[Percutaneous treatment of post-acute myocardial infarction mechanical complications: state of the art]. / Trattamento percutaneo delle complicanze meccaniche dell'infarto miocardico acuto: stato dell'arte.

Left ventricular free wall rupture, ventricular pseudoaneurysm, papillary muscle rupture and ventricular septal rupture are life-threatening mechanical complications of acute myocardial infarction. Despite significant improvements over the last decades in overall mortality for patients with myocardial infarction, the outcome of subjects who develop post-infarction mechanical complications remains poor. Surgical treatment is considered the standard of care. However, percutaneous approaches (such as pericardial fibrin-glue injection for left ventricular free wall rupture, transcatheter edge-to-edge mitral repair for papillary muscle rupture and device closure for ventricular pseudoaneurysm or septal rupture) have been proposed in selected high-risk or inoperable patients, or in subjects with ideal characteristics for feasibility, as therapeutic alternatives to open surgery. The aim of the present review is to provide a comprehensive overview of the percutaneous strategies for the management of post-acute myocardial infarction mechanical complications.

Mechanical Complications of Acute Myocardial Infarction: A Review.

Importance: Mechanical complications of acute myocardial infarction include left ventricular free-wall rupture, ventricular septal rupture, papillary muscle rupture, pseudoaneurysm, and true aneurysm. With the introduction of early reperfusion therapies, these complications now occur in fewer than 0.1% of patients following an acute myocardial infarction. However, mortality rates have not decreased in parallel, and mechanical complications remain an important determinant of outcomes after myocardial infarction. Early diagnosis and management are crucial to improving outcomes and require an understanding of the clinical findings that should raise suspicion of mechanical complications and the evolving surgical and percutaneous treatment options. Observations: Mechanical complications most commonly occur within the first week after myocardial infarction. Cardiogenic shock or acute pulmonary edema are frequent presentations. Echocardiography is usually the first test used to identify the type, location, and hemodynamic consequences of the mechanical complication. Hemodynamic stabilization often requires a combination of medical therapy and mechanical circulatory support. Surgery is the definitive treatment, but the optimal timing remains unclear. Percutaneous therapies are emerging as an alternative treatment option for patients at prohibitive surgical risk. Conclusions and Relevance: Mechanical complications present with acute and dramatic hemodynamic deterioration requiring rapid stabilization. Heart team involvement is required to determine appropriate management strategies for patients with mechanical complications after acute myocardial infarction.

[A septal rupture of atypical location after myocardial infarction. A clinical case]. / Ruptura septal de localización atípica posterior a infarto del miocardio. Caso clínico

Paciente masculino de 46 años de edad con antecedentes personales de hipertensión arterial sistémica, tabaquismo y etilismo y heredofamiliares de hipertensión arterial sistémica. El padecimiento inició con cuadro de astenia, adinamia, disnea progresiva, edema de miembros inferiores y aumento del volumen abdominal, por lo que acudió con el médico, quien decidió hospitalizarlo. El paciente recibió tratamiento médico con captopril, furosemida y espironolactona, sin mejoría de los síntomas, motivo por el cual se lo refirió a la institución de los autores. Al llegar al servicio de urgencias, el sujeto se encontraba estable.

Cardiac Lymphoma Presenting with Recurrent STEMI.

The incidence of primary cardiac tumors is exceedingly rare, whereas secondary cardiac tumors are more common in the global population. Cardiac involvement is seen in approximately 18% of patients with non-Hodgkin's lymphoma at the time of autopsy. Clinical manifestations of cardiac involvement are subtle and often go unrecognized until advanced stages of the disease. We present a rare case of metastatic cardiac lymphoma that presented as an ST-segment elevation myocardial infarction complicated by left ventricular free wall rupture and cardiogenic shock due to transmural myocardial necrosis from malignant cell infiltration.

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.

Temporal Trends in Mechanical Complications of Acute Myocardial Infarction in the Elderly.

