Self-limiting left ventricular wall rupture following myocardial infarction: a case report and literature review.

We report the case of a 62-year-old woman presenting with symptoms and findings of myocardial infarction and a left ventricular free wall rupture. Coronary angiography revealed a critical stenosis in the middle right coronary artery. A contrast left ventriculogram revealed extravasation of contrast through the inferolateral wall of the left ventricle. Left ventricular free wall rupture is a rare complication of acute myocardial infarction, occurring in approximately 2% of cases. It is often fatal because of the development of haemopericardium and tamponade. Some patients, like the one described in this case, may present with small leaks that might close spontaneously by epicardial fibrin deposits, thus self-limiting, without requiring surgical intervention. This patient received only intense medical treatment. Indeed, blood clots at the endocardial and the epicardial site of the rupture have often been identified, suggesting protection for further rupture.

Post-infarct cardiac rupture: recent insights on pathogenesis and therapeutic interventions.

Ventricular wall rupture represents a catastrophic complication of myocardial infarction (MI) in the clinic while research has long been hampered due to absence of suitable animal models. Since late 1990s, the mouse has become a suitable model for human post-infarct cardiac rupture. Here we review the clinical features of post-infarct rupture, factors associated with a higher risk of rupture, and findings from clinical trials on the incidence of post-infarct rupture. The features of the mouse model of post-infarct cardiac rupture are discussed. Research using this model suggests acute ventricular remodeling as the fundamental change leading to rupture, and has defined several key factors that determine the risk of rupture. We then provide a comprehensive review of the progress of experimental research in this field focusing on recent findings from genetically modified mouse models and experimental therapeutic interventions that reveal molecular mechanisms of post-infarct rupture. Genetic and pharmacological interventions targeting key inflammatory mediators, regulatory factors of extracellular matrix collagen and healing process effectively reduced the risk of rupture. These findings convincingly demonstrate that cardiac inflammation, damage to extracellular matrix proteins or blunted fibrotic healing constitute the central mechanisms for the pathogenesis of cardiac rupture and acute ventricular remodeling. Studies using the mouse model have also identified novel molecular mechanisms and therapeutic targets as well as suitable interventional regimens providing useful clues for clinical translation.

Matrix metalloproteinases as valid clinical targets.

The matrix metalloproteinase family of enzymes has been a pharmaceutical target for over 20 years. In that time, many drugs have been developed but none have successfully passed clinical trials. A significant problem has been development of dose-limiting side-effects that were revealed during long-term clinical trials in diseases such as arthritis and various cancers. There are, however, other clinical settings where evidence for MMP function contributing to the pathophysiology of disease is strong. A number of these settings will be discussed here together with evidence from animal models that MMP inhibition is a valid strategy to be considered. A major advantage with many of these settings is that drug exposure may not have to be long-term and/or systemic thus reducing the possibility that side-effects will stymie MMPI-based therapy.

Eplerenone : a pharmacoeconomic review of its use in patients with post-myocardial infarction heart failure.

Eplerenone (Inspra) is a selective aldosterone blocker. When added to standard medical therapy, eplerenone significantly improved morbidity and mortality in patients with left ventricular (LV) systolic dysfunction and clinical evidence of heart failure following acute myocardial infarction (MI), in a well designed, placebo-controlled trial known as EPHESUS (Eplerenone Post-acute myocardial infarction Heart failure Efficacy and SUrvival Study). Although eplerenone was generally well tolerated, it was associated with a higher incidence of hyperkalaemia than placebo.Cost-effectiveness analyses based on this trial have been performed in the US, The Netherlands, Germany, France and Spain. Direct medical costs were analysed based on prospectively collected resource-use data with local costs applied; modelling was conducted to calculate incremental costs per life-year or QALY gained, with survival curves assumed to remain parallel after treatment ended. Eplerenone was associated with a gain of 0.0304 life-years (approximately 11 days) compared with placebo during the study period. Based on these analyses, eplerenone was cost effective compared with placebo in patients with LV systolic dysfunction and heart failure after an MI when added to standard therapy for 16 months. The incremental cost per life-year gained for eplerenone versus placebo (for a range of three different life-expectancy projections) was 10,402-21,876 US dollars in the US (year 2001 costs, except for eplerenone [2004]) [equivalent to 12,274-25,814 euro; mid-2001 exchange rate], 5,365-12,795 euro for The Netherlands (year 2003 costs), 6,956-14,628 euro for Germany, 5,432-11,423 euro for France and 8,626-18,141 euro for Spain (year of costing not reported). The US, Dutch, French and Spanish analyses estimated that >90% of observations for incremental cost per life-year gained were below a threshold of 50,000 US dollars or 50,000 euro. Incremental costs per QALY gained for eplerenone versus placebo in the US, Dutch, French and Spanish analyses were 15,330-32,405 US dollars (18,089-38,238 euro), 12,148, 8,005-16,922 euro and 12,713-26, 873 euro, respectively. Clinical and pharmacoeconomic data comparing eplerenone with another active drug, such as spironolactone, in this patient population are not available. In conclusion, when added to standard therapy in patients with LV systolic dysfunction and heart failure after an acute MI, eplerenone was associated with significant reductions in mortality and morbidity compared with placebo. Despite some inherent limitations, available pharmacoeconomic data from Europe and the US indicate that eplerenone is a cost-effective treatment compared with placebo in terms of incremental cost per life-year gained in this patient population.

