Left ventricular filling patterns in patients with systemic hypertension and left ventricular hypertrophy (the LIFE study). Losartan Intervention For Endpoint

Abnormal left ventricular (LV) filling may exist in early stages of hypertension. Whether this finding is related to LV hypertrophy is currently controversial. This study was undertaken to assess relations between abnormal diastolic LV filling and LV geometry in a large series of hypertensive patients with electrocardiographic LV hypertrophy. M-mode, 2-dimensional, and pulsed Doppler echocardiographic recordings of mitral inflow velocity and isovolumetric relaxation time (IVRT) were obtained in 750 patients with stage I to III hypertension and LV hypertrophy determined by electrocardiography (sex-adjusted Cornell voltage duration criteria or Sokolow-Lyon voltage criteria) after 14 days of placebo treatment. The patients' mean age was 67+/-7 years and 44% were women. One hundred forty patients (19%) had normal LV geometric pattern, 79 (11%) had concentric remodeling, 342 (45%) had eccentric LV hypertrophy, and 189 (25%) had concentric LV hypertrophy. A normal LV filling pattern was found in 116 patients (16%), abnormal relaxation in 519 (69%), "pseudonormal" filling was found in 83 (11%), and a restrictive filling pattern in 32 (4%). Prolonged IVRT was associated with LV hypertrophy (p<0.01) as well as elevated relative wall thickness (p<0.05). A stronger difference (p<0.01) in IVRT was found between groups with and without LV hypertrophy. Multiple regression analysis revealed that increased LV mass correlated with prolonged IVRT, whereas LV mass and geometry were not associated with peak early LV filling velocity (E), peak atrial filling velocity (A) ratio or mitral valve E-peak deceleration time, although IVRT was found to be an independent correlate of E/A ratio and deceleration time. Thus, abnormal IVRT was highly prevalent in all LV geometric subgroups among hypertensive patients with electrocardiographic LV hypertrophy, even in those with normal LV geometry determined by echocardiography. We found that IVRT differed significantly among patient groups with different LV geometric patterns, primarily because of the association of IVRT to LV mass.     

Left atrial systolic force in hypertensive patients with left ventricular hypertrophy: the LIFE study

In hypertensive patients without prevalent cardiovascular disease, enhanced left atrial systolic force is associated with left ventricular hypertrophy and increased preload. It also predicts cardiovascular events in a population with high prevalence of obesity. Relations between left atrial systolic force and left ventricular geometry and function have not been investigated in high-risk hypertrophic hypertensive patients. Participants in the Losartan Intervention For Endpoint reduction in hypertension echocardiography substudy without prevalent cardiovascular disease or atrial fibrillation (n = 567) underwent standard Doppler echocardiography. Left atrial systolic force was obtained from the mitral orifice area and Doppler mitral peak A velocity. Patients were divided into groups with normal or increased left atrial systolic force (>14.33 kdyn). Left atrial systolic force was high in 297 patients (52.3%), who were older and had higher body mass index and heart rate (all P < 0.01) but similar systolic and diastolic blood pressure, in comparison with patients with normal left atrial systolic force. After controlling for confounders, increased left atrial systolic force was associated with larger left ventricular diameter and higher left ventricular mass index (both P < 0.01). Prevalence of left ventricular hypertrophy was greater (84 vs. 64%; P < 0.001). Participants with increased left atrial systolic force exhibited normal ejection fraction; higher stroke volume, cardiac output, transmitral peak E velocities and peak A velocities; and lower E/A ratio (all P < 0.01). Enhanced left atrial systolic force identifies hypertensive patients with greater left ventricular mass and prevalence of left ventricular hypertrophy, but normal left ventricular chamber systolic function with increased transmitral flow gradient occurring during early filling, consistent with increased preload.     

