Association between angiotensin-converting enzyme gene polymorphisms and regression of left ventricular hypertrophy in patients treated with angiotensin-converting enzyme inhibitors.

PURPOSE: An insertion/deletion (ID) polymorphism of the angiotensin-converting enzyme (ACE) gene is associated with left ventricular hypertrophy. The present study examined polymorphisms of the ACE gene in patients with essential hypertension and left ventricular hypertrophy who were participants in a long-term trial of therapy with an ACE inhibitor. PATIENTS AND METHODS: ACE inhibitor therapy was administered for >2 years to 54 patients with hypertension who had moderate or severe left ventricular hypertrophy. Cardiac dimensions were monitored by echocardiography before the initiation of therapy and after 1 and 2 years of treatment. Serum ACE activity and plasma concentrations of brain natriuretic peptide, a marker for left ventricular hypertrophy, were also monitored. RESULTS: Eighteen patients had the II genotype for the angiotensin-converting enzyme gene, 19 had the ID genotype, and 17 had the DD genotype. Baseline (mean +/- SD) serum ACE activity was significantly greater (P <0.05) in the DD (18 +/- 7 IU/L) group than in the II (7 +/- 4 IU/L) or ID (12 +/- 6 IU/L) groups. ACE inhibitor therapy was effective in controlling blood pressure, and it reduced posterior and septal wall thickness, left ventricular mass index, and plasma brain natriuretic peptide concentration in all three groups. Despite similar blood pressure reductions, after 2 years, mean (+/- SD) regression in posterior wall thickness was significantly less (P <0.05) in the DD group (-9% +/- 5%) than in the ID (-21% +/- 7%) and II (-21% +/- 9%) groups. Similar results were seen for the reductions in brain natriuretic peptide levels. The magnitudes of regression of septal wall thickness and left ventricular mass index during therapy were less in the DD group than the II group (P <0.05). CONCLUSION: Hypertensive patients with the DD genotype are less likely to have regression of left ventricular hypertrophy when treated with ACE inhibitors than are patients with other ACE genotypes.     

Angiotensin-converting enzyme gene polymorphism and geometric patterns of hypertensive left ventricular hypertrophy

Polymorphism in the angiotensin-converting enzyme (ACE) gene has been found to be associated with left ventricular hypertrophy (LVH) in patients with essential hypertension (EHT) in certain populations. We sought to evaluate, in a Japanese population, whether ACE genotype is related to left ventricular mass, or to the geometry of LVH in EHT. Eighty-seven patients with EHT were examined. Their relative wall thickness (RWT) and left ventricular mass index (LVMI), determined by echocardiogram, were used to divide them into 4 groups: normal (normal RWT and LVMI, n = 35); concentric remodeling (increased RWT but normal LVMI, n= 10); eccentric hypertrophy (increased LVMI but normal RWT, n = 20); and concentric hypertrophy (increased LVMI and RWT, n = 22). Genetic analysis for ACE genotypes was performed on peripheral leukocytes using PCR techniques. Interventricular septal thickness and RWT were significantly greater in the patients with the DD genotype than in those with the II genotype, but LVMI did not differ among the three ACE genotypes. The frequency of the DD genotype was higher in the concentric hypertrophy group than in each of the other groups, and the frequency of the II genotype was lower in the concentric hypertrophy group than in either the normal or eccentric hypertrophy group. The geometric pattern of hypertensive LVH was associated with ACE genotype in a Japanese population. The DD genotype may contribute to concentric hypertrophy, but not to eccentric hypertrophy.     

