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Eva Gerdts

Publications and source records attributed to Eva Gerdts.

30 records · Page 2Linked to original sources
PubMed2003

Left ventricular mass regression in the LIFE study: effect of previous antihypertensive treatment.

BACKGROUND: Whether to include only those patients who have not had prior hypertension treatment in clinical trials of left ventricular (LV) mass reduction is controversial. Accordingly, our aim was to study the relationship between prior treatment and both baseline and 1-year echocardiographic LV mass in subjects enrolled in the Losartan Intervention For Endpoint reduction (LIFE) study. METHODS: We studied clinical and baseline echocardiographic data on 960 patients with electrocardiographically confirmed left ventricular hypertrophy enrolled in the electrocardiographic substudy of the LIFE study, 847 of whom had LV mass remeasured after 1 year of blinded treatment. The majority (75%) of these patients had prior medical treatment for hypertension. RESULTS: In multivariable regression analysis, controlling for age, sex, blood pressure (BP), body mass index, and indices of pump and myocardial function, prior antihypertensive treatment was not associated with either greater LV mass or relative wall thickness on the baseline study. Moreover, there was no significant difference between the 637 subjects who were previously treated and the 210 who were not treated with regard to the mean reduction in systolic or diastolic pressures (-25 +/- 17 v -24 +/- -16 and -13 +/- 9 mm Hg v -12 +/- 9 mm Hg), LV mass (-27 +/- 38 v -29 +/- 34 g), or LV mass/body surface area (-14 +/- 20 v -15 +/- 18 g/m(2)), all P >.05. CONCLUSIONS: Prior treatment is not associated with either greater LV mass or greater relative wall thickness when age, body mass index, sex, systolic BP, heart rate, or indices of LV volume load and systolic function are taken into account. In addition, prior treatment is not associated with lesser degrees of LV mass reduction. For design of future clinical trials, restriction of inclusion criteria to only previously untreated patients does not appear to be necessary when the selection criterion is electrocardiographically determined left ventricular hypertrophy.

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PubMed2003

Pulse pressure/stroke index and left ventricular geometry and function: the LIFE Study.

OBJECTIVE: To evaluate the relationship between arterial stiffness estimated by the pulse pressure/stroke index ratio (PP/SVi) and prognostically relevant abnormalities of left ventricular geometry and function. METHODS: Baseline data from the echocardiographic substudy of the Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study were used. Patients involved in the present study had stage II-III hypertension and electrocardiographic left ventricular hypertrophy; those with a history of coronary heart disease or segmental wall motion abnormalities were excluded. Plasma glucose, total and high-density lipoprotein (HDL) cholesterol and creatinine concentrations and urinary albumin/creatinine were assessed by standard methods. RESULTS: The study sample (n = 667) was subdivided into tertiles of PP/SVi. With greater PP/SVi, age, proportion of women and prevalence of type 2 diabetes, systolic and mean blood pressures were greater, whereas body mass index, body height and diastolic blood pressure were lower. Total and HDL cholesterol, creatinine and albuminuria did not differ among the three groups. After adjustment for age, sex and body size, greater PP/SVi was related to concentric left ventricular geometry, but showed a weak negative relationship to left ventricular mass and aortic root diameter; the prevalence of aortic fibrocalcification and left atrial diameter did not differ among tertiles of PP/SVi. PP/SVi was related to greater left ventricular end-systolic stress; stress-corrected left ventricular chamber function was greater with greater PP/SVi, whereas myocardial contractility did not differ significantly among the three groups. Greater PP/SVi was related to greater mitral E-wave/A-wave ratio and shorter isovolumic relaxation time independently of age, sex, left ventricular geometry, systolic function and other confounders. CONCLUSION: Increased estimated arterial stiffness is associated with concentric left ventricular geometry and with diastolic left ventricular abnormalities suggestive of increased diastolic left ventricular stiffness.

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PubMed2003

Echocardiographic wall motion abnormalities in hypertensive patients with electrocardiographic left ventricular hypertrophy: the LIFE Study.

