TRANSESOPHAGEAL echocardiography (TEE) is a new tool for the perioperative treatment of cardiac surgery patients. We report a clinical case to illustrate the usefulness of TEE for evaluating morphologic and functional features of a cardiac graft. Mitral regurgitation (MR) secondary to left ventricular outflow tract obstruction with systolic anterior motion (SAM) of the anterior mitral leaflet was diagnosed preoperatively with TEE. Medical treatment of the recipient was changed consequently to prevent hemodynamic deterioration.

J Vasc Res 1998;35:372–393 Joint Meeting of the British Microcirculation Society and the Northern Vascular Biology Group Manchester, UK, March 30–31, 1998 Editor Barbara Ward, London, UK

Background-It has been suggested that oxidant stress may play a role in the pathophysiology of heart failure. However, no definitive information is available because most previous approaches used to measure oxidant stress are nonspecific, inaccurate, and unreliable.Methods and Results-To evaluate oxidant stress in the heart, we measured pericardial fluid levels of 8-iso-prostaglandin F-2 alpha (8-iso-PGF(2 alpha)), a specific and quantitative marker of oxidant stress in vivo, in a series of 51 consecutive patients with ischemic and/or valvular heart disease referred for cardiac surgery. Pericardial levels of 8-iso-PGF(2 alpha) were correlated with the functional severity of heart failure (NYHA classification) and with echocardiographic indices of ventricular dilatation measured by independent physicians. Pericardial levels of 8-iso-PGF(2 alpha) were significantly increased in patients with symptomatic heart failure compared with asymptomatic patients and gradually increased with the functional severity of heart failure (P=.0003). In addition, pericardial levels of 8-iso-PGF(2 alpha) were significantly correlated with left ventricular end-diastolic and end-systolic diameters (P=.008 and .026, respectively).Conclusions-Pericardial levels of 8-iso-PGF(2 alpha) increase with the functional severity of heart failure and are associated with ventricular dilatation. These data suggest an important role for in vivo oxidant stress on ventricular remodeling and the progression to heart failure.

The authors report the anatomo-clinical features of aortic insufficiency complicating atrophic polychondritis, a rare inflammatory disease affecting mainly cartilaginous tissues. This case illustrates the inflammatory changes of the aortic wall, particularly progressive during this disease, responsible for aortic insufficiency and aneurysmal dilatation of the ascending aorta which required aortic valve replacement and prosthetic replacement of the ascending aorta. Histological analysis showed inflammatory lesions of the aortic wall comparable to the cartilaginous lesions described in this condition and suggesting a common physiopathogenic mechanism.

A gene polymorphism of the angiotensin II (AII) type 1 receptor has been described previously (A to C transversion at position 1166). Besides the epidemiological studies needed to determine a possible relationship between the polymorphism and some cardiovascular diseases, no study has been conducted to determine the impact of the polymorphism on vascular functions. At subthreshold concentrations, within the physiological range, AII potentiates alpha-adrenergic-dependent vascular tone. We investigated phenylephrine-induced tone and its amplification by AII (10 pmol/l) in human internal mammary artery rings mounted in organ baths. We performed concentration-response curves to phenylephrine (0.1-100 micromol/l) before and after pretreatment with AII (10 pmol/l). Patients had the genotype AA (n = 20) or the A to C transversion (AC/CC, n = 30). Contractions to phenylephrine (0.1-100 micromol/l) were significantly higher in rings from AC/CC than from AA patients (maximum response: 1.47+/-0.07 vs. 1.22+/-0.06 mN/mg, p < 0.001). AII (10 pmol/l) induced a significant potentiation of phenylephrine-induced contraction (e.g. 58.9% increase in tone with 1 micromol/l phenylephrine, p < 0.001) which was significantly lower in the AC/CC than in the AA group (46+/-9 vs. 66+/-7% with 1 micromol/l phenylephrine, p < 0.01). Contractions to AII (1 or 100 nmol/l) were not significantly affected by the genotype. Although the study was performed in arteries from patients with a coronary artery disease, these changes in vascular reactivity might be of interest in the understanding of the relationship between a possible higher probability of cardiovascular disorder and the genetic polymorphism of the AII type 1 receptor.

