Summary
Background
Ventricular septal defect (VSD) after acute myocardial infarction is a catastrophic event.
Aims
We describe our multicentre experience of a defect closure strategy that combined surgery and transcatheter closure.
Methods
Data were obtained by retrospective chart review.
Results
Twenty patients (mean age, 67 years) from three centres were studied. Median time from myocardial infarction to VSD was 6 (range, 3–9) days. Acute cardiogenic shock occurred in 12 (60%) patients. Median defect diameter by echocardiography was 18 (range, 12–28) mm. Median time to first surgical or percutaneous closure was 18 (range, 4–96) days. Twenty-seven procedures were performed in the 20 patients. Surgical closure was undertaken in 14 patients and contraindicated in eight, six of whom underwent percutaneous closure; the other two, after reconsideration, proceeded to surgical closure. No procedural complications occurred with percutaneous closure. Percutaneous closure patients were older than surgical patients (75 vs. 64 years; P = 0.01) and had a higher mean logistic EuroSCORE (87% vs. 67%; P = 0.02). Rates of residual shunt and mortality did not differ between surgical and percutaneous patients ( P = 0.12 and 0.3, respectively). Those who underwent early VSD closure (< 21 days after myocardial infarction) had higher rates of residual shunt ( P = 0.09) and mortality ( P = 0.01), irrespective of closure strategy. The mortality rate was also higher after early percutaneous closure ( P = 0.001), but not after early surgery. Finally, predicted mortality (logistic EuroSCORE) was higher than hospital mortality (≤ 30 days) in our patient population (75% vs. 30%; P = 0.01).
Conclusion
Vigorous pursuit of closure of post-myocardial infarction VSD with a sequential surgical and/or percutaneous approach is recommended for improved outcomes.
Résumé
Contexte
Les communications interventriculaires post-infarctus myocardique ont un pronostic catastrophique.
Objectifs
Nous décrivons notre expérience multicentrique combinant la chirurgie et le cathétérisme interventionnel.
Méthodes
Les données ont été obtenues par l’étude rétrospective des dossiers des patients.
Résultats
Vingt patients dans 3 centres ont été étudiés à l’âge moyen de 67 ans. Le délai médian entre la survenue de l’infarctus du myocarde et le diagnostic de la communication interventriculaire était de 6 (3–9) jours. Un choc cardiogénique est survenu dans 12 cas (60 %). Le diamètre médian du défaut septal à l’échocardiographie était de 18 (12–28) mm. Le délai médian de la première fermeture de la communication interventriculaire était de 18 (4–96) jours. Au total, 27 procédures ont été réalisées chez 20 patients dont une fermeture chirurgicale dans 14 cas. Cette dernière étant contre-indiquée chez 8 patients, une fermeture par cathétérisme a été pratiquée dans 6 cas, les 2 derniers patients initialement contre-indiqués à la chirurgie ayant finalement été fermés chirurgicalement après rediscussion de leur opérabilité. Aucune complication n’est survenue lors des cathétérismes. Les patients dont la communication interventriculaire a été fermée par cathétérisme étaient plus âgés que les patients chirurgicaux (75 vs 64 ans ; p = 0,01) et l’EuroSCORE logistique pour le groupe cathétérisme était significativement plus élevé, reflétant une population plus grave (87 % vs 67 % ; p = 0,02). Le taux de shunts résiduels et la mortalité ne différaient pas significativement entre les 2 groupes chirurgie et cathétérisme ( p = 0,12 et 0,3, respectivement). Les patients dont la communication interventriculaire a été fermée précocement (< 21 jours après l’infarctus) avaient taux de shunts résiduels et de décès plus important ( p = 0,09 et 0,01, respectivement) quelle que soit la stratégie de fermeture. Le décès était plus fréquent après une fermeture percutanée ( p = 0,001) précoce mais pas après la chirurgie précoce. Enfin, la mortalité prédictive (EuroSCORE logistique) était de 75 %, significativement plus élevée que la mortalité hospitalière à 30 % dans notre population de patients ( p = 0,01).
Conclusion
La poursuite d’une prise en charge agressive de fermeture des communications interventriculaires post-infarctus, combinant de manière séquentielle la chirurgie et le cathétérisme interventionnel, est recommandée pour continuer d’améliorer le pronostic.
Background
Ischaemic ventricular septal rupture after acute myocardial infarction (AMI) is a catastrophic event. The resulting ventricular septal defect (VSD) imposes an acute left-to-right shunt, precipitating or exaggerating cardiogenic shock and compounding the preexisting cardiac disease burden . The incidence of post-AMI VSD (PMI-VSD) appears to have declined in recent times to 0.2% ; however, mortality remains high in patients with PMI-VSD . Management of these patients presents complex challenges. Urgent surgical repair of PMI-VSD was first proposed in the early 1980s, because nearly 100% mortality was reported with medical management alone . The American Heart Association/American College of Cardiology practice guidelines recommend urgent surgical repair of PMI-VSD as a class I indication . However, early surgical repair (from 3 days to within 4 weeks after AMI) has a 52% operative in-hospital mortality rate, while delayed surgical repair has an overall in-hospital mortality rate of 8% . Yet there is often an urgent need to proceed with PMI-VSD closure to avert a fatality, despite early surgical closure being associated with a high incidence (20%) of residual shunt, leaving an additional disease burden . Thus the concept of an ‘optimal time’ for PMI-VSD closure is misleading.