There is limited information on correlates of left ventricular wall motion (WM) abnormalities in ambulatory patients with hypertension and ECG left ventricular hypertrophy by Cornell voltage-duration product and/or Sokolow-Lyon voltage criteria. Therefore, we assessed the prevalence and the correlates of echocardiographic global and segmental left ventricular WM abnormalities in 942 hypertensive patients with hypertrophy enrolled in the Losartan Intervention For End-point reduction in hypertension (LIFE) echo substudy. Patients were separated into groups of those with normal WM or those with segmental or global WM abnormalities. Segmental and global WM abnormalities were mostly of mild degree and were detected in 7% and 6% of the study sample. Compared with subjects with normal motion, those with WM abnormalities were mostly men and had higher prevalences of self-reported coronary heart disease, ECG signs of myocardial infarction, ST-strain pattern, and higher Cornell voltage-duration product, echo-left ventricular mass, and albuminuria, but lower total and high-density lipoprotein cholesterol. Blood pressure was similar among groups. No significant differences were found between patients with global or segmental WM abnormalities. Only half of patients with WM abnormalities had a history or ECG signs of coronary heart disease. Independent correlates of WM abnormalities were higher albuminuria and Cornell voltage-duration product, male gender, and echo-left ventricular hypertrophy, but lower cholesterol. In a subanalysis restricted to patients with WM abnormalities, those with evident cardiovascular disease had a higher prevalence of ST-strain pattern than those with subclinical WM abnormalities, but other clinical, ECG, or echocardiographic parameters were indistinguishable between the 2 groups. Thus, in hypertensives with ECG left ventricular hypertrophy, WM abnormalities, mostly of mild degree, occurred in one eighth of the patients and were associated with male gender, left ventricular hypertrophy, and albuminuria. No significant differences were found between patients with global or segmental wall motion abnormalities.

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PubMed2002

Change in systolic left ventricular performance after 3 years of antihypertensive treatment: the Losartan Intervention for Endpoint (LIFE) Study.

BACKGROUND: We have shown that hypertensive patients with left ventricular (LV) hypertrophy have decreased LV midwall mechanics, but the effect of antihypertensive therapy remains unclear. METHODS AND RESULTS: Echocardiograms were recorded at baseline in 679 hypertensive patients and ECG LV hypertrophy and repeated yearly during 3 years of blinded treatment to achieve target blood pressures (BPs) of 140/90 mm Hg. On average, BP was reduced from 174+/-21 to 147+/-19 over 95+/-11 to 82+/-10 mm Hg and LV mass from 234+/-56 to 194+/-50 g. Endocardial fractional shortening (FS) decreased slightly, whereas midwall FS increased from 15.4+/-2.0% to 16.8+/-2.1% and stress-corrected midwall FS increased from 97+/-13 to 105+/-12% (all P<0.001). Change in midwall FS was related inversely to change in LV mass (LVM), relative wall thickness (RWT), and diastolic BP and directly to change in Doppler stroke volume (SV, all P<0.001). Multivariate analysis showed that change in MWS was independently inversely related to changes in LVM (beta=-0.211), RWT (beta=-0.334, all P<0.001), and diastolic BP (beta=-0.088, P<0.05) and directly related to SV (beta=0.192, P<0.001) with control for blinded therapy. Change in stress-corrected midwall shortening was inversely independently associated with changes in LVM (beta=-0.153) and RWT (beta=-0.562) and directly with changes in SV (beta=0.145) and systolic BP (beta=0.s221, all P<0.001) with control for blinded therapy. CONCLUSIONS: Antihypertensive therapy reduced LVM and increased LV midwall shortening and contractility with a small decrease in LV chamber function and significant increase in SV. Change in systolic LV performance was independently associated inversely with change in LVM, RWT, and BP and directly with change in SV.

Antihypertensive Agents↗
PubMed2002

Change in diastolic left ventricular filling after one year of antihypertensive treatment: The Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study.