Left ventricular systolic response to exercise in patients with systemic hypertension without left ventricular hypertrophy

Supine exercise radionuclide angiography was performed in 367 men to assess left ventricular (LV) systolic response to exercise; 58 had systemic hypertension without LV hypertrophy on a resting electrocardiogram and 309 were normotensive. All patients met the following criteria defining a low pretest likelihood of coronary artery disease: age less than 50 years; normal electrocardiographic response to exercise; absence of typical or atypical chest pain; and exercise heart rate greater than 120 beats/min. Patients taking beta-receptor blockers were excluded. There were no significant differences between hypertensive and normotensive groups in peak exercise heart rate, workload or exercise duration. However, hypertensive patients had significantly higher peak exercise systolic blood pressures and peak exercise rate-pressure products. There were no differences between patients with and without hypertension in resting ejection fraction, peak exercise ejection fraction (hypertensive patients 0.71 +/- 0.01, normotensive patients 0.70 +/- 0.05) or change in ejection fraction at peak exercise (hypertensive patients 0.07 +/- 0.01, normotensive patients 0.07 +/- 0.04). Diastolic and systolic ventricular volumes tended to be smaller in the hypertensive patients, but the difference was not statistically significant. The change in systolic volume with exercise was similar in the 2 groups (hypertensive -10 +/- 3 ml/m2, normotensive -10 +/- 1 ml/m2). In the absence of electrocardiographic evidence of LV hypertrophy, systemic hypertension does not influence LV systolic response to exercise.     

Left ventricular performance in patients with left ventricular hypertrophy caused by systemic arterial hypertension.

To assess the adaptation of the left ventricle to a chronic pressure overload we used echocardiography to study 18 patients with left ventricular hypertrophy caused by systemic arterial hypertension. Increased values for either posterior wall or interventricular septal thickness or both confirmed the presence of left ventricular hypertrophy in all patients and an increase in the average wall thickness to radius ratio was consistent with the development of concentric hypertrophy. No patient had clinical evidence of ischaemic heart disease. Ejection phase indices of left ventricular performance (mean Vcf, fractional per cent of shortening, normalised posterior wall velocity, and ejection fraction) were within the normal range in the basal state in 16 of the 18 patients. The hypothesis is advanced that patients with concentric left ventricular hypertrophy resulting from systemic arterial hypertension usually have normal left ventricular performance in the basal state because values for wall stress remain within the normal range. We conclude that the hypertrophic response to a chronic increase in systemic arterial pressure does not per se result in depression of the basal inotropic state of the left ventricle.     

Left ventricular performance in patients with left ventricular hypertrophy caused by systemic arterial hypertension.

To assess the adaptation of the left ventricle to a chronic pressure overload we used echocardiography to study 18 patients with left ventricular hypertrophy caused by systemic arterial hypertension. Increased values for either posterior wall or interventricular septal thickness or both confirmed the presence of left ventricular hypertrophy in all patients and an increase in the average wall thickness to radius ratio was consistent with the development of concentric hypertrophy. No patient had clinical evidence of ischaemic heart disease. Ejection phase indices of left ventricular performance (mean Vcf, fractional per cent of shortening, normalised posterior wall velocity, and ejection fraction) were within the normal range in the basal state in 16 of the 18 patients. The hypothesis is advanced that patients with concentric left ventricular hypertrophy resulting from systemic arterial hypertension usually have normal left ventricular performance in the basal state because values for wall stress remain within the normal range. We conclude that the hypertrophic response to a chronic increase in systemic arterial pressure does not per se result in depression of the basal inotropic state of the left ventricle.     

Electrocardiographic strain pattern and left ventricular diastolic function in hypertensive patients with left ventricular hypertrophy: the LIFE study

BACKGROUND: Whether the typical electrocardiographic (ECG) strain pattern (Strain, in leads V5 and/or V6), which is associated with left ventricular hypertrophy (LVH) and LV systolic dysfunction, is independently associated with LV diastolic dysfunction is unknown. METHODS: The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study enrolled hypertensive patients with ECG-LVH, of whom 10% underwent Doppler echocardiography. LV diastolic function measures included peak mitral E and A wave velocities and their ratio (E/A); E wave deceleration time (EDT); atrial filling fraction (AFF); and isovolumic relaxation time (IVRT). Normal filling pattern was defined by E/A < 1 with EDT >or= 150 and or=60 ms; abnormal relaxation by E/A < 1 with EDT > 250 ms or IVRT > 100 ms; pseudonormal filling pattern by E/A >or= 1 associated with IVRT > 100 ms or EDT > 250 ms; restrictive pattern by E/A >or= 1 with IVRT < 100 ms and EDT < 250 ms. A combined index of LV systolic-diastolic function was also computed (isovolumic time/ejection time, modified myocardial performance index). Of LIFE echo substudy participants with all needed ECG and Doppler data (n = 791), 110 (14%) had Strain. RESULTS: Strain was associated with male gender, African-American race, diabetes, history of coronary heart disease (CHD), higher systolic blood pressure (BP), LV mass and relative wall thickness, and higher prevalences of echo-LV hypertrophy and wall motion abnormalities, and with slower heart rate (all P < 0.05). Age, diastolic BP and LV ejection fraction were similar in patients with or without Strain. Diastolic parameters, and prevalences of different LV filling patterns, did not differ significantly between patients with versus those without Strain (all P > 0.1), but modified myocardial performance index was higher with Strain (P < 0.05). Findings were consistent in multivariate analyses. The association of Strain with higher modified myocardial performance index was no longer statistically significant after accounting for LV systolic function and wall motion abnormalities. CONCLUSIONS: In hypertensive patients with ECG-LVH, the ECG Strain pattern did not identify independently those with more severe LV diastolic abnormalities.     