The aim of the study was to compare the supra-annular and intra-annular implantation techniques by evaluating the differences in early haemodynamic outcome (gradients, effective orifice area, regurgitation). Since August 1991, 200 stentless Bravo model 300 valves have been implanted. Patients were divided into three groups of consecutive cases: group 1 (n = 50) represents exclusively intra-annular implantation; group 2 (n = 50) is a transitional period: and group 3 (n = 100) comprises only patients with supra-annular implantation. Significant differences were found (P<0.001) in low postoperative gradients (mean < or = 10 mmHg): 24% in group 1, 42% in group 2, and 95% in group 3. Comparing groups 1 and 3, gradients were lower and effective orifice area was augmented in all valve sizes in group 3. Trivial central regurgitation was present in groups 1-3 (6%, 12% and 0% respectively). Peripheral regurgitation was trivial in 6%, 8% and 0% and mild to moderate in 4%, 2% and 0% (P<0.001).

The authors report the anatomo-clinical features of aortic insufficiency complicating atrophic polychondritis, a rare inflammatory disease affecting mainly cartilaginous tissues. This case illustrates the inflammatory changes of the aortic wall, particularly progressive during this disease, responsible for aortic insufficiency and aneurysmal dilatation of the ascending aorta which required aortic valve replacement and prosthetic replacement of the ascending aorta. Histological analysis showed inflammatory lesions of the aortic wall comparable to the cartilaginous lesions described in this condition and suggesting a common physiopathogenic mechanism.

