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.

Transcatheter edge-to-edge mitral valve repair for post-myocardial infarction papillary muscle rupture and acute heart failure: A systematic review.

Papillary muscle rupture (PMR) is a rare complication of acute myocardial infarction (AMI) associated with high mortality and morbidity. Surgery is the gold-standard treatment for these patients, but it is burdened by a high perioperative risk due to hemodynamic instability. Mitral transcatheter edge-to-edge repair (M-TEER) was reported to be safe and effective in unstable patients with significant mitral regurgitation. However, data in patients with post-AMI PMR are limited to a few case reports. In this review, we summarized all data available regarding percutaneous treatment of post-AMI PMR. These results show that M-TEER is safe and effective in this setting with low in-hospital mortality and complications and high rate of significant mitral regurgitation reduction.

Recent insights into pathophysiology and management of mechanical complications of myocardial infarction.

PURPOSE OF REVIEW: Mechanical complications of myocardial infarction are a group of postischemic events and include papillary muscle rupture resulting in ischemic mitral regurgitation, ventricular septal defect, left ventricle free wall rupture, pseudoaneurysm, and true aneurysm. Advances made in management strategies, such as the institution of 'Code STEMI' and percutaneous interventions, have lowered the incidence of these complications. However, their presentation is still associated with increased morbidity and mortality. Early diagnosis and appropriate management is crucial for facilitating better clinical outcomes. RECENT FINDINGS: Although the exact timing of a curative intervention is not known, emerging percutaneous and transcatheter approaches and improving mechanical circulatory support (MCS) devices have greatly enhanced our ability to manage and treat some of the complications postinfarct. SUMMARY: Although the incidence of mechanical complications of myocardial infarction has decreased over the past few decades, these complications are still associated with high rates of morbidity and mortality. The combination of early and accurate diagnosis and subsequent appropriate management are imperative for optimizing clinical outcomes. Although more randomized clinical trials are needed, mechanical circulatory support devices and emerging therapeutic strategies can be offered to carefully selected patients.

Survival after left ventricular free wall rupture following acute myocardial infarction by conservative treatment.

Left ventricular free wall rupture (LVFWR) is a rare and fatal mechanical complication following an acute myocardial infarction (AMI). Cases of survival after LVFWR due to ST-segment elevation myocardial infarction (STEMI) treated with a conservative treatment strategy are extremely rare. In this case, a 55-year-old male patient with several cardiovascular risk factors presented to the emergency department with symptoms of ongoing chest pain and syncope. The patient's electrocardiogram was in sinus rhythm with ST-elevation on I, aVL, and V4-6 leads. His myoglobin and troponin I levels were elevated. Due to the unstable hemodynamic state of the patient, bedside echocardiography was performed. The echocardiography indicated LVFWR after AMI. Pericardiocentesis was used to restore a satisfactory hemodynamic state in the patient. Following the initial treatment, the patient opted for a conservative treatment strategy and was uneventfully discharged after 19 days.

Unusual presentations of cardiac rupture during COVID-19 pandemic.

The Covid-19 pandemia has many other undesirable consequences apart of virus infection. Less people is hospitalized due to acute coronary syndrome and the delay to seek medical attention has increased. Patients with ST segment elevation myocardial infarction arrive at the hospital too late to be timely treated and we have recently seen mechanical complications that were more frequent in the past decades before the use of reperfusion strategies. In this report we describe the presentation, evolution and detailed imaging evaluation of two patients with unusual presentations of cardiac rupture: left ventricular pseudoaneurysm and left ventricular intramyocardial dissecting hematoma.

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.

Cardiac rupture complicating acute myocardial infarction: the clinical features from an observational study and animal experiment.

