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Background The prognostic value of aortic valve calcification (AVC) measured by using multidetector computed tomography imaging has been well validated in native aortic stenosis, and sex-specific thresholds have been proposed. However, few data are available regarding the impact of leaflet calcification on outcomes after biological aortic valve replacement (AVR). Objectives The goal of this study was to analyze the association of quantitative bioprosthetic leaflet AVC with hemodynamic and clinical outcomes, as well as its possible interaction with sex. Methods From 2008 to 2010, a total of 204 patients were prospectively enrolled with a median of 7.0 years (interquartile range: 5.1 to 9.2 years) after biological surgical AVR. AVC measured by using the Agatston method was indexed to the cross-sectional area of aortic annulus measured by echocardiography to calculate the AVC density (AVCd). Presence of hemodynamic valve deterioration (HVD; increase in mean gradient [MG] ≥10 mm Hg and/or increase in transprosthetic regurgitation ≥1) was assessed by echocardiography in 137 patients at the 3-year follow-up. The primary clinical endpoint was mortality or aortic valve re-intervention. Results There was no significant sex-related difference in the relationship between bioprosthetic AVCd and the progression of MG. Baseline AVCd showed an independent association with HVD at 3 years. During follow-up, there were 134 (65.7%) deaths (n = 100) or valve re-interventions (n = 47). AVCd ≥58 AU/cm2 was independently associated with an increased risk of mortality or aortic valve re-intervention (adjusted hazard ratio: 2.23; 95% confidence interval: 1.44 to 3.35; p Conclusions Aortic bioprosthetic leaflet calcification is strongly and independently associated with HVD and the risk of death or aortic valve re-intervention. As opposed to native aortic stenosis, there is no sex-related differences in the relationship between AVCd and hemodynamic or clinical outcomes.

Background Mitral leaflet enlargement has been identified as an adaptive mechanism to prevent mitral regurgitation in dilated left ventricles (LVs) caused by chronic aortic regurgitation (AR). This enlargement is deficient in patients with functional mitral regurgitation, which remains frequent in the population with ischemic cardiomyopathy. Maladaptive fibrotic changes have been identified in post-myocardial infarction (MI) mitral valves. It is unknown if these changes can interfere with valve growth and whether they are present in other valves. Objectives This study sought to test the hypothesis that MI impairs leaflet growth, seen in AR, and induces fibrotic changes in mitral and tricuspid valves. Methods Sheep models of AR, AR + MI, and controls were followed for 90 days. Cardiac magnetic resonance, echocardiography, and computed tomography were performed at baseline and 90 days to assess LV volume, LV function, mitral regurgitation and mitral leaflet size. Histopathology and molecular analyses were performed in excised valves. Results Both experimental groups developed similar LV dilatation and dysfunction. At 90 days, mitral valve leaflet size was smaller in the AR + MI group (12.8 ± 1.3 cm2 vs. 15.1 ± 1.6 cm2, p = 0.03). Mitral regurgitant fraction was 4% ± 7% in the AR group versus 19% ± 10% in the AR + MI group (p = 0.02). AR + MI leaflets were thicker compared with AR and control valves. Increased expression of extracellular matrix remodeling genes was found in both the mitral and tricuspid leaflets in the AR + MI group. Conclusions In these animal models of AR, the presence of MI was associated with impaired adaptive valve growth and more functional mitral regurgitation, despite similar LV size and function. More pronounced extracellular remodeling was observed in mitral and tricuspid leaflets, suggesting systemic valvular remodeling after MI.