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

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 66+/-7 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 (126+/-25 vs 124+/-26 g/m(2)) and relative wall thickness (0.41+/-0.07 vs 0.41+/-0.07, P=NS), patients with LBBB had lower LV fractional shortening (30+/-6 vs 34+/-6%), ejection fraction (56+/-10 vs 61+/-8%), midwall shortening (14+/-2 vs 16+/-2%), stress-corrected midwall shortening (90+/-13 vs 97+/-13%) (all P<0.001), and lower LV stroke index (38+/-7 vs 42+/-9 ml/m(2)) (P<0.05). Patients with LBBB also had reduced LV inferior wall and lower mitral E/A ratio (0.75+/-0.18 vs 0.87+/-0.38) (all P<0.05). 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.     

Impact of valvular regurgitation on left ventricular geometry and function in hypertensive patients with left ventricular hypertrophy: the LIFE study

Mild-to-moderate aortic and mitral regurgitation are frequently detected by echocardiogram in asymptomatic hypertensive patients. Our goal was to assess the prevalence and impact of mild-to-moderate mitral and/or aortic regurgitation on left ventricular (LV) structure and function in patients with hypertension and LV hypertrophy (LVH). Hypertensive patients with ECG LVH enrolled in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography substudy were evaluated. Among 939 patients with needed LV measurements and Doppler data, 242 had mild (1+) valvular regurgitation, and 51 patients had moderate (2+ or 3+) regurgitation of one or both valves. In analyses adjusting for gender, patients with mild mitral and/or aortic regurgitation had larger LV internal dimensions (5.25 vs 5.33 cm, P<0.05), higher LV mass indexed for body surface area (122 vs 125 g/m(2), P<0.05) or height(2.7) (55.4 vs 57.3, P<0.05), and larger left atrial diameter. Patients with moderate regurgitation of one or both valves had larger LV chambers (5.25 vs 5.9 cm, P<0.001), greater mean LV mass (232 vs 248 g, P<0.001) and LV mass indexed for body surface area or height(2.7), and higher Doppler stroke volume. Patients with moderate valvular regurgitation also had a higher prevalence of LVH due to an increased prevalence of eccentric LVH. There were no differences among groups defined by the presence and severity of valvular regurgitation in cardiac output, total peripheral resistance, or pulse pressure/stroke volume, indicating that the observed inter-group differences in LV geometry were not due to differences in the haemodynamic severity of hypertension. Hypertensive patients with mild-to-moderate mitral or aortic valvular insufficiency have additional LV structural and functional changes that may affect prognosis.     

Effects of indapamide on left ventricular mass and function in systemic hypertension with left ventricular hypertrophy

Left ventricular hypertrophy (LVH) is frequently associated with hypertension and constitutes a major cardiovascular risk factor, the reduction of which should be considered when initiating antihypertensive therapy. To assess the effects of indapamide on LVH, 18 hypertensive patients were included in the study (11 men and 7 women, age 53.6 +/- 2.9 years, mean +/- standard deviation) whose supine diastolic blood pressure was greater than 95 mm Hg without (n = 11) or with (n = 7:6 beta blockers, 1 calcium antagonist) antihypertensive therapy. All presented with LVH, echocardiographically defined by a left ventricular mass index greater than 110 g/m2. After a 2-week preinclusion period, all patients received indapamide, 2.5 mg/day, for a period of 6 months. Physical examination including blood pressure measurement was performed on selection (M-1/2), before (M0), and after 1 (M1), 3 (M3) and 6 (M6) months of indapamide treatment, and echocardiography was performed at M0 and M6. Quality of life was evaluated by means of questionnaires completed by the patient and the physician, and a visual analog scale was completed by the patient at M-1/2, M0 and M6. All clinical parameters remained stable during the 2-week preinclusion period. Indapamide administration induced a highly significant reduction in both supine systolic and diastolic blood pressures from 173.9 +/- 2.9/100.5 +/- 1.2 mm Hg at M0 to 150.9 +/- 1.9/90.5 +/- 1.3 mm Hg at M1 (p less than 0.001), and 145.0 +/- 1.7/86.0 +/- 1.5 mm Hg at M6 (p less than 0.001). Similar favorable effects were observed in the upright position.(ABSTRACT TRUNCATED AT 250 WORDS)     

