Optimal role of rest and stress echocardiography in cardiac resynchronization therapy.

Cardiac resynchronization therapy (CRT) is an effective treatment for patients with advanced heart failure (HF), depressed left ventricular (LV) function and wide QRS complex. CRT improves symptoms, exercise capacity, LV function and reduces HF hospitalization and mortality rates. However, in parallel with the impressive results for CRT in several large trials, a consistent percentage of patients do not respond to CRT when the traditional patient selection criteria are applied. The prevalence of non-responders is about 30% when clinical end-points are considered but it is much higher (≥ 45%) if echocardiographic end-points are used. Reduction of the number of non-responders is currently one of the main challenges in the field of CRT. Response to CRT has been related to the presence of cardiac dyssynchrony prior to implantation. LV dyssynchrony can be evaluated using different echocardiographic methods. When LV dyssynchrony is added to traditional patient selection criteria, the prevalence of non-responders decreases considerably. However, the value of LV dyssynchrony to predict response to CRT has shown some limitations and is possibly not sufficient. CRT response is clearly modulated by several factors. Regional and global myocardial viability are key pieces of the puzzle as well as the presence and severity of mitral regurgitation (MR). Echocardiography thus plays an important role in the care of HF patients treated with cardiac resynchronization therapy and is useful to assess acute and long-term beneficial effects of CRT. Numerous recent published reports have used echocardiographic techniques to potentially help patient selection for CRT prior to implantation and to optimize device settings afterwards. These topics are discussed in this review.

Deep sternal wound infection due to Pasteurella multocida: the first case report and review of literature.

Pasteurella multocida is a Gram-negative bacterium recovered from a wide variety of wild and domestic animals and has mostly been associated with infection following animal bites. We present the first reported case of a patient who developed a postoperative sternal wound infection due to P. multocida complicated by bloodstream infection. The outcome was favorable following surgical debridement and antimicrobial therapy. We also review the literature regarding P. multocida postoperative wound infections.

Enhancement of non-coronary collateral blood flow from the internal thoracic arteries: the theoretical and practical basis of an alternative method of myocardial blood supply.

Non-coronary collateral blood flow arrives to the heart from mediastinal, bronchial, and pericardial channels. These enter the heart through the pericardial reflections surrounding the pulmonary and systemic veins, as well as from the vasa vasorum of the aorta and the pulmonary artery leading to and from the myocardium. Before the advent of cardiopulmonary bypass surgery, surgical bilateral ligature of the internal thoracic arteries (ITAs) was performed in patients with ischemic heart disease to increase the perfusion pressure within the channels leading to the heart. Nowadays, the occurrence of natural collaterals between coronary and extracardiac arteries including the ITAs, the potential hemodynamic effects of ITA ligation, the potential of ITAs for developing important collateral branches, and the current availability of angiogenic growth factors could pave the way for the development of a new field in cardiovascular research aimed at developing an alternative strategy of myocardial blood supply by means of the surgical and biological enhancement of non-coronary collateral circulation.

Lipid-mediated inflammation and degeneration of bioprosthetic heart valves.

BACKGROUND: The durability of bioprosthetic valves is limited by structural valve degeneration (SVD) leading to bioprostheses (BPs) stenosis or regurgitation. We hypothesized that a lipid-mediated inflammatory mechanism is involved in the SVD of BPs. MATERIAL AND METHODS: Eighteen Freestyle stentless BP valves were explanted for SVD at a mean time of 5.9 +/- 3 years after implantation and were analysed by immunohistochemistry and transmission electron microscopy (TEM). RESULTS: The mean age of the patients was 65 +/- 8 years and there were 11 male and seven female patients. Two of the 18 BPs had macroscopic calcification, whereas the other valves had minimal or no macroscopic calcification. Tears at the commissures leading to regurgitation was present in 16 BPs. Immunohistochemistry showed the presence of oxidized low-density lipoprotein (ox-LDL) and glycosaminoglycans in the fibrosa layer of 13 BPs. Areas with ox-LDL were infiltrated by macrophages (CD68(+)) co-expressing the scavenger receptor CD36 and metalloproteinase-9 (MMP-9). Zymogram showed the active form of MMP-9 within explanted BPs. EM studies revealed the presence of lipid-laden cells featuring foam cells and fragmented collagen. Nonimplanted control BPs obtained from the manufacturer (n = 4) had no evidence of lipid accumulation, inflammatory cell infiltration or expression of MMP9 within the leaflets. CONCLUSIONS: These results support the concept that lipid-mediated inflammatory mechanisms may contribute to the SVD of BPs. These findings suggest that modification of atherosclerotic risk factors with the use of behavioural or pharmacological interventions could help to reduce the incidence of SVD.