BACKGROUND: Reperfusion therapy led to an important decline in mortality after ST-segment elevation myocardial infarction (STEMI). Because the rate of cardiogenic shock has not changed dramatically, the authors speculated that a reduction in the incidence or fatality rate of mechanical complications (MCs), the second cause of death in these patients, could explain this decrease. OBJECTIVES: This study sought to assess time trends in the incidence, management, and fatality rates of MC, and its influence on short-term mortality in old patients with STEMI. METHODS: Trends in the incidence and outcomes of MC between 1988 and 2008 were analyzed by Mantel-Haenszel linear association test in 1,393 consecutive patients ≥75 years of age with first STEMI. RESULTS: Overall in-hospital mortality decreased from 34.3% to 13.4% (relative risk reduction, 61%; p < 0.001). Although the absolute mortality due to MC decreased from 9.6% to 3.3% (p < 0.001), the proportion of deaths due to MC among all deaths did not change (28.1% to 24.5%; p = 0.53). The incidence of MC decreased from 11.1% to 4.3% (relative risk reduction 61%) with no change in their hospital fatality rate over time (from 87.1% to 82.4%; p = 0.66). The proportion of patients undergoing surgical repair decreased from 45.2% to 17.6% (p = 0.04), with no differences in post-operative survival (from 28.6% to 33.3%; p = 0.74). CONCLUSIONS: Although the incidence of MC has decreased substantially since the initiation of reperfusion therapy in elderly STEMI patients, this reduction was proportional to other causes of death and was not accompanied by an improvement in fatality rates, with or without surgery. MCs are less frequent but remain catastrophic complications of STEMI in these patients.

Off-pump hemostasis for left ventricular rupture after myocardial infarction with Hydrofit® and Surgicel®.

Left ventricular free wall rupture (LVFWR) is a catastrophic complication of myocardial infarction. In these cases, cardiopulmonary bypass (CPB) should be performed for left ventricular repair, but can impact hemodynamic stability. An 87-year-old man presented with acute shock. He was diagnosed with LVFWR after myocardial infarction. We describe a simple, effective, and reproducible technique to achieve hemostasis at the LVFWR site during emergency operation using Hydrofit® and Surgicel® surgical hemostatic agents. We simply placed and manually pressed the Hydrofit® and Surgicel® composite on the bleeding site. This technique provides complete hemostasis without CPB establishment.

Lateral left ventricular wall rupture following acute myocardial infarction: pathophysiological interpretation by multimodality imaging approach.

Lateral left ventricular wall rupture (LVWR) is a rare complication following acute myocardial infarction (AMI) less than 1%. After cardiogenic shock, LVWR constitutes the most common cause of in-hospital death in AMI patients. Around 40% of all LVWR occurred during the first 24 hours and 85% within the first week. In the present case, 76 hours following the intervention, LVWR was observed likely due to a small infarction at the lateral left ventricular wall possibly due to the marginal lesion. Our patient refused surgery and was followed clinically. Eighteen months later, real time three-dimensional echocardiography showed a pseudoaneurysm.

Successful percutaneous mitral valve repair with the MitraClip system of acute mitral regurgitation due to papillary muscle rupture as complication of acute myocardial infarction.

Percutaneous mitral valve repair with the MitraClip is a new promising therapeutic option for symptomatic severe mitral regurgitation (MR). Acute myocardial infarction (MI) is a well recognized cause of papillary muscle rupture (PMR). If PMR is untreated, the prognosis is poor and the mortality could be as high as 80% during the first week of post MI. For patients with PMR, the standard therapy for MR is open surgical repair or replacement. However, in our case, percutaneous mitral valve repair with the MitraClip was chosen technique because of the metastatic colon cancer. We report the case of a 60-year-old woman who underwent successful percutaneous mitral valve repair with the MitraClip system for the treatment of acute MI complicated by PMR.

