Clinical Data

Our patient was a 72-year-old man who had been followed for 4 years at an outside hospital for severe chronic systolic heart failure due to dilated cardiomyopathy and mitral regurgitation (MR). He had been diagnosed with atrial fibrillation four years ago, but the exact time of onset was unknown. With medical management (carvedilol 5 mg, enalapril maleate 5 mg, telmisartan 40 mg, furosemide 20 mg, metildigoxin 0.05 mg, warfarin 2 mg) alone, his disease had progressed, leading to exertional dyspnea. From these findings, our policy was to treat with surgery. On admission to our institution, his height was 153.5 cm, body weight 59.1 kg, blood pressure 98/64 mmHg, heart rate 64 bpm and the rhythm was atrial fibrillation. Electrocardiography revealed atrial fibrillation without f-wave and no left bundle branch block. Echocardiography showed severe MR resulting from tethering and moderate tricuspid regurgitation (TR). Left ventricular (LV) end-diastolic and end-systolic dimensions (LVEDD/LVESD) were 75/66 mm, left ventricular volumetry were 341/225 mL, interventricular septal wall thickness in the end diastole (IVSd) was 11 mm, left ventricular posterior wall thickness in the end diastole (LVPWd) was 5 mm, interpapillary muscle distance was 39 mm and the LV ejection fraction was 28% (modified Simpson’s method). Peak early diastolic filling velocity (E-wave), peak late diastolic filling velocity (A-wave) and their ratio (E/A) was 1.37. The E/e’ (the ratio between early mitral inflow velocity and mitral annular early diastolic velocity) was 14.43. The LV wall showed global hypokinesia and inferoposterior dyskinesia. The chest X-ray revealed bilateral pulmonary congestion. The chest thoracic ratio was 72%. His preoperative BNP was 1155 pg/mL. Coronary computed tomography (CT) revealed no vascular stenoses. Cardiac catheterization showed left ventricular end-systolic volume (LVESV) 267.6 mL, left ventricular end-diastolic volume (LVEDV) 395.2 mL, left ventricular end-systolic volume index (LVESVI) 180 mL/m², cardiac output (CO) 2.2 L/minute, cardiac index (CI) 1.5 L/minute/m². Single-photon emission computed tomography image of exercise 99mTc-methoxy isobutyl isonitrile (MIBI) scintigraphy revealed defect of concentration in the posterior wall and myocardial infarction tracer showed a negative scintigram.

Surgical Plan

The patient’s dilated cardiomyopathy was due to global hypokinesia and lateral wall dyskinesia. We thus decided to perform the Batista procedure. We did not choose maze procedure and cardiac resynchronization therapy because both were thought to be not effective. To establish a postoperative LVEDD of 62 mm, 40 mm of ventricular tissue needed to be removed (Figure 1). As a practical matter, we needed an incision line of less than 40 mm to establish the marginal area of the suture zone.

Fig. 1 - Mathematical modeling of posterior ventricular restoration. Preoperative LVEDD=75 mm. To establish a postoperative LVEDD of 62 mm, 40 mm of ventricular tissue needed to be removed.
LVDD=left ventricular end-diastolic diameter

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Fig. 1 - Mathematical modeling of posterior ventricular restoration. Preoperative LVEDD=75 mm. To establish a postoperative LVEDD of 62 mm, 40 mm of ventricular tissue needed to be removed.
LVDD=left ventricular end-diastolic diameter

Surgery

Under local anesthesia, an intra-aortic balloon pump (IABP) was inserted into the left femoral artery. The IABP was initiated before the introduction of general anesthesia. The procedure was performed on-pump, with a beating heart and without aortic cross-clamp (Video1). The anterior and posterior pupillary muscles were visualized with epicardial echocardiography (SonoSite S Series, Fujifilm, Washington) (Video 2). The posterior wall was noted to be thin in the region between the posterior descending artery and the obtuse marginal artery. A wedge resection was performed under echocardiogram guidance. A deep and wide mattress suture was performed with 3-0 hexafluoropropylene in an interrupted and continuous fashion to exclude the posterolateral dyskinetic lesion of the left ventricle. The patient was also noted to have moderate-to-severe mitral and tricuspid regurgitation, so mitral valve repair with Physio II ring 26 mm (Edwards Lifesciences Corporation, Irvine, CA) and tricuspid annuloplasty with MC332 mm (Edwards Lifesciences Corporation, Irvine, CA) were performed (Video 3).