Distribution of SPARC during neovascularisation of degenerative aortic stenosis.

OBJECTIVE: To examine the hypothesis that degenerative aortic stenosis (AS) is associated with the development of blood vessels and the expression of the secreted protein, acidic and rich in cysteine/osteonectin (SPARC), a matricellular protein that is involved in ossification, the modulation of angiogenesis and the production of metalloproteinases. METHODS: 30 surgically excised AS valves and 20 normal aortic valves were studied. RESULTS: Blood vessels were detected in the aortic valves from patients with degenerative AS, whereas normal valves were avascular structures. Blood vessels in AS valves expressed endothelial nitric oxide synthase, CD34 and von Willebrand factor (vWF). Blood vessels were located in three distinct regions: near calcified nodules, under the leaflet border and in rich cellular areas forming cell islands. Blood vessels were predominantly present in early and intermediate grades of calcification. Cell islands were densely populated by CD45-positive cells where endothelial cells (CD34+, vWF+) forming cord-like structures were present. Immunoblotting detected SPARC only in AS valves and immunohistological analysis located SPARC in mature blood vessels. The proportion of blood vessels positive for SPARC was higher in valves with a lower grade of calcification. In cell islands, SPARC was distributed to mature blood vessels and to macrophages, where it co-located with matrix metalloproteinase-9, whereas no expression was detected in endothelial cells forming cord-like structures. CONCLUSION: The localisation of SPARC to mature blood vessels and its predominant expression in AS valves with a lower calcification grade suggest that the spatial and temporal distribution of this matricellular protein is tightly controlled to participate in the neovascularisation of AS valves.

Expression of bone-regulatory proteins in human valve allografts.

OBJECTIVE: To test the hypothesis that valve allograft (VA) calcification results from an ossification process in which bone-regulatory proteins are expressed. METHODS: 15 VA that were explanted at the time of surgery for dysfunction were studied. VA were analysed and compared with normal aortic valves (n = 20). RESULTS: All the VA (5 aortic, 10 pulmonary) exhibited heavy calcification and important fibrosis. Immunohistochemistry studies showed that the bone-specific transcription factor Cbfa-1 was expressed by stromal cells. Bone alkaline phosphatase was expressed in calcified regions. Immunostaining for alpha smooth muscle (alpha-SM) actin was increased in VA compared with normal valves and in 6 of the 15 valves formed cellular clusters close to the calcified nodules. In VA osteopontin and osteonectin were expressed by stromal cells, whereas osteocalcin was closely associated with the calcified regions. Furthermore, analysis of the bone-regulatory proteins that control bone resorption showed that receptor activator of nuclear factor kappaB ligand (RANKL), receptor activator of nuclear factor kappaB (RANK) and osteoprotegerin (OPG) were differentially expressed in calcified VA and normal valves. Normal valve leaflets expressed OPG, whereas OPG expression was absent or faint in calcified VA. RANKL and RANK were not detected in normal valves, whereas calcified VA expressed RANKL and RANK. CONCLUSION: These data suggest that calcification of VA results from an ossification process, which relies on tight control of bone-regulatory protein expression. The expression pattern of the RANKL/RANK/OPG system suggests that it may have a regulatory role not only in osteoclastogenesis but also in the calcification of human VA.

Which biologic valve should we select for the 45- to 65-year-old age group requiring aortic valve replacement?