In the past decade, percutaneous device closure of PMI-VSD has emerged as an alternative strategy, with a high procedural success rate . A management strategy that considers application of both techniques has not been explored extensively to date. It has been suggested that defects < 15 mm should be treated with percutaneous therapy, either as a temporary strategy, to stabilize the patient until a definitive surgical repair can be accomplished, or as a definitive therapy . However, percutaneous closure of larger defects is feasible . Residual shunts after surgical closure, which are not uncommon, can undergo percutaneous closure . We believe that a management algorithm that applies surgical and/or percutaneous closure of PMI-VSD for the best potential management of a patient needs to be delineated. In this report, we describe our experience of a management algorithm that applies surgical and/or percutaneous closure of PMI-VSD for the best management of any patient. ‘Best’ management was defined as amelioration or elimination of the haemodynamic burden related to the shunt resulting from PMI-VSD.
Methods
In our practice, we offered surgical closure of PMI-VSD in accordance with the American College of Cardiology/American Heart Association recommendations . Percutaneous closure was pursued when surgical closure was contraindicated or declined by the patient. Additionally, we offered percutaneous closure in patients with residual shunt after surgical closure.
A retrospective review of charts was conducted at the participating centres, to identify patients presenting with AMI who developed PMI-VSD between April 2006 and May 2012. Data pertaining to clinical presentation, co-morbidities, echocardiography, haemodynamic findings, clinical course, technical details of surgical or/and transcatheter closure, acute outcome and the most recent follow-up were obtained.
Surgical closure was performed under cardiopulmonary bypass. The defect was approached through the left ventricle, except in posterior PMI-VSD, in which case an incision was made into the posterior left ventricular infarct. The double-patch concept was applied. After patch closure of PMI-VSD, patch closure of the approach incision was performed. Small defects were closed by application of a single patch. Associated large ventricular aneurysm underwent an endoexclusion .
Percutaneous closure was carried out when there was a contraindication to surgical closure or for patient preference. Percutaneous closure was performed under ultrasound guidance (transoesophageal and transthoracic) in accordance with the techniques described previously . Antibiotic prophylaxis was administered in the form of a single dose of cefamandole (1.5 g). Heparin was administered in standard doses. Patients with heparin-induced thrombocytopoenia received intravenous anti-factor Xa (2500 units). Clopidogrel and aspirin were given to all patients.
Statistical analysis: PASW Statistics 17.0 (SPSS, Inc., Chicago, IL, USA) was used for statistical analysis. Nominal variables are expressed as numbers and percentages, and were compared by Fisher’s exact test. Continuous and ordinal variables are presented as means ± standard deviations or medians (ranges), and were compared by the Mann-Whitney test. Survival probabilities were calculated using the Kaplan–Meier method, and were compared using the log-rank test. All tests were two-sided and a P -value < 0.05 was considered statistically significant.
Results
Between April 2006 and May 2012, 20 patients underwent closure of PMI-VSD in three centres (University Hospital of La Timone, Marseille; University Hospital of Arnaud-de-Villeneuve, Montpellier; le Millénaire Private Hospital, Montpellier). The mean age of the patients was 67 (range, 52–85) years and there were nine (45%) women. Preexisting cardiovascular co-morbid states were hypertension ( n = 9), diabetes ( n = 6), history of smoking ( n = 9) and hypercholesterolaemia ( n = 9). In addition, two patients had a history of angina.
Acute myocardial infarction presentation
Most patients ( n = 16, 80%) were diagnosed with AMI more than 24 hours after onset of symptoms. No patient had cardiogenic shock at presentation. All patients received standard medical therapy for AMI in accordance with the recommendations . The AMI location was anterior in 45% and inferior in 55%. Single-vessel disease was present on coronary angiography in 14 (70%) patients, while four (20%) had two-vessel disease and two (10%) had triple-vessel disease. The right coronary artery was most commonly involved ( n = 11, 55%), followed by the left anterior descending artery ( n = 8, 40%) and the circumflex artery ( n = 1, 5%). None of the patients received intravenous thrombolysis. All patients underwent cardiac catheterization for coronary angiography. Percutaneous coronary revascularization was performed in 13 (65%) patients. One (5%) patient underwent a coronary revascularization procedure at the time of surgical PMI-VSD closure, with a bypass graft. Revascularization was not performed in six (30%) patients.
Post-acute myocardial infarction ventricular septal defect presentation
The median time from onset of AMI to development of PMI-VSD was 6 (range, 3–9) days. Right heart failure was noted in nine (45%) patients, severe left ventricular dysfunction in six (30%) patients and biventricular systolic dysfunction in four (20%) patients. Only one patient had no cardiac failure with normal biventricular function. Acute cardiogenic shock manifested with ventricular septal rupture in 12 (60%) patients, 11 of whom required intra-aortic balloon counterpulsation (55%), while one was managed with intravenous inotropic therapy. No patient had disruption of atrioventricular conduction. Transthoracic echocardiography was performed in all patients on clinical suspicion of ventricular septal rupture ( Fig. 1 ). The defect was located in the anterior apical septum in 12 (60%) patients and posteriorly in eight (40%) patients. The median VSD diameter by echocardiographic evaluation was 18 (range, 12–28) mm. No patient had mitral valve dysfunction, papillary muscle or free wall rupture. Cardiac catheterization was performed in 11 patients with onset of PMI-VSD, six of whom proceeded to device closure.
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