Long-term usefulness of percutaneous intrapericardial fibrin-glue fixation therapy for oozing type of left ventricular free wall rupture: a case report.

This report describes a long-term survival case of left ventricular free wall rupture treated with percutaneous intrapericardial fibrin-glue fixation therapy. A 82-year-old woman was admitted to the emergency room because of vomiting and syncope diagnosed as acute posterolateral myocardial infarction complicated by cardiac tamponade. After her hemodynamic condition was stabilized by drawing off the bloody pericardial effusion, fibrin-glue was injected into pericardial space with the expectation that the glue would cover the oozing site of the left ventricular epicardium. After this therapy, the patient recovered and did not have any no recurrent cardiac events for 1 year. Serial echocardiographic studies revealed a preserved left ventricular function and no development of left ventricular restriction. This case suggests that percutaneous intrapericardial fibrin-glue fixation therapy is an effective treatment for the oozing type of left ventricular free wall rupture and that there is no risk of left ventricular restriction during long-term follow-up.

Medical management of selected patients with left ventricular free wall rupture during acute myocardial infarction.

OBJECTIVES: This study sought to evaluate the effects of prolonged rest and blood pressure control on survival of patients in whom left ventricular free wall rupture (LVFWR) was strongly suspected. BACKGROUND: Left ventricular free wall rupture in myocardial infarction is often fatal, and only a few patients may undergo operation. However, survival without surgical repair has not yet been evaluated. METHODS: Eighty-one consecutive patients with a first transmural acute myocardial infarction in Killip class I or II who presented with acute hypotension due to cardiac tamponade, with electromechanical dissociation (EMD) in 72, were prospectively evaluated. Patients with early recovery were managed with prolonged bed rest and blood pressure control with beta-blockade as tolerated. RESULTS: Forty-seven patients died within 2 h of acute tamponade, and autopsy in 21 showed LVFWR in all. In 15 others, an emergency surgical repair resulted in 2 survivors. The remaining 19 patients, 10 with EMD, had early recovery with dobutamine and colloid solution, and 15 required pericardiocentesis. Shortly thereafter, these 19 patients still showed a paradoxic pulse > or = 20 mm Hg, relevant pericardial effusion (24 +/- 7 mm [mean +/- SD]) and comparable elevation of right and left ventricular filling pressures (15.8 +/- 3.9 and 15.9 +/- 3.8 mm Hg, respectively). Subsequent management included bed rest (8.2 +/- 4.8 days) and control of systolic blood pressure (< or = 120 mm Hg) with beta-adrenergic blocking agents as tolerated (n = 12). Four patients died, and autopsy in three revealed a rupture that was sealed in two. A sealed rupture was also seen at thoracotomy in 2 other patients who, like the remaining 13, survived for 52.5 +/- 35.2 months. CONCLUSIONS: Long-term survival of selected patients with prompt hemodynamic recovery after LVFWR is possible without surgical repair. Prolonged bed rest and blood pressure control are likely to contribute favorably to their initial outcome.

Rotura cardíaca após infarto agudo do miocárdio (IAM): uma complicaçäo passível de correçäo cirúrgica? / Cardiac rupture after acute myocardial infarction (AMI): may it have a surgical repair?