Background Elevated lipoprotein(a) (Lp[a]) is associated with aortic stenosis (AS). Oxidized phospholipids (OxPL) are key mediators of calcification in valvular cells and are carried by Lp(a). Objectives This study sought to determine whether Lp(a) and OxPL are associated with hemodynamic progression of AS and AS-related events. Methods OxPL on apolipoprotein B-100 (OxPL-apoB), which reflects the biological activity of Lp(a), and Lp(a) levels were measured in 220 patients with mild-to-moderate AS. The primary endpoint was the progression rate of AS, measured by the annualized increase in peak aortic jet velocity in m/s/year by Doppler echocardiography; the secondary endpoint was need for aortic valve replacement and cardiac death during 3.5 ± 1.2 years of follow-up. Results AS progression was faster in patients in the top tertiles of Lp(a) (peak aortic jet velocity: +0.26 ± 0.26 vs. +0.17 ± 0.21 m/s/year; p = 0.005) and OxPL-apoB (+0.26 ± 0.26 m/s/year vs. +0.17 ± 0.21 m/s/year; p = 0.01). After multivariable adjustment, elevated Lp(a) or OxPL-apoB levels remained independent predictors of faster AS progression. After adjustment for age, sex, and baseline AS severity, patients in the top tertile of Lp(a) or OxPL-apoB had increased risk of aortic valve replacement and cardiac death. Conclusions Elevated Lp(a) and OxPL-apoB levels are associated with faster AS progression and need for aortic valve replacement. These findings support the hypothesis that Lp(a) mediates AS progression through its associated OxPL and provide a rationale for randomized trials of Lp(a)-lowering and OxPL-apoB-lowering therapies in AS. (Aortic Stenosis Progression Observation: Measuring Effects of Rosuvastatin [ASTRONOMER]; NCT00800800)

BACKGROUND: Dysmetabolic profile has been associated with native aortic valve stenosis. However, there are limited data on the effects of an atherogenic milieu and its potential implications on the structural and hemodynamic deterioration of aortic bioprosthetic valves. OBJECTIVES: This prospective longitudinal study sought to determine the predictors and impact on outcomes of hemodynamic valve deterioration (HVD) of surgically implanted aortic bioprostheses. METHODS: A total of 137 patients with an aortic bioprosthesis implanted for a median time of 6.7 (interquartile range: 5.1 to 9.1) years prospectively underwent a first (baseline) assessment with complete Doppler echocardiography, quantitation of bioprosthesis leaflet calcification by multidetector computed tomography (CT), and a fasting blood sample to assess cardiometabolic risk profile. All patients underwent a second (follow-up) Doppler echocardiography examination at 3 (interquartile range: 2.9 to 3.3) years post-baseline visit. HVD was defined by an annualized change in mean transprosthetic gradient ≥3 mm Hg/year and/or worsening or transprosthetic regurgitation by ≥1/3 class. The primary endpoint was a nonhierarchical composite of death from any cause or aortic reintervention procedure (redo surgical valve replacement or transcatheter valve-in-valve implantation) for bioprosthesis failure. RESULTS: Thirty-four patients (25.6%) had leaflet calcification on baseline CT, and 18 patients (13.1%) developed an HVD between baseline and follow-up echocardiography. Fifty-two patients (38.0%) met the primary endpoint during subsequent follow-up after the second echocardiographic examination. Leaflet calcification (hazard ratio [HR]: 2.58; 95% confidence interval [CI]: 1.35 to 4.82; p = 0.005) and HVD (HR: 5.12; 95% CI: 2.57 to 9.71; p \textless 0.001) were independent predictors of the primary endpoint. Leaflet calcification, insulin resistance (homeostatic model assessment index ≥2.7), lipoprotein-associated phospholipase A2 activity (Lp-PLA2 per 0.1 nmol/min/ml increase), and high level of proprotein convertase subtilisin/kexin 9 (PCSK9) (≥305 ng/ml) were associated with the development of HVD after adjusting for age, sex, and time interval since aortic valve replacement. CONCLUSIONS: HVD identified by Doppler echocardiography is independently associated with a marked increase in the risk of valve reintervention or mortality in patients with a surgical aortic bioprosthesis. A dysmetabolic profile characterized by elevated plasma Lp-PLA2, PCSK9, and homeostatic model assessment index was associated with increased risk of HVD. The presence of leaflet calcification as detected by CT was a strong predictor of HVD, providing incremental risk-predictive capacity.