I/D gene polymorphism of the angiotensin-converting enzyme and left ventricular hypertrophy. Response to converting enzyme inhibitors

BACKGROUND: The present study was designed to assess whether the angiotensin-converting enzyme (ACE) gene I/D polymorphism influence the ACE inhibitors effect on the regression of left ventricular hypertrophy. METHODS: Sixty hypertensive subjects never treated by antihypertensive drugs, aged 46 +/- 11 years, were included in the study. Follow-up with ACE inhibitor treatment was 60 +/- 26 months. Genotypes for ACE I/D polymorphism (DD, ID or II) were determined by PCR. The left ventricular mass index (LVMI) was assessed by two-dimensional directed M-mode echocardiography. RESULTS: ACE genotype distribution was in agreement with the Hardy-Weinberg equilibrium: 21 patients had the DD genotype, 29 were ID, and 10 were II. At baseline, age, systolic arterial pressure and LVMI didn't differ on the basis of genotype. Body mass index was significantly higher in II than in ID and DD groups. Regression of LVMI with ACE inhibitor treatment was similar in the 3 genotypes (-8.9%, -0.6%, -12.1% in DD, ID and II groups respectively). In addition, decrease of systolic arterial pressure was identical in 3 groups. CONCLUSION: ACE gene I/D polymorphism seems not to influence regression of left ventricular hypertrophy by ACE inhibitors in essential hypertension.     

The ACE/DD genotype is associated with the extent of exercise-induced left ventricular growth in endurance athletes

OBJECTIVES: We studied the impact of the angiotensin-converting enzyme (ACE)/DD genotype on morphologic and functional cardiac changes in adult endurance athletes. BACKGROUND: Trained athletes usually develop adaptive left ventricular hypertrophy (LVH), and ACE gene polymorphisms may regulate myocardial growth. However, little is known about the impact of the ACE/DD genotype and D allele dose on the cardiac changes in adult endurance athletes. METHODS; Echocardiographic studies (including tissue Doppler) were performed in 61 male endurance athletes ranging in age from 25 to 40 years, with a similar period of training (15.6 +/- 4 h/week for 12.6 +/- 5.7 years). The ACE genotype (insertion [I] or deletion [D] alleles) was ascertained by polymerase chain reaction (DD = 27, ID = 31, and II = 3). Athletes with the DD genotype were compared with their ID counterparts. RESULTS: The DD genotype was associated with a higher left ventricular mass index (LVMI) than the ID genotype (162.6 +/- 36.5 g/m(2) vs. 141.6 +/- 34 g/m(2), p = 0.031), regardless of other confounder variables. As a result, 70.4% of DD athletes and only 42% of ID athletes met the criteria for LVH (p = 0.037). Although systolic and early diastolic myocardial velocities were similar in DD and ID subjects, a more prolonged E-wave deceleration time (DT) was observed in DD as compared with ID athletes, after adjusting for other biologic variables (210 +/- 48 ms vs. 174 +/- 36 ms, respectively; p = 0.008). Finally, a positive association between DT and myocardial systolic peak velocity (medial and lateral peak S(m)) was only observed in DD athletes (p = 0.013, r = 0.481). CONCLUSIONS: The ACE/DD genotype is associated with the extent of exercise-induced LVH in endurance athletes, regardless of other known biologic factors.     

No correlation of polymorphism of angiotensin-converting enzyme genes with left ventricular hypertrophy in essential hypertension.

To investigate the correlation of polymorphism of angiotensin-converting enzyme (ACE) genes with left ventricular hypertrophy in essential hypertension, 151 patients with essential hypertension were studied. ACE genotypes were determined by PCR technology and diastolic left ventricular diameter (DLVd), systolic left ventricular diameter (SLVd), interseptal ventricular thickness (IVS), and left ventricular posterior wall thickness (LVPW) were scanned by echocardiography. Left ventricular mass (LVM) and the left ventricular mass index (LVMI) were calculated from echocardiographic findings. Results revealed that DLVd, SLVd, IVS, LVPW, LVM, and LVMI of the DD genotype group were 49.9 +/- 5.6 mm, 30.5 +/- 6.5 mm, 11.2 +/- 1.6 mm, 11.7 +/- 1.5 mm, 259.5 +/- 62.1 g, 92.7 +/- 23.5 g/m2, respectively. DLVd, SLVd, IVS, LVPW, LVM, and LVMI of the ID genotype group were 8.9 +/- 5.3 mm, 31.5 +/- 5.2 mm, 11.4 +/- 1.7 mm, 11.9 +/- 1.6 mm, 261.3 +/- 70.3 g, and 94.9 +/- 25.8 g/m2, respectively, and DLVd, SLVd, IVS, LVPW, LVM, and LVMI of the II genotype group are 48.9 +/- 5.5 mm, 31.8 +/- 6.5 mm, 11.1 +/- 1.9 mm, 11.5 +/- 1.8 mm, 250.8 +/- 82.5 g and 90.8 +/- 30.1 g/m2 respectively. There was no significant difference between the ID, DD and II genotype groups as regards DLVd, SLVd, IVS, LVPW, LVM, and LVMI (p > 0.05). These findings indicate that there is no association between the ACE gene and left ventricular hypertrophy in essential hypertension occurring in the Chinese population.     

