141 research outputs found

    Infective endocarditis caused by Pseudomonas stutzeri in a patient with Marfan syndrome: Case report and brief literature review

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    Invasive infections due to Pseudomonas stutzeri have rarely been described and mainly occur in immunocompromised individuals. We report a case of infective endocarditis caused by P. stutzeri after previous cardiac surgery in a Lebanese patient with Marfan syndrome. We review the literature and conclude that this pathogen may be of particular medical relevance in the Mediterranean Basin

    Late-onset native valve endocarditis caused by Corynebacterium kroppenstedtii

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    Corynebacterium kroppenstedtii is an emerging cause of granulomatous mastitis and recurrent breast abscesses in women, but data on its clinical relevance in nongynecological disease conditions are limited. Here, we report the first case of a late-onset endocarditis of a native aortic valve in a 73-year-old male patient who presented with symptomatic aortic insufficiency. Echocardiography and cardiac computed tomography revealed the perforation of the noncoronary cusp and a large perivalvular abscess cavity. Hence, the surgical replacement of the aortic valve and aortic root were performed. Intraoperatively obtained tissue specimens grew C. kroppenstedtii and the patient made a full recovery after a 6-week course of antibiotic treatment. We briefly review the literature pertaining to antimicrobial susceptibility patterns of C. kroppenstedtii and available treatment recommendations. Our report calls for further studies to assess the role of this bacterium as a causative agent of infections other than granulomatous mastitis

    Age-dependent phenotypic modulation of smooth muscle cells in the normal ascending aorta

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    Objectives: Ascending aortic aneurysms are associated with pre-existing conditions, including connective tissue disorders (i.e., Marfan syndrome) and bicuspid aortic valves. The underlying mechanisms remain uncertain. Even less is known regarding ascending aortic aneurysms in individuals with normal (i.e., tricuspid) aortic valves (TAV), and without known aneurysm-associated disorders. Regardless of etiology, the risk of aortic complications increases with biological age. Phenotypic modulation of smooth muscle cells (SMCs) is a feature of ascending aortic aneurysms, whereby contractile SMCs are replaced with synthetic SMCs that are capable of degrading the aortic wall. We asked whether age itself causes dysfunctional SMC phenotype modulation, independent of aortic dilatation or pre-existing aneurysm-associated diseases. Methods: Non-dilated ascending aortic samples were obtained intra-operatively from 40 patients undergoing aortic valve surgery (range: 20–82 years old, mean: 59.1 ± 15.2). Patients with known genetic diseases or aortic valve malformations were excluded. Tissue was divided, and a portion was formalin-fixed and immunolabeled for alpha-smooth muscle actin (ASMA), a contractile SMC protein, and markers of synthetic (vimentin) or senescent (p16/p21) SMCs. Another fragment was used for SMC isolation (n = 10). Cultured SMCs were fixed at cell passage 2 and stained for phenotype markers, or were cultured indefinitely to determine replicative capacity. Results: In whole tissue, ASMA decreased (R2 = 0.47, P < 0.0001), while vimentin increased (R2 = 0.33, P = 0.02) with age. In cultured SMCs, ASMA decreased (R2 = 0.35, P = 0.03) and vimentin increased (R2 = 0.25, P = 0.04) with age. p16 (R2 = 0.34, P = 0.02) and p21 (R2 = 0.29, P = 0.007) also increased with age in SMCs. Furthermore, the replicative capacity of SMCs from older patients was decreased compared to that of younger patients (P = 0.03). Conclusion: By investigating non-dilated aortic samples from individuals with normal TAVs, we found that age itself has a negative impact on SMCs in the ascending aortic wall, whereby SMCs switched from the contractile phenotype to maladaptive synthetic or senescent states with increased age. Therefore, based on our findings, modification of SMC phenotype should be studied as a therapeutic consideration against aneurysms in the future, regardless of etiology

    Aortic regurgitation provokes phenotypic modulation of smooth muscle cells in the normal ascending aorta

