Factors Influencing Left Ventricular Structure and Stress-Corrected Systolic Function in Men and Women With Asymptomatic Aortic Valve Stenosis (a SEAS Substudy)

Cramariuc, Dana; Rieck, Ashild E; Staal, Eva M.; Wachtell, Kristian; Eriksen, Erlend; Rossebø, Anne B.; Gerdts, Eva

doi:10.1016/j.amjcard.2007.09.100

Cited by 71 publications

(56 citation statements)

References 28 publications

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“…First, low pressure gradient in the presence of a severe aortic stenosis may be the result of reduced stroke volume despite preserved ejection fraction due to decreased ventricular size and/or impaired myocardial function. 3,16 However, a low stroke volume index was found in only one half of patients with low-gradient "severe" aortic stenosis in the present study, confirming previous findings that low stroke volume may only partly explain this constellation. 1 Second, low-gradient "severe" aortic stenosis in the presence of a normal stroke volume may be due to inconsistencies in current guidelines regarding the partition value for severe stenosis.…”

Section: Mechanisms Of Low-gradient "Severe" Aortic Stenosissupporting

confidence: 80%

Outcome of Patients With Low-Gradient “Severe” Aortic Stenosis and Preserved Ejection Fraction

et al. 2011

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Background— Retrospective studies have suggested that patients with a low transvalvular gradient in the presence of an aortic valve area <1.0 cm 2 and normal ejection fraction may represent a subgroup with an advanced stage of aortic valve disease, reduced stroke volume, and poor prognosis requiring early surgery. We therefore evaluated the outcome of patients with low-gradient “severe” stenosis (defined as aortic valve area <1.0 cm 2 and mean gradient ≤40 mm Hg) in the prospective Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study. Methods and Results— Outcome in patients with low-gradient “severe” aortic stenosis was compared with outcome in patients with moderate stenosis (aortic valve area 1.0 to 1.5 cm 2 ; mean gradient 25 to 40 mm Hg). The primary end point of aortic valve events included death from cardiovascular causes, aortic valve replacement, and heart failure due to aortic stenosis. Secondary end points were major cardiovascular events and cardiovascular death. In 1525 asymptomatic patients (mean age, 67±10 years; ejection fraction, ≥55%), baseline echocardiography revealed low-gradient severe stenosis in 435 patients (29%) and moderate stenosis in 184 (12%). Left ventricular mass was lower in patients with low-gradient severe stenosis than in those with moderate stenosis (182±64 versus 212±68 g; P <0.01). During 46 months of follow-up, aortic valve events occurred in 48.5% versus 44.6%, respectively ( P =0.37; major cardiovascular events, 50.9% versus 48.5%, P =0.58; cardiovascular death, 7.8% versus 4.9%, P =0.19). Low-gradient severe stenosis patients with reduced stroke volume index (≤35 mL/m 2 ; n=223) had aortic valve events comparable to those in patients with normal stroke volume index (46.2% versus 50.9%; P =0.53). Conclusions— Patients with low-gradient “severe” aortic stenosis and normal ejection fraction have an outcome similar to that in patients with moderate stenosis.

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Section: Mechanisms Of Low-gradient "Severe" Aortic Stenosissupporting

confidence: 80%

Outcome of Patients With Low-Gradient “Severe” Aortic Stenosis and Preserved Ejection Fraction

et al. 2011

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“…Our finding that women had higher end-study scMWS compared with men also when LV size was taken into account is in accordance with results published recently from our echocardiography laboratory demonstrating that, among 1720 patients with asymptomatic mild-to-moderate aortic stenosis, women have higher scMWS at any given LV internal diameter, in particular, in eccentric LV geometry, as well as results from the community-based Olmsted County Study. 31,32 Although a higher prevalence of LV systolic dysfunction was reported in men than in women in the Hypertension Genetic Epidemiology Network cohort, 7 the present analysis, using gender-specific partition values, found comparable prevalences of low end-study EF and scMWS in women and men. A similar prevalence of LV dysfunction in both genders was also reported in a population sample of 274 healthy Italian hypertensive subjects by Celentano et al 8 However, compared with previous reports, low end-study scMWS was less frequent, whereas low end-study EF was more common in the present study population, possibly as a consequence of effective antihypertensive treatment used in the LIFE Study, as well as differences in population characteristics, including higher prevalences of LV hypertrophy and lower prevalences of diabetes, obesity, and history of previous myocardial infarction, all important covariates of LV systolic dysfunction in hypertension.…”