BACKGROUND: Cardiac rupture (CR) is a fatal complication of ST-elevation myocardial infarction (STEMI) with its incidence markedly declined in the recent decades. However, clinical features of CR patients now and the effect of reperfusion therapy to CR remain unclear. We investigated the clinical features of CR in STEMI patients and the effect of reperfusion therapy to CR in mice. METHODS: Two studies were conducted. In clinical study, data of 1456 STEMI patients admitted to the First Hospital, Xi'an Jiaotong University during 2015.12. ~ 2018.12. were analyzed. In experimental study, 83 male C57BL/6 mice were operated to induce MI. Of them, 39 mice were permanent MI (group-1), and remaining mice received reperfusion after 1 h ischemia (21 mice, group-2) or 4 h ischemia (23 mice, group-3). All operated mice were monitored up to day-10. Animals were inspected three times daily for the incidence of death and autopsy was done for all mice found died to determine the cause of death. RESULTS: CR was diagnosed in 40 patients: free-wall rupture in 17, ventricular septal rupture in 20, and combined locations in 3 cases. CR presented in 19 patients at admission and diagnosed in another 21 patients during 1 ~ 14 days post-STEMI, giving an in-hospital incidence of 1.4%. The mortality of CR patients was high during hospitalization accounting for 39% of total in-hospital death. By multivariate logistic regression analysis, older age, peak CK-MB and peak hs-CRP were independent predictors of CR post-STEMI. In mice with non-reperfused MI, 17 animals (43.6%) died of CR that occurred during 3-6 days post-MI. In MI mice received early or delayed reperfusion, all mice survived to the end of experiment except one mouse died of acute heart failure. CONCLUSION: CR remains as a major cause of in-hospital death in STEMI patients. CR patients are characterized of being elderly, having larger infarct and more server inflammation. Experimentally, reperfusion post-MI prevented CR.

The evolution of left ventricular pseudoaneurysm from the rupture of left ventricular free wall following acute myocardial infarction: a case report.

BACKGROUND: Left ventricular pseudoaneurysm is a very rare complication following acute myocardial infarction, which results from a free wall rupture. Hemopericardium and cardiac tamponade caused by rupture of the free wall after acute myocardial infarction are often fatal. It is difficult to fully document the evolution of left ventricular pseudoaneurysm resulted from acute myocardial infarction with conservative treatment. CASE PRESENTATION: Herein, we followed a 75-year-old female patient for 3 years. Recorded the evolution of the disease: acute lateral myocardial infarction - emergency reperfusion therapy - cardiac rupture - positive successful rescue - the pseudoaneurysm formation - maintaining conservative treatment - gradual enlargement of the pseudoaneurysm - thrombosis in pseudoaneurysm - thrombus filling with pseudoaneurysm - finally stabilized condition - the treatment of coronary revascularization. CONCLUSIONS: This case is reported here because of its scarcity, which provides provides us with a complete record of the entire evolution and an astonishing indication of the long-term prognosis of non-surgical treatment for pseudoventricular.

Combination of eosinophil percentage and high-sensitivity C-reactive protein predicts in-hospital major adverse cardiac events in ST-elevation myocardial infarction patients undergoing primary percutaneous coronary intervention.

BACKGROUND: Eosinophil levels predict prognosis in ST-segment elevation myocardial infarction (STEMI) patients. Both eosinophils and high-sensitivity C-reactive protein (hs-CRP) play a major role in the acute inflammatory response of myocardial infarction. The purpose of this study was to evaluate eosinophil percentage (EOS%) and hs-CRP as prognostic markers for in-hospital adverse events in STEMI patients undergoing primary percutaneous coronary intervention. METHODS: We retrospectively analyzed the clinical data of 518 patients. Major adverse cardiac events (MACEs) were defined as cardiac rupture, cardiac arrest, malignant arrhythmia, and cardiac death. Based on the receiver operating characteristic (ROC) analysis, all patients were regrouped into 3 groups (None, One, and Two) according to cutoff EOS% value (≤0.3%) and hs-CRP value (>11.8 mg/L). Both Cox regression analyses and the KM (Kaplan-Meier) survival curve were used to examine the prognostic role of combined hs-CRP and EOS% in cardiovascular events. RESULTS: Of the 518 STEMI patients, 50 of them developed MACEs. Patients who developed MACEs had a significantly lower EOS% and higher hs-CRP than patients who remained MACE-free. In the multivariable Cox regression analysis, the highest risk of in-hospital MACEs was constantly observed in patients with a combined low EOS% and elevated hs-CRP. Patients with reduced EOS% and high hs-CRP had significantly higher incidence rates of cardiac rupture (P = .001), cardiac arrest (P = .001), and malignant arrhythmia (P < .001); furthermore, they had the worst cumulative survival compared with the other two groups. CONCLUSION: Combined reduced EOS% and elevated hs-CRP were valuable tools for identifying patients at risk of in-hospital MACEs.

