a traditional autopsy and histopathology examination, which confirmed the presence of hemopericardium and left ventricular rupture associated with acute coronary insufficiency. Such cases with an indicative history, circumstantial evidence, and PMCT findings can be considered for minimal invasive autopsy. If the external findings indicate the application of physical force, then an explorative dissection could be done. Therefore, we conclude that PMCT can be used as a reliable tool for determining the cause of death in SCDs on a case-to-case basis.

Left Ventricular Pseudoaneurysm: A Rare Cause of Chest Pain to Keep in Mind

A man in his 80s presented with sharp central chest pain, diaphoresis, and dyspnea. He had a remote history of coronary artery bypass graft. Results of the physical examination were unremarkable, and initial vital signs were stable. Electrocardiogram was unrevealing. Troponins were elevated and flat. He was initiated on intravenous nitroglycerin, after which his symptoms resolved. However, his blood pressure decreased to a minimal systolic of 76 and diastolic of 50 mm Hg. Because of the resolution of his symptoms, immediate angiography was deferred, and the patient was admitted to the cardiac intensive care unit. Transthoracic echocardiography (TTE) showed a loculated pericardial fluid collection adjacent to the anterolateral left ventricular (LV) wall (Figure; Video 1, available online at http://www.mayoclinicproceedings.org). Contrast TTE showed extension of the contrast from the main LV cavity to the adjacent pericardial cavity, consistent with pseudoaneurysm (Figure; Video 2, available online at http://www.mayoclinicproceedings.org). Computed tomography angiography of the thoracic aorta confirmed LV myocardial rupture along the anterolateral wall with active extravasation of contrast (Supplemental Figure 1A-D, available online at http://www.mayoclinicproceedings.org). The patient’s hospital stay was complicated by acute kidney injury. In the setting of increased risk for dialysis, he opted for conservative management. He remained hemodynamically stable, and pericardiocentesis was not indicated. He was discharged 1 week later. Predismissal TTE redemonstrated the contained LV anterolateral wall rupture with systolic and end-diastolic flow through the myocardial defect (Supplemental Figure 2; Video 3, available online at http://www.mayoclinicproceedings.org). He did well after discharge and died 4 years later of metastatic bladder cancer. Left ventricular pseudoaneurysms develop when LV free-wall rupture is contained by adherent pericardium or scar tissue and is most commonly secondary to myocardial infarction.1Frances C. Romero A. Grady D. Left ventricular pseudoaneurysm.J Am Coll Cardiol. 1998; 32: 557-561https://doi.org/10.1016/s0735-1097(98)00290-3Crossref PubMed Scopus (0) Google Scholar Mortality rate is high both with surgically (23%) and medically (48%) managed patients. Our patient’s previous cardiac surgery was thought to provide him with protection against complete rupture owing to scar tissue formation along the pericardium. The authors have no competing interests. eyJraWQiOiI4ZjUxYWNhY2IzYjhiNjNlNzFlYmIzYWFmYTU5NmZmYyIsImFsZyI6IlJTMjU2In0.eyJzdWIiOiIxNTQxZDIwOGFjOGU1NzExNTdlMjNhZjAyYmQzOWFjZiIsImtpZCI6IjhmNTFhY2FjYjNiOGI2M2U3MWViYjNhYWZhNTk2ZmZjIiwiZXhwIjoxNjcyMjg1NzkzfQ.bVK6mgeslM0bvj2ghgDzATVaMK2nN-hvkaaOINrhzerjUTY0BhHMM0RiEzxLzEbBfhrwaelJakGbXXQRNll3c1A4XIQPAMOuOb2WwBwZngrk3sZqt9PQ4-QR1521dLqyo87FedzewHEVHQp1u1-hU63njZ80S64gIww7AGwvm1GYVyG_PUqN2dsULzDkhx0u4N5mSlj1ic-GJziWbDQxyp_vNNXowt-C79lK4_irrwGt4gwiXrVTBjmVW7EKxw5UnOPiqxuUal_anvunu52uzNW3lrhjfMSIvZiK_HwBXn1MpYIpEXuY1maXiO04cZRMuJsbkyi_csiLCsenlZMhWQ Download .mp4 (0.63 MB) Help with .mp4 files Supplemental Video 1eyJraWQiOiI4ZjUxYWNhY2IzYjhiNjNlNzFlYmIzYWFmYTU5NmZmYyIsImFsZyI6IlJTMjU2In0.eyJzdWIiOiJmNmU1ZDFjYzFjN2ZjM2EwMWM5NDQwZTRiMmVjZTQwMyIsImtpZCI6IjhmNTFhY2FjYjNiOGI2M2U3MWViYjNhYWZhNTk2ZmZjIiwiZXhwIjoxNjcyMjg1NzkzfQ.Llq0S-_MHJRqyeGeS8Jl1MGMOD3jHXaMnSq2_kq2VhClHCQx7UQu2w1bavnJDzW-urKRKWcnlXxIP6c8ScTvUdDnqtsubhEVrzHW2JY3Z0uOy9wcg6B_njlmvDJ7DjHkNV_Wg1UShZnAe4D0BMcCn1xyOhNhnmdAmi6V4c4-scHYs1f39hzgdjf9w5F7dKcuSbIKlkrjtEY_qTeY2cR1xdts7_cPrryda-lMKtQI_u3_dJVyf6V98uOfmi83dlBu4IKiMAQTQqVhegEmZZMM2zW5oeMHuoJNa_Aucg2BGVfu0eSp_755fOFZplx8a3eJo6XSzsB117uy6si2bN1Rig Download .mp4 (1.19 MB) Help with .mp4 files Supplemental Video 2Supplemental Figure 2Predismissal transthoracic echocardiography demonstrating contained left ventricular anterolateral wall rupture with systolic flow through the myocardial defect (green arrow).View Large Image Figure ViewerDownload Hi-res image Download (PPT)eyJraWQiOiI4ZjUxYWNhY2IzYjhiNjNlNzFlYmIzYWFmYTU5NmZmYyIsImFsZyI6IlJTMjU2In0.eyJzdWIiOiI0ZmEyNTIzYzc5NzdlNjg0NTUzNmI2MDcxMDM2ZTcxNSIsImtpZCI6IjhmNTFhY2FjYjNiOGI2M2U3MWViYjNhYWZhNTk2ZmZjIiwiZXhwIjoxNjcyMjg1NzkzfQ.CLfwOf7c_tQ5ApbvTOhJiynY9JIChxJ0Ho88bUeccmwEp0wB49X9Fp6UwMS-Qib5WLnv2_nCIlFxES7Q4iG6BIz_EeZA793g_oji_oHVeYoGnFheqPblch42qUSdCpa-xMBwZcZ8c-gzQhvpS3I5zNtDduAhHgYApS4ZAabBZ_mf8tP7br0YwC9bwnbMsA_bSc96LWkKylKVzz_u0U1GrNP9PsBT48qp0Gx1eVFZH__eZ7YuQ8oU67aqRZrGIWmPiVzth5eA72Hj4DjTmNP5QgIm_xzs2b015kbpEQSmn5UIU2iD4DPfCHR1S9woNUB6-DHnncT-Dl6Z2dLsB5WWeA Download .mp4 (0.57 MB) Help with .mp4 files Supplemental Video 3

