SURGICAL TREATMENT OF PSEUDOANEURYSM OF THE FREE LEFT VENTRICLE WALL: A CLINICAL CASE

Today diseases of the cardiovascular system are the leading cause of death in many countries. The key role in this pathology is played by ischemic heart disease. An extreme manifestation of ischemic heart disease - myocardial infarction is one of the main causes of complications and mortality in patients with ischemic heart disease. One of the most formidable complications of acute myocardial infarction is heart rupture, which most often leads to death, more than 60% of cases occurring in the prehospital stage. Many studies of similar groups of patients show a wide spread in assessing the incidence and mortality of this pathology. The development of myocardial ruptures has two frequency peaks: the first day and 5-7 days from the onset of AMI. The most common case is acute rupture of the free wall of the left ventricle with extensive hemorrhage in the pericardium leading to a fulminant death. The development of a pseudoaneurysm of the left ventricle is a very rare outcome of the myocardial rupture. There are no convincing data on the incidence of pseudoaneurysms as a result of myocardial infarction (according to many authors, it is less than 0.5% of all cases of myocardial infarction). This type of rupture is most favorable in terms of the possibility of providing assistance. The complexity of providing care to patients with pseudoaneurysms of the left ventricle lies in their low frequency of occurrence and often asymptomatic nature of the course, which complicates the diagnosis of this pathology. Timely diagnosis plays a key role in avoiding a fatal outcome, since the vast majority of pseudoaneurysms are extremely unstable and, except occasional cases, require urgent surgical intervention. This article describes a clinical case of a patient who underwent surgical treatment for pseudoaneurysm of the free wall of the left ventricle as a result of myocardial infarction. The article also presents a brief literature review of the available isolated data on risk factors for myocardial rupture, methods of diagnosis and treatment of this pathology.

Left-sided primary cardiac lymphoma: a case report

Background Primary cardiac lymphoma (PCL) is a rare neoplasm, defined as lymphoma with the main bulk localized in the heart; diffuse large B cell lymphoma (DLBCL) is the most common type. It usually involves the pericardium and the right heart and has a poor prognosis with a median survival of less than 1 year. Case presentation A 62-year-old female presented to the emergency department for palpitations and recent-onset dyspnea. The echocardiogram showed a round-shaped mass (33 x 32 mm) in the left atrium, a mild circumferential pericardial effusion, and a hyperechogenic mass at the level of the atrio-ventricular junction. A thoracic CT scan demonstrated the presence of a bulky mediastinal mass, strictly attached to the left heart and infiltrating its posterior wall, the left pulmonary veins, and the inferior lobar bronchus. The patient underwent CT-guided biopsy, and the diagnosis of double-expressor DLBCL was made. Given the potential risk of heart rupture during chemotherapy, the first cycle of R-CHOP was performed in an in-hospital setting, with initial benefit. After completing 6 cycles of R-CHOP, imaging studies showed rapid progression of the disease; the patient was started on the salvation protocol R-DHAOX but died of septic shock 10 months later. Conclusions PCL is rare and accounts for less than 2% of primary cardiac tumors; double-expressor DLBCL carries a poor prognosis. As in most cases, the diagnosis was made after the onset of nonspecific symptoms (dyspnea) but—despite the strong predilection for right heart involvement reported in literature—our patient had a predominant left atrial infiltration.

Blood group A: a risk factor for heart rupture after acute myocardial infarction

Introduction Studies have been performed to identify the association between ABO blood groups and coronary artery disease. However, data is scarce about the impact of ABO blood groups on heart rupture (HR) after acute myocardial infarction (AMI). Methods We conducted a retrospective case–control study that included 61 consecutive patients with HR after AMI during a period from 1 January 2012 to 1 December 2019. The controls included 600 patients who were selected randomly from 8143 AMI patients without HR in a ratio of 1:10. Univariate and multivariate logistic regression analysis were used to identify the association between ABO blood groups and HR. Results Patients with blood group A had a greater risk of HR after AMI than those with non-A blood groups (12.35% vs 7.42%, P < 0.001). After adjusting for age, gender, heart rate at admission, body mass index (BMI), and systolic blood pressure (SBP), blood group A was independently related to the increased risk of HR after AMI (OR = 2.781, 95% CI 1.174–7.198, P = 0.035), and remained as an independent risk factor of HR after AMI in different multivariate regression models. Conclusion Blood group A is significantly associated with increased HR risk after AMI.