Clinical Manifestation, Timing Course, Precipitating Factors, and Protective Factors of Ventricular Free Wall Rupture Following ST-Segment Elevation Myocardial Infarction.

Ventricular free wall rupture (FWR) is a catastrophic complication of that occurs after acute myocardial infarction (AMI), and at present, its clinical characteristics are unclear. We analyzed a total of 6,712 consecutive patients who presented with ST-segment elevation myocardial infarction (STEMI), and 78 patients with FWR after STEMI were enrolled in the study. Patients' demographic data, clinical manifestation, laboratory test results, and angiographic features were then collected and analyzed. FWR occurred in 78 cases (1.16%), and the inhospital mortality of FWR was up to 92.3%. Among the 78 FWR patients, 72 obtained accurate rupture time. FWR typically occurred within the first week after the infarct. Compared to late-phase FWR (more than 48 hours after STEMI) patients, early-phase FWR (during 48 hours after STEMI) patients showed significantly higher random glucose and higher percentage of anterior myocardial infarction. Besides, dual antiplatelet therapy (DAPT), ß-blockers, and angiotensin-converting enzyme inhibitors/angiotensin receptor blocker (ACEI/ARB) were used less frequently in early-phase FWR patients. Moreover, we first reported the precipitating factors of FWR. Defecating, transporting, acute emotional upset, diets, and invasive treatment turned out to be the main triggers for FWR. Furthermore, we found that patients who survived from FWR were younger, had higher ß-blocker coverage in the inhospital treatment, and had a higher frequency of primary PCI. FWR remains an infrequent but devastating complication of STEMI. We have found several factors related to the occurrence and prognosis of FWR. This study provides evidence for a better understanding of FWR.

Ventricular free wall rupture-a rare under-diagnosed fatal complication of myocardial infarction.

Ventricular free wall rupture is a rare complication of acute myocardial infarction (MI) i.e. <1.7% of cases, although it occurs more frequently than might be expected. Without imaging evidence or autopsy, sudden cardiac death in acute MI setting is commonly attributed to fatal dysrhythmias, high degree atrio-ventricular blocks or pulmonary embolism resulting in underdiagnosis of free wall rupture. Modern therapies have probably reduced the incidence but not eliminated the problem. We present a case of left ventricular free wall rupture in acute MI setting and syncopal presentation. The diagnosis was established during left heart catheterisation and further confirmed on transthoracic echocardiography. The patient deteriorated abruptly, pericardial window was made to bridge for surgical repair. Unfortunately, the patient died before surgical intervention.

Myeloid receptor CD36 is required for early phagocytosis of myocardial infarcts and induction of Nr4a1-dependent mechanisms of cardiac repair.