Intra-pericardial thrombin injection as bailout strategy in iatrogenic pericardial tamponade.

Cardiac tamponade is arare but life-threatening complication of cardiac interventions. Despite prompt pericardiocentesis, clinical management can be challenging and sometimes haemodynamic stabilisation is difficult to achieve. Intra-pericardial thrombin injection after pericardiocentesis promotes haemostasis and acts as asealing agent, as previously described for left ventricular free-wall rupture. We aimed to evaluate intra-pericardial thrombin injection as abailout strategy for pericardial tamponade following percutaneous cardiac interventions. In a5-year single-centre retrospective analysis we identified 31patients with cardiac tamponade due to percutaneous intracardiac procedures. Intra-pericardial thrombin injection as abailout strategy was administered in 5of 31patients (16.1%). Patients receiving intra-pericardial thrombin were in amore critical state when thrombin was applied, as demonstrated by ahigher rate of resuscitation (40% versus 26.9%) and atrend toward aprolonged stay in the intensive care unit (177.6 ± 84.0 vs 98.0 ± 31.4 h). None of the patients with pericardial tamponades treated with intra-pericardial thrombin needed cardiothoracic surgery. Mortality after 30days was lower with intra-pericardial thrombin injection than with standard treatment (0% vs 15.4%). We observed no complications using intra-pericardial thrombin. Intra-pericardial thrombin injection could be considered as abailout strategy for patients with iatrogenic pericardial tamponade due to percutaneous procedures. We recommend further evaluation of this technique in the clinical management of refractory pericardial tamponade.