Objectives This study sought to document the presence and role of lipoprotein-associated phospholipase A2 (Lp-PLA2) in calcific aortic valve disease (CAVD). Background CAVD is a chronic disorder characterized by pathological mineralization and remodeling. Studies have indicated that human CAVD tissues are infiltrated by lipids and that inflammation may play a role in the pathobiology. We hypothesized that Lp-PLA2 (encoded by the PLA2G7 gene) is expressed in CAVD and may play a role in the mineralization of valve interstitial cells. Methods We have documented the expression of the phospholipase A2 family of genes in aortic valves by using a transcriptomic assay. Messenger ribonucleic acid and protein expression were confirmed in aortic valves explanted from 60 patients by quantitative polymerase chain reaction and immunohistochemistry, respectively. The effect of lysophosphatidylcholine, the product of Lp-PLA2 activity, was documented on the mineralization of valve interstitial cell cultures. Results Transcriptomic analyses of CAVD and control nonmineralized aortic valves revealed that Lp-PLA2 was increased by 4.2-fold in mineralized aortic valves. Higher expression of Lp-PLA2 in stenotic aortic valves was confirmed by quantitative polymerase chain reaction, immunohistochemistry, and enzymatic Lp-PLA2 activity. The number of Lp-PLA2 transcripts correlated with several indexes of tissue remodeling. In vitro, lysophosphatidylcholine increased the expression of alkaline phosphatase, the ectonucleotide pyrophosphatase/phosphodiesterase 1 enzyme, sodium-dependent phosphate cotransporter 1 (encoded by the SLC20A1 gene), and osteopontin. We then showed that lysophosphatidylcholine-induced mineralization involved ectonucleotidase enzyme as well as apoptosis through a protein-kinase-A-dependent pathway. Conclusions Together, these results demonstrated that Lp-PLA2 is highly expressed in CAVD, and it plays a role in the mineralization of valve interstitial cells. Further work is necessary to document whether Lp-PLA2 could be considered as a novel target in CAVD.

ObjectivesThe aim of this case match study was to compare the outcome of patients with paradoxical low-flow (left ventricular ejection fraction [LVEF] ≥50% but stroke volume index 1.0 cm2 and MG

Objectives The aims of this study were to examine prospectively the relationship between metabolic syndrome (MetS) and aortic stenosis (AS) progression and to evaluate the effect of age and statin therapy on AS progression in patients with or without MetS. Background Despite the clear benefits of statin therapy in primary and secondary coronary heart disease prevention, several recent randomized trials have failed to demonstrate any significant effect of this class of drugs on the progression of AS. Previous retrospective studies have reported an association between MetS and faster AS progression. Methods This predefined substudy included 243 of the 269 patients enrolled in the ASTRONOMER (AS Progression Observation: Measuring Effects of Rosuvastatin) trial. Follow-up was 3.4 ± 1.3 years. AS progression rate was measured by calculating the annualized increase in peak aortic jet velocity measured by Doppler echocardiography. Results Patients with MetS (27%) had faster stenosis progression (+0.25 ± 0.21 m/s/year vs. +0.19 ± 0.19 m/s/year, p = 0.03). Predictors of faster AS progression in multivariate analysis were older age (p = 0.01), higher degree of valve calcification (p = 0.01), higher peak aortic jet velocity at baseline (p = 0.007), and MetS (p = 0.005). Impact of MetS on AS progression was most significant in younger ( Conclusions MetS was found to be a powerful and independent predictor of faster AS progression, with more pronounced impact in younger patients. These findings emphasize the importance of routinely identifying and treating MetS in AS patients. The apparent faster stenosis progression in the subset of normocholesterolemic patients with MetS receiving the statin will need to be confirmed by future studies.

Objectives: The aim of this study was to examine the relationship between metabolic syndrome (MetS) and left ventricular (LV) geometry and function in patients with asymptomatic aortic stenosis (AS...