HomeCirculationVol. 96, No. 10False Aortic Aneurysm due to Rupture of an Aortocoronary Saphenous Vein Bypass Graft Free AccessResearch ArticleDownload EPUBAboutView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticleDownload EPUBFalse Aortic Aneurysm due to Rupture of an Aortocoronary Saphenous Vein Bypass Graft Philippe Gabriel Steg, Marc Benacerraf, Didier Chatel and Jean-Pierre Laissy Philippe Gabriel StegPhilippe Gabriel Steg From the Cardiology (P.G.S., M.B.), Cardiac Surgery (D.C.), and Radiology (J.-P.L.) Departments, Hôpital Bichat, Paris, France. , Marc BenacerrafMarc Benacerraf From the Cardiology (P.G.S., M.B.), Cardiac Surgery (D.C.), and Radiology (J.-P.L.) Departments, Hôpital Bichat, Paris, France. , Didier ChatelDidier Chatel From the Cardiology (P.G.S., M.B.), Cardiac Surgery (D.C.), and Radiology (J.-P.L.) Departments, Hôpital Bichat, Paris, France. and Jean-Pierre LaissyJean-Pierre Laissy From the Cardiology (P.G.S., M.B.), Cardiac Surgery (D.C.), and Radiology (J.-P.L.) Departments, Hôpital Bichat, Paris, France. Originally published18 Nov 1997https://doi.org/10.1161/01.CIR.96.10.3778Circulation. 1997;96:3778A 40-year-old man was admitted for atypical chest pain. Eight years earlier, he had undergone coronary artery bypass graft surgery, with two saphenous vein grafts placed on the left anterior descending coronary artery and on the obtuse marginal artery. The ECG was unremarkable, but chest radiographs showed a left anterior paracardiac mass.Contrast-enhanced CT at the level of the anastomotic sites between the ascending aorta and the grafts (Fig 1) shows a large para-aortic mass that filled with dye (in white). The leakage site on the ascending aorta is clearly visible. There appear to be several layers of low-density thrombus filling the mass (black arrowheads).A coronal spin-echo ECG-gated MRI (Fig 2) shows the mass filled with several layers of distinct signals (black arrowheads), which probably represent progressive aneurysm thrombosis. The absence of signal at the central part of the false aneurysm represents blood flowing in from the ascending aorta (A). Signal void is also present at the site of anastomotic leakage.Successive frames of a right anterior oblique view aortogram (Fig 3) show a patent saphenous vein graft to the left anterior descending artery but also contrast leakage in the form of a small anterior jet (white arrow) at the anastomotic site of the left marginal graft.The patient underwent repeat coronary artery surgery. There was rupture of the proximal anastomosis of the saphenous vein graft and development of a large para-aortic false aneurysm. The aneurysm was resected, and a left internal mammary artery graft was placed on the left anterior descending coronary artery. The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke's Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.Circulation encourages readers to submit cardiovascular images to Dr Hugh A. McAllister, Jr, St Luke's Episcopal Hospital and Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.Download figureDownload PowerPoint Figure 1. Download figureDownload PowerPoint Figure 2. Download figureDownload PowerPoint Figure 3. FootnotesCorrespondence to Prof P.G. Steg, MD, Cardiology, Hôpital Bichat, 46 rue H. Huchard, 75018, Paris, France. Previous Back to top Next FiguresReferencesRelatedDetailsCited By Mezzetti E, Maiese A, Spina F, Del Duca F, De Matteis A, Di Paolo M, La Russa R, Turillazzi E and Fineschi V (2023) Early Saphenous Vein Graft Aneurysm Rupture: A Not So-Late Complication. Case Report and Comprehensive Literature Review, Biomedicines, 10.3390/biomedicines11010220, 11:1, (220) Bansal R, Lafian H and Kirk S (2021) Aortocoronary Saphenous Vein Graft Aneurysm: Diagnosis Using Color Doppler and Contrast Transesophageal Echocardiography, CASE, 10.1016/j.case.2021.09.008, 5:6, (368-372), Online publication date: 1-Dec-2021. Fohlen A, Tager P, Lognoné T and Pelage J (2016) Acute chest pain with elevated troponin due to rupture of previously stented saphenous vein graft aneurysm, Diagnostic and Interventional Imaging, 10.1016/j.diii.2016.06.014, 97:11, (1183-1185), Online publication date: 1-Nov-2016. Kashima K, Yotsumoto G, Miyajima R, Nuruki N, Sonoda M and Yamashita M (2010) Successful treatment of spontaneous coronary bypass rupture using a polytetrafluoroethylene-covered stent, Cardiovascular Intervention and Therapeutics, 10.1007/s12928-010-0015-2, 25:2, (122-125), Online publication date: 1-Jul-2010. Kaehler J, Franzen O, Regier M, Lorenzen J, Meinertz T, Reichenspurner H and Detter C (2008) Spontaneous Coronary Bypass Rupture, The Annals of Thoracic Surgery, 10.1016/j.athoracsur.2007.10.006, 86:2, (664), Online publication date: 1-Aug-2008. Kishore R and Losordo D (2007) Gene therapy for restenosis: Biological solution to a biological problem, Journal of Molecular and Cellular Cardiology, 10.1016/j.yjmcc.2006.11.012, 42:3, (461-468), Online publication date: 1-Mar-2007. Kurozumi K, Izumi C, Goto K, Hashiwada S, Takahashi S and Matsumoto M (2004) Pseudoaneurysm of Left Internal Thoracic Artery Graft After Coronary Artery Bypass Grafting: Diagnosis by Transthoracic Echocardiography, Journal of Echocardiography, 10.2303/jecho.2.80, 2:3, (80-82), . MEMON A, HUANG R, MARCUS F, XAVIER L and ALPERT J (2003) Saphenous Vein Graft Aneurysm, Cardiology in Review, 10.1097/00045415-200301000-00006, 11:1, (26-34), Online publication date: 1-Jan-2003. Harada T, Ida T, Koyanagi T, Kasahara K, Naganuma F and Hosoda S (2016) Pseudoaneurysm of the Saphenous Vein Graft Related to Artificial Rubber Pericardium, Angiology, 10.1177/000331970205300618, 53:6, (741-743), Online publication date: 1-Nov-2002. Bansal R (2002) Echocardiographic diagnosis of an asymptomatic aneurysm of a saphenous vein graft, Journal of the American Society of Echocardiography, 10.1067/mje.2002.118175, 15:6, (661-664), Online publication date: 1-Jun-2002. November 18, 1997Vol 96, Issue 10 Advertisement Article InformationMetrics Copyright © 1997 by American Heart Associationhttps://doi.org/10.1161/01.CIR.96.10.3778 Originally publishedNovember 18, 1997 Advertisement