Microalbuminuria in hypertensive patients with electrocardiographic left ventricular hypertrophy: the LIFE study

OBJECTIVES : Left ventricular hypertrophy and albuminuria have both been shown to predict increased cardiovascular morbidity and mortality. However, the relationship between these markers of cardiac and renal glomerular damage has not been evaluated in a large hypertensive population with target organ damage. The present study was undertaken to determine whether albuminuria is associated with persistent electrocardiographic (ECG) left ventricular hypertrophy, independent of established risk factors for cardiac hypertrophy, in a large hypertensive population with left ventricular hypertrophy who were free of overt renal failure. METHODS : Patients with stage II-III hypertension were enrolled in the study if they had left ventricular hypertrophy on a screening ECG by Cornell voltage-duration product and/or Sokolow-Lyon voltage criteria, and clinic blood pressures between 160 and 200/95-115 mmHg and plasma creatinine < 160 mmol/l. A second ECG and morning spot urine were obtained after 14 days of placebo treatment. Renal glomerular permeability was evaluated by urine albumin/creatinine (UACR, mg/mmol). Microalbuminuria was present if UACR > 3.5 mg/mmol and macroalbuminuria if UACR > 35 mg/mmol. RESULTS : The mean age of the 8029 patients was 66 years, 54% were women. Microalbuminuria was found in 23% and macroalbuminuria in 4% of patients. Microalbuminuria was more prevalent in patients of African American (35%), Hispanic (37%) and Asian (36%) ethnicity, heavy smokers (32%), diabetics (36%) and in patients with ECG left ventricular hypertrophy by both ECG-criteria (29%). Urine albumin/creatinine was positively related to Sokolow-Lyon voltage criteria and Cornell voltage-duration product criteria. In multiple regression analysis, higher UACR was independently associated with older age, diabetes, higher blood pressure, serum creatinine, smoking and left ventricular hypertrophy. Patients smoking > 20 cigarettes/day had a 1.6-fold higher prevalence of microalbuminuria and a 3.7-fold higher prevalence of macroalbuminuria than never-smokers. ECG left ventricular hypertrophy by Cornell voltage-duration product or Sokolow-Lyon criteria was associated with a 1.6-fold increased prevalence of microalbuminuria and a 2.6-fold increase risk of macroalbuminuria compared to no left ventricular hypertrophy on the second ECG. CONCLUSIONS : In patients with moderately severe hypertension, left ventricular hypertrophy on two consecutive ECGs is associated with increased prevalences of micro- and macroalbuminuria compared to patients without persistent ECG left ventricular hypertrophy. High albumin excretion was related to left ventricular hypertrophy independent of age, blood pressure, diabetes, race, serum creatinine or smoking, suggesting parallel cardiac damage and albuminuria.     

Left ventricular midwall function improves with antihypertensive therapy and regression of left ventricular hypertrophy in patients with asymptomatic hypertension

Recent evidence suggests that regression of left ventricular hypertrophy (LVH) with antihypertensive therapy improves prognosis. The mechanism for this benefit is unknown but may be related to effects on myocardial performance. Midwall fractional shortening (mFS) is often depressed in patients with asymptomatic hypertension, is associated with LVH, and is a potent, independent predictor of outcome. We therefore examined whether antihypertensive therapy may improve midwall performance. mFS as well as conventional echocardiographic parameters were measured serially among 29 hypertensive persons during 6 months of drug therapy. Stress-adjusted and absolute midwall function improved by 10% and 11%, respectively (p <0.05), whereas no significant changes were detected in other measures of chamber function. Improvement in function was more pronounced in patients with concentrically remodeled ventricular geometry and in those who achieved greater reductions in left ventricular (LV) mass. Antihypertensive therapy and LV mass regression is associated with demonstrable improvements in cardiac performance when assessed using mFS. Determinations of mFS may have a promising role in identifying patients with early hypertensive heart disease, tracking responses to therapy, and in elucidating the potential beneficial effects associated with LV mass regression.     

