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Background: Thromboembolic events (TEs) are frequent after mechanical mitral valve replacement (MVR), but their association to anticoagulation quality is unclear and has never been studied in a population-based setting with patients who have a complete anticoagulation record.Methods: We compiled a complete record of all residents of Olmsted County, MN, who underwent mechanical MVR between 1981 and 2004, for all TE, bleeding episodes, and international normalized ratios (INRs) measured from prosthesis implantation.Results: In the 112 residents (mean [+/- SD] age, 57 +/- 16 years; 60% female residents) who underwent mechanical MVR, 19,647 INR samples were obtained. While INR averaged 3.02 +/- 0.57, almost 40% of INRs were < 2 or > 4.5. Thirty-four TEs and 28 bleeding episodes occurred during a mean duration of 8.2 +/- 6.1 years of follow-up. There was no trend of association of INR (average, SD, growth variance rate, or intensity-specific incidence of events) with TE. Previous cardiac surgery (p = 0.014) and ball prosthesis (hazard ratio [HR], 2.92; 95% CI, 1.43 to 5.94; p = 0.003) independently determined TE. With MVR using a ball prosthesis, despite higher anticoagulation intensity (p = 0.002), the 8-year rate of freedom from TE was considerably lower (50 +/- 9% vs 81 +/- 5%, respectively; p < 0.0001). Compared with expected stroke rates in the population, stroke risk was elevated with non-ball prosthesis MVR (HR 2.6; 95% CI, 1.3 to 5.2; p = 0.007) but was considerable with ball prosthesis MVR (HR 11.7; 95% CI, 7.5 to 18.4; p < 0.0001). INR variability (SD) was higher with a higher mean INR value (p < 0.0001). INR variability (HR 2.485; 95% CI, 1.11 to 5.55; p = 0.027) and cancer history (p < 0.0001) independently determined bleeding rates.Conclusion: This population-based comprehensive study of anticoagulation and TE post-MVR shows that, in these closely anticoagulated patients, anticoagulation intensity was highly variable and not associated with TE incidence post-MVR. Higher anticoagulation intensity is linked to higher variability and, thus, to bleeding. The MVR-ball prosthesis design is associated with higher TE rates notwithstanding higher anticoagulation intensity, and its use should be retired worldwide. [ABSTRACT FROM AUTHOR]

Objectives: To analyse clinical, echocardiographic, and prognostic characteristics of Staphylococcus aureus infective endocarditis (IE) compared with endocarditis caused by other pathogens. Design: Cohort study. Methods: 194 consecutive patients with definite IE according to the Duke criteria prospectively examined by transthoracic and transoesophageal echocardiography were enrolled. Patients without identified microorganisms were excluded. The S aureus IE group (n = 61) was compared with the group with IE caused by other pathogens (n = 133). Results: Compared with IE caused by other pathogens, S aureus IE was characterised by severe comorbidity, a shorter duration of symptoms before diagnosis, and a higher prevalence of right sided IE, cutaneous portal of entry, and history of renal failure. Severe sepsis, major neurological events, and multiple organ failure were more frequent during the acute phase in S aureus IE. In-hospital mortality (34% v 10%, p < 0.001) was higher in patients with S aureus IE and the 36 month actuarial survival rate was lower in S aureus IE than in IE caused by other pathogens (47% v 68%, p = 0.002). Multivariate analyses identified S aureus infection as a predictive factor for in-hospital mortality and for overall mortality. Conclusions: S aureus IE compared with IE caused by other pathogens occurs in a more debilitated clinical setting and is characterised by a higher prevalence of severe sepsis, major neurological events, and multiple organ failure leading to higher mortality. [ABSTRACT FROM AUTHOR]