Immediate primary transcatheter closure of left ventricular free wall rupture after myocardial infarction.

Left ventricular free wall rupture due to acute myocardial infarction (MI) is an infrequent but fatal complication that occurs especially during the 1st week of MI. Emergency surgical intervention is essential but conveys significant operative mortality. Most of the patients die before they reach the operating room. We present a case of percutaneous left ventricular free wall rupture closure complicating acute inferior MI to bridge the time until the patient can be transferred to the surgical department and subjected to surgery.

Intramural myocardial hemorrhagic rupture in a patient with metastatic cancer and myocardial infarction.

A 77-year-old man with anterior ST-elevated myocardial infarction and lateral myocardial rupture underwent successful percutaneous revascularization. Cardiac magnetic resonance imaging (MRI) and positron emission tomography (PET) unveiled a disseminated metastatic cancer, likely responsible not only for a prothrombotic paraneoplastic syndrome but also for ventricular metastasis and myocardial rupture. The patient unfortunately died because of noncardiovascular complications of cancer.

Postinfarction left ventricular rupture salvaged by resuscitation induced pericardial tear.

A 73-year-old diabetic, hypertensive man sustained acute inferolateral wall myocardial infarction 2 days before a syncopal episode, and he was resuscitated on the way to the hospital and during the preoperative examination. An extensive tear of the left posterolateral pericardium with massive left hemothorax and left ventricular free wall rupture with pulsatile bleeding were found during surgery. Iatrogenic pericardial tear due to vigorous cardiac massage could temporarily relieve the pericardial tamponade due to the postinfarction ventricular rupture and allowed the timely surgery to be conducted.

[Successful surgical repair of left ventricular free wall rupture after acute myocardial infarction].

Left ventricular free wall rupture (LVFWR) after acute myocardial infarction (AMI) is a fatal complication. We report emergency surgery for 2 blow out cases and 2 oozing cases during the 5-year period from 2003. After percutaneous coronary intervention (PCI), subacute thrombosis (SAT) occurred before operation in 2 oozing cases. To the blow out cases, both percutaneous cardiopulmonary support system (PCPS) and intra-aortic balloon pumping (IABP) were applied. The actively bleeding site was approximated by a large mattress suture with felt strips. To the oozing cases, only IABP was applied, and sutureless technique was used for hemostasis. They all survived the operation

Left ventricular oozing rupture following acute myocardial infarction.

We describe the case of an 85-year-old woman in whom pericardiocentesis, prolonged bed rest and blood pressure control were performed without surgery to successfully treat an oozing-type myocardial rupture due to myocardial infarction.

Early Amplatzer occluder closure of a postinfarct ventricular septal defect as a bridge to surgical procedure.

The management of postinfarction ventricular septal defects represents a challenge to both cardiologists and surgeons due to the high morbidity and mortality rate. We report the case of a 79-year-old patient who developed an apical rupture of the ventricular septum, nine days after an anterior myocardial infarction. As the patient was in cardiogenic shock and developed acute pulmonary edema we chose to perform a percutaneous closure of the septal defect using an Amplatzer occluder (AO). Despite the incomplete closure, the placement of the device greatly improved the patient's clinical condition allowing the delay of the surgical procedure, which could be performed ten days later with an excellent result.

Pseudoaneurisma ventricular. Evolución clínica y ecocardiográfica / Ventricular pseudoaneurysm. Clinical and echocardiographic evolution

Presentamos el caso de un paciente con una ruptura cardíaca secundaria a un infarto miocárdico al nivel del ápex del ventrículo izquierdo. La complicación mecánica condicionó la formación de un pseudoaneurisma que fue ocupado por un trombo que selló el punto de ruptura. El paciente sobrevive sin tratamiento quirúrgico tras 5 años de seguimiento.