Association of the angiotensin-converting enzyme gene polymorphism with chronic heart failure in Chinese Han patients

BACKGROUND: An insertion/deletion (I/D) polymorphism is present in the 16th intron of the angiotensin-converting enzyme (ACE) gene and is associated with serum and tissue ACE level. Some studies have shown that the DD genotype is associated with some cardiovascular diseases; while ACE polymorphism's effect on chronic heart failure (CHF) remains uncertain. AIM: To investigate the association of the ACE gene I/D polymorphism with CHF in the Chinese Han population. METHODS: The genotype was determined by polymerase chain reaction in 102 normal controls and in 79 patients with CHF. Plasma angiotensin (Ang) levels were assessed by radio-immunity assay. Left ventricular end-diastolic diameters (LVDD) and left ventricular ejection fractions were assessed by echocardiography. RESULTS: The ACE gene polymorphism distribution was similar in patients and control subjects. However, ACE gene DD polymorphism was associated with a more severe condition, greater LVDD [mm: DD: 71+/-7, ID: 62+/-5, II: 60+/-5, P<0.001 DD vs. ID, P<0.001 DD vs. II] and higher plasma Ang II level [pg/ml DD: 92+/-19, ID: 79+/-21, II: 65+/-17 P<0.05 DD vs. ID, P<0.001 DD vs. II]. CONCLUSION: In Chinese Han patients with CHF, ACE gene DD polymorphism might be a marker of a more severe condition, and a higher level of activation of the renin-angiotensin system.     

Left ventricular remodeling impairs coronary flow reserve in hypertensive patients

BACKGROUND : In arterial hypertension, changes in both left ventricular mass and geometry may occur. Concentric left ventricular remodeling (i.e. an increased wall thickness relative to end diastolic diameter) has been implicated as an independent cardiovascular risk factor in hypertensive patients. The influence of concentric remodeling on the coronary microcirculation is not known. OBJECTIVE : To investigate the impact of left ventricular geometry on coronary flow reserve in patients with arterial hypertension and angiographically normal coronary arteries. METHODS : Following exclusion of coronary artery disease by cardiac catheterization, coronary flow reserve (dipyridamole, 0.5 mg/kg body weight intravenously; argon gas-chromatographic method) was measured in 49 patients with arterial hypertension and in six age-matched controls. Hypertensive patients were grouped by echocardiographic findings according to left ventricular mass and relative left ventricular wall thickness (i.e. left ventricular posterior wall plus septal thickness divided by end diastolic diameter): seven patients had normal left ventricular mass and geometry, 19 had eccentric hypertrophy (i.e. normal relative wall thickness but increased mass), concentric remodeling (i.e. normal mass but increased relative wall thickness) was present in nine patients, and 14 patients had concentric hypertrophy. RESULTS : There was a marked reduction in coronary flow reserve in all hypertensive groups as compared with control values (4.2 +/- 0.5). Within the hypertensive subgroups, the coronary flow reserve was differentially reduced in the following rank order: concentric remodeling (2.0 +/- 0.7) approximately concentric hypertrophy (2.3 +/- 0.8) < eccentric hypertrophy (2.9 +/- 0.6) mu normal geometry (2.7 +/- 0.4). Multi-factorial regression analysis showed that the relative wall thickness but not left ventricular mass was independently linked to the coronary flow reserve. CONCLUSIONS : Concentric left ventricular remodeling is an independent predictor of the coronary flow reserve in hypertensive patients with chest pain and normal coronary angiogram. The impairment of the coronary microcirculation may contribute to the excess cardiovascular event rate associated with hypertensive concentric left ventricular remodeling.     