BACKGROUND: It is well established that hypertensive patients with left ventricular (LV) hypertrophy have impaired diastolic filling. However, the impact of antihypertensive treatment and LV mass reduction on LV diastolic filling remains unclear. METHODS AND RESULTS: Echocardiograms were recorded in 728 hypertensive patients with ECG-verified LV hypertrophy (Cornell voltage-duration or Sokolow-Lyon) at baseline and after 1 year of blinded treatment with either losartan or atenolol-based regimen. Systolic and diastolic blood pressures (BP) were reduced on average 23/11 mm Hg; isovolumic relaxation time and E/A ratio became more normal, and LV inflow deceleration time prolonged (all P<0.001). Directionally opposite changes in isovolumic relaxation time (IVRT) and deceleration time indicate improvement in active LV relaxation and passive chamber stiffness during early diastole. Prevalences of normal LV filling increased, abnormal relaxation and pseudonormalization decreased, and restrictive filling pattern remained unchanged (P<0.05). Patients with reduction in LV mass had smaller left atrial diameter, shortened IVRT, increased E/A ratio, and prolonged LV inflow deceleration time (all P<0.001). Patients without LV mass reduction had no change in diastolic filling parameters (P=NS). IVRT shortening was independently associated with reduction in LV mass. Increase in E/A ratio was independently associated with reduction in diastolic BP, and increase in the deceleration time was independently associated with reduced end-systolic relative wall thickness. CONCLUSIONS: Antihypertensive therapy resulting in LV mass or relative wall thickness regression is associated with significant improvement of diastolic filling parameters related to active relaxation and passive chamber stiffness compared with patients without regression, independent of BP reduction; however, abnormalities of diastolic LV filling remain common.

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PubMed2002

Correlates of left atrial size in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study.

Left ventricular hypertrophy has been suggested to mediate the relation between hypertension and left atrial enlargement, with associated risks of atrial fibrillation and stroke. However, less is known about correlates of left atrial size in hypertensive patients with left ventricular hypertrophy. We assessed left atrial size by echocardiography in 941 hypertensive patients, age 55 to 80 (mean, 66) years, with electrocardiographic left ventricular hypertrophy at baseline in the Losartan Intervention For Endpoint reduction in hypertension study. Enlarged left atrial diameter (women, >3.8 cm; men, >4.2 cm) was present in 56% of women and 38% of men (P<0.01). Compared with the 512 patients with normal left atrial size, the 429 patients with enlarged left atrium more often had mitral regurgitation, atrial fibrillation, and echocardiographic left ventricular hypertrophy. They also had higher age, systolic blood pressure, pulse pressure, weight, body mass index, left ventricular internal chamber dimension, stroke volume, and mass and lower relative wall thickness and ejection fraction (all, P<0.05). In logistic regression analysis, left atrial enlargement was related to left ventricular hypertrophy and eccentric geometry; greater body mass index, systolic blood pressure, and age; female gender; mitral regurgitation; and atrial fibrillation (all, P<0.05). Thus, left atrial size in hypertensive patients with electrocardiographic left ventricular hypertrophy is influenced by gender, age, obesity, systolic blood pressure, and left ventricular geometry independently of left ventricular mass and presence of mitral regurgitation or atrial fibrillation.

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PubMed2002

Correlates of pulse pressure reduction during antihypertensive treatment (losartan or atenolol) in hypertensive patients with electrocardiographic left ventricular hypertrophy (the LIFE study).

In hypertensive patients, pulse pressure has been related to hypertension-induced target organ damage and risk of cardiovascular events. However, correlates of pulse pressure reduction during antihypertensive treatment have been less extensively investigated. We related pulse pressure changes to clinical and echocardiographic findings before and after 2 years of antihypertensive treatment in 767 patients aged 55 to 80 years (mean 66) in the Losartan Intervention For End point reduction in hypertension study. Over 2 years, blood pressure and pulse pressure were reduced from 173/98 to 147/84 mm Hg and from 75 to 63 mm Hg, respectively, both p <0.001. In linear multivariate analysis controlling for initial pulse pressure, 2-year reduction in pulse pressure correlated negatively with age and concomitant diabetes mellitus, and positively with body height and 2-year reduction in mean blood pressure (multiple R(2) = 0.42, p <0.01). When dividing the study population into 2 groups using a prognostically validated partition for pulse pressure, patients with pulse pressure > or =63 mm Hg after 2 years of antihypertensive treatment (n = 349) were older and shorter, included more women and patients with isolated systolic hypertension, diabetes mellitus, albuminuria, and echocardiographic left ventricular hypertrophy at baseline, and also had a smaller decrease in mean blood pressure and the urinary albumin/creatinine ratio over 2 years (all p <0.05). Thus, in hypertensive patients with electrocardiographic left ventricular hypertrophy, older age, less reduction in mean blood pressure, concomitant diabetes mellitus, and shorter stature are associated with attenuated pulse pressure reduction during antihypertensive treatment.

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PubMed2002

Urine albumin/creatinine ratio and echocardiographic left ventricular structure and function in hypertensive patients with electrocardiographic left ventricular hypertrophy: the LIFE study. Losartan Intervention for Endpoint Reduction.