老年高血压伴左室肥厚对左心功能的影响

目的 :探讨老年高血压伴左室肥厚对心功能的影响。方法 :应用核素心血池扫描的方法 ,对老年高血压伴左室肥厚和无左室肥厚的患者 ,进行了左室射血分数 (LVEF)、左室高峰射血率 (PER)、左室高峰充盈率(PFR)、1/ 3充盈分数 (1/ 3FF)及相角程 (PA)的测定 ,并进行比较。结果 :伴左室肥厚的患者PFR、1/ 3FF明显低于无左室肥厚的患者 ,PA明显高于无左室肥厚的患者。结论 :老年高血压伴左室肥厚对心功能的影响 ,主要表现为对舒张功能的影响 ;左室肥厚导致的心室肌纤维化、顺应性下降和运动协调性异常 ,是影响舒张功能的重要原因     

Gender differences in systolic left ventricular function in hypertensive patients with electrocardiographic left ventricular hypertrophy (the LIFE study)

Echocardiography was performed in 944 untreated hypertensive patients (391 women and 553 men, mean age 66 years) who had electrocardiographic left ventricular (LV) hypertrophy at baseline in the Losartan Intervention For End point reduction in hypertension (LIFE) study to evaluate gender-associated differences in systolic LV function. Women had significantly lower diastolic blood pressure (175/97 vs 173/99 mm Hg) and body surface area and a higher body mass index (all p < 0.01). Women also had higher LV ejection fraction (EF), endocardial and midwall fractional shortening (63% vs 60%, 35% and 33%, and 16% vs 15%, respectively, all p < 0.01), higher stress-corrected midwall fractional shortening (98% vs 96%, p < 0.05), and lower circumferential end-systolic wall stress (178 vs 187 kdynes/cm(2), p < 0.01). There was no difference in age or LV mass indexed for height(2.7), but relative wall thickness was higher in women (0.42 vs 0.41, p < 0.05). In multiple regression analyses: (1) EF and endocardial fractional shortening were 2% to 3% higher in women than men, independent of the effects of LV stress, body mass index, and height (multiple r = 0.77 and 0.75, respectively, gender p < 0.02 in both models); (2) midwall fractional shortening was 0.5% higher in women, independent of the effects of age, body mass index, circumferential end-systolic stress, and absence of diabetes (multiple r = 0.36, p = 0.014 for gender); and (3) stress-corrected LV midwall fractional shortening was 2% higher (p = 0.004) in women, independent of the effects of age, height, heart rate, body mass index, and diabetes (multiple r = 0.33). Thus, female gender is an independent predictor of higher systolic LV function in hypertensive patients with electrocardiographic LV hypertrophy.     

老年高血压病人左室肥厚与左室舒张功能的关系

目的：研究老年高血压病人左室肥厚与左室舒张功能各参数的关系,探讨在老年人左室肥厚对左室舒张功能的影响。方法：用彩色多普勒超声心动图测量101例老年高血压病人左心室结构及舒张功能参数。结果：101例高血压病人中,左室肥厚组（48例）的左房内径指数（LADI）、等容舒张时间（IVRT）、舒张期二尖瓣E波减速时间（EDT）显著大于左室正常组（53例,P〈0．05～〈0．01）．多元逐步回归分析发现,左室质量指数（LVMI）与左房射血分数（LAEF）、LADI、IVRT和EDT有明显的相关关系（r分别为0．213,0．251．0．450．0．338．P〈0．05～0．001）结论：老年高血压病人的左室增厚可进一步降低左室舒张功能。     

Left ventricular hypertrophy and myocardial ischemia in systemic hypertension

Considerable attention has properly been focused in recent years on electrocardiographic abnormalities in patients with essential hypertension. It has been well established that both voltage evidence of left ventricular (LV) hypertrophy and LV hypertrophy and strain are ominous risk factors. A better understanding of the strain pattern in patients with LV hypertrophy has arisen from experimental animal studies showing how an increase in cardiac mass can lead to myocardial ischemia and from clinical studies showing that the patient with LV hypertrophy and strain is at risk from myocardial ischemia as a consequence of both associated coronary artery disease and increased LV mass. All the clinical syndromes associated with myocardial ischemia are increased in patients with LV hypertrophy and therefore earlier recognition of both cardiac involvement and myocardial ischemia is likely to improve survival in this particularly high-risk group of patients.     