Left Ventricular Free-Wall Rupture After Late-Admission STEMI.

This case illustrates a rare but catastrophic complication of acute myocardial infarction, ie, acute rupture of the left ventricular free wall. The majority of patients have hemodynamic impairment on arrival, and a high level of suspicion is needed. Point-of-care echocardiogram is valuable for prompt diagnosis. Management is very challenging and is based on fluid infusion, inotropic support, and pericardiocentesis. Emergency coronary artery bypass grafting and ventricular wall suture may be the only definitive treatment available, although in the majority of cases timely treatment is not possible.

Effects of concomitant coronary artery bypass grafting on early and late mortality in the treatment of post-infarction mechanical complications: a systematic review and meta-analysis.

Mechanical complications of acute myocardial infarction represent life-threatening events, including ventricular septal rupture (VSR), left ventricular free-wall rupture (LVFWR) and papillary muscle rupture (PMR). In-hospital mortality is high, even when prompt surgery can be offered. The role of concomitant coronary artery bypass grafting (CABG) in the surgical treatment of these conditions is still debated. A systematic review of the literature, from 2000 onwards, about these complications was performed, analyzing data of subjects receiving versus not-receiving concomitant CABG. Primary outcome was early mortality. Secondary outcome was late mortality for hospital survivors. Subgroup analysis for VSR, LVFWR and PMR was also performed. Thirty-six studies were identified, including 4,321 patients (mostly VSR-related). Preoperative coronarography was performed in 92.2% of the cases, showing single-vessel disease in 54.3% of patients. Concomitant CABG rate was 49.0%. Early mortality was 32.6% and late mortality was 40.0% with 5.2 years of mean follow-up. The analysis showed no difference in early (OR 0.96; P=0.60) or late mortality (RR 0.91; P=0.49) between CABG and non-CABG group. In subgroup analysis, concomitant CABG was associated with significantly lower mortality at long term for PMR (RR 0.42; P=0.001), although it showed a higher, but not significant, mortality in VSR (RR 1.24; P=0.20). Concomitant CABG in the treatment for post-infarction mechanical complications showed no significant impact on both early and late mortality, although deserving some distinctions among different types of complication and single versus multiple vessel disease. However, larger, dedicated studies are required to provide more consistent data and evidence.

Left ventricular pseudoaneurysm: the niche of post-infarction mechanical complications.

Left ventricular pseudoaneurysm (LVP) is a very rare, but potentially lethal mechanical complication of acute myocardial infarction (AMI). Despite representing a unique subset of cardiac rupture, it presents peculiar features that distinguish it from both ventricular free-wall rupture (FWR) and ventricular true aneurysm. LVP occurs in less than 0.5% of patients affected by AMI. However, LVP is generally burdened by high mortality, often related to false cavity rupture, leading to catastrophic and often irreversible consequences. The risk of rupture is inversely proportional to the timing from AMI onset, which also determines both the classification of LVP and drives the indication for treatment. Despite the lack of a current consensus on LVP management, urgent surgery is the treatment of choice for LVPs occurring within 3 months from AMI, especially if larger than 3 cm in diameter. A matter of debate, however, is represented by chronic LVPs, especially because the risk of rupture decreases progressively as time passes and left ventricular (LV) false cavity stabilizes. Surgical mortality rate remains not negligible (more than 20%), but these suboptimal results may be considered acceptable, especially considering the lethality associated with the occurrence of pseudoaneurysm rupture. Diagnostic workup is essential for anatomical characterization of LV rupture, which is mandatory to guide the decision on surgical approach and technique for pseudoaneurysm repair. Finally, for a subset of patients with anterior LVP and a well-defined fibrotic neck, and deemed at excessively high surgical risk, percutaneous closure of the cavity has been described with encouraging results.

