Left ventricular filling patterns in patients with systemic hypertension and left ventricular hypertrophy (the LIFE study)

Wachtell, Kristian; Smith, Geoffrey; Gerdts, Eva; Dahlöf, Björn; Nieminen, Markku S.; Papademetriou, Vasilios; Bella, Jonathan N.; Ibsen, Hans; Rokkedal, Jens; Devereux, Richard B.

doi:10.1016/s0002-9149(99)00773-0

Cited by 151 publications

(112 citation statements)

References 28 publications

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“…Echocardiographic methods and performance protocol were based on procedures used as in previous studies 7,8 and have been described in detail. 6,9,10 The echocardiograms were sent to Cornell Medical Center in New York City for blinded interpretation by experienced physicians, and blinded verification, and correction of measurements if necessary, by highly experienced investigators.…”

Section: Echocardiographic Methods and Performance Protocolmentioning

confidence: 99%

“…[8][9][10] Linear LV internal dimension and interventricular septal and posterior wall thickness were measured at end-diastole and end-systole according to American Society of Echocardiography recommendations. 11,12 Left atrial end-systolic dimension was measured from the trailing edge of the posterior aortic-anterior left atrial complex to avoid erroneously including the variable size of the connective tissue-filled space between these structures in atrial size.…”

Section: Echocardiographic Measurementsmentioning

confidence: 99%

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Association of left bundle branch block with left ventricular structure and function in hypertensive patients with left ventricular hypertrophy: the LIFE study

Wachtell

Okin

et al. 2004

J Hum Hypertens

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Electrocardiographic (ECG) left bundle branch block (LBBB) is associated with left ventricular hypertrophy (LVH), but its relation to left ventricular (LV) geometry and function in hypertensive patients with ECG LVH is unknown. Echocardiograms were performed in 933 patients (548 women, mean age 6677 years) with essential hypertension and LVH by baseline ECG in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. LBBB, defined by Minnesota code 7.1, was present in 47 patients and absent in 886 patients. Patients with and without LBBB were similar in age, gender, body mass index, blood pressure, prevalence of diabetes, and history of myocardial infarction. Despite similarly elevated mean LV mass (126725 vs 124726 g/m 2 ) and relative wall thickness (0.4170.07 vs 0.4170.07, P ¼ NS), patients with LBBB had lower LV fractional shortening (3076 vs 3476%), ejection fraction (56710 vs 6178%), midwall shortening (1472 vs 1672%), stress-corrected midwall shortening (90713 vs 97713%) (all Po0.001), and lower LV stroke index (3877 vs 4279 ml/m 2 ) (Po0.05). Patients with LBBB also had reduced LV inferior wall and lower mitral E/A ratio (0.7570.18 vs 0.8770.38) (all Po0.05). The above univariate results were confirmed by multivariate analyses adjusted for gender, age, blood pressures, height, weight, body mass index, heart rate, and LV mass index. Among hypertensive patients at high risk because of ECG LVH, the presence of LBBB identifies individuals with worse global and regional LV systolic function and impaired LV relaxation without more severe LVH by echocardiography.

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Section: Echocardiographic Methods and Performance Protocolmentioning

confidence: 99%

Section: Echocardiographic Measurementsmentioning

confidence: 99%

Association of left bundle branch block with left ventricular structure and function in hypertensive patients with left ventricular hypertrophy: the LIFE study

Wachtell

Okin

et al. 2004

J Hum Hypertens

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“…[15][16][17][18] However, 168 echocardiography substudy participants were ineligible for the present study because of one or more of the following: inability to obtain either baseline or year-3 minus baseline measurements of LV dimensions (nϭ22 and 24, respectively) or Doppler stroke volume (SV) (nϭ95 and nϭ59, respectively), or lack of year-3 studies because of death (nϭ10), disability, or failure to cooperate (nϭ77). Compared with the ineligible patients, the present study population (nϭ831) were at enrollment younger (mean 66.2Ϯ6.7 versus 68.4Ϯ7.7 years, PϽ0.01) but did not differ in sex, body mass index, LVM, LVM/body surface area (LVMI), RWT, SV, or systolic and diastolic BP (data not shown).…”

Section: Methodsmentioning

confidence: 99%

“…[15][16][17][18] End-diastolic LV dimensions were used to calculate LVM by an anatomically validated formula (rϭ0.90 versus necropsy LVM). 20 LV hypertrophy was considered present when LVMI Ͼ116 g/m 2 for men and Ͼ104 g/m 2 for women.…”

Section: Echocardiographic Methodsmentioning

confidence: 99%

Change in Systolic Left Ventricular Performance After 3 Years of Antihypertensive Treatment

et al. 2002

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“…10,11 All studies were sent to the Cornell Echocardiography Reading Center for blinded interpretation by an experienced echocardiographer. Measurements were made according to the American Society of Echocardiography standards.…”

Section: Doppler Echocardiographymentioning

confidence: 99%

Impact of age on left ventricular hypertrophy regression during antihypertensive treatment with losartan or atenolol (the LIFE study)

et al. 2004

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To assess the influence of age on changes in left ventricular (LV) mass and geometry during antihypertensive treatment, we related age to clinical and echocardiographic findings before and after 4 years of antihypertensive treatment in a subset of 560 hypertensive patients without known concurrent disease in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, which randomized patients to blinded losartan-or atenolol-based treatment. Patients X65 years (older group) included more women and patients with isolated systolic hypertension or albuminuria (all Po0.05). Compared to patients o65 years, older patients had higher pulse pressure, LV mass, and prevalence of concentric hypertrophy at baseline (78 vs 69 mmHg, 234 vs 224 g, and 28 vs 16%, respectively, all Po0.01), while the mean blood pressure did not differ. Over 4 years, reductions in LV mass and the mean blood pressure were similar in both groups, but older patients more often had residual hypertrophy (31 vs 15%, Po0.001) with a preponderance of eccentric geometry. In multivariate analysis of 4-year change in LV mass controlling for baseline mass, larger hypertrophy reduction was associated with losartan treatment, while age, gender, body mass index, and 4-year change in pulse pressure and albuminuria did not enter (Multiple R 2 ¼ 0.40, Po0.001). Thus, in up-to-80-year-old hypertensive patients with left ventricular hypertrophy, age did not significantly attenuate hypertrophy reduction during antihypertensive treatment, although residual hypertrophy was more prevalent in older patients as a consequence of higher initial LV mass.

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Left ventricular filling patterns in patients with systemic hypertension and left ventricular hypertrophy (the LIFE study)

Cited by 151 publications

References 28 publications

Association of left bundle branch block with left ventricular structure and function in hypertensive patients with left ventricular hypertrophy: the LIFE study

Association of left bundle branch block with left ventricular structure and function in hypertensive patients with left ventricular hypertrophy: the LIFE study

Change in Systolic Left Ventricular Performance After 3 Years of Antihypertensive Treatment

Impact of age on left ventricular hypertrophy regression during antihypertensive treatment with losartan or atenolol (the LIFE study)

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