Effect of electrocardiographic left ventricular hypertrophy on left ventricular systolic function in systemic hypertension (The LIFE Study). Losartan Intervention For Endpoint

Left ventricular (LV) ejection fraction is normal in most patients with uncomplicated hypertension, but the prevalence and correlates of decreased LV systolic chamber and myocardial function, as assessed by midwall mechanics, in hypertensive patients identified as being at high risk by the presence of LV hypertrophy on the electrocardiogram has not been established. Therefore echocardiograms were obtained in 913 patients with stage I to III hypertension and LV hypertrophy determined by electrocardiographic (Cornell voltage duration or Sokolow-Lyon voltage) criteria after 14 days' placebo treatment. The 913 patients' mean age was 66 years, and 42% were women. Fourteen percent had subnormal LV endocardial shortening, 24% had subnormal midwall shortening, and 13% had reduced stress-corrected midwall shortening. Nineteen percent had normal LV geometry, 11% had concentric remodeling, 47% had eccentric hypertrophy, and 23% had concentric hypertrophy. LV systolic performance evaluated by LV endocardial shortening and midwall shortening was impaired in 10% of patients with normal geometry, 20% with concentric remodeling, 27% with eccentric hypertrophy, and 42% with concentric hypertrophy. Relative wall thickness, an important independent correlate of LV chamber function, was related directly to endocardial shortening and negatively to midwall shortening and stress-corrected midwall shortening. LV mass was the strongest independent correlate of impaired endocardial shortening, midwall shortening, or both. In hypertensive patients with electrocardiographic LV hypertrophy, indexes of systolic performance are subnormal in 10% to 42% with different LV geometric patterns. Depressed endocardial shortening is most common in patients with eccentric LV hypertrophy, whereas impaired midwall shortening is most prevalent in patients with concentric remodeling or hypertrophy. Thus, in hypertensive patients with electrocardiographic LV hypertrophy, impaired LV performance occurs most often, and is associated with greater LV mass and relative wall thickness and may contribute to the high rate of cardiovascular events.     

N-terminal pro-brain natriuretic peptide predicts cardiovascular events in patients with hypertension and left ventricular hypertrophy: a LIFE study

BACKGROUND: N-terminal pro-brain natriuretic peptide (Nt-proBNP) and N-terminal pro-atrial natriuretic peptide (Nt-proANP) are strong cardiovascular risk markers in patients with chronic heart failure, as well as in the general population. We investigated whether high Nt-proBNP or Nt-proANP could also predict the composite endpoint (CEP) of cardiovascular death, non-fatal stroke or non-fatal myocardial infarction in patients with hypertension and left ventricular (LV) hypertrophy. METHODS: After 2 weeks of placebo treatment, clinical, laboratory and echocardiographic variables were assessed in 183 hypertensive participants in the LIFE echo substudy with electrocardiographic LV hypertrophy. Nt-proBNP and Nt-proANP were measured by immunoassay at baseline. The patients were followed for 60 +/- 5 months. RESULTS: Using Cox regression analysis, the 25 CEP were predicted by ln(Nt-proBNP) (hazard ratio 1.61 per 2.73-fold increase, P < 0.01) as well as ln(Nt-proANP) (hazard ratio 2.93, P < 0.05). Nt-proBNP above the median value of 21.8 pmol/ml was associated with higher incidence of CEP (19.6 versus 7.7%, P < 0.05). Nt-proBNP above the median value was associated with higher incidence of CEP in the 123 patients without history of diabetes or cardiovascular disease (14.8 versus 4.3%, P < 0.05), but the association was insignificant in the 60 patients with a history of diabetes or cardiovascular disease (26.3 versus 18.2%, NS). Nt-proANP showed the same tendency. CONCLUSION: Nt-proBNP, more than Nt-proANP, strongly predicts cardiovascular events in patients with hypertension and LV hypertrophy, especially in patients without diabetes or clinically overt cardiovascular disease.     

Left ventricular structure and function in sedentary and physically active subjects with left ventricular hypertrophy (the LIFE Study)

Patients with left ventricular hypertrophy had higher heart rates, left ventricular mass, and left atrial size independent of gender, blood pressure, or body mass index than physically active patients.