Deletion Polymorphism of Angiotensin-Converting Enzyme Gene and Left Ventricular Hypertrophy in Southern Italian Patients

Objectives. This study sought to evaluate the possible association of polymorphism of the angiotensin-converting enzyme (ACE) gene with blood pressure and left ventricular mass index (LVMI).Background. The renin–angiotensin system seems to be involved in the pathogenesis of essential hypertension. Moreover, recent epidemiologic observations demonstrate that many subjects with left ventricular hypertrophy have normal blood pressure levels, suggesting that factors other than hemodynamic overload may contribute to the hypertrophy.Methods. The study included 140 untreated hypertensive outpatients who underwent ambulatory blood pressure monitoring, echocardiographic evaluation and analysis for insertion (I)/deletion (D) polymorphism in intron 16 of the ACE gene by polymerase chain reaction. Blood pressure was measured at 24 h, and LVMI was calculated by the Devereux formula, in each patient.Results. Left ventricular mass index values (mean ± SD) were 137 ± 28 g/m²in patients with the DD genotype, 125 ± 27 g/m²in those with the ID genotype and 115 ± 27 g/m²in those with II genotype. The frequencies of the DD, ID and II genotypes were 45.71% (n = 64), 46.42% (n = 65) and 7.85% (n = 11), respectively, and were in Hardy-Weinberg equilibrium. The strongest association between left ventricular mass and DD genotype in our cohort appeared to be an independent cardiovascular risk factor (DD vs. ID: odds ratio [OR] 2.497, 95% confidence interval [CI] interval 1.158 to 5.412, p < 0.05; DD vs. II: OR 6.577, 95% CI 1.169 to 28.580, p < 0.02).Conclusions. Our data show that the LVMI was significantly enhanced in patients with the DD genotype.(J Am Coll Cardiol 1997;29:365–9)     

N-terminal atrial natriuretic peptide and left ventricular geometry and function in a population sample of elderly males

OBJECTIVES: To investigate the relationships between N-terminal atrial natriuretic peptide (N-ANP) and left ventricular geometry and function. DESIGN: A cross-sectional study of a population-based cohort. SETTING: Follow-up of a health survey in Uppsala county, Sweden. SUBJECTS: Two hundred and five men aged 70. MAIN OUTCOME MEASURES: A Delfia sandwich immunoassay was used to measure the plasma levels of N-ANP. M-mode and Doppler echocardiographic examinations were used to measure left ventricular dimensions, mass, geometry and systolic function and to classify the subjects into four groups (normal geometry, concentric remodelling, concentric hypertrophy or eccentric hypertrophy). Left ventricular systolic dysfunction was defined as a left ventricular ejection fraction 相似文献   

Usefulness of the I/D angiotensin-converting enzyme genotype for detecting the risk of left ventricular hypertrophy in pharmacologically treated hypertensive men

The insertion/deletion polymorphism (I/D) of the angiotensin-converting enzyme (ACE) gene has been associated in some studies with a higher prevalence of left ventricular hypertrophy (LVH), but few of them were performed on pharmacologically treated hypertensive patients. The present study was undertaken to determine whether ACE genotype determination could help in the identification of pharmacologically treated hypertensive patients at a higher risk of LVH. Ninety-six consecutive men with essential hypertension were selected for the study. Left ventricular mass (LVM) was assessed by echocardiography and indexed by body surface area and 82 patients were considered suitable for the study. Three groups of patients were defined on the basis of their I/D ACE genotype: DD (n = 39), ID (n = 33) and II (n = 10). There were no statistically significant differences between the three groups regarding to the severity of hypertension at diagnosis, degree of control of blood pressure or type of antihypertensive drug therapy used. No statistically significant differences were found between the three groups regarding to LVM index (total 124 +/- 31, DD 121 +/- 29, ID 127 +/- 35 and II 122 +/- 18 g/m2), relative wall thickness (total 0.5 +/- 0. 2, DD 0.5 +/- 0.3, ID 0.48 +/- 0.07 and II 0.47 +/- 0.04) or prevalence of LVH (total 34%, DD 31%, ID 39% and II 30% by Cornell criteria and total 39%, DD 33%, ID 45% and II 40% by Framingham criteria). Furthermore, the I and D allele frequency distribution was similar in the whole group of patients, in patients with LVH, and in a control group of healthy volunteers. Our data do not support that the I/D ACE genotype determination helps in identifying treated hypertensive patients at higher risk of LVH. Journal of Human Hypertension (2000) 14, 327-331     