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    Background: Aortic complications are more likely to occur in patients with ascending aortic aneurysms and concomitant aortic regurgitation (AR). AR may have a negative influence on the aortic wall structure even in patients with tricuspid aortic valves and absence of aortic dilatation. It is unknown whether smooth muscle cell (SMC) changes are a feature of AR-associated aortic remodeling. Methods: Nondilated aortic samples were harvested intraoperatively from individuals with normal aortic valves (n ÂĽ 10) or those with either predominant aortic stenosis (AS) (n ÂĽ 20) or AR (n ÂĽ 35). Tissue from each patient was processed for immunohistochemistry or used for the extraction of medial SMCs. Tissue and cells were stained for markers of SMC contraction (alpha-smooth muscle actin), synthesis (vimentin) and senescence (p16INK4A and p21Cip1 [p16/p21]). Replicative capacity was analyzed in cultured SMCs from AS- and AR-associated aortas. A subanalysis compared SMCs from individuals with either tricuspid aortic valves or bicuspid aortic valves to evaluate the effect of aortic valve morphology. Results: In aortic tissue samples, AR was associated with decreased alpha-smooth muscle actin and increased vimentin, p16 and p21 compared with normal aortic valves and AS. In cell culture, SMCs from AR-aortas had decreased alpha-smooth muscle actin and increased vimentin compared with SMCs from AS-aortas. ARassociated SMCs had increased p16 and p21 expression, and they reached senescence earlier than SMCs from AS-aortas. In AR, SMC changes were more pronounced with the presence of a bicuspid aortic valve. Conclusions: AR itself negatively influences SMC phenotype in the ascending aortic wall. This AR-specific effect is independent of aortic diameter and aortic valve morphology, although it is more pronounced with bicuspid aortic valves. These findings provide insight into the mechanisms of AR-related aortic remodeling, and they provide a model for studying SMC-specific therapies in culture. (J Thorac Cardiovasc Surg 2023;166:1604-16

    The Ross procedure versus repair for treatment of a unicuspid aortic valve in adults

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    OBJECTIVES Aortic stenosis or regurgitation in patients with a unicuspid valve morphology requires interventions early in life. We have performed either primary valve repair or the Ross procedure. The goal of this study was to compare the midterm results of repair and pulmonary autograft replacement. METHODS Between December 1998 and April 2022, a total of 345 patients (77% male; mean age 34 ± 9.7 years) underwent treatment of a unicuspid aortic valve. Patients were excluded if they were 54 years (n = 3) at the time of the operation. The remaining cohort was divided into 2 groups: 167 (64%) patients underwent valve repair; 91 (36%) patients underwent pulmonary autograft replacement. The indications for surgery were aortic regurgitation (n = 104), aortic stenosis (n = 45), combined disease (n = 103) and endocarditis (n = 6). Fifty-one patients had root dilatation (>43 mm) with aortic regurgitation (repair n = 23; Ross n = 28). Mean follow-up was 5.9 years (SD: 5 years) [range 0.1–22.3 years]. RESULTS There were 1 early and 3 late deaths; 47 patients required reintervention. Survival at 10 years was 95% in the Ross group and 97% after valve repair (P = 0.769). Freedom from reintervention at 10 years was 98% in the Ross group and 80% after valve repair (P = 0.012). A receiver operating characteristics curve analysis showed a trend towards better durability in patients < 26 years. CONCLUSIONS The ideal treatment of the unicuspid aortic valve remains debatable. Repair of a unicuspid valve can be considered a bridge to pulmonary autograft replacement, at least in younger patients. The appropriate times to replace and to repair require further investigation

    Autograft reoperations after the Ross procedure

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    OBJECTIVES: After a Ross procedure, autograft failure can occur. At reoperation, repair of the autograft preserves the advantages of the Ross procedure. The aim of this retrospective study was to assess mid-term results after reoperation of a failed autograft. METHODS: Between 1997 and 2022, 30 consecutive patients (83% male; age 41 ± 11 years) underwent autograft reintervention between 60 days and 24 years (median 10 years) after a Ross procedure. The initial technique varied, full-root replacement (n = 25) being the most frequent. The indication for reoperation was isolated autograft regurgitation (n = 7), root dilatation (>43 mm) with (n = 17) or without (n = 2) autograft regurgitation, mixed dysfunction (n = 2) and endocarditis (n = 2). In 4 instances, the valve was replaced by valve (n = 1) or combined valve and root replacement (n = 3). Valve-sparing procedures consisted of isolated valve repair (n = 7) or root replacement (n = 19), and tubular aortic replacement. Cusp repair was performed in all but 2. Mean follow-up was 5.4 ± 6 years (35 days to 24 years). RESULTS: Mean cross-clamp and perfusion times were 74 ± 26 and 132 ± 64 min. There were 2 perioperative deaths (7%; both valve replacement) and 2 patients died late (32 days to 1.2 years postoperatively). Freedom from cardiac death at 10 years was 96% after valve repair and 50% after replacement. Two patients required reoperation (1.68 and 16 years) following repair. One underwent valve replacement for cusp perforation, the other, root remodelling for dilatation. Freedom from autograft reintervention at 15 years was 95%. CONCLUSIONS: Autograft reoperations after the Ross procedure can be performed as valve-sparing operations in the majority of cases. With valve-sparing, long-term survival and freedom from reoperation are excellent

    SMAD3 contributes to ascending aortic dilatation independent of transforming growth factor-beta in bicuspid and unicuspid aortic valve disease