BACKGROUND: Albuminuria, reflecting systemic microvascular damage, and left ventricular (LV) geometric abnormalities have both been shown to predict increased cardiovascular morbidity and mortality. However, the relationship between these markers of cardiovascular damage has not been evaluated in a large hypertensive population. METHODS: The urine albumin/creatinine ratio (UACR) and echocardiographic measures of LV structure and function were obtained in 833 patients with stage I to III hypertension and LV hypertrophy determined by electrocardiogram (ECG) (Cornell voltage-duration or Sokolow-Lyon voltage criteria) after 14 days of placebo treatment. RESULTS: Patients' mean ages were 66 years, 42% were women, 23% had microalbuminuria, and 5% had macroalbuminuria. Patients with eccentric or concentric LV hypertrophy had higher prevalences of microalbuminuria (average 26%-30% vs 9%, P <.001) and macroalbuminuria (6%-7% vs <1%, P <.001). Furthermore, patients with microalbuminuria and macroalbuminuria had a significantly higher LV mass and lower endocardial and midwall fractional shortening. Patients with abnormal diastolic LV filling parameters had a significantly increased prevalence of microalbuminuria. In univariate analyses, UACR correlated positively to LV mass, systolic blood pressure, age (all P <.001) and pulse pressure/stroke volume and negatively to relative wall thickness (both P <.01) and endocardial (P <.05) and midwall shortening (P <.001) but not to diastolic filling parameters. In multiple regression analysis higher UACR was associated with higher LV mass (beta=.169, P <.001) independently of older age (beta =.095, P <.01), higher systolic pressure (beta=.163), black race (beta=.186), and diabetes (beta=.241, all P <.001). CONCLUSIONS: In hypertensive patients with ECG LV hypertrophy, abnormal LV geometry and high LV mass are associated with high UACR independent of age, systolic blood pressure, diabetes, and race, suggesting parallel cardiac and microvascular damage.

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PubMed2002

Change of left ventricular geometric pattern after 1 year of antihypertensive treatment: the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study.

BACKGROUND: Patients with hypertension have different types of left ventricular (LV) geometry, but the impact of blood pressure (BP) reduction on LV geometry change during antihypertensive treatment remains unclear. METHODS: Two-dimensional and M-mode echocardiograms were recorded at baseline in 853 unmedicated patients with stage II to III hypertension and LV hypertrophy determined by electrocardiography (Cornell voltage duration > or =2440 mV x ms or modified Sokolow-Lyon criteria: SV1 + RV5/RV6 >38 mV) after 14 days of placebo treatment. Follow-up echocardiography was done after 1 year of blinded treatment with either losartan or atenolol, in some cases supplemented with thiazide and calcium antagonist to reach target a BP of 140/90 mm Hg. RESULTS: Baseline systolic/diastolic BP were reduced from 174 +/- 20/95 +/- 11 to 151 +/- 19/84 +/- 11 mm Hg. LV mass was reduced from 234 +/- 56 to 207 +/- 51 g and relative wall thickness from 0.41 +/- 0.07 to 0.38 +/- 0.06 (all P <.001). Prevalence of concentric LV hypertrophy decreased from 24% to 6%, eccentric LV hypertrophy from 46% to 37%, and concentric LV remodeling from 10% to 6%; normal geometry increased from 20% to 51%. A shift toward lower LV mass and relative wall thickness was found, as approximately 73% of those with concentric LV remodeling at baseline shifted to normal geometric pattern, whereas only 7% of those with normal pattern at baseline shifted to concentric LV remodeling. Of patients with concentric LV hypertrophy at baseline, 34% shifted to eccentric LV hypertrophy, whereas only 3% with eccentric LV hypertrophy at baseline had concentric LV hypertrophy. Furthermore, multiple regression analysis showed that Doppler stroke volume reduction was a significant correlate of LV mass reduction (beta = 0.108, P <.001) independent of BP, heart rate change, and assigned drug treatment. CONCLUSIONS: Antihypertensive treatment reduces LV mass and decreases the prevalence of LV hypertrophy and concentric LV remodeling. Additional control of Doppler stroke volume potentiates the effect of BP reduction on LV mass regression independent of the BP reduction per se.

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PubMed2002

Impact of diastolic Doppler indices on exercise capacity in hypertensive patients with electrocardiographic left ventricular hypertrophy (a LIFE substudy).