Angiotensin-converting enzyme gene polymorphism influences degree of left ventricular hypertrophy and its regression in patients undergoing operation for aortic stenosis.

Insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been associated with increased left ventricular hypertrophy (LVH) in patients with cardiomyopathy and congestive heart failure. Patients with aortic stenosis (AS) have varying degrees of LVH at a given valve area. The aim of this study was to examine the relation between ACE gene polymorphism and the degree of LVH in patients undergoing operation for AS. Eighty-two patients who underwent operation for AS with a stentless valve were followed prospectively with echocardiographic assessments of left ventricular mass index (LVMI). ACE gene polymorphism was determined by polymerase chain reaction. The genotype (DD, ID, and II) frequency was the same as in healthy controls. The pressure difference across the aortic valve did not differ between genotypes. Patients with the DD genotype of the ACE gene had a higher LVMI (197 +/- 47 g/m2) preoperatively than those with ID (175 +/- 41 g/m2) or II (155 +/- 43 g/m2) genotypes (p = 0.01). LVMI decreased significantly in DD (p <0.001) and ID (p <0.001) genotypes but not in the II genotype during follow-up (mean 15 months). There was a significant difference in regression of LVMI over time between genotypes (p = 0.0056), with no significant difference between genotypes at follow-up. The DD genotype of the ACE gene is associated with increased preoperative LVH in patients treated surgically for AS. The DD genotype appears to be an important factor which increases hypertrophic myocardial reactivity to pressure overload.     

Soluble cell adhesion molecules in hypertensive concentric left ventricular hypertrophy

OBJECTIVE : Concentric left ventricular (LV) hypertrophy is an important cardiovascular risk factor. We investigated whether concentric LV hypertrophy is associated with activation of the vascular endothelium, as assessed by measurements of soluble cell adhesion molecules. DESIGN : E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1) were measured in serum from hypertensive patients with LV hypertrophy (64 with concentric and 47 with eccentric hypertrophy) and from two matched control groups consisting of 38 hypertensive patients without LV hypertrophy and 38 normotensive subjects. Carotid artery intima-media thickness (IMT) was examined by ultrasonography and LV mass by echocardiography. Neurohormone activities of the renin-angiotensin-aldosterone system were also measured. RESULTS : E-selectin levels were higher in hypertensive than in normotensive subjects (56 +/- 19 versus 49 +/- 11 ng/ml, P = 0.031). Patients with concentric LV hypertrophy had higher levels of E-selectin (61 +/- 21 versus 49 +/- 15 ng/ml, P < 0.001), ICAM-1 (273 +/- 49 versus 254 +/- 49 ng/ml, P = 0.043), VCAM-1 (591 +/- 131 versus 544 +/- 78 ng/ml, P = 0.038) and greater carotid artery IMT (0.99 +/- 0.26 versus 0.83 +/- 0.15 mm, P = 0.018) than eccentric LV hypertrophy patients. E-selectin and VCAM-1 correlated positively to LV relative wall thickness (P = 0.040 and 0.037, respectively), with a similar trend for ICAM-1 (P = 0.083). E-selectin correlated with serum aldosterone (P < 0.001), and E-selectin and ICAM-1 with plasma angiotensin converting enzyme activity (P = 0.003 and 0.036, respectively). CONCLUSION : Increased levels of soluble cell adhesion molecules and an increased carotid artery IMT characterize concentric LV hypertrophy. This indicates perturbations at the vascular level, involving activation of the vascular endothelium in hypertensive patients with concentric LV hypertrophy.     

Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension.

The spectrum of left ventricular geometric adaptation to hypertension was investigated in 165 patients with untreated essential hypertension and 125 age- and gender-matched normal adults studied by two-dimensional and M-mode echocardiography. Among hypertensive patients, left ventricular mass index and relative wall thickness were normal in 52%, whereas 13% had increased relative wall thickness with normal ventricular mass ("concentric remodeling"), 27% had increased mass with normal relative wall thickness (eccentric hypertrophy) and only 8% had "typical" hypertensive concentric hypertrophy (increase in both variables). Systemic hemodynamics paralleled ventricular geometry, with the highest peripheral resistance in the groups with concentric remodeling and hypertrophy, whereas cardiac index was super-normal in those with eccentric hypertrophy and low normal in patients with concentric remodeling. The left ventricular short-axis/long-axis ratio was positively related to stroke volume (r = 0.45, p less than 0.001), with cavity shape most elliptic in patients with concentric remodeling and most spheric in those with eccentric hypertrophy. Normality of left ventricular mass in concentric remodeling appeared to reflect offsetting by volume "underload" of the effects of pressure overload, whereas eccentric hypertrophy was associated with concomitant pressure and volume overload. Thus, arterial hypertension is associated with a spectrum of cardiac geometric adaptation matched to systemic hemodynamics and ventricular load. Concentric left ventricular remodeling and eccentric hypertrophy are more common than the typical pattern of concentric hypertrophy in untreated hypertensive patients.     

Echocardiographic assessment of the different left ventricular geometric patterns in middle-aged men and women in Tallinn

The aim of this study was to determine the association of left ventricular (LV) geometry with sex, age, arterial hypertension and obesity in Tallinn. In a framework of a population study for cardiovascular risk factors, echocardiography was carried out in 325 men and 398 women (69.3% of all 1043 participants aged 35-59) in 1999-2001. Left ventricular hypertrophy was defined if left ventricular mass (LVM), LVM/height and LVM/body surface area were 294 g, 163 g/m and 150 g/m2 in men, and 198 g, 121 g/m and 120 g/m2 in women, respectively. LV geometry was analysed according to four types generally recognized (with regard to relative wall thickness > 0.45). The prevalence of concentric hypertrophy was similar in men and women: 7.7% and 9.1%. The prevalence of eccentric hypertrophy was significantly higher in women than in men (33.3% vs 4.9%). Concentric remodelling was also found in women more often than in men (9.5 vs 5.5%; p < 0.05). Regardless of sex and age, concentric hypertrophy was never found in participants with blood pressure < 140/90. In hypertensives, there was a tendency for age-related increase of concentric hypertrophy prevalence: the latter was higher in women than in men: 39.1% vs 25.5%; p < 0.05. In examinees with BMI < 30, this type of LV geometry was seldom found: in 3.1% of men and 5.0% of women; p < 0.05. In obese persons, it increased with age, reaching 26.5% in men and 21.2% in women (p < 0.05). The prevalence of eccentric hypertrophy in men increased with age, and with hypertension and obesity. The prevalence of concentric remodelling in men was not related to BMI; it was significantly more often found in older age groups and in hypertensives. In women, the prevalence of eccentric hypertrophy and concentric remodelling was not related to age, hypertension or obesity.     