Clinical experience of surgical repair left ventricular rupture after mitral valve replacement

Background: Left ventricular rupture after mitral valve replacement is very rare but often leads to death. This study aimed to report one center experience.
 Methods: Retrospective case series from 2001 to 2021 at the Heart Institute.
 Results: There had 18 cases of left ventricular rupture after mitral valve replacement (0.2%). 94% of patients were female, the mean age at surgery was 57. Rheumatic mitral stenosis (11) or mitral disease (6) occurred in the majority of cases. 6/18 has posterior annulus calcification; 3/18 cases had reoperation after previous mitral valve replacement. The median valve size was 27 (25-29mm). Type I rupture 03; type II: 1 and type III: 14. Time of left ventricular rupture occurrence: early in 5; late in 2 and intermediate in 11 cases. The mortality rate was 61% (11/18). Regarding the repair technique, 8 cases of external repairs, without opening the heart and 10 cases of combined internal and external repairs, reinforced with bio-glue. 100% had supported by extracorporeal circulation and 15/18 cases had inserted intra-aortic balloon counterpulsation.
 Conclusion: preserve the posterior valve as much as possible, gentle resection of the diseased valve, and no need for radical decalcification of the posterior annulus are measures to prevent left ventricular rupture. The combined technique of internal and external repairs with bio-glue coating has shown a good hemostatic and high success rate.

Localized absence of myocardium mimicking a contained left ventricular rupture.

Localized absence of myocardium mimicking a contained left ventricular rupture.

Mechanical complications of acute myocardial infarction: from diagnosis to treatment

Post-infarction mechanical complications include left ventricular free-wall rupture, ventricular septal rupture, and papillary muscle rupture. With the advent of early reperfusion strategies, including thrombolysis and percutaneous coronary intervention, these events now occur in fewer than 0.3% of patients following acute myocardial infarction. However, unfortunately, there has been no parallel decrease in associated mortality rates over the past two decades. Moreover, during the ongoing COVID-19 pandemic the incidence of mechanical complications resulting from ST-elevation myocardial infarction has possibly risen. Early diagnosis and prompt management are crucial to improving outcomes. Although some percutaneous device repair approaches are available, surgical treatment remains the gold standard for these catastrophic post-infarction complications. The timing of surgery, also related to the type of complication and patient's clinical conditions, and the possible role of mechanical circulatory supports before and after surgery, represent main topics of debate that still need to be fully addressed.

ADAM15 is required for optimal collagen cross-linking and scar formation following myocardial infarction

Collagen cross-linking is an important step in optimal scar formation. Myocardial infarction (MI) results in loss of cardiomyocytes that are replaced with a scar (infarct) tissue. Disintegrin and metalloproteinases (ADAMs) are membrane-bound proteases that can interact with molecules intra- and extra-cellularly to mediate various cellular functions. ADAM15 is expressed in the myocardium, however its function in heart disease has been poorly explored. We utilized mice lacking ADAM15 (Adam15−/−) and wildtype (WT) mice. MI, induced by ligation of the left anterior descending artery, resulted in a transient but significant rise in ADAM15 protein in the WT myocardium at 3-days. Following MI, Adam15−/− mice exhibited markedly higher rate of left ventricular (LV) rupture compared to WT mice (66% vs. 15%, p<0.05). Echocardiography and strain analyses showed worsened LV dysfunction in Adam15−/− mice at 3days, prior to the onset of LV rupture. Second harmonic generation imaging revealed significant disarray and reduction in fibrillar collagen density in Adam15−/− compared to WT hearts. This was associated with lower insoluble and higher soluble collagen fractions, reduced cross-linking enzyme, lysyl oxidase-1 (LOX-1), and fibronectin which is required for LOX-1 function, in Adam15−/−-MI hearts. Post-MI myocardial inflammation was comparable between the genotypes. In vitro, primary adult cardiac fibroblasts from Adam15−/− mice showed suppressed activation in response to ischemia (hypoxia+nutrient depletion) compared to WT fibroblasts. Adam15-deficiency was associated with reduced PAK1(p21-activated kinase-1) levels, a regulator of fibronectin and LOX-1 expression. In female mice, the rate of post-MI LV rupture, PAK1 signaling, LOX-1 and fibronectin protein levels were comparable between Adam15−/− and WT, indicating less impact of ADAM15 loss in females post- MI. This study reports a novel function for ADAM15 in collagen cross-linking and optimal scar formation post-MI which may also apply to scar formation in other tissues.