Background: The clinical outcome of asymptomatic mitral regurgitation is poorly defined, and the treatment is uncertain. We studied the effect on the outcome of quantifying mitral regurgitation according to recent guidelines. Methods: We prospectively enrolled 456 patients (mean [+/-SD] age, 63+/-14 years; 63 percent men; ejection fraction, 70+/-8 percent) with asymptomatic organic mitral regurgitation, quantified according to current recommendations (regurgitant volume, 66+/-40 ml per beat; effective regurgitant orifice, 40+/-27 mm2). Results: The estimated five-year rates (+/-SE) of death from any cause, death from cardiac causes, and cardiac events (death from cardiac causes, heart failure, or new atrial fibrillation) with medical management were 22+/-3 percent, 14+/-3 percent, and 33+/-3 percent, respectively. Independent determinants of survival were increasing age, the presence of diabetes, and increasing effective regurgitant orifice (adjusted risk ratio per 10-mm2 increment, 1.18; 95 percent confidence interval, 1.06 to 1.30; P<0.01), the predictive power of which superseded all other qualitative and quantitative measures of regurgitation. Patients with an effective regurgitant orifice of at least 40 mm2 had a five-year survival rate that was lower than expected on the basis of U.S. Census data (58+/-9 percent vs. 78 percent, P=0.03). As compared with patients with a regurgitant orifice of less than 20 mm2, those with an orifice of at least 40 mm2 had an increased risk of death from any cause (adjusted risk ratio, 2.90; 95 percent confidence interval, 1.33 to 6.32; P<0.01), death from cardiac causes (adjusted risk ratio, 5.21; 95 percent confidence interval, 1.98 to 14.40; P<0.01), and cardiac events (adjusted risk ratio, 5.66; 95 percent confidence interval, 3.07 to 10.56; P<0.01). Cardiac surgery was ultimately performed in 232 patients and was independently associated with improved survival (adjusted risk ratio, 0.28; 95 percent confidence interval, 0.14 to 0.55; P<0.01). Conclusions: Quantitative grading of mitral regurgitation is a powerful predictor of the clinical outcome of asymptomatic mitral regurgitation. Patients with an effective regurgitant orifice of at least 40 mm2 should promptly be considered for cardiac surgery. [ABSTRACT FROM AUTHOR]

Thromboembolism, valve thrombosis and haemorrhagic events have been compared in 356 Starr-Edwards (SE) 1260, 113 Björk-Shiley (BS), and 178 aortic bioprostheses operated upon between 1968 and 1982, and reviewed by the same group with less than 2% of patients lost of follow-up. Expressed in actuarial rate at 7 years the percentage of patients free of thromboembolism event is 87% for SE, 86% for BS. 94% for bioprostheses; the linearized rate is 2·9%/patient/year for SE, 2·2 for BS, 1·9 for bioprostheses (NS).Valve thrombosis was not observed in bioprostheses; 97·9% of patients with mechanical valves were free of valve thrombosis at 6·5 years.Haemorrhagic risk was lower with bioprostheses than with mechanical valves 0·2% patient/year vs 2·33 (P<0·005).The most important factor influencing thromboembolic and haemorrhagic risks is the quality of anticoagulant therapy. Other contributing factors are the date of the operation and associated mitral disease. [ABSTRACT FROM PUBLISHER]

Among 1436 patients who underwent valve replacement, the 400 first cases were studied to assess the features of recurrent systemic embolic event. The mean follow-up was 87 months. Three groups of patients were compared: group A — 289 patients without any thromboembolic event (72·25%); group B—78 patients with only one embolic event (19·5%); group C—33 patients with several embolic events (8·25%).The frequency of recurrence was high: one patient out oj three (linearized mean 8·9% in group C considering only one recurrence, vs 3·8% in group B). The recurrence have the same location in 45% of patients. The consequences of these embolisms are serious: each event has a 30 to 40% risk of death or major disability. Four variables seem statistically to promote the occurrence of embolic events: mitral prostheses, pre-operative fibrillation, left atrial enlargement, poor anticoagulant therapy. 54 months after the first embolic event, 60% of the patients with poor anticoagulant therapy experience a recurrent thromboembolism vs 20% with adequate therapy.Twenty-six patients of groups B and C had a pathological study of prostheses. Thrombosis of the prostheses was found in 12 out of 18 patients in group B and in 7 out of 8 patients; in group C.Strict observance of anticoagulant therapy is the better way to prevent thromboembolism and especially recurrences. A reoperation is sometimes necessary. Valve re-replacement was performed in 27 cases out of 1436 patients. [ABSTRACT FROM PUBLISHER]

The article presents the study "Natural History of Asymptomatic Mitral Valve Prolapse in the Community" by J. F. Avierinos and colleagues. It examines the prognosis of the disease in patients with asymptomatic mitral valve prolapse (MVP). It indicates that clinical and echocardiographic variables have predicted mortality and cardiovascular (CV) morbidity in patients with MVP.