OBJECTIVE: The diversity of biologic valves available to replace the aortic valve renders selection difficult for the 45- to 65-year-old patient. To evaluate and compare the results of biologic valves in the 45- to 65-year-old patient, we reviewed our experience (1991-2004). METHODS: Three hundred thirty-two patients between 45 and 65 years old with isolated aortic valve disease had a biologic valve implanted: Freestyle valve in 140 patients, a homograft in 54 patients, a stented Mosaic or Perimount valve (stented xenograft) in 62 patients, and a Ross procedure in 76 patients. RESULTS: Perioperative mortality was comparable for all groups (Freestyle, 2.1%; homograft, 3.7%; stented xenograft, 3.2%; Ross procedure, 1.3%; P = .8). Echocardiographically determined valve performance at discharge was significantly enhanced in the Ross procedure and homograft groups (indexed effective orifice area: Freestyle, 0.9 +/- 0.3 cm 2 /m 2 ; homograft, 1.3 +/- 0.3 cm 2 /m 2 ; stented xenograft, 0.8 +/- 0.2 cm 2 /m 2 ; Ross procedure, 1.4 +/- 0.4; P < .0001; mean gradient: Freestyle, 12.0 +/- 6.6 mm Hg; homograft, 7.4 +/- 4.0 mm Hg; stented xenograft, 15.4 +/- 5.4 mm Hg; Ross procedure, 4.6 +/- 3.2 mm Hg; P < .0001). For all yearly follow-up, freedom from New York Heart Association class III or IV was comparable and greater than 95% for all groups. At 7 years, cardiac survival (homograft, 96.3% +/- 3.7%; Ross procedure, 90.6% +/- 6.3%; stented xenograft, 86.0% +/- 10.3%; Freestyle, 89.2% +/- 10.8%; P = .7) and freedom from reoperation (Ross procedure, 98.5% +/- 1.4%; homograft, 90.6% +/- 5.7%; Freestyle, 88.0% +/- 4.9%; stented xenograft, 90.0% +/- 8.0%; P = .4) were comparable. Freedoms from significant bleeding events, valve-related neurologic events, or endocarditis were comparable and greater than 95% for all groups. CONCLUSION: Type of aortic biologic valve for the 45- to 65-year-old patient does not affect midterm survival or valve-related morbidity. Thus the choice of biologic valve for the 45- to 65-year-old patient should be dictated by patient-surgeon preference, ease of implantation, and reoperation until longer comparative studies are available.

[Cardiac surgery in renal transplant patients. Apropos of 24 cases]. / La chirurgie cardiaque chez le patient greffé rénal. A propos de 24 cas.

UNLABELLED: Results of cardiac surgery in renal transplant patients are not well documented. Immunosuppression as well as associated conditions in these patients, and the increased susceptibility of the renal allograft to the extracorporeal circulation (ECC) may alter the prognosis of renal transplant patients submitted to cardiac surgery. To evaluate this hypothesis, we reviewed the files of 24 patients (18 Male, 6 Female; age: 49 +/- 12 years) operated under ECC between 1978 and 1997. Twenty patients underwent coronary artery bypass surgery, 5 patients a valve replacement procedure (aortic and/or mitral), and one patient necessitated a Cabrol procedure for an ascending aorta aneurysm. Preoperatively, the majority of patients were in functional class (NYHA) IV (16 patients), and ejection fraction was > 50% in 18 patients. Two operative deaths secondary to cardiogenic shock were encountered. Five patients (23%) were reoperated for bleeding; 5 patients (23%) sustained a major infection (2 pneumonias, 2 mediastinitis and one wound infection) resulting in death in one patient; 5 patients (23%) were treated for arythmia; and 2 patients (9%) suffered a perioperative myocardial infarction. Serum creatinine levels did not increase significantly during hospitalization (p = 0.41 between extreme values). Mean follow-up (41 +/- 28 months) of the 20 survivors revealed recurrent angina in 5 patients and late death in 4 patients, cardiac-related in 3 cases. CONCLUSION: Cardiac surgery in renal transplant patients is subjected to a high morbidity and mortality. Mid-term prognosis is reserved especially in presence of associated conditions.