Foram estudados 9162 pacientes atendidos no INCOR, com o diagnóstico de IAM, de janeiro de 1983 a dezembro de 1993. Deste, 1,05 por cento apresentaram rotura cardíaca de origem isquêmica como complicaçäo do infarto miocárdico. A faixa etária foi de 69,5 anos, predominando os pacientes de raça branca (93,74 por cento)e do sexo feminino (55,3 por cento). Os dados estudados incluíram história clínica, exames laboratoriais subsidiários, drogas utilizadas e achados cirúrgicos ou de necropsia. As roturas cardíacas foram classificadas, de acordo com a literatura, em agudas e sub-agudas. Observamos 72 casos de rotura miocárdica aguda com taxa de mortalidade de 98,6 por cento e 24 casos de rotura sub-aguda com 41,6 por cento de óbitos.Foram operados 4 pacientes na forma aguda e 15 na forma sub-aguda, resultando em 78,9 por cento de sobrevida pós-operatória. Dos pacientes que receberam terapia trombolítica com sucesso, 76,4 por cento faleceram, enquanto que, dos pacientes tratados convenciomalmente, esse número chegou a 86,1 por cento . Quando a terapia trombolítica foi administrada até 1 hora após o IAM, a mortalidade foi de 33,3 por cento dentre 3 e 6 horas foi de 60 por cento e após 6 horas foi de 100 por cento. A rotura ocorreu após 5 dias do IAM somente em 5,9 por cento que receberam trombolíticos, enquanto que nos pacientes submetidos à terapêutica convencional esse índice elevou-se para 40,5 por cento. Concluímos pela gravidade e necessidade de atuaçäo imediata nos pacientes com rotura cardíaca, mesmo nos casos sub-agudos, quando 30 por cento dos pacientes com suspeita ecocardiográfica de expansäo em área isquêmica transmural falecem. Nas roturas agudas, a situaçäo agudas, a situaçäo é dramática, e a sobrevida está associada a fatores logísticos. Em condiçöes sub-agudas, entretando, pode-se dispor de técnicas que dispensam suturas e circulaçäo extracorpórea, constituindo um importante recursos para o tratamento dessa grave complicaçäo do IAM.

Management of uncomplicated acute myocardial infarction: are there differences in patterns of care between VAMC physicians and private practice physicians?

Uncomplicated acute myocardial infarction is a diagnostic category in which significant changes in patterns of care have occurred in the past 17 years. In this retrospective study, a comparison has been made between actual practice patterns of VA physicians and those reported in literature. Findings demonstrated differences in: length of stay in a monitored bed-5 days vs. 2.8 days; drug preferences--calcium antagonists and nitrates vs. nitrates and plasminogen activators; pre-discharge diagnostic studies--cholesterol/triglyceride levels and coronary angiography vs. lipid levels and exercise electrocardiograms; and patient education--follow-up appointments and diet vs. smoking cessation, diet, and exercise programs.

Medical interventions in acute myocardial infarction.

Streptokinase, APSAC, and rtPA clearly reduce mortality in acute myocardial infarction. rtPA is definitely superior at recanalization; it does it faster and more effectively in the first 1-2 h after infusion. There is no evidence that it causes less bleeding, but rather that the proneness to bleeding might be a little higher. rtPA is expensive. Therefore, on the whole, physicians in the United Kingdom mainly use streptokinase and some APSAC. rtPA is probably the best agent for second-time use within 6-12 months of the first use of streptokinase or APSAC, when antibodies may limit the effectiveness of these agents. Aspirin is clearly useful, and one should remember to use it long term in any patient who has had a vascular event. It should not be used for primary prevention except where there is a clear vascular risk. For secondary prevention, it is very effective. Intravenous beta-blockers should be considered for less ill patients, who amount to about 50% of all patients admitted. Beta-blocker treatment reduces cardiac rupture and should be used in conjunction with thrombolysis and continued long term in patients without contraindications. It also has proven antiarrhythmic benefit (sudden death). Anticoagulants are promising but yet to be proven. Nitrates may have a place in the acute therapy of myocardial infarction, but calcium blockers and lidocaine are definitely not suited for routine use. Lidocaine should generally be used only in patients who already have ventricular fibrillation or severe or symptomatic ventricular arrhythmia. Finally, before getting too enthusiastic, one should remember that this overview deals only with those people who reach the hospital alive. There is a huge number of patients at least equal to those admitted who die before reaching medical help. They have to be prevented from getting a myocardial infarction. Therefore, along with better treatment, we need to focus on prevention, with arguments against smoking, excess weight, and in favor of more exercise. These arguments are still very important.

[Drug optimization of the healing of complicated forms of large-focus myocardial infarct]. / Medikamentoznaia optimizatsiia zazhivleniia oslozhnennykh form krupnoochagovogo infarkta miokarda.

The authors give a description of methods of diagnosis and drug optimization of complicated forms of healing of myocardial infarction. It is emphasized that measures of optimization facilitate the clinical course of the disease, reduce the frequency of development of postinfarction aneurysms and further the decrease of lethality.