Less invasive surgery of the proximal aorta : From 23rd World Congress of the World Society of Cardio-Thoracic Surgeons. Split, Croatia. 12-15 September 2013

Oral presentation: 23rd World Congress of the World Society of Cardio-Thoracic Surgeons. Split, Croatia. 12-15 September 2013. Background: Partial upper sternotomy (PUS) is established less invasive approach for single and double valve surgery. Reports of aortic surgery performed through PUS are rare. Methods: The records of 52 patients undergoing primary elective surgery on the proximal aorta through PUS between 2005 and 2011 were reviewed. Patients mean age was 57 years, 35% were in NYHA Class III or IV, 59% had recent cardiac decompensation, and 17% had pulmonary hypertension. The PUS was taken down to the 4th left intercostal space in 44 patients (85%). Results: No conversion to full sternotomy was necessary. The aortic cross-clamp, cardiopulmonary bypass and operative times averaged 136 ± 20 min., 186 ± 36 min. and 327 ± 83 min., respectively. In eight patients, the right axillary artery was cannulated for establishing cardiopulmonary bypass; the others were cannulated centrally. All patients except one received a procedure on the ascending aorta, either replacement in 30 (58%) or reduction aortoplasty in 21 (40%). Aortic root replacement was additionally performed in 31 patients (60%), including David in 20 (38%) and Ross procedure in 6 (11.5%). The aortic arch was replaced either partially in 5 (10%) or totally in 3 (6%) patients, in moderate hypothermia employing antegrade cerebral perfusion. Additional procedures, included mitral valve repair in 15 (29%) patients and coronary grafting. Ventilation time, intensive care unit and hospital stay averaged 17 ± 12 hours, 2 ± 1, and 11 ± 9 days. Chest drainage was 470 ± 380 ml/24 hours. Permanent neurologic deficit did not occur. Wound dehiscence was observed in a single patient (2%). Thirty-day and hospital mortality were not observed. Conclusions: Less invasive surgery on the aortic root, ascending aorta and aortic arch can be performed safely and reproducibly. Potential benefits include a minimized risk of wound dehiscence and reduced postoperative bleeding. The PUS does not compromise the quality of the operation

Permanent biventricular ICD-implantation in a heart failure second re-do-CABG patient: a case report

Biventricular pacing has been suggested in end-stage heart failure. We present a 59-year-old patient undergoing second re-do CABG (coronary artery bypass graft) and carotid artery endarterectomy. Ejection fraction was 15%, QRS-width 175 ms. Following the carotid and CABG procedure, an implanted single-chamber ICD (implantable cardioverter defibrillator) was upgraded to permanent biventricular DDD pacing by implantation of one epicardial left ventricular and one epicardial atrial electrode. At follow-up two months postoperatively ejection fraction had significantly improved to 45%, the patient underwent stress test with adequate load and reported a good quality of life

Cardiac metastasis causes paradoxical malignant embolism

Background Embolic events play an important role in clinical everyday practice. Malignant arterial embolism is a rare nevertheless often fatal entity for cardiac, cerebral or systemic ischemia, requiring immediate diagnosis and treatment. Case This is a case report of a 65 years-old female, suffering from pulmonal adenocarcinoma, who was hospitalized due to neurological deficits caused by an acute ischemic stroke, followed by anterior myocardial infarction within 3 days. Diagnostic work-up revealed metastasis of the pulmonal adenocarcinoma in the right atrium and a patent foramen ovale. Histopathological examination of the coronary embolus verified paradoxical arterial embolism of the pulmonal adenocarcinoma into a coronary vessel and consequently cerebral arteries. Conclusion The present case underlines the need for (i), consideration of malignant embolism, (ii) histopathological examination of the embolus to determine its etiology, and (iii) interdisciplinary discussion of individual therapeutic and prevention strategies in cancer patients with cerebral, cardiac or systemic embolic events

Longer-term outcomes after bicuspid aortic valve repair in 142 patients

Background: The aim of this study was to evaluate the longer-term results of bicuspid aortic valve (BAV) repair with or without aortic root replacement. Methods: From 1999 to 2017, 142 patients with or without aortic root dilatation who underwent repair of a regurgitant BAV were included in the study. Ninety-four patients underwent isolated BAV repair (Group 1; median age 43 years) and 48 patients underwent valve-sparing aortic root replacement plus BAV repair (aortic valve reimplantation—Group 2; median age 48 years). Median clinical follow-up time was 5.9 years (range 0.5–15) in Group 1 and 3 years (range 0.5–16) in Group 2, respectively. Results: In-hospital mortality was 1% in Group 1, and 2% in Group 2 (p = .6). The 5- and 10-year survival was 93 ± 2.9% and 81 ± 5.8% in Group 1 and 96 ± 3.1% and 96 ± 3.1% in Group 2, respectively (p = .31). Eleven patients of Group 1 (1.7%/patient-year) and five patients of Group 2 (2.2%/patient-year) underwent reoperation of the aortic valve (p = .5). The 5- and 10-year freedom from reoperation were 93.0 ± 2.1% and 77.1 ± 7.1% in Group 1 and 93.0 ± 5.0% and 76.7 ± 9.6% in Group 2 (p = .83), respectively. At the latest follow-up, only two patients of Group 1 and 1 patient of Group 2 had AV regurgitation = 2° (p = .7). The cumulative linearized incidence of all valve-related complications (bleeding, stroke, endocarditis, and reoperation) was 2.9%/patient-year in Group 1% and 4%/patient-year in Group 2, respectively (p = .6). Conclusions: Isolated BAV repair and combined aortic valve reimplantation plus BAV repair provide good clinical longer-term outcomes with relatively low reoperation rate and durable valve function