Objectives This study was designed to evaluate the effect of valve prosthesis-patient mismatch (PPM) on late survival after aortic valve replacement (AVR) and to determine if this effect is modulated by patient age, body mass index (BMI), and pre-operative left ventricular (LV) function. Background We recently reported that PPM is an independent predictor of operative mortality after AVR, particularly when associated with LV dysfunction. Methods The indexed valve effective orifice area (EOA) was estimated in 2,576 patients having survived AVR and was used to define PPM as not clinically significant if it was >0.85 cm2/m2, as moderate if >0.65 and ≤0.85 cm2/m2, and severe if ≤0.65 cm2/m2. Results After adjustment for other risk factors, severe PPM was associated with increased late overall mortality (hazard ratio [HR]: 1.38; p = 0.03) and cardiovascular mortality (HR: 1.63; p = 0.0006) in the whole cohort. Severe PPM was also associated with increased overall mortality in patients Conclusions Moderate PPM is associated with increased late mortality in patients with LV dysfunction, but with normal prognosis in those with preserved LV function. Notwithstanding the previously demonstrated deleterious effect of severe PPM on early mortality, this factor appears to increase late mortality only in patients

ObjectivesThe purpose of this study was to evaluate mitral valve hemodynamic performance and functional capacity in patients with ischemic mitral regurgitation (MR) who underwent restrictive mitral valve annuloplasty (MVA).BackgroundRestrictive MVA combined with coronary artery bypass graft is the conventional approach for the surgical management of patients with ischemic MR. We hypothesized that the restriction of the mitral annulus could cause an obstruction to antegrade mitral flow that may affect the patient's functional capacity.MethodsA dobutamine stress echocardiography (DSE) and a 6-min walk test (6MWT) were performed in 24 patients with ischemic MR 13 ± 3 months after restrictive MVA and coronary artery bypass graft and in 20 control patients with coronary artery disease matched for age, gender, and left ventricular ejection fraction.ResultsNone of the 24 MVA patients had significant MR after operation. Compared with control patients, MVA patients had significantly (p < 0.001) higher resting and stress peak gradients (rest: 13 ± 4 mm Hg vs. 4 ± 1 mm Hg; DSE: 19 ± 6 mm Hg vs. 6 ± 3 mm Hg) and systolic pulmonary arterial pressures (PAP) (rest: 42 ± 13 mm Hg vs. 27 ± 8 mm Hg; DSE: 58 ± 12 mm Hg vs. 38 ± 11 mm Hg) and lower (p = 0.01) 6MWT distance (358 ± 95 m vs. 433 ± 61 m). The resting peak mitral gradient correlated with systolic PAP (r = −0.67; p = 0.001) and 6MWT distance (r = −0.78; p < 0.0001) in the MVA group.ConclusionsThe results suggest that performing a restrictive MVA in patients with ischemic MR may create a functional mitral stenosis. This hemodynamic sequel is associated with higher PAP and a worse functional capacity.

With the current shift toward an older population, calcific aortic valve stenosis (AVS) is likely to become a major societal and economic burden. For many years, AVS was regarded as a degenerative and nonmodifiable process. However, molecular studies unanimously demonstrated that AVS is an actively regulated disorder with several potential therapeutic targets. Many factors are predicted to cause AVS, and an important genetic predisposition is anticipated. In this review, we describe candidate genes and signaling pathways identified by genetic research and incorporate this new knowledge into a more comprehensive picture of factors involved in the pathogenesis of AVS. We also emphasize the need for additional studies to elucidate its complete genetic architecture. Recent advances in genomic research offer a remarkable opportunity to investigate AVS at the most fundamental level. The benefits of these new approaches can be observed in many complex diseases, but the field of AVS is trailing behind. We discuss the future utility of these new genomic approaches to improve our understanding of AVS and to refine the management of patients in terms of diagnosis, prevention, and treatment.

Post-operative atrial fibrillation (POAF) is a frequent complication occurring in 30% to 50% of patients after cardiac surgery. It is associated with an increased risk of mortality and morbidity, predisposes patients to a higher risk of stroke, requires additional treatment, and increases the costs of the post-operative care. The aim of this review is to present the current state of knowledge about the risk factors, mechanisms, prevention, and treatment of this complication. In addition to the well known risk factors for the development of POAF such as age, left atrial enlargement, and valvular surgery, new metabolic risk factors related to visceral obesity have been identified. With regard to the prevention of POAF, beta-blocker drugs are effective and safe and can be used in most patients, whereas amiodarone can be added in high-risk patients. Biatrial pacing was shown to be effective; however, its complexity might limit its application. Although there are only few data regarding the usefulness of magnesium, statins, N-3 polyunsaturated fatty acids, and corticosteroids, their addition to beta-blocker drugs might be of benefit for further reducing POAF. Treatment includes the use of an AV nodal blocking agent to achieve the rate control. If AF does not spontaneously convert to sinus rhythm within 24 h, anticoagulation should be initiated and a rhythm control strategy should be attempted. More investigations are warranted to explore mechanisms by which POAF occurs. This new knowledge would undoubtedly translate into a more efficient prevention and treatment of this common post-operative complication that is associated with a major health and economic burden.