OBJECTIVE: To assess whether Doppler evidence of impaired early diastolic relaxation during exercise is associated with lesser exercise capacity in hypertensive patients. DESIGN: Single center addition to the echocardiographic substudy in the Losartan Intervention For Endpoint (LIFE) reduction in hypertension study. SETTING: University hospital out-patient clinic. METHODS: A total of 60 patients (29 women and 31 men) with essential hypertension and electrocardiographic LV hypertrophy. INTERVENTIONS: Assessment of Doppler echocardiography and ergospirometry during semi-upright bicycling. MAIN OUTCOME MEASURE: Exercise capacity and its relation to diastolic Doppler indices at rest and during exercise. RESULTS: Average resting blood pressure was 181/97 +/- 18/9 mmHg, LV mass/body surface area 127 +/- 26 g/m2, midwall shortening 16 +/- 2%, and isovolumic relaxation time (IVRT) and transmitral early to atrial filling velocity (E/A) ratio 121 ms and 0.80, respectively. Exercise capacity, assessed as peak oxygen uptake and exercise load at exhaustion in all patients, were 20 and 25% higher, respectively, in men than women (both P < 0.01). In multivariate analysis, higher peak exercise load was related to male gender, higher E/A ratio at rest, greater reduction in IVRT during exercise and higher peak exercise heart rate (multiple R2 = 0.59, P < 0.01). Younger age, greater reduction in IVRT during exercise, higher midwall shortening and peak exercise heart rate were associated with higher peak oxygen uptake (multiple R2 = 0.47, P < 0.01). CONCLUSION: Diastolic LV performance significantly influences exercise capacity in hypertensive patients with LV hypertrophy. Impaired exercise capacity is more strongly associated with blunted reduction in IVRT during exercise than with lower E/A ratio at rest.

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PubMed2002

Progressive hypertrophy regression with sustained pressure reduction in hypertension: the Losartan Intervention For Endpoint Reduction study.

OBJECTIVE: To examine the time course of left ventricular (LV) geometric response to blood pressure (BP) control during 2 years of systematic antihypertensive treatment. DESIGN: A total of 754 hypertensive patients with left ventricular hypertrophy (LVH) by Cornell voltage-duration product or Sokolow-Lyon voltage criteria on a screening electrocardiogram had their LV mass measured by echocardiogram at enrolment in the Losartan Intervention For Endpoint Reduction (LIFE) trial, and after 12 and 24 months of blinded therapy with losartan-based or atenolol-based regimens. SETTING: The LIFE trial, in which hypertensive patients with electrocardiographic LVH (Cornell voltage-duration product > 2440 mm x ms and/or Sokolow-Lyon voltage criteria SV1 + RV5-6 > 38 mm) were randomized to >or= 4 years double-blinded treatment with losartan or atenolol. PARTICIPANTS: A total of 754 LIFE participants with serial echocardiographic measurements of LV geometry. INTERVENTIONS: None. MAIN OUTCOME MEASURES: LV wall thicknesses, diameter and mass, and its indices. RESULTS: Mean systolic/diastolic BP fell from 173/95 to 150/84 mmHg after 1 year (P < 0.001) and to 148/83 mmHg at year 2 (P = not significant). Mean echocardiographic LV mass fell from 233 g at baseline to 206 g after 1 year (P < 0.001, adjusted for change in systolic BP) and to 195 g at year 2 (P < 0.001 versus year 1), with a parallel decrease in indexed LV mass [from 56.1 to 49.7 g/m2.7 (P < 0.001), to 47.1 g/m2.7 (P < 0.001 versus year 1)]. Relative wall thickness decreased from 0.41 at baseline to 0.37 at year 1 (P < 0.001), to 0.36 at year 2 (P < 0.001 versus year 1). As a result, there were serial decreases in prevalences of eccentric LVH [44 to 38%, and to 30% (P < 0.001 versus year 1)] and concentric LVH [24 to 7% (P < 0.001), to 2% (P < 0.05 versus year 1)], and increases in the proportion with normal LV geometry [22 to 50% (P < 0.001), and to 64% (P < 0.01 versus year 1)]. CONCLUSIONS: Sustained BP reduction in hypertensive patients with target organ damage causes continued decrease in echocardiographic LV mass and prevalence of anatomic LVH for at least 2 years despite only small BP decreases after the first year of blinded therapy. These data document cardiac benefit of sustained BP control and suggest that maximum LVH regression with effective antihypertensive treatment requires at least 2 years.

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