A 57 y/o Caucasian male patient was referred to our hospital with pronounced motor aphasia and unilateral right sensorimotor performance deficits after having been found unconscious at home. In the ER the patient was awake and oriented to person, place and time. Due to the severe dynamic aphasia and agitation it was not possible to obtain a sufficient patient history. According to the patient’s relatives the onset of neurological symptoms was the evening before, however less pronounced and progressed to an unconscious state the next morning. Initially the patient and his family denied any history of chest pain, orthopnea, and lower extremities edema, however eventually the patient recalled an episode of chest pain and lightheadedness as angina pectoris equivalent two years before. Coronary angiography revealed a three vessel disease with a total occlusion of the first marginal branch of circumflex artery which apparently lead to transmural infarction and subsequent aneurysm formation. His past medical history was otherwise remarkable for essential hypertension and intermittent atrial fibrillation. On physical exam his pupils were equal round and reactive to light and accommodation. He manifested a unilateral faciobrachial weakness as well as a unilateral faciobrachial sensory loss. His cardiac risk factors were significant for tabacco abuse (50 pack years), essential hypertension, unhealthy diet and physical inactivity.
The electrocardiogram showed atrial fibrillation at 120 beats/min and pathologic Q-waves in leads I and aVL consistent with a non-recent lateral myocardial infarction. The tachycardic supraventricular arrhythmia was successfully converted with 300 mg of amiodarone. Cranial computed tomography was immediately initiated and revealed a large left frontotemporal and right parietal hypoattenuation consistent with cerebral infarction. The patient was started on high molecular weight heparin. Chest X-rays showed a massive cardiomegaly with a bulging protrusion along the left ventricular shadow (Figure 1). Comparison to prior X-ray studies raised the suspicion of a giant ventricular aneurysm. There was associated pulmonary venous congestion due to heart failure.
The preoperative echocardiographic evaluation and magnetic resonance imaging confirmed the diagnosis of a 15×10×8cm left ventricular aneurysm along the left ventricular wall (Figure 2 and Additional file 1: Video 1). Spontaneous echo contrast was clearly visible as a dynamic sign of blood stasis in the aneurysmal sac. Despite the huge size of the aneurysm the mitral valve was competent due to the fact that the neck of the aneurysm which extended from the base of the heart to the apex and was located exactly in-between the anterolateral und posteromedial papillary muscles. This way the submitral apparatus was spared from any tethering and necrosis. Again the neck was only 2 cm wide but 8 cm long, stretching in length from the apex up to 1 cm below the mitral valve annulus with the aneurysmal sac bulging to the thoracic wall (Figure 2). The left ventricular (LV) ejection fraction was estimated at 10-15% with an akinetic lateral wall and a grade one LV diastolic dysfunction. No intracardiac thrombus was appreciated, however a sponatanous contrast was visible in the aneurysmal sac. All four valves were competent and the estimated pulmonary artery systolic pressure was 24 mm Hg.
Cardiac catheterization showed 3-vessel disease with 60% stenosis of the proximal right coronary artery (RCA) as well as a 60% stenosis of the proximal posterior descending artery, a 30% stenosis of the left anterior descending artery (LAD), a 75% stenosis of the first diagonal branch and a proximal total occlusion of the first obtuse marginal branch the circumflex artery (OM).
The patient was in NYHA class III. He was diagnosed with a giant ventricular aneurysm 2 years after his myocardial infarction and underwent surgical lateral ventricular restoration 2 months after the initial neurologic presentation. The patient was put on pump via a standard bicaval cannulation and aortic cannulation. A left ventricular vent was installed via the right superior pulmonary vein. There were extensive adhesions between the heart and entire pericardium that could only be detached after aortic cross-clamping. Care was taken to keep the 2 mm thin aneurysm wall intact for later hemostasis. After liberating the heart from the pericardial sac the aneurysm was incised and the situs inspected. The entry of the aneurysm had a neck between the papillary muscles and extended from the apex to within 1 cm of the posterior mitral valve leaflets (Figure 3A). Ventricular restoration was done using the Dor procedure with a Dacron patch tailored from a 34 mm tube graft in order to mimick the geometry of the heart (Figure 3B). The thin wall of the giant aneurysm was partially resected and the limbus was sown together buttressed with a felt strip with 3/0 prolene for hemostatic purposes (Figure 3C). Thereafter coronary revascularization was performed with a saphenous vein graft to the first diagonal branch and the right coronary artery, respectively. Myocardial protection was achieved with antegrade aortic and vein graft blood cardioplegia, as well as retrograde blood cardioplegia via the coronary sinus.
The patient was off all inotropes and pressors on postoperative day two and transferred to an outside neurology department on post-operative day ten. He was eventually discharged home in good clinical condition and with almost normal ejection fraction. Of note, the neurological situation improved dramatically with only minor sequelae. The patient was followed 9 months upon surgery, his neurological sequelae continued to improve with no residual cardiac impairment.