Ulf Kjellman

Endograft therapy for diseases of the descending thoracic aorta: results in 43 high-risk patients.

Purpose: To report an initial experience with endovascular stent-graft implantation for diseases of the descending thoracic aorta in high-risk patients. Methods: Forty-three patients (28 men; mean age 67 years, range 17–82) with 16 descending thoracic aortic dissections, 14 aneurysms, 7 contained ruptures, 3 mycotic aneurysms, 2 posttraumatic pseudoaneurysms, and an aneurysm of an anomalous right subclavian artery were treated between June 1999 and July 2001. Twenty-three (53%) patients were treated emergently. Results: There were no conversions to open repair, but 3 (7%) patients died during the first 30 days (pneumonia, multiorgan failure, and acute bowel ischemia). Thirteen (30%) patients suffered 18 major complications (8 strokes, paraplegia in 3, respiratory insufficiency in 6, and 1 renal failure). Of 7 (16%) endoleaks detected in the early postoperative period, 3 required additional stents, while the other 4 were treated conservatively. Follow-up, which averaged 19 ± 6 months (median: 13; range 0–34), was 100% complete. Five (12%) patients died: 3 of aortic rupture at 34, 47, and 139 days, respectively, and 2 from heart failure at 3 and 15 months, respectively. No late migration or endoleaks have been detected in the remaining 35 patients; however, 1 (2%) patient showed progressive aortic dissection proximal to the stent-graft. In all other cases, the size of the aneurysm or the false lumen was unchanged or diminished. Conclusions: Treatment of descending thoracic aortic diseases with an endovascular approach has acceptable early mortality and morbidity in high-risk patients. In selected cases, stent-grafts may afford the best therapy.

Does pretransplant left ventricular assist device therapy improve results after heart transplantation in patients with elevated pulmonary vascular resistance

OBJECTIVE Pulmonary hypertension (PH), defined as a pulmonary vascular resistance (PVR) >2.5 Wood units (WU) and (or) a transpulmonary gradient (TPG) >12 mmHg, is an established risk factor for mortality in heart transplantation. Elevated PVR in heart transplant candidates can be reduced using a left ventricular assist device (LVAD), and LVAD is proposed to be the treatment of choice for candidates with PH. We analyzed the effect on PVR of pretransplant LVAD therapy in patients with PH and compared posttransplant outcome with matched controls. Long-term survival was compared between heart transplant recipients with mild, moderate or severe PH and patients with no PH. METHODS Heart transplant recipients 1988-2007 (n=405) were reviewed and divided into two groups with respect to pretransplant PVR: <2.5 WU (n=148) and >2.5 WU (n=158). From the group with PH, patients subjected to pretransplant LVAD therapy (n=11) were analyzed with respect to PVR at implant and at transplant and, with respect to outcome, compared to matched historical controls (n=22). Patients with PH without LVAD treatment (n=147) were stratified into three subgroups: mild, moderate and severe PH and survival according to Kaplan-Meier was analyzed and compared to patients with no PH. RESULTS LVAD therapy reduced PVR from 4.3+/-1.6 to 2.0+/-0.6 WU, p<0.05. Three cases of perioperative heart failure required mechanical support whereas one control patient developed perioperative right heart failure requiring mechanical support. The incidence of other perioperative complications was comparable between groups. There was no difference in survival between LVAD patients and controls, 30-day survival was 82% and 91%, respectively and 4-year survival was 64% and 82%, respectively. CONCLUSIONS Pretransplant LVAD therapy reduces an elevated PVR in heart transplant recipients, but there was no statistically significant difference in posttransplant survival in patients with PH with, or without LVAD therapy. The study revealed no differences in survival in patients regardless of the severity of the PH.