The CX3C chemokine fractalkine mediates platelet adhesion via the von Willebrand receptor glycoprotein Ib

The membrane-anchored CX3C chemokine fractalkine (FKN) is expressed on activated endothelium and is associated with the development of atherosclerosis. The potential of FKN in mediating platelet adhesion beyond platelet activation remains unexplored to date. A flow-based adhesion assay was used to study the adhesion of platelets to immobilized FKN under physiologic flow conditions. Platelet adhesion to von Willebrand factor (VWF) was increased in the presence of FKN at 600 inverse seconds. Additional platelet adhesion to FKN coimmobilized with VWF was dependent on the FKN receptor CX3CR1 and activation of glycoprotein (GP) IIb/IIIa. The number of platelets rolling on VWF was likewise enhanced in the presence of FKN. The enhancement of rolling on FKN and VWF was insensitive to anti-CX3CR1 antibody but was fully inhibited by neutralizing GPIb alpha function. The extracellular domain of GPIb alpha was covalently coupled to fluo-rescent microspheres, and microsphere binding was significantly higher in the presence of FKN. Platelet adhesion to activated endothelium in vitro and to intact human arteries was substantially increased in an FKN-dependent manner. These data demonstrate that endothelial expressed FKN activates platelets via its cognate receptor CX3CR1, whereas platelet adhesion is predominantly mediated by GPIb alpha and independent of CX3CR1. (Blood. 2011;117(18):4999-5008)status: publishe

Platelets from flowing blood attach to the inflammatory chemokine CXCL16 expressed in the endothelium of the human vessel wall

Endothelial chemokine CXC motif ligand 16 (CXCL16) expression is associated with atherosclerosis, while platelets, particularly those attaching to atherosclerotic plaque, contribute to all stages of atherosclerotic disease. This investigation was designed to examine the role of CXCL16 in capturing platelets from flowing blood. CXCL16 was expressed in human atherosclerotic plaques, and lesion severity in human carotid endarterectomy specimens was positively correlated with CXCL16 levels. CXCL16 expression in plaques was co-localised with platelets deposited to the endothelium. Immobilised CXCL16 promoted CXCR6-dependent platelet adhesion to the human vessel wall, endothelial cells and von Willebrand factor during physiologic flow. At low shear, immobilised CXCL16 captured platelets from flowing blood. It also induced irreversible platelet aggregation and a rise in intra-platelet calcium levels. These results demonstrate that endothelial CXCL16's action on platelets is not only limited to platelet activation, but that immobilised CXCL16 also acts as a potent novel platelet adhesion ligand, inducing platelet adhesion to the human vessel wall.status: publishe

Hepatocyte growth factor mobilizes non-bone marrow-derived circulating mesoangioblasts

AIMS: The identification of factors that mobilize subsets of endogenous progenitor cells may provide new therapeutic tools to enhance the repair of ischaemic tissue. We previously identified circulating mesenchymal cells that co-express endothelial markers (so-called circulating mesoangioblasts, cMABs) in children undergoing heart surgery with cardiopulmonary bypass (CPB). However, the mechanisms by which these cells are mobilized and their origin is unclear. METHODS AND RESULTS: Circulating CD73(+)CD45(-)KDR(+) cMABs were analysed in adults undergoing heart surgery with (n = 21) or without CPB (n = 8). During surgery with CPB, cMABs are mobilized with a maximal response at the end of the operation. In contrast, off-pump heart surgery does not stimulate cMAB mobilization, indicating that the stress mediated by CPB induces the mobilization of cMAB. Circulating mesoangioblasts were enriched in blood obtained from the coronary sinus. Histologically, CD73(+) cells were detected around vessels in the heart, indicating that the heart is one of the niches of cMABs. Consistently, studies in gender mismatched bone marrow transplanted patients demonstrated that cMABs did not originate from the bone marrow. Cytokine profiling of serum samples revealed that hepatocyte growth factor (HGF) was profoundly increased at the time point of maximal mobilization of cMABs. Hepatocyte growth factor stimulated the migration of cMABs. Importantly, injection of recombinant HGF increased cMABs in rats. CONCLUSIONS: Hepatocyte growth factor induces mobilization of non-haematopoietic progenitor cells with a cardiac repair capacity. This newly identified function together with the known pleiotrophic effects of HGF makes HGF an attractive therapeutic option for the treatment of ischaemic heart disease