Section: End-study LV Systolic Functionmentioning

confidence: 52%

Gender Differences in Left Ventricular Structure and Function During Antihypertensive Treatment

et al. 2008

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Abstract-In hypertensive patients with left ventricular hypertrophy, antihypertensive treatment induces changes in left ventricular structure and function. However, less is known about gender differences in this response. Baseline and annual echocardiograms until the end of study or a primary end point occurred were assessed in 863 hypertensive patients with electrocardiographic left ventricular hypertrophy aged 55 to 80 years (mean: 66 years) during 4. in women and men, respectively, and systolic function as ejection fraction and stress-corrected midwall fractional shortening. Women included more patients with obesity, isolated systolic hypertension, and mitral regurgitation (all PϽ0.01). Ejection fraction, stress-corrected midwall shortening, and prevalence of left ventricular hypertrophy were higher in women at baseline and at the end of study (all PϽ0.01). In particular, more women had residual eccentric hypertrophy (47% versus 32%; PϽ0.01) in spite of similar in-treatment reduction in mean blood pressure. In logistic regression, left ventricular hypertrophy at study end was more common in women (odds ratio: 1.61; 95% CI: 1.16 to 2.26; PϽ0.01) independent of other significant covariates. In linear regression analyses, female gender also predicted 2% higher mean in-treatment ejection fraction and 2% higher mean stress-corrected midwall shortening (both ␤ϭ0.07; PϽ0.01). Hypertensive women in this study retained higher left ventricular ejection fraction and stress-corrected midwall shortening in spite of less hypertrophy regression during long-term antihypertensive treatment. t is well documented that aggressive antihypertensive treatment reduces left ventricular (LV) mass and improves myocardial function in a majority of hypertensive patients with LV hypertrophy. Less LV hypertrophy reduction has been described in subgroups of patients, including patients with obesity, diabetes, or renal disease. 1-5 Several studies have reported gender differences in LV adaptation to chronic pressure overload in hypertension: women exhibit a greater prevalence of concentric LV geometry, as well as better indices of LV systolic chamber and myocardial function evaluated by echocardiography. 6 -8 Little is known about the impact of gender on changes in LV structure and systolic function during long-term antihypertensive treatment.Accordingly, the present analysis was undertaken to assess gender differences in LV structure and systolic function during 4.8 years of losartan-or atenolol-based antihypertensive therapy in hypertensive patients with electrocardiographic LV hypertrophy recruited in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography substudy. Methods Patient PopulationThe present analysis was carried out in the LIFE echocardiography substudy, which enrolled 960 of the 9193 participants in the parent trial for annual echocardiographic follow-up. 9,10 This analysis was not prespecified as part of the LIFE protocol but added to the data analysis plan before completion of the LIFE Stud...

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“…In Cox regression analyses, 1-cm 2 /m 2 lower baseline ELI predicted a 2-fold higher risk both for aortic valve events and for combined total mortality and hospitalization for heart failure independently of baseline peak aortic jet velocity or mean aortic gradient and independently of aortic root size (all P<0.05). In reclassification analysis, ELI improved the prediction of aortic valve events by 13% (95% confidence interval, [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19], whereas the prediction of combined total mortality and hospitalization for heart failure resulting from the progression of AS did not improve significantly. patients with asymptomatic AS, defined as aortic valve thickening and peak aortic jet velocity ≥2.5 and ≤4.0 m/s.…”

Section: Study Populationmentioning

confidence: 99%

“…14,15 A copy of all echocardiograms was sent for expert interpretation at the SEAS echocardiography core laboratory at Haukeland University Hospital, Bergen, Norway. Management of patients in the study was based on local clinical and echocardiographic interpretation at the study centers.…”

Section: Echocardiographymentioning

confidence: 99%

Prognostic Value of Energy Loss Index in Asymptomatic Aortic Stenosis

et al. 2013

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Background— Aortic valve area index adjusted for pressure recovery (energy loss index [ELI]) has been suggested as a more accurate measure of aortic stenosis (AS) severity, but its prognostic value has not been determined in a prospective study. Methods and Results— The relation between baseline ELI and rate of aortic valve events and combined total mortality and hospitalization for heart failure resulting from the progression of AS was assessed by multivariate Cox regression and reclassification analysis in 1563 patients with initial asymptomatic AS in the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study. During 4.3 years follow-up, a total of 498 aortic valve events and 181 combined total mortalities and hospitalizations for heart failure caused by the progression of AS occurred. In Cox regression analyses, 1-cm 2 /m 2 lower baseline ELI predicted a 2-fold higher risk both for aortic valve events and for combined total mortality and hospitalization for heart failure independently of baseline peak aortic jet velocity or mean aortic gradient and independently of aortic root size (all P <0.05). In reclassification analysis, ELI improved the prediction of aortic valve events by 13% (95% confidence interval, 5–19), whereas the prediction of combined total mortality and hospitalization for heart failure resulting from the progression of AS did not improve significantly. Conclusions— In asymptomatic AS patients without known atherosclerotic disease or diabetes mellitus, ELI provides independent and additional prognostic information to that derived from conventional measures of AS severity, suggesting that ELI should be measured in such patients. Clinical Trial Registration Information— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00092677.

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Factors Influencing Left Ventricular Structure and Stress-Corrected Systolic Function in Men and Women With Asymptomatic Aortic Valve Stenosis (a SEAS Substudy)

Cited by 71 publications

References 28 publications

Outcome of Patients With Low-Gradient “Severe” Aortic Stenosis and Preserved Ejection Fraction

Outcome of Patients With Low-Gradient “Severe” Aortic Stenosis and Preserved Ejection Fraction

Gender Differences in Left Ventricular Structure and Function During Antihypertensive Treatment

Prognostic Value of Energy Loss Index in Asymptomatic Aortic Stenosis

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