α-ketoglutarate for myocardial protection in heart surgery

Abstract A low myocardial content of α-ketoglutarate during heart surgery might aggravate ischaemic injury. 24 men undergoing coronary surgery participated in a randomised controlled study. 28 g α-ketoglutarate was added to blood cardioplegia for intermittent antegrade intracoronary perfusion in 13 cases. α-ketoglutarate reduced the appearance in blood of the ischaemic markers creatine kinase MB and troponin T (at 4 h after release of aortic cross-clamp; median [95% Cl] 49 [37-60] μg/L in controls vs 32 [27-37] μg/L for creatine kinase MB, 2·0 [1·2-2·8] vs 1·1 [0·8-1·4] μg/L for troponin T). These findings signify attenuated ischaemic injury, possibly secondary to enhanced myocardial oxidative capacity.

Addition of α-Ketoglutarate to Blood Cardioplegia Improves Cardioprotection

Abstract Background . We hypothesized that myocardial content of α-ketoglutarate (α-KG), an intermediate of the Krebs cycle, can be critically low during heart operations, and that provision of α-KG could reduce metabolic abnormalities and lead to improved myocardial protection. Methods . Twenty-four men aged 46 to 78 years who were undergoing heart operations participated in a prospective, controlled, randomized study. In 13 patients, an average of 28 g of α-KG was added to blood cardioplegia. Plasma creatine kinase isoenzyme MB and troponin T, and myocardial extraction of oxygen, substrates, and amino acids were measured. Results . α-Ketoglutarate treatment was associated with lower creatine kinase isoenzyme MB (F = 39.6, df=1.172, p p p p = 0.016). There were no other differences after 30 minutes of reperfusion. Conclusion . Provision of α-KG during blood cardioplegia improves myocardial protection in patients undergoing coronary operations. This may be linked to enhanced oxidation. (Ann Thorac Surg 1997;63:1625–34)

Insulin(GIK) improves myocardial metabolism in patients during blood cardioplegia.

The aim of this study was to test the hypothesis that abnormalities of myocardial substrate metabolism during blood cardioplegic aortic cross-clamping and early reperfusion are attenuated further by insulin(GIK) than by alpha-ketoglutarate enrichment of blood cardioplegia alone. Twenty-eight males (47 to 78 years) undergoing coronary artery bypass grafting (CABG) participated in a prospective, controlled, randomized study. All patients had alpha-ketoglutarate-enriched blood cardioplegia. Insulin(GIK) was infused in 13 patients during aortic cross-clamping. Insulin(GIK) prevented lactate release during cardioplegia (1.5+/-15 vs -44+/-14 micromol/min, p = 0.04), and a significant extraction of lactate was induced shortly after declamping the aorta (15+/-3 vs 2+/-1%, p = 0.001). Free fatty acid uptake was reduced after cardioplegic cross-clamping (5.7+/-1.6 vs 16.0+/-3.8 micromol/min, p = 0.02). More positive/less negative levels of alanine, aspartate, glutamine, glycine, ornithine, taurine and tyrosine were found in all the insulin-treated patients. We conclude that insulin(GIK) attenuates abnormalities of myocardial substrate metabolism during blood cardioplegic aortic cross-clamping and early reperfusion further than is obtained with alpha-ketoglutarate enrichment of blood cardioplegia alone.

Anatomical mismatch of the pulmonary autograft in the aortic root may be the cause of early aortic insufficiency after the Ross procedure

OBJECTIVE Early aortic insufficiency can be a problem after the Ross procedure. Anatomical mismatch and an inexact surgical technique may lead to distortion of the normal pulmonary valve geometry and subsequent incorrect leaflet coaptation and valve insufficiency. In this study, we assessed the efficacy of changing and improving the surgical technique to minimize the early pulmonary autograft valve failure. The modifications and the strategy are discussed. METHODS From January 1995 to February 1999, a total of 77 adults underwent the Ross procedure for aortic valve replacement at Sahlgrenska University Hospital. The operative technique used was full free-standing aortic root replacement with a pulmonary autograft in all cases. In the first 24 cases, the diameter of the pulmonary roots was seldom measured, eye-balling was used to exclude anatomical mismatch due to a dilated aortic root, and only one attempt of correction was made, which failed. In the other 53 cases, the technique was improved by: (1) reducing the aortic anulus diameter in cases with moderate dilatation; (2) excluding cases with severe dilatation of the aortic annulus; (3) adjusting the diameter of the sinotubular junction of the aorta to the diameter of the sinotubular junction of the pulmonary artery; (4). reimplanting the left ostium in the autograft, and (5) changing the proximal anastomosis technique. RESULTS In this study, we had an early aortic incompetence of grade 2 in eight patients among the first 24 patients. In the other 53 patients, postoperative echocardiography at 1 week revealed aortic insufficiency of grade 2 in two patients. CONCLUSIONS Aortic insufficiency after the Ross procedure can be minimized by patient selection, intraoperative correction of anatomical mismatch and improved surgical technique.