Objectives This study sought to examine the association between the metabolic syndrome (MS) and the progression of aortic stenosis (AS). Background It has been suggested that aortic valve sclerosis and its progression to AS are caused by an atherosclerotic process. Metabolic syndrome is associated with a higher risk of vascular atherosclerosis. Thus, we hypothesized that the atherogenic features of MS could negatively influence disease progression and prognosis in patients with AS. Methods We retrospectively analyzed the data of 105 consecutive patients (age 69 ± 12 years, 64 men) with at least moderate AS. Of these patients, 40 (38%) had MS identified according to the modified clinical criteria proposed by the National Cholesterol Education Program-Adult Treatment Panel III. The hemodynamic progression of AS was assessed by the measurement of the annualized decrease in valve area during the follow-up period of the study, which averaged 28 ± 13 months. Event-free survival was defined as the absence of death or aortic valve replacement during follow-up. Results The hemodynamic progression of the stenosis was twice as fast (−0.14 ± 0.13 cm2/year vs. −0.08 ± 0.08 cm2/year, p = 0.008) and the three-year event-free survival was markedly lower (44 ± 8% vs. 69 ± 6%, p = 0.002) among patients with MS. In multivariate analysis, MS was found to be a strong independent predictor of both stenosis progression (p = 0.006) and event-free survival (odds ratio 3.85, 95% CI 1.96 to 7.58, p Conclusions The present study is the first to report that MS is associated with a faster disease progression and worse outcome in patients with AS. Such findings open new avenues of research and provide a strong impetus for the elaboration of additional prospective studies focusing on this association.

BackgroundLow flow (LF) can occur with reduced (classic) or preserved (paradoxical) left ventricular ejection fraction (LVEF).ObjectivesThe objective of this study was to compare outcomes of patients with low ejection fraction (LEF), paradoxical low flow (PLF), and normal flow (NF) after aortic valve replacement (AVR).MethodsWe examined 1,154 patients with severe aortic stenosis (AS) who underwent AVR with or without coronary artery bypass grafting.ResultsAmong these patients, 206 (18%) had LEF as defined by LVEF of 35 ml ∙ m2. Aortic valve area was lower in low flow/LVEF groups (LEF: 0.71 ± 0.20 cm2 and PLF: 0.65 ± 0.23 cm2 vs. NF: 0.77 ± 0.18 cm2; p < 0.001). The 30-day mortality was higher (p < 0.001) in LEF and PLF groups than in the NF group (6.3% and 6.3% vs. 1.8%, respectively). SVi and PLF group were independent predictors of operative mortality (odds ratio [OR]: 1.18, p < 0.05; and OR: 2.97, p = 0.004; respectively). At 5 years after AVR, overall survival was 72 ± 4% in LEF group, 81 ± 2% in PLF group, and 85 ± 2% in NF group (p < 0.0001).ConclusionsPatients with LEF or PLF AS have a higher operative risk, but pre-operative risk score accounted only for LEF and lower LVEF. Patients with LEF had the worst survival outcome, whereas patients with PLF and normal flow had similar survival rates after AVR. As a major predictor of perioperative mortality, SVi should be integrated in AS patients’ pre-operative evaluation.

