Acute Left Ventricular Failure After Transcatheter Closure of a Secundum Atrial Septal Defect in a Patient With Coronary Artery Disease: a Critical Reappraisal

We report a case of acute left ventricular failure after transcatheter closure of a single secundum atrial septal defect in a 68-year-old man with coronary artery disease. Just before the procedure two coronary lesions had been treated with direct stenting. Transcatheter closure of atrial septal defects should always be deferred in ischemic heart disease patients who need percutaneous myocardial revascularization.

Transcatheter closure of a single secundum atrial septal defect is an accepted alternative to surgical repair (1,2), with similar complete closure rates and complications but shorter duration of hospital stay and less morbidity (3). Closure of an atrial septal defect, concomitant to the sudden interruption of the left-to-right shunt, causes an abrupt overloading of the left ventricle with a consequent increase in myocardial oxygen consumption. Such acute hemodynamic changes are usually well tolerated in patients with normal left ventricular function (4), but could be harmful in elderly patients (5), in patients with reduced left ventricular function and even more in patients with ischemic heart disease. In these patients, in fact, coronary revascularization is always performed before or immediately before atrial septal defect closure. We report a case of acute left ventricular failure after transcatheter closure of a single secundum atrial septal defect in a patient with coronary artery disease.

Introduction

Summary

A 68-year-old man was referred to our institution for transcatheter closure of a single secundum atrial septal defect. Two years before he suffered from a lateral myocardial infarction. On admission he complained dyspnoea for mild effort (NYHA class III) and physical examination revealed fixed splitting of second sound and a midsystolic murmur on the second intercostal space. Electrocardiogram showed a common atrial flutter with a ventricular heart rate of 70 beats per minute. 2D-echocardiography showed a large atrial septal defect (maximal diameter of 28 mm), enlarged right chambers, mildly reduced left ventricular function (ejection fraction of 50%) and severe lateral hypokinesia. The day after the admission the patient was brought to the catheterization laboratory for transcatheter closure of the atrial septal defect. According to standard procedure, the patient was sedated and intubated. Atrial flutter was successfully reverted to sinus rhythm by DC shock (100 joule). Subsequently, coronary angiography was performed. It showed a severe stenosis on the proximal tract of the left anterior descending coronary artery, a severe stenosis on the proximal tract of the left circumflex coronary artery and a total occlusion of the first obtuse marginal branch (Figure 1, left panel). Therefore, direct stenting of both lesions was successfully performed with a 3.5/13 mm Multilink Tetra and a 3.5/13 mm BxVelocity stents, respectively (Figure 1, right panel). Then, we proceeded to transcatheter closure of the atrial septal defect by using the self-centering Amplatzer septal occluder, whose technical details of the implantation have been described elsewhere (6). After positioning of the transesophageal echocardiographic probe for continuous monitoring and balloon-stretched sizing of the atrial septal defect by transesophageal echocardiography, the atrial septal defect was successfully closed with a 32 mm Amplatzer septal occluder (Figure 2). At the end of the procedure, after weaning of anesthesia the patient was extubated and transferred in intensive care unit with dopamine infusion (3mg/Kg/min). One hour later, however, patient exhibited progressive reduction of oxygen saturation, cough and pulmonary rales. The administration of high doses of diuretics and the institution of adrenaline infusion did not prevent the progression towards a massive pulmonary edema which needed reintubation and mechanical ventilation. Twelve hours later the patient exhibited improvement of clinical conditions, reduction of pulmonary congestion at chest X-ray and satisfactory blood gas analyses and was extubated. In the following days, 2D-echocardiography showed an improvement of the left ventricular function and after 7 days the patient was discharged in good clinical conditions.

The present clinical case clearly demonstrates the need to defer transcatheter closure of atrial septal defects in patients with associated ischemic heart disease suitable for coronary revascularization. In fact, the closure of a large atrial septal defect causes an abrupt increase of left ventricular pre-load and myocardial oxygen consumption which could be not acutely tolerated by a dysfunctional left ventricle. Several reasons could have caused the acute left ventricular failure. This includes the reduced left ventricular function at baseline, myocardial stunning following coronary stenting of both coronary arteries (7) and, possibly, DC shock (8). Moreover, as previously reported (5), a reduced diastolic elasticity of the left ventricle due to aging could have also contributed to develop pulmonary congestion following the atrial septal defect closure. Therefore, the present clinical case provides the following clinical implications. First, transcatheter closure of atrial septal defects should always be deferred in ischemic heart disease patients who need percutaneous myocardial revascularization. Noteworthy, differently from a standard surgical approach, percutaneous treatment of both ischemic and congenital pathologies offers the possibility to space out the two procedures, thus decreasing the chance of acute left ventricular failure. Second, in patients with atrial septal defect and mildly reduced left ventricular function, a provisional inotropic support (i.e., dopamine or dobutamine infusion) might be advisable before the procedure. Third, the opportunity to perform coronary angiography immediately before atrial septal defect closure in adult patients, even in the absence of previous coronary events, to rule out the presence of coronary artery disease. Finally, as previously suggested for elderly patients (5), acute left ventricular failure should be taken into account as a potential complication of transcatheter closure of atrial septal defects in patients with left ventricular dysfunction.

Introduction

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2. Chatterjee T, Windecker S, Seiler C, Meier B. Nonsurgical closure of secundum atrial septal defect and patent foramen ovale. J Clin Basic Cardiol 2001;4:35-38.

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8. Allan JJ, Feld RD, Russell AA, Ladenson JH, Rogers MA, Kerber RE, Jaffe AS. Cardiac troponin I levels are normal or minimally elevated after transthoracic cardioversion. J Am Coll Cardiol 1997;30(4):1052-1056.

Table 1 - Coronary angiograms show severe stenoses on the proximal tracts of the left anterior descending and of the left circumflex coronary arteries (arrows, left panel), successfully treated with direct stenting (right panel).

Table 2- Transesophageal echocardiography shows a large atrial septal defect (ASD) (left panel), successfully closed with a 32 mm Amplatzer septal occluder (ASO) (right panel).