Pulmonary venous flow (PVF) reversal is observed in mitral regurgitation (MR) and can be detected by Doppler echocardiography. However, the determinants of PVF alterations in MR have not been analyzed with simultaneous quantitative methods, and the diagnostic accuracy of flow reversal is uncertain. Prospectively, in 128 patients with isolated MR of various degrees (regurgitant fraction 4% to 81%), Doppler echocardiography was used to measure PVF velocity simultaneously to quantify MR by 2 methods and to perform a comprehensive hemodynamic assessment. Systolic PVF velocity was 4 +/- 56 cm/s (systolic flow reversal in 39 patients) and showed the strongest correlations with mitral effective regurgitant orifice (r = -0.56, p <0.0001). In multivariate analysis, larger effective regurgitant orifice (p <0.0001), eccentric jets (p = 0.0023), longer jets (p = 0.0033), and lower mitral regurgitant velocity (p = 0.0015) were independent determinants of decreased systolic PVF velocity. In organic MR, increased filling pressures were associated with systolic PVF reversal. Blunted systolic flow was associated with shorter mitral deceleration time (p <0.0001) and enlarged left atrium (p = 0.0007). For the diagnosis of severe MR (regurgitant orifice > or = 35 mm2, regurgitant fraction > or = 50%), systolic flow reversal sensitivity was 61% and 60%, and specificity was 92% and 85%, respectively. Among 29 patients in whom surgery demonstrated severe mitral lesions, 12 (41%) had no systolic flow reversal preoperatively. In patients with MR, the determinants of systolic PVF are complex and, in addition to the degree of MR, include the hemodynamic consequences of MR, jet characteristics, left ventricular filling, and left atrial volume alterations. Consequently, systolic PVF reversal is a useful sign of severe MR but of relatively low sensitivity, emphasizing the importance of quantifying MR. [ABSTRACT FROM AUTHOR]

Objectives: This study analyzed the association of left ventricular end-systolic diameter (LVESD) with survival after diagnosis in organic mitral regurgitation (MR) due to flail leaflets. Background: LVESD is a marker of left ventricular function in patients with organic MR but its association to survival after diagnosis is unknown. Methods: The MIDA (Mitral Regurgitation International Database) registry is a multicenter registry of echocardiographically diagnosed organic MR due to flail leaflets. We enrolled 739 patients with MR due to flail leaflets (age 65 +/- 12 years; ejection fraction: 65 +/- 10%) in whom LVESD was measured (36 +/- 7 mm). Results: Under conservative management, 10-year survival and survival free of cardiac death were higher with LVESD <40 mm versus > or =40 mm (64 +/- 5% vs. 48 +/- 10%; p < 0.001, and 73 +/- 5% vs. 63 +/- 10%; p = 0.001). LVESD > or =40 mm independently predicted overall mortality (hazard ratio [HR]: 1.95, 95% confidence interval [CI]: 1.01 to 3.83) and cardiac mortality (HR: 3.09, 95% CI: 1.35 to 7.09) under conservative management. Mortality risk increased linearly with LVESD >40 mm (HR: 1.15, 95% CI: 1.04 to 1.27 per 1-mm increment). During the entire follow-up (including post-surgical), LVESD > or =40 mm independently predicted overall mortality (HR: 1.86, 95% CI: 1.24 to 2.80) and cardiac mortality (HR: 2.14, 95% CI: 1.29 to 3.56), due to persistence of excess mortality in patients with LVESD > or =40 mm after surgery (HR: 1.86, 95% CI: 1.11 to 3.15 for overall death, and HR: 1.81, 95% CI: 1.05 to 3.54 for cardiac death). Conclusions: In MR due to flail leaflets, LVESD > or =40 mm is independently associated with increased mortality under medical management but also after mitral surgery. These findings support prompt surgical rescue in patients with LVESD > or =40 mm but also suggest that best preservation of survival is achieved in patients operated before LVESD reaches 40 mm. [ABSTRACT FROM AUTHOR]