The aims of this study were to examine prospectively the relationship between metabolic syndrome (MetS) and aortic stenosis (AS) progression and to evaluate the effect of age and statin therapy on AS progression in patients with or without MetS.Despite the clear benefits of statin therapy in primary and secondary coronary heart disease prevention, several recent randomized trials have failed to demonstrate any significant effect of this class of drugs on the progression of AS. Previous retrospective studies have reported an association between MetS and faster AS progression.This predefined substudy included 243 of the 269 patients enrolled in the ASTRONOMER (AS Progression Observation: Measuring Effects of Rosuvastatin) trial. Follow-up was 3.4 ± 1.3 years. AS progression rate was measured by calculating the annualized increase in peak aortic jet velocity measured by Doppler echocardiography.Patients with MetS (27%) had faster stenosis progression (+0.25 ± 0.21 m/s/year vs. +0.19 ± 0.19 m/s/year, p = 0.03). Predictors of faster AS progression in multivariate analysis were older age (p = 0.01), higher degree of valve calcification (p = 0.01), higher peak aortic jet velocity at baseline (p = 0.007), and MetS (p = 0.005). Impact of MetS on AS progression was most significant in younger (57 years) patients (MetS: +0.24 ± 0.19 m/s/year vs. no MetS: +0.13 ± 0.18 m/s/year, p = 0.008) and among patients receiving statin therapy (+0.27 ± 0.23 m/s/year vs. +0.19 ± 0.18 m/s/year, p = 0.045). In multivariate analysis, the MetS-age interaction was significant (p = 0.01), but the MetS-statin use interaction was not.MetS was found to be a powerful and independent predictor of faster AS progression, with more pronounced impact in younger patients. These findings emphasize the importance of routinely identifying and treating MetS in AS patients. The apparent faster stenosis progression in the subset of normocholesterolemic patients with MetS receiving the statin will need to be confirmed by future studies.

The aim of this study was to examine the relationship between metabolic syndrome (MetS) and left ventricular (LV) geometry and function in patients with asymptomatic aortic stenosis (AS).Recent experimental studies reveal that, among animals with sustained pressure overload, those with insulin resistance induced by a high-carbohydrate/high-fat diet have more severe LV hypertrophy and dysfunction compared to animals fed with standard diet.Among the 272 patients who were recruited in the ASTRONOMER (Aortic Stenosis Progression Observation Measuring Effects of Rosuvastatin) study, none had hypercholesterolemia, diabetes mellitus, or coronary artery disease (exclusion criteria) at baseline. However, 33% had systemic hypertension and 27% had MetS as identified by the National Cholesterol Education Program, Adult Treatment Panel III, clinical criteria.Patients with MetS had higher LV mass index (53 +/- 14 g/m(2.7) vs. 47 +/- 15 g/m(2.7); p = 0.002), relative wall thickness ratio (0.47 +/- 0.09 vs. 0.42 +/- 0.09; p = 0.001), and prevalence of LV concentric hypertrophy (42% vs. 23%) and lower peak early diastolic (8.2 +/- 2.4 cm/s vs. 9.6 +/- 3.1 cm/s, p = 0.001) and peak systolic (7.9 +/- 1.7 cm/s vs. 8.7 +/- 2.2 cm/s, p = 0.009) mitral annular myocardial velocities compared to patients without MetS. After adjustment for age, sex, low-density lipoprotein cholesterol, hypertension, and valvuloarterial impedance (i.e., global LV hemodynamic load), MetS was independently associated with higher relative wall thickness ratio (p = 0.01), higher prevalence of concentric hypertrophy (p = 0.03), and reduced diastolic (p = 0.01) and systolic (p = 0.03) myocardial velocities.Notwithstanding AS severity and increase in hemodynamic load, MetS is independently associated with more pronounced LV concentric hypertrophy and worse myocardial function in patients with AS, which may, in turn, predispose them to the occurrence of adverse events. (Effects of Rosuvastatin on Aortic Stenosis Progression [ASTRONOMER]; NCT00800800).