Left ventricular adaptation to hypertension and plasma renin activity

Chronic pressure and volume overload result in morphologically and functionally distinct forms of myocardial hypertrophy. In essential hypertension, the respective effect of these factors on the morphology of the left ventricle remains unknown. In the present study, we hypothesised that activity of the renin angiotensin system (assessed by plasma renin activity) may be associated to the variability of the left ventricular adaptation to essential hypertension. To assess this relation, we categorised by echocardiography 333 never-treated hypertensive patients, according to values of left ventricular mass and relative wall thickness. Higher systolic and pulse arterial pressure was strongly associated with concentric left ventricular hypertrophy (27% of hypertensives). When compared to the normal left ventricle group, patients with eccentric left ventricular hypertrophy (15% of hypertensives) had a high cardiac index (5 +/- 1 vs 4 +/- 0.8 L/min/m2; P = 0.0001), a lower basal plasma renin activity (0.81 +/- 0.63 vs 1.45 +/- 1.3 ng/ml/h; P = 0.02) and similar mean values of left ventricular performance and glomerular filtration rate. A tendency for depressed myocardial contractility assessed by the midwall shortening/end-systolic stress was associated with concentric left ventricular remodelling and hypertrophy when compared to hypertensive with a normal left ventricle. In conclusion, at the early phase of essential hypertension, in patients without renal dysfunction, each anatomic pattern of cardiac adaptation to hypertension was associated with a distinct profile of haemodynamics, myocardial function and activity of the renin-angiotensin system. Journal of Human Hypertension (2000) 14, 181-188.     

血管紧张素转换酶基因型与高血压左室肥厚的相关性研究

目的研究血管紧张素转换酶（ＡＣＥ）基因型与高血压患者左室肥厚的关系。方法用ＰＣＲ方法分别检测１５１例原发高血压患者ＡＣＥ基因型,并做超声心动图检查,测量左室舒张末径（ＤＬＶｄ）、左室收缩末径（ＳＬＶｄ）、心脏室间隔厚度（ＩＶＳ）及左室后壁厚度（ＬＶＰＷ）,计算左室重量（ＬＶＭ）。结果各基因型组中ＤＤ型的ＤＬＶｄ、ＳＬＶｄ、ＩＶＳ、ＬＶＰＷ、ＬＶＭ分别为４９．９±５．６ｍｍ、３０．５±６．５ｍｍ、１１．２±１．６ｍｍ、１１．７±１．５ｍｍ、２５９．５±６２．１ｇ,ＩＤ型组的ＤＬＶｄ、ＳＬＶｄ、ＩＶＳ、ＬＶＰＷ、ＬＶＭ分别为４８．９±５．３ｍｍ、３１．５±５．２ｍｍ、１１．４±１．７ｍｍ、１１．９±１．６ｍｍ、２６１．３±７０．３ｇ,Ｉ型组的ＤＬＶｄ、ＳＬＶｄ、ＩＶＳ、ＬＶＰＷ、ＬＶＭ分别为４８．９±５．５ｍｍ、３１．８±６．５ｍｍ、１１．１±１．９ｍｍ、１１．５±１．８ｍｍ、２５０．８±８２．５ｇ,各基因型组间ＤＬＶｄ、ＳＬＶｄ、ＩＶＳ、ＬＶＰＷ、ＬＶＭ并无显著性差异（Ｐ＞０．０５）。结论国人ＡＣＥ基因型与高血压左室肥厚无关。     

Effects of angiotensin-converting enzyme polymorphism on aortic elastic parameters in athletes

BACKGROUND: Physiologic adaptations in an athlete's heart include increased left and right ventricular chamber size, left ventricular wall thickness and mass. Angiotensin-converting enzyme (ACE) is a key enzyme in angiotensin II production causing cardiac hypertrophy. The cloning of the ACE gene has made it possible to identify a deletion (D)-insertion (I) polymorphism that appears to affect the level of serum ACE activity. Therefore, the ACE genes, which have been shown to be polymorphic, could be candidate genes for large-artery stiffness. METHODS: 56 endurance athletes and 46 sedentary subjects were included in this study, and they underwent both complete echocardiographic examination, and analysis of ACE insertion (I) and deletion (D) allele frequencies in peripheral blood. The aortic diameter was recorded by M-mode echocardiography at a level 3 cm above the aortic valve. Aortic systolic diameter was measured at the time of full opening of the aortic valve, and diastolic diameter was measured at the peak of QRS. Aortic strain, stiffness index and distensibility were calculated. RESULTS: Left ventricular mass index and left ventricular ejection fraction were significantly higher in athletes than controls (p < 0.001). The aortic distensibility index and strain were significantly greater in athletes compared with controls (respectively: 5.8 +/- 2.7 vs. 4.7 +/- 1.8 cm(-2) dyn(-1) 10(-6), p = 0.017; 12.3 +/- 2.4 vs. 9.3 +/- 3.1, p < 0.001). The aortic stiffness index was significantly lower in athletes than in controls (4.8 +/- 1.9 vs. 6.1 +/- 2.1, p < 0.001). The aortic distensibility index and strain were statistically different in ACE DD vs. DI groups and DD vs. II groups of athletes. The aortic stiffness index was statistically different in ACE DD vs. II groups of athletes. Aortic parameters were similar according to ACE genotypes in controls. CONCLUSION: The results of this study indicate that aortic distensibility was increased by prolonged training in endurance athletes, particularly in those with the ACE II genotype. This effect represents an extracardiac adaptation to chronic prolonged training in athletes.     