Abstract 223: Yap and Its Homolog Wwtr1 Are Regulators of Myofibroblast Activation Following Ischemic Injury

Introduction: Following ischemic injury in adult mammals, cardiac fibroblasts differentiate into myofibroblasts and promote secretion of matrix fibers. Myofibroblast activation is critical for initial scar formation and preventing heart rupture, however, extended activity can lead to heart failure progression. Thus, there is a need to identify the mechanisms mediating persistent activation of myofibroblasts to prevent excessive fibrosis and adverse cardiac remodeling. Here we demonstrate that Hippo-Yap pathway offers a target for modulating myofibroblast activation and thus the fibrotic response. Methods and Results: We tested the hypothesis that Yap and its homolog Wwtr1 (known as ‘Taz’) are regulators of myofibroblast activation following ischemic injury. We implemented a Cre-lox system whereby Yap alone or both Yap and Wwrt1 were depleted using an inducible Cre expressed under a myofibroblast specific promoter ( Postn MCM ). Following permeant ligation of the left anterior descending artery in adult mice, we found that myofibroblast depletion of Yap alone resulted in a significant reduction in left ventricular dilation 28 days post injury (dpi) and decreased proliferation of scar associated cells. Strikingly, myofibroblast specific depletion of Yap and one copy of Wwrt1 resulted in further attenuation of left ventricular dilation as well as improved fractional shortening and ejection fraction at 28 and 60 dpi. Histological assessment revealed that depletion of both Yap and Wwrt1 resulted in greater than 50% reduction in scar size (by midline) at 60 dpi. RNAseq of whole hearts collected at 4 dpi suggested that Hippo-Yap pathway expression specifically in myofibroblasts facilitates immune cell recruitment in the heart. Collectively These data illustrate a role for Hippo-Yap signaling mediating myofibroblast activity and immune cell coordination following injury and therefore cardiac fibrosis and remodeling. Conclusions: Our data demonstrate that endogenous Yap and Wwrt1 deletion in myofibroblasts suppresses the fibrotic response, mediates inflammation, and improves cardiac function after ischemic injury. These results therefore offer a regulatory pathway that can be targeted therapeutically to prevent progressive heart failure.

Interventricular Septal Rupture in a 62-Year-Old Man With Familial Amyloid Polyneuropathy

Cardiac involvement in familial amyloid polyneuropathy consists of arrhythmias, conduction disturbances, and heart failure. To our knowledge, heart rupture has never been described in association with this condition. We report the case of a 62-year-old man with a 6-year history of refractory familial amyloid polyneuropathy who underwent liver transplantation. The operation was complicated by severe hypotension because the neuropathy involved the autonomic system. Perioperatively, the patient had a myocardial infarction, and during the next 10 days, a complete interventricular septal rupture developed, resulting in a systemic-to-pulmonary shunt. Coronary angiographic findings were normal. However, the shunt caused unstable hemodynamics, resulting in cardiogenic shock. An attempt to close the rupture percutaneously failed. The patient underwent successful heart transplantation 50 days later. Macroscopic examination of the explanted heart showed thickening of both ventricles, septal rupture, and a gray scar in the interventricular septum around the cavity. Histopathologic examination revealed intramural amyloid angiopathy. Our case shows that heart rupture can occur in patients with familial amyloid polyneuropathy who have no history of obstructive coronary artery disease, perhaps as a result of tissue fragility caused by amyloid angiopathy. Therefore, autonomic disturbances should be regarded with concern and promptly treated in the perioperative period.

TIMING OF SURGICAL INTERVENTION AFTER VENTRICULAR SEPTAL RUPTURE

Ventricular septal rupture (VSR) is a rare but lethal complication of acute myocardial infarction (AMI). patients presenting with ST-elevation MI (STEMI) were evaluated for heart rupture (VSR ) based on reperfusion strategy. , After undergoing a primary percutaneous coronary intervention (PCI), VSR was reported to occur in 0.23-0.71% of patients. Post-infarction VSR carries significant mortality (36.%) despite aggressive surgical management. Rupture develops after full-thickness (transmural) infarction of the ventricular septum and can occur at any anatomic location. Ventricular septal rupture is likely to be associated with total occlusion of the infarct-related artery. the newly formed communication results in left to right shunting of oxygenated blood from the high-pressure left ventricle to the lower-pressure right ventricle. .Mortality was highest in patients who underwent operation in the first 24 h, consistent with other investigators. The case reflects the important problem after myocardial infarction , ventricular septal rupture and challenges the timing of intervention Patient 70 year old,male,caucasion was admitted in our hospital with encephalopathy and hypotension.ECG revealed ST segment elevation in II,III,AVF,V4-V6 lead,ST segment depression in AVL,V1-V3 lead. Koronarography detected left main artery without important stenosis, 95 % stenosis of middle segment and 75% stenosis of distal part of left anterior descending artery.40% stenosis of middle segment of right coronary artery, occlusion of posterior descending artery.After recanalization and balloon predilatation of posterior descending artery, was parformed drug eluted stant implantation. transthoracic echocardiography (TTE) detected of postinfarction VSR (pict 3). The Colour Doppler was demonstrated of flow across the septum and left to rigt shunt. Conclusion: Ventricular septal rupture (VSR) is a rare but lethal complication of acute myocardial infarction (AMI). Mortality of patients is significantly depending o n timing of surgery. Operative management of patients can be complex, and having a systematic approach is helpful. The cornerstone of medical management of VSR is afterload reduction, and may be considered routine care.. According our case , surgical intervention was delayed and dispite adequate treatment patient was died . There is no clear evidence to guide the surgical management of patients who are in shock, as all approaches have shown extremely high mortality. Possible strategies include emergent surgery on individuals with marked haemodynamic instability and circulatory compromise.