This study was designed to evaluate the effect of valve prosthesis-patient mismatch (PPM) on late survival after aortic valve replacement (AVR) and to determine if this effect is modulated by patient age, body mass index (BMI), and pre-operative left ventricular (LV) function.We recently reported that PPM is an independent predictor of operative mortality after AVR, particularly when associated with LV dysfunction.The indexed valve effective orifice area (EOA) was estimated in 2,576 patients having survived AVR and was used to define PPM as not clinically significant if it was0.85 cm(2)/m(2), as moderate if0.65 andor =0.85 cm(2)/m(2), and severe ifor =0.65 cm(2)/m(2).After adjustment for other risk factors, severe PPM was associated with increased late overall mortality (hazard ratio [HR]: 1.38; p = 0.03) and cardiovascular mortality (HR: 1.63; p = 0.0006) in the whole cohort. Severe PPM was also associated with increased overall mortality in patients70 years old (HR: 1.77; p = 0.002) and in patients with a BMI30 kg/m(2) (HR: 2.1; p = 0.006), but had no impact in older patients or in obese patients. Moderate PPM was a predictor of mortality in patients with LV ejection fraction50% (HR: 1.21; p = 0.01), but not in patients with preserved LV function.Moderate PPM is associated with increased late mortality in patients with LV dysfunction, but with normal prognosis in those with preserved LV function. Notwithstanding the previously demonstrated deleterious effect of severe PPM on early mortality, this factor appears to increase late mortality only in patients70 years old and/or with a BMI30 kg/m(2) or an LV ejection fraction50%.

ObjectivesThe aim of this study was to determine the impact of the metabolic syndrome (MS) on operative mortality after a coronary artery bypass grafting surgery (CABG).BackgroundDiabetes and obesity are highly prevalent among patients undergoing CABG. However, it remains unclear whether these factors have a significant impact on operative mortality after this procedure. We hypothesized that the metabolic abnormalities associated with MS could negatively influence the operative outcome of CABG surgery.MethodsWe retrospectively analyzed the data of 5,304 consecutive patients who underwent an isolated CABG procedure between 2000 and 2004. Of these 5,304 patients, 2,411 (46%) patients met the National Cholesterol Education Program–Adult Treatment Panel III criteria for MS. The primary end point was operative mortality.ResultsThe operative mortality after CABG surgery was 2.4% in patients with MS and 0.9% in patients without MS (p < 0.0001). The MS was a strong independent predictor of operative mortality (relative risk 3.04 [95% confidence interval (CI) 1.73 to 5.32], p = 0.0001). After adjusting for other risk factors, the risk of mortality was increased 2.69-fold (95% CI 1.43 to 5.06; p = 0.002) in patients with MS and diabetes and 2.36-fold (95% CI 1.26 to 4.41; p = 0.007) in patients with MS and no diabetes, whereas it was not significantly increased in the patients with diabetes and no MS.ConclusionsThis is the first study to report that MS is a highly prevalent and powerful risk factor for operative mortality in patients undergoing a CABG surgery. Thus, interventions that could contribute to reduce the prevalence of MS in patients with coronary artery disease or that could acutely modify the metabolic perturbations of MS at the time of CABG might substantially improve survival in these patients.

Discordant findings between aortic valve area (AVA

ObjectivesWe sought to determine the impact of valve prosthesis-patient mismatch (PPM) on pulmonary arterial (PA) pressure after mitral valve replacement (MVR).BackgroundPulmonary arterial hypertension is a serious complication of mitral valve disease, and it is a major risk factor for poor outcome after MVR. We hypothesized that valve PPM might be a determinant of PA hypertension after MVR.MethodsSystolic PA pressure was measured by Doppler echocardiography in 56 patients with normally functioning mitral prosthetic valves. Mitral valve effective orifice area (EOA) was determined by the continuity equation and indexed for body surface area.ResultsThirty patients (54%) had PA hypertension defined as systolic PA pressure >40 mm Hg, whereas 40 patients (71%) had PPM defined as an indexed EOA ≤1.2 cm2/m2. There was a significant correlation (r = 0.64) between systolic PA pressure and indexed EOA. The average systolic PA pressure and prevalence of PA hypertension were 34 ± 8 mm Hg and 19% in patients with no PPM versus 46 ± 8 mm Hg and 68% in patients with PPM (p < 0.001). In multivariate analysis, the indexed EOA was by far the strongest predictor of systolic PA pressure.ConclusionsPersistent PA hypertension is frequent after MVR and strongly associated with the presence of PPM. The clinical implications of these findings are important given that PPM can largely be avoided by using a simple prospective strategy at the time of operation.