Video 1 - Intraoperative diagnosis with using cardiopulmonary bypass.

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Video 1 - Intraoperative diagnosis with using cardiopulmonary bypass.

Video 2 - Epicardial echocardiography.

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Video 2 - Epicardial echocardiography.

Video3 - Performing Partial Left Ventriculectomy.

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Video3 - Performing Partial Left Ventriculectomy.

Postoperative Course

Postoperative echocardiography revealed LVEDD/LVESD of 62/43 mm and LV ejection fraction of 30% (modified Simpson’s method). Mitral regurgitation was not observed (tethering was improving). Three weeks after surgery, the patient was discharged from our hospital without further complication. Histopathological findings revealed the presence of abnormal nuclei (swollen nuclei with an altered structure surrounded by a halo) and loss of striation. Fibrosis was characteristically interstitial and began to surround and isolate individual myocytes. There was no contradiction as a finding of dilated cardiomyopathy.

Two years later, the patient had no symptom and his BNP level decreased from 1155 to 49.3 pg/mL (Figure 2). Echocardiography showed LVEDD/LVESD of 67/41 mm, left ventricular volumetry were 176/138 mL, E/A was 1.22, E/e’ was 1.3 and an LV ejection fraction of 31% (modified Simpson’s method). Mitral regurgitation was trivial and tricuspid regurgitation was none. In the short axis view, the anterior and posterior papillary muscle was approximate compared to preoperative echocardiography (interpapillary muscle distance was reduced from 39 mm to 18 mm) (Figure 3).

Fig. 2 - Timeline. On postoperative day (POD) 4, the patient presented abdominal distension. Follow-up computed tomography suggested a segmental lack of enhancement in the intestinal wall without superior mesenteric artery (SMA) occlusion. The patient was diagnosed with nonocclusive mesenteric ischemia (NOMI). We performed selective mesenteric angiography and transcatheter prostaglandin infusion via SMA. Seventeen days after treatment, mesenteric blood flow improved and enteral nutrition was resumed. The patient was discharged from the hospital 2 months after surgery. His outpatient course was good, and his heart failure symptoms gradually improved.
BNP=brain natriuretic peptide; NYHA=New York Heart Association

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Fig. 2 - Timeline. On postoperative day (POD) 4, the patient presented abdominal distension. Follow-up computed tomography suggested a segmental lack of enhancement in the intestinal wall without superior mesenteric artery (SMA) occlusion. The patient was diagnosed with nonocclusive mesenteric ischemia (NOMI). We performed selective mesenteric angiography and transcatheter prostaglandin infusion via SMA. Seventeen days after treatment, mesenteric blood flow improved and enteral nutrition was resumed. The patient was discharged from the hospital 2 months after surgery. His outpatient course was good, and his heart failure symptoms gradually improved.
BNP=brain natriuretic peptide; NYHA=New York Heart Association

Fig. 3 - Pre and postoperative transthoracic echocardiography. In the short axis view, the anterior and posterior papillary muscle distance (interpapillary muscle distance) was 39 mm in preoperative echocardiography. Two years later, interpapillary muscle distance was 18 mm.

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Fig. 3 - Pre and postoperative transthoracic echocardiography. In the short axis view, the anterior and posterior papillary muscle distance (interpapillary muscle distance) was 39 mm in preoperative echocardiography. Two years later, interpapillary muscle distance was 18 mm.