A 58-year-old man previously underwent axillobifemoral bypass at another hospital for atypical coarctation of the aorta due to Takayasu’s arteritis. He was re-hospitalized approximately 10 years later due to heart failure, and a progressive decrease in left ventricular contractility was observed, along with a decrease in the left ventricular ejection fraction (LVEF) from 54–28%. Multiple antihypertensive drugs were administered, and he was referred to our hospital to investigate the cause of the progressive decrease in left ventricular contractility and repeated heart failure due to poor blood pressure control. 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) performed at the previous hospital did not detect 18F-FDG accumulation in the aorta. His laboratory data were as follows: creatinine, 2.93 mg/dL; blood urea nitrogen, 65.7 mg/dL; estimated glomerular filtration rate, 19 mL/min/1.73 m2; C-reactive protein (CRP), 0.54 mg/dL; N-terminal pro-brain natriuretic peptide (NT-proBNP), 17,014 pg/mL; aldosterone, 119 (reference values 36–240) pg/ml; and plasma renin activity, 10.6 (reference values 0.2–2.3) ng/ml/h. His blood pressure values were as follows: right upper limb, 168/108 mmHg; upper left limb, 169/99 mmHg; right lower limb, 143/98 mmHg; and left lower limb, 131/101 mmHg. The right and left ankle brachial index (ABI) values were 0.85 and 0.78, respectively. Preoperative transthoracic echocardiography revealed a LVEF of 28%. There was no left ventricular asynergy, and the wall motion showed severe diffuse hypokinesis. Left ventricular wall thickness of the interventricular septum (IVS) and posterior wall (PW) were 13 and 12 mm, respectively. Left ventricular hypertrophy was also observed. Further, the left ventricular end-diastolic and systolic diameters (LVEDD and LVESD) were 57.4 and 47.5 mm, respectively, and left ventricular hypertrophy was detected. However, no significant valvular dysfunction was observed. Contrast-enhanced CT showed a patent axillobifemoral bypass and collateral circulation to the arteries of the lower extremity (Fig. 1a). Significant calcification was observed from the distal descending thoracic aorta to the abdominal aorta, and severe stenosis was suspected at the same site (Fig. 1b). Aortography showed severe stenosis of the aorta from below the celiac artery to the abdominal aorta below the renal arteries. We also noticed that collateral circulation from the celiac artery to the superior mesenteric artery was well developed Blood flow in the superior mesenteric artery passed from the developed collateral circulation from the celiac artery, and flow imaging of both renal arteries was delayed (Fig. 2a). Coronary angiography showed no abnormal findings, including at the entrance. Contrast-enhanced cardiac magnetic resonance imaging (MRI) revealed no apparent delayed contrast on the left ventricular wall, and T1 mapping images of cardiac MRI presented no significant increase in the T1 value on the left ventricular wall (1,050 ms by 1.5T modified Look-Locker inversion recovery method; the average value of normal control at our hospital was 1,000 ms), and fibrosis of the left ventricular wall was considered mild (Fig. 2b). Although CRP was weakly positive, CT only showed severe calcification of the aorta, and PET-CT performed at the previous hospital did not show active inflammation of the aorta due to Takayasu’s arteritis. Therefore, we decided to perform open surgery for uncontrolled renal hypertension and a progressive decrease in left ventricular contractility due to decreased bilateral renal blood flow. To reliably reduce afterload, we performed descending thoracic aorta–abdominal aorta bypass using a large-diameter graft and revascularization of both renal arteries via great saphenous vein grafts.
Thoracotomy was performed under general anesthesia via the left lower 7th intercostal space, and the retroperitoneal approach was used to access the abdominal aorta. A skin incision was then made across the axillobifemoral bypass. To secure blood flow to the lower limbs during aortic clamping, surgery was performed without transection of the axillobifemoral bypass graft. The thoracic and abdominal aorta approach was performed without incising the diaphragm. In the retroperitoneal space, the dorsal side of the kidney was dissected, and the diaphragm was incised on the left side of the aortic hiatus to create a tunnel that connected the left thoracic cavity and retroperitoneal space. After systemic heparinization, the descending thoracic aorta was clamped at the Th9 level, and a proximal anastomosis was performed using a 12-mm woven graft (Intergard®, Maquet, Sunderland, UK). The anastomosed woven graft was guided into the retroperitoneal space through the tunnel in the diaphragm, and a distal anastomosis was performed just above the bifurcation of the abdominal aorta. During this period, blood flow to the lower limb was maintained by the patent left axilobifemoral artery bypass. The anterior side of the left kidney was peeled off to expose the anterior surface of the abdominal aorta and the left and right renal arteries. The great saphenous vein was collected and anastomosed to the left and right renal arteries, and the vein graft stump was anastomosed to the woven graft. Next, the left leg of the exposed axillobifemoral bypass graft was resected just below the wound to reduce the risk of postoperative infection. The operative time was 388 minutes.
No postoperative complications were observed. Postoperative 3D-CT showed that the bypass graft from the descending thoracic aorta to the abdomen ran parallel to the aorta on the dorsal side of the left renal artery and was patent. The great saphenous vein graft to both renal arteries was also patent (Fig. 2c). Postoperative ABI improved to 1.12 on the right and 1.06 on the left; the upper-limb blood pressure improved to 128/91 mmHg with good control, and the dose of antihypertensive drugs could be reduced. He was discharged from the hospital 16 days postoperatively. Blood test findings after discharge showed a decrease in NT-proBNP level (78 pg/dL), aldosterone level (58 pg/mL), and plasma renin activity (1.1 ng/ml/h). Transthoracic echocardiography performed 1.5 years postoperatively showed marked improvement in LVEF of 58% (Fig. 3). Furthermore, left ventricular wall thickness and left ventricular diameter decreased: IVS, 9.0 mm; PW, 8.7 mm; LVEDD, 41.6 mm; and LVESD, 28.6 mm. Left ventricular reverse remodeling had also occurred.