Phagocytosis after myocardial infarction (MI) is a prerequisite to cardiac repair. Recruited monocytes clear necrotic cardiomyocytes and differentiate into cardiac macrophages. Some studies have linked apoptotic cell receptors on cardiac macrophages to tissue repair; however, the contribution of precursor monocyte phagocytic receptors, which are the first to interact with the cardiac parenchyma, is unclear. The scavenger receptor cluster of differentiation (CD)36 protein was detected on cardiac Ly6cHI monocytes, and bone marrow-derived Cd36 was essential for both early phagocytosis of dying cardiomyocytes and for smaller infarct sizes in female and male mice after permanent coronary ligation. Cd36 deficiency led to reduced expression of phagocytosis receptor Mertk and nuclear receptor Nr4a1 in cardiac macrophages, the latter previously shown to be required for phagocyte survival. Nr4a1 was required for phagocytosis-induced Mertk expression, and Nr4a1 protein directly bound to Mertk gene regulatory elements. To test the overall contribution of the Cd36-Mertk axis, MI was induced in Cd36-/- Mertk-/- double-knockout mice and led to increases in myocardial rupture. These data implicate monocyte CD36 in the mitigation of early infarct size and transition to Mertk-dependent macrophage function. Increased myocardial rupture in the absence of both Cd36 and Mertk underscore the physiologic significance of phagocytosis during tissue injury.-Dehn, S., Thorp, E. B. Myeloid receptor CD36 is required for early phagocytosis of myocardial infarcts and induction of Nr4a1-dependent mechanisms of cardiac repair.

Left ventricular free-wall rupture, a potentially lethal mechanical complication of acute myocardial infarction: an unusual and illustrative case report.

BACKGROUND: There are three major mechanical complications after acute myocardial infarction: left ventricular free-wall rupture, ventricular septum rupture and acute mitral valve regurgitation. The left ventricular free-wall rupture is a serious and often lethal complication following an ST elevation myocardial infarction. However, very rarely this rupture can be contained by the pericardium, forming a pseudoaneurysm. CASE PRESENTATION: We report a case of a 66-year-old man with multiple cardiovascular risk factors and previous ST elevation myocardial infarction, complaining of atypical chest pain. His electrocardiogram was in normal sinus rhythm, with the presence of Q wave in inferior leads and T-wave inversion in lateral leads. A transthoracic echocardiogram showed a left ventricular pseudoaneurysm. In the coronary angiography, multi-vessel disease was found. On-pump CABG was performed and a posterolateral left ventricular giant pseudoaneurysm were observed. Due its "petrous" consistency it was impossible to perform an aneurysmectomy. CONCLUSIONS: The diagnosis of left ventricular pseudoaneurysm can be difficult, as patients often present either asymptomatic or with non-specific symptoms attributed to other causes. A multimodality imaging diagnostic approach can be necessary. Immediate surgery is considered the treatment of choice because untreated pseudoaneurysms have a high risk of rupture leading to cardiac tamponade, shock and death.

Mechanical, inflammatory, and embolic complications of myocardial infarction: An emergency medicine review.

INTRODUCTION: Despite the declining incidence of coronary heart disease (CHD) in the United States, acute myocardial infarction (AMI) remains an important clinical entity, with many patients requiring emergency department (ED) management for mechanical, inflammatory, and embolic complications. OBJECTIVE: This narrative review provides an evidence-based summary of the current data for the emergency medicine evaluation and management of post myocardial infarction mechanical, inflammatory, and embolic complications. DISCUSSION: While 30-day mortality rate after AMI has decreased in the past two decades, it remains significantly elevated at 7.8%, owing to a wide variety of subacute complications evolving over weeks. Mechanical complications such as ventricular free wall rupture, ventricular septal rupture, mitral valve regurgitation, and formation of left ventricular aneurysms carry significant morbidity. Additional complications include ischemic stroke, heart failure, renal failure, and cardiac dysrhythmias. This review provides several guiding principles for management of these complications. Understanding these complications and an approach to the management of various complications is essential to optimizing patient care. CONCLUSIONS: Mechanical, inflammatory, and embolic complications of AMI can result in significant morbidity and mortality. Physicians must rapidly diagnose these conditions while evaluating for other diseases. In addition to understanding the natural progression of disease and performing a focused physical examination, an electrocardiogram and bedside echocardiogram provide quick, noninvasive determinations of the underlying pathophysiology. Management varies by presentation and etiology, but close consultation with cardiology and cardiac surgery is recommended.