Weaning from mechanical support in a patient with acute heart failure and multiple sclerosis

We describe a 19-year-old woman developing acute left ventricular heart failure during her first exacerbation of multiple sclerosis. Histopathologic examination of myocardial tissue showed extensive myocytolysis. A left ventricular assist device was implanted. Three months later the cardiac function was restored and the left ventricular assist device was explanted. After 1 year the patient still remains well and her cardiac function is normal.

Successful Outcome After Massive Bleeding in A Heart Transplant Recipient With Mycotic Aortitis

Sudden mediastinal haemorrhage one month after heart transplantation in an 18-year-old youth was found to originate from a rupture of the ascending aorta associated with mycotic aortitis. Aortic continuity was restored with a Dacron graft. Cultures from the resected vessel wall showed Candida albicans. The patient recovered, and 11 months later is well.

Extracorporeal membrane oxygenation as a bridge to lung transplantation in a patient with persistent severe porto-pulmonary arterial hypertension following liver transplantation

Idiopathic pulmonary artery hypertension (IPAH) is a progressive disease with a dismal prognosis and lung transplantation is often the only option for patients, who do not respond to pharmacological therapy. We report the use of an extracorporeal membrane oxygenation (ECMO) system in a 49-year-old woman with primary pulmonary hypertension, previously liver transplanted. The patient, listed for lung transplantation, developed respiratory and circulatory failure despite maximal pharmacological therapy and was successfully bridged to emergent bilateral lung transplantation with veno-arterial ECMO. Emergent veno-arterial ECMO was able to rescue the patient and bridge her to bilateral lung transplantation and should therefore be an option for patients with PAH and circulatory collapse.

Predictors of allograft ischemic injury in clinical heart transplantation.

Objectives: 1. Identify clinical, biochemical and inflammatory predictors of allograft ischemic injury in clinical heart transplantation. 2. Evaluate the impact of high dose insulin (GIK) on allograft metabolism during blood cardioplegia and post-ischemic injury. Design: A clinical, prospective, randomized open trial comprising 25 consecutive heart transplantations at a university hospital. Ischemic injury was evaluated from plasma levels of creatine kinase isoenzyme MB (CK-MB). Blood cardioplegic arterial and coronary sinus concentrations of C3a, IL-6, substrates, amino acids and blood gases were measured at the end of the implantation period, prior to reperfusion. Twelve patients received high dose insulin with glucose, potassium and amino acids. Results: CK-MB increased from 1.9 - 0.2 to 161 - 13 µ g/l (range 47-293 µ g/l). The peak level of CK-MB correlated with donor age ( r = 0.48, p = 0.02) and implantation time ( r = 0.53, p = 0.02); and with recipient plasma IL-6 ( r = 0.56, p = 0.02), allograft oxygen extraction ( r = 0.56, p = 0.02), lactate release ( r = 0.47, p = 0.02) and allograft arterial-coronary sinus (cs) pH ( r = 0.47, p = 0.02) all during final cardioplegia before reperfusion. Seventy-two percent of the variance of CK-MB was explained by a model which included donor age, art-cs pH difference and arterial IL-6. In contrast, CK-MB was unrelated to total ischemic time ( r = -0.17, p = 0.38). Insulin infusion had no effect on myocardial substrates during cardioplegia, or on post-ischemic CK-MB. Conclusion: Donor age, duration and quality of the implantation period are significant predictors of allograft ischemic injury in heart transplantation. High dose insulin had no detectable effects on allograft metabolism during cardioplegia, or on subsequent ischemic injury.