The case of a patient with cardiac rupture following a myocardial infarction is presented. The rupture led to the formation of a ventricular pseudoaneurysm that was occupied by a thrombus that sealed the breakthrough point. The patient has survived without surgical treatment during the last 5 years. (Arch Cardiol Mex 2005; 75: 182-183).

Targeted overexpression of leukemia inhibitory factor to preserve myocardium in a rat model of postinfarction heart failure.

OBJECTIVE: Myocardial infarction leads to cardiomyocyte loss. The cytokine leukemia inhibitory factor regulates the differentiation and growth of embryonic and adult heart tissue. This study examined the effects of gene transfer of leukemia inhibitory factor in infarcted rat hearts. METHODS: Lewis rats underwent ligation of the left anterior descending coronary artery and direct injection of adenovirus encoding leukemia inhibitory factor (n = 10) or null transgene as control (n = 10) into the myocardium bordering the ischemic area. A sham operation group (n = 10) underwent thoracotomy without ligation. After 6 weeks, the following parameters were evaluated: cardiac function with a pressure-volume conductance catheter, left ventricular geometry and architecture by histologic methods; myocardial fibrosis by Masson trichrome staining, apoptosis by terminal deoxynucleotidal transferase-mediated deoxyuridine triphosphate nick-end labeling assay, and cardiomyocyte size by immunofluorescence. RESULTS: Rats with overexpression of leukemia inhibitory factor had more preserved myocardium and less fibrosis in both the infarct and its border zone. The border zone in leukemia inhibitory factor-treated animals contained fewer apoptotic nuclei (1.6% +/- 0.1% vs 3.3% +/- 0.2%, P < .05) than that in control animals and demonstrated cardiomyocytes with larger cross-sectional areas (910 +/- 60 microm 2 vs 480 +/- 30 microm 2 , P < .05). Leukemia inhibitory factor-treated animals had increased left ventricular wall thickness (2.1 +/- 0.1 mm vs 1.8 +/- 0.1 mm, P < .05) and less dilation of the left ventricular cavity (237 +/- 22 microL vs 301 +/- 16 microL, P < .05). They also had improved cardiac function, as measured by maximum change in pressure over time (3950 +/- 360 mm Hg/s vs 2750 +/- 230 mm Hg/s, P < .05) and the slopes of the maximum change in pressure over time-end-diastolic volume relationship (68 +/- 5 mm Hg/[s . microL] vs 46 +/- 6 mm Hg/[s . microL], P < .05) and the preload recruitable stroke work relationship (89 +/- 10 mm Hg vs 44 +/- 4 mm Hg, P < .05). CONCLUSIONS: Myocardial gene transfer of leukemia inhibitory factor preserved cardiac tissue, geometry, and function after myocardial infarction in rats.

Cardiac rupture complicating myocardial infarction.

Rupture of the ventricular free wall is a leading cause of death in patients with acute myocardial infarction (MI). There are a number of risk indicators that are associated with cardiac rupture, such as female gender, old age, hypertension, and first MI. Typical symptoms of cardiac rupture are recurrent or persistent chest pain, syncope, and distension of jugular veins. Electrocardiographic signs may include sinus tachycardia, new Q-waves in 2 or more leads, persistent or recurrent ST segment elevation, deviation of expected evolutionary T-wave pattern, and electromechanical dissociation in end-stage cases. Once patients at risk have been identified using clinical symptoms and electrocardiographic signs, a fast and sensitive diagnostic test to confirm cardiac rupture is transthoracic echocardiography (TTE). New insights in the etiology of subacute myocardial rupture suggests that defective cardiac remodeling may predispose the heart for rupture. The matrix metalloproteinase (MMP) system has been shown to play an important role in cardiac extracellular matrix (ECM) remodeling and cardiac rupture. Current therapy of cardiac rupture consists mainly of surgery, and conservative management with hemodynamic monitoring, prolonged bed rest, beta-blockers, and angiotensin-converting enzyme (ACE) inhibitors in selected cases.