Intramyocardial dissecting hematoma: Two case reports and a meta-analysis of the literature.

Until recently, diagnosis of intramyocardial dissecting hematoma (IDH) was performed during necropsy or at surgery. During the recent years, echocardiography has permitted clinical suspicion, which usually needed confirmation with magnetic resonance imaging (MRI). In this study, we tried to define clinical and imaging features of IDH and predictors of mortality. We searched the literature for proven cases of IDH and analyzed them together with 2 of our cases. A total of 40 cases of IDH (2 our original and 38 literature cases) were included. Mean age was 60. In 32 cases, IDH was a complication of myocardial infarction (MI), in 66% anterior, a mean time from symptoms to diagnosis was 9 days. Thirty-eight % underwent surgery. In-hospital mortality was 23%. Multivariate analysis showed that the strongest independent predictor of mortality (42%) was EF < 35%; in patients with age >60, mortality risk was 44%; and in the presence of MI or late diagnosis (>24 hours since symptoms started), mortality risk was 50%. In summary, IDH is a diagnostic challenge. A high level of suspicion is needed for prompt diagnosis. Management of these patients is based on individual clinical and imaging parameters. Low EF, age > 60, and late diagnosis, all are predictors of in-hospital mortality.

Inhibition of the Renin-Angiotensin System Post Myocardial Infarction Prevents Inflammation-Associated Acute Cardiac Rupture.

PURPOSE: Inhibition of the renin-angiotensin system (RAS) is beneficial in patient management after myocardial infarction (MI). However, whether RAS inhibition also provides cardiac protection in the acute phase of MI is unclear. METHODS: Male 129sv mice underwent coronary artery occlusion to induce MI, followed by treatment with losartan (L, 20 and 60 mg/kg), perindopril (P, 2 and 6 mg/kg), amlodipine (20 mg/kg as a BP-lowering agent) or vehicle as control. Drug effects on hemodynamics were examined. Effects of treatments on incidence of cardiac rupture, haematological profile, monocyte and neutrophil population in the spleen and the heart, cardiac leukocyte density, expression of inflammatory genes and activity of MMPs were studied after MI. RESULTS: Incidence of cardiac rupture within 2 weeks was significantly and similarly reduced by both losartan (L) and perindopril (P) in a dose-dependent manner [75% (27/36) in vehicle, 40-45% in low-dose (L 10/22, P 8/20) and 16-20% (L 5/32, P 4/20) in high-dose groups, all P < 0.05]. This action was independent of their BP-lowering action, as amlodipine reduced BP to a similar degree without effect on rupture (70%, 21/30). Compared to the control group, high dose losartan and perindopril decreased counts of white blood cells, neutrophils and lymphocytes (all P < 0.05), and inhibited splenic monocyte and neutrophil release into the circulation. Consequently, monocyte, neutrophil and leukocyte infiltration, inflammatory gene expressions (IL-1ß, IL-6, MMP9, MCP-1, TNF-α and TGFß1) and activity of MMP2 and MMP9 in the infarct tissue were attenuated by losartan and/or perindopril treatment (all P < 0.05). CONCLUSIONS: RAS inhibition by losartan or perindopril prevented cardiac rupture at the acute phase of MI through blockade of splenic release of monocytes and neutrophils and consequently attenuation of systemic and regional inflammatory responses.

A Case of Anterolateral Papillary Muscle Rupture Caused by Isolated First Diagonal Branch Occlusion.

A 74-year-old man hospitalized due to acute myocardial infarction (AMI) of the first diagonal branch developed cardiogenic shock. Ultrasonography showed anterolateral papillary muscle rupture (PMR) which caused anterior mitral leaflet prolapse and severe mitral valve regurgitation, and he successfully underwent mitral valve replacement. Anterolateral PMR causing anterior mitral leaflet prolapse due to obstruction of the first diagonal branch is rare and should be considered in such an AMI case.