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    We sought to determine whether there are differences in transforming growth factor-beta (TGFß) signaling in aneurysms associated with bicuspid (BAV) and unicuspid (UAV) aortic valves versus normal aortic valves. Ascending aortic aneurysms are frequently associated with BAV and UAV. The mechanisms are not yet clearly defined, but similarities to transforming growth factor-beta TGFß vasculopathies (i.e. Marfan, Loeys-Dietz syndromes) are reported. Non-dilated (ND) and aneurysmal (D) ascending aortic tissue was collected intra-operatively from individuals with a TAV (N = 10ND, 10D), BAV (N = 7ND, 8D) or UAV (N = 7ND, 8D). TGFß signaling and aortic remodeling were assessed through immuno-assays and histological analyses. TGFß1 was increased in BAV/UAV-ND aortas versus TAV (P = 0.02 and 0.04, respectively). Interestingly, TGFß1 increased with dilatation in TAV (P = 0.03) and decreased in BAV/UAV (P = 0.001). In TAV, SMAD2 and SMAD3 phosphorylation (pSMAD2, pSMAD3) increased with dilatation (all P = 0.04) and with TGFß1 concentration (P = 0.04 and 0.03). No relationship between TGFß1 and pSMAD2 or pSMAD3 was observed for BAV/UAV (all P > 0.05). pSMAD3 increased with dilatation in BAV/UAV aortas (P = 0.01), whereas no relationship with pSMAD2 was observed (P = 0.56). Elastin breaks increased with dilatation in all groups (all P < 0.05). In TAV, elastin degradation correlated with TGFß1, pSMAD2 and pSMAD3 (all P < 0.05), whereas in BAV and UAV aortas, elastin degradation correlated only with pSMAD3 (P = 0.0007). TGFß signaling through SMAD2/SMAD3 contributes to aortic remodeling in TAV, whereas TGFß-independent activation of SMAD3 may underlie aneurysm formation in BAV/UAV aortas. Therefore, SMAD3 should be further investigated as a therapeutic target against ascending aortic dilatation in general, and particularly in BAV/UAV patients

    Which Aortic Valve Can Be Surgically Reconstructed?

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    Purpose of Review Preservation or repair of the aortic valve has evolved dynamically in the past 20 years. It leads to a high freedom from valve-related complications if an adequate valve durability can be achieved; it may possibly also improve survival. To date, little structured information is available about which valves can be repaired and which should better be replaced. Recent Findings For surgical decision-making, the size of the aortic root is important and the anatomy of the aortic valve must be considered. In the presence of root aneurysm, most tricuspid and bicuspid aortic valves can be preserved. In aortic regurgitation and normal aortic dimensions, the majority of tricuspid and bicuspid aortic valves can be repaired with good long-term durability. In bicuspid aortic valves, the morphologic characteristics must be taken into consideration. Unicuspid and quadricuspid aortic valves can be repaired in selected cases. Generally, cusp calcification is a sign of a poor substrate for repair; the same is true for cusp retraction and cusp destruction due to active endocarditis. They are associated with limited valve durability. Summary Using current concepts, many non-calcified aortic valves can be repaired. Modern imaging, in particular three-dimensional transesophageal echocardiography (TEE), should be able to define repairable aortic valves with a high probability

    Preoperative aortic root geometry and postoperative cusp configuration primarily determine long-term outcome after valve-preserving aortic root repair

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    ObjectiveTechnical controversies exist in valve-preserving aortic root replacement. We sought to determine predictors of long-term stability of the aortic valve.MethodsA total of 430 patients (aged 57 ± 15 years, 323 male) underwent valve-preserving aortic root surgery (remodeling in 401, reimplantation in 29) between 1995 and 2009 and were followed echocardiographically. Factors influencing late recurrence of aortic valve regurgitation grade II or greater (n = 45) or need for reoperation on the aortic valve (n = 25) were analyzed.ResultsEarly mortality was 2.8% (1.9% for elective cases), and actuarial survival at 10 years was 83.5% ± 2.4%. Ten-year freedom from aortic valve regurgitation grade II or greater was 85.0% ± 2.5%. Preoperative aortoventricular junction diameter greater than 28 mm and postoperative effective height of the aortic cusp less than 9 mm were identified as significant predictors for late aortic valve regurgitation grade II or greater in multivariate analysis (both P < .001). Ten-year freedom from reoperation on the aortic valve was 89.3% ± 2.5%. Preoperative aortoventricular junction diameter greater than 28 mm (P < .001), use of pericardial patch (P = .022), and effective height of the aortic cusp less than 9 mm (P = .049) were identified as significant predictors for reoperation in multivariate analysis. Operative technique (remodeling, reimplantation), Marfan syndrome, bicuspid valve anatomy, concomitant central cusp plication, size of prosthesis used, and acute dissection were not associated with an increased risk of late aortic valve regurgitation grade II or greater or reoperation. In patients with preoperative aortoventricular junction diameter greater than 28 mm (n = 94), the addition of central cusp plication significantly improved freedom from aortic valve regurgitation grade II or greater (P = .006) regardless of root procedures (remodeling, P = .011; reimplantation, P = .053).ConclusionsLong-term stability of valve-preserving aortic root replacement was influenced not by the technique of root repair but by the preoperative aortic root geometry and postoperative cusp configuration
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