The Relationship Between High‐Sensitivity C‐Reactive Protein Levels and Left Ventricular Hypertrophy in Patients With Newly Diagnosed Hypertension

The authors aimed to evaluate the relationship between high‐sensitivity C‐reactive protein (hs‐CRP) and presence of left ventricular hypertrophy and diastolic dysfunction in patients with hypertension. A total of 95 newly diagnosed hypertensive patients (mean age, 54±10 years) and 20 controls were included in this study. Patients were divided into four groups according to relative wall thickness as normal, concentric remodeling, concentric, and eccentric hypertrophy. hs‐CRP was measured in all patients and serum hs‐CRP level was shown to be increased in patients with hypertension compared with controls (0.57 mg/dL vs 0.25 mg/dL, respectively; P<.001). The hs‐CRP level was highest in patients with concentric hypertrophy. When compared with controls, serum hs‐CRP level was significantly higher in patients with concentric remodeling (0.61±0.3 mg/dL vs 0.43±0.5 mg/dL, P<.030) and concentric hypertrophy (0.69±0.3 mg/dL vs 0.43±0.5 mg/dL, P<.032). The present study shows that serum hs‐CRP is significantly associated with left ventricular diastolic function and concentric hypertrophy in patients with hypertension.     

Usefulness of stress echocardiography for risk stratification and prognosis of patients with left ventricular hypertrophy

The purpose of this study was to evaluate the role of stress echocardiography in the risk stratification and prognosis of patients with left ventricular (LV) hypertrophy. One thousand two patients (mean age 62 +/- 13 years, 35% men) with LV hypertrophy (defined by LV mass index >115 g/m(2) for men and >95 g/m(2) for women) were evaluated. LV mass was calculated using the linear dimension method, as recommended by the American Society of Echocardiography. The calculation of relative wall thickness was performed using the formula (2 x posterior wall thickness)/LV internal diameter. Concentric and eccentric LV hypertrophy were defined as relative wall thicknesses > or =0.42 and <0.42 cm, respectively. Follow-up (2.6 +/- 1.1 years) for confirmed myocardial infarction and cardiac death (n = 71) was obtained. Four hundred seventy-three patients (47%) had concentric hypertrophy, and 529 patients (53%) had eccentric hypertrophy. In patients with either concentric or eccentric LV hypertrophy, stress echocardiography was able to effectively risk-stratify normal versus abnormal subgroups (event rate 1.1% vs 4.9% per year, p <0.0001), whereas stress electrocardiography was unable to do so. In the cohort with normal stress echocardiographic results, patients with concentric LV hypertrophy had an event rate 5 times higher than those with eccentric LV hypertrophy (event rate 1.7% vs 0.3% per year, p = 0.007). In conclusion, stress echocardiography effectively risk-stratifies patients with LV hypertrophy compared with stress electrocardiography. Normal stress echocardiographic results in patients with concentric LV hypertrophy indicate a worse prognosis than in patients with eccentric LV hypertrophy, probably reflecting decreased sensitivity in this cohort. However, abnormal stress echocardiographic results portend a worse prognosis in patients with either concentric or eccentric LV hypertrophy.