Objective: To assess blood polymorphonuclear neutrophil (PMN) activation status during normothermic cardiopulmonary bypass (CPB), the expression of the PMN adhesion molecule CD11b/CD18 was measured. Basal state as well as ex vivo capacity of PMN to be stimulated by a bacterial peptide (FMLP) were investigated. Because interleukin-8 (IL-8) is known to induce CD11b/CD18 expression in vitro in PMN, IL-8 plasma levels were concomitantly measured.Design: Prospective study.Setting: University hospital.Participants: Thirteen patients scheduled for cardiac surgery.Interventions: Systemic arterial and pulmonary arterial blood samples were withdrawn at the same moment during the first 4 hours after the onset of CPB.Measurements and Main Results: Twenty minutes after the onset of CPB, basal expression of PMN CD11b/CD18 was upregulated, whereas IL-8 plasma levels remained unchanged. The increase in PMN CD11b expression was maintained until the fourth hour after the onset of CPB. At this time, elevation of IL-8 plasma levels was maximal, No differences were found between pulmonary and systemic arterial IL-8 plasma levels, even after aortic unclamping. The capacity of PMN to be stimulated ex vivo by FMLP remained normal.Conclusions: Normothermic CPB induced a fast increase in CD11b expression, which appeared to be similar to that observed during hypothermia. IL-8 was probably not related to the very early CD11b upregulation, but could be involved in pulmonary PMN sequestration during pulmonary reperfusion and contribute to the maintained expression of PMN CD11b. Although partially activated, PMNs maintain a normal capacity to respond to a further FMLP stimulation and thus to bacterial infection. Copyright (C) 1997 by W.B. Saunders Company.

The authors report their experience with a simple and efficient technique for repair of left ventricular free wall rupture complicating myocardial infarction. The technique consists, with the aid of cardiopulmonary bypass, in suturing a plaque of the patients own pericardium (6 to 8 cm in diameter) to the more normal tissue encircling the pathologic myocardium, and by injecting five ml of human fibrin glue as a cement under the pericardium to reinforce the remair and prevent leaking throughout the suture line. With a 10 year follow-up, we are able to be confident with the long term results. The five patients, at the time of operation were aged 46 to 74 years. The post-operative results and the annual echocardiographic controls have proved the technique to be sound without recurrences and without late complications such as pseudo aneurysms at the site of the repair.

Mitral valve repair was performed in six patients by transferring the posterior tricuspid leaflet with its sub-valvular apparatus onto the mitral valve. This new technique considers the tricuspid valve as the patients own tissue bank where the posterior leaflet and eventually the adjacent part of the anterior leaflet is used as a ''donor'' valve, based on the knowledge that the right atrio-ventricular valve can be efficiently repaired with a very low risk of significant dysfunction. The mitral repair consists of incorporating the tricuspid autograft by securing the tricuspid papillary muscle to the mitral papillary muscle and by suturing the leaflet tissue where required. A mitral annuloplasty ring reinforces the repair. The tricuspid valve is subsequently repaired by annular plication and leaflet suture. A tricuspid ring is necessary to maintain efficient remodeling. The six patients ages ranged from 20 to 70 years. A etiology, was rheumatic in the first case and degenerative in the following. In three cases, sterilised endocarditis was responsible for ruptured chordae and leaflet destruction. The mitral insufficiency was located in a commissural area in 4 cases, and was due to a widespread posterior prolapse in 2. Post-operative control transesophageal echocardiography confirmed the excellent results of the repair and proved that, in selected cases, the tricuspid leaflet inserted onto the mitral apparatus is very efficient in correcting mitral insufficiency, without causing significant tricuspid impairement. With a 3 to 7 month follow-up, the results are stable.