Nausea and Dyspnea on Exertion: Left Ventricular Free-wall Rupture.

Case PresentationA 53-year-old female presented to the emergency department with three days of nausea and dyspnea on exertion after using methamphetamine. Initial electrocardiogram revealed an ST-elevation myocardial infarction. While awaiting transfer to the cardiac catheterization lab the patient suffered a witnessed cardiac arrest. During resuscitative efforts an enlarging pericardial effusion on point-of-care ultrasound led to the detection of a left ventricular free-wall rupture (LVFWR). This case illustrates the progression of a left ventricular free-wall rupture using point-of-care ultrasound.DiscussionLeft ventricular free-wall rupture has a low incidence rate in the setting of an acute myocardial infarction. Ultrasonography is the tool of choice for detecting a LVFWR.

Acute Myocardial Infarction with Microthrombi in Cardiac Small Vessels after COVID-19 Vaccination (ChAdOx1 nCov-19): A Case Report

We present the postmortem findings of an unexpected death due to acute myocardial infarction (AMI) with microthrombi and thrombosis in other vessels after the first dose of coronavirus disease 2019 (COVID-19) vaccination (ChAdOx1 nCov-19). The deceased was a 69-year-old woman who complained of nonspecific symptoms shortly after vaccination and was found dead on the sixth day. Postmortem examination revealed AMI and complications (left ventricular rupture, hemopericardium) with microthrombi in small cardiac vessels, which are similar to the characteristic findings of myocardial injury caused by microthrombi in patients with COVID-19. Nonobstructive thromboembolism in the pulmonary arteries and inferior vena cava, and fibrin microthrombi in some small vessels in the brain were also observed. It is unclear whether these findings are associated with COVID-19 vaccination, and further comprehensive studies are needed.

All left ventricular free wall ruptures are not the same: Our experience

All left ventricular free wall ruptures are not the same: Our experience

Left Ventricular Pseudoaneurysm and Left Ventricular Thrombus in a Patient Presenting with an Acute ST-Elevation Myocardial Infarction

Patient: Male, 73-year-old Final Diagnosis: Pseudoaneurysm • thrombus Symptoms: Chest pain • sycope Medication: — Clinical Procedure: — Specialty: General and Internal Medicine Objective: Unusual clinical course Background:ST-elevation myocardial infarction (STEMI), when associated with acute left ventricular (LV) free-wall rupture, is often a lethal complication, and if not followed by sudden death, the rupture may be contained by the parietal pericardium and a local thrombus, leading to the formation of a left ventricular (LV) pseudoaneurysm. The incidence of LV pseudoaneurysm after STEMI is ~ 0.3%.Case Report:A 73-year-old man who presented with an acute syncopal episode and intermittent chest pain for 7 days was found to have an anterolateral myocardial infarction (MI) with lateral wall rupture and pseudoaneurysm formation. He had an LV thrombosis in the LV aneurysm. While this increased his risk of thromboembolic events, it likely stopped the evolution of the rupture and stabilized the pericardial effusion size. The patient underwent coronary artery bypass grafting (CABG), thrombectomy, and lateral wall repair.Conclusions:Left ventricular pseudoaneurysm and left ventricular thrombus in a patient presenting with an acute ST-elevation myocardial infarction is a rare complication of myocardial infraction, with an incidence of <1%. It is often a lethal complication and requires stabilization and repair if not followed by sudden death.

Double-patch repair of left ventricular rupture after mitral valve replacement

Cardiovascular Surgery and Interventions publishes original articles on topics in cardiovascular surgery, cardiovascular anesthesia and cardiology. These encompass all relevant clinical, surgical and laboratory studies, editorials, current and collective reviews, technical know-how papers, case reports, interesting images, “How to Do It” papers, correspondence and commentary.