Objectives: This study was designed to analyze the association among cholesterol levels, lipid-lowering treatment, and progression of aortic stenosis (AS) in the community.Background: Aortic stenosis is a progressive disease for which there is no known medical treatment to prevent or slow progression. Despite plausible pathologic mechanisms linking hypercholesterolemia to AS progression, clinical studies have been inconsistent and affected by referral bias, and the role of lipid-lowering therapy is uncertain.Methods: We determined the association between blood cholesterol levels and progression of native AS (assessed by Doppler echocardiography at baseline and at least six months later; mean interval, 3.7 +/- 2.3 years) in a community-based study of 156 patients (age 77 +/- 12 years; 90 men). Thirty-eight patients received statin treatment during follow-up.Results: In untreated subjects, mean gradient increased from 22 +/- 12 mm Hg to 39 +/- 19 mm Hg, and aortic valve area (AVA) decreased from 1.20 +/- 0.35 cm(2) to 0.91 +/- 0.33 cm(2) (both p < 0.001). The annualized change in AVA was -0.09 +/- 0.17 cm(2)/year (-7% +/- 13%/year). Neither total cholesterol (r = -0.01, p = 0.92) nor low-density lipoprotein cholesterol (r = 0.01; p = 0.88) showed a significant correlation to AS progression. Nevertheless, progression of AS was slower in patients receiving statins compared with untreated patients (decrease in AVA -3 +/- 10% vs. -7 +/- 13% per year, respectively; p = 0.04), even when adjusted for age, gender, cholesterol, and baseline valve area (p = 0.04). The association of statin treatment with slower progression was confirmed when analysis was restricted to patients coming for a systematic follow-up (p=0.02). The odds ratio of AS progression with statin treatment was 0.46 (95% confidence interval, 0.21 to 0.96).Conclusions: In the community, progression of AS shows no trend of association with cholesterol levels. Statin treatment, however, is associated with slower progression, suggesting that the effects of statin treatment on progression of AS should be pursued with appropriate clinical trials. [ABSTRACT FROM AUTHOR]

The objective of this study was to determine the effect of oral losartan on the degree of mitral regurgitation (MR). The regurgitant volume and effective regurgitant orifice were quantified using 3 methods (flow convergence, quantitative Doppler, and quantitative 2-dimensional echocardiography) in 32 patients (26 men, mean age 67 +/- 14 years) with MR, both at baseline and 4 hours after losartan (50 mg orally). Twenty-eight patients were also reevaluated after 1 month of continued treatment with losartan (50 mg/day). With treatment, systolic blood pressure decreased from 143 +/- 16 to 130 +/- 18 mm Hg and left ventricular end-systolic wall stress from 173 +/- 46 to 156 +/- 44 g/cm2 (both p < 0.001). With treatment, regurgitant volume decreased (from 77 +/- 28 to 64 +/- 26 ml, - 18 +/- 10%; p < 0.001) in direct relation to the effective regurgitant orifice change (from 43 +/- 16 to 37 +/- 15 mm2, -17 +/- 10%; p < 0.001) but without significant change in regurgitant gradient or duration. Wide individual variability in response was observed unrelated to the magnitude of blood pressure changes. Larger reduction in regurgitant volume was observed in patients with a marked decrease in wall stress (r = 0.47, p = 0.01) and higher baseline end-diastolic volume index (r = -0.38, p = 0.03) and regurgitant volume (r = -0.45, p = 0.01). Acute improvements were sustained and unchanged at 1 month (all p > 0.15). Treatment of MR using the angiotensin receptor antagonist losartan produces a significant and sustained decrease in the degree of MR, with decreases in regurgitant volume and effective regurgitant orifice. However, the changes are of modest and variable magnitude. [ABSTRACT FROM AUTHOR]