The authors report two cases of pulmonary valve endocarditis which required emergency surgical treatment. A 74 year old patient with trivalvular endocarditis (pulmonary, aortic, mitral), due to Sptreptococcus D bovis, developed cardiogenic shock with acute pulmonary oedema and underwent double aortic and pulmonary valve replacement with Carpentier-Edwards prostheses and simple resection of a mitral valve vegetation. Another 36 year old drug addict developed isolated pulmonary valve endocarditis due to Staphylococcus aureus infection complicated by pulmonary regurgitation with right ventricular failure and by septic pulmonary embolism with persistent sepsis: he underwent pulmonary valve replacement with a Brave 300 bioprosthesis. The postoperative course was uncomplicated in both cases, with interruption of the infection and normalisation of the hemodynamic status. The insidious and severe nature of pulmonary valve endocarditis is demonstrated by these two cases, confirming previous reports which have underlined the poor prognosis of this condition. Surgery has been shown to be effective and well tolerated and should be integrated early in the therapeutic strategy, the results being all the better when an aggressive attitude is taken.

The authors report two cases of pulmonary valve endocarditis which required emergency surgical treatment. A 74 year old patient with trivalvular endocarditis (pulmonary, aortic, mitral), due to Sptreptococcus D bovis, developed cardiogenic shock with acute pulmonary oedema and underwent double aortic and pulmonary valve replacement with Carpentier-Edwards prostheses and simple resection of a mitral valve vegetation. Another 36 year old drug addict developed isolated pulmonary valve endocarditis due to Staphylococcus aureus infection complicated by pulmonary regurgitation with right ventricular failure and by septic pulmonary embolism with persistent sepsis: he underwent pulmonary valve replacement with a Bravo 300 bioprosthesis. The postoperative course was uncomplicated in both cases, with interruption of the infection and normalisation of the haemodynamic status. The insidious and severe nature of pulmonary valve endocarditis is demonstrated by these two cases, confirming previous reports which have underlined the poor prognosis of this condition. Surgery has been shown to be effective and well tolerated and should be integrated early in the therapeutic strategy, the results being all the better when an aggressive attitude is taken.

The authors report a case of tricuspid endocarditis complicating a congenital coronary artery fistula to the right ventricle in an eight-year-old female. The patient underwent valve replacement using a cryopreserved mitral homograft. Six months later, clinical and echocardiographic status are excellent. Using a mitral homograft for tricuspid endocarditis is a recognized approach in adults, whereas in pediatric cases it is exceptional. Homografts could prove to be a valid procedure in children when repair is not feasible, although one could expect a more rapid deterioration.

The authors report their experience with a simple and efficient technique for repair of left ventricular free wall rupture complicating myocardial infarction. The technique consists, with the aid of cardiopulmonary bypass, in suturing a plaque of the patients own pericardium (6 to 8 cm in diametre) to the more normal tissue encircling the pathologic myocardium, and by injecting five mi of human fibrin glue as a cement under the pericardium to reinforce the remair and prevent leaking throught the suture line. With a 10 year follow-up, we are able to be confident with the long term results. The five patients, at the time of operation were aged 46 to 74 years. The post-operative results and the annual echocardiographic controls have proved the technique to be sound without recurrences and without late complications such as pseudo aneurisms at the site of the repair.

OBJECTIVE: Some mitral lesions are still out of reach of conventionalrepairs. Transferring the posterior leaflet of the tricuspid valve with itssubvalvular apparatus to the mitral valve is a new autograft techniquewhich has allowed us a conservative approach in cases where repair seemedless predictable. METHODS: After removing the posterior tricuspid leafletwith its subvalvular apparatus, the tricuspid autograft was inserted byimplanting its papillary muscle onto the mitral papillary muscle and thenby suturing the leaflet tissue in place. The tricuspid valve wassubsequently repaired by annular plication and leaflet suture. A tricuspidring was used in all but the first case. RESULTS: The age of the sevenpatients ranged from 20 to 70 years. Postoperative controls bytransesophageal echocardiography showed no leaks in five and trivial in oneon the site of the mitral repair. On the tricuspid valve, we found amoderate leak in the first case and trivial or none in the following cases,where a tricuspid ring was used. With a 3-12 month follow-up the resultsare stable. CONCLUSIONS: This autograft technique is reproducible, andextends the field of mitral valve repairs. Compared to segments of mitralhomografts, we prefer the intraoperative availability of natural chordaeand valvular leaflet that have no immunological interference. The patientis his own tissue bank and the tricuspid valve can be repaired with a verylow risk of significant dysfunction.