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.     

Association of angiotensin converting enzyme gene polymorphisms with left ventricular hypertrophy.

The angiotensin converting enzyme gene (ACE) is of much interest as a candidate gene conferring an individual's genetic susceptibility to left ventricular hypertrophy (LVH). LVH has long been thought to be an end point of essential hypertension (EH), rather than a separate entity, though it is influenced by a unique set of hormonal, vascular and genetic factors. In this study, we attempted to determine whether two representative polymorphisms of the ACE gene, ACE I/D and 2350 G>A, known to be associated with EH and to have a highly significant influence on plasma ACE levels, could implicate ACE as a quantitative trait locus (QTL) for LVH. We carried out a retrospective, case-control study of the two ACE polymorphisms amongst 180 nationals (50 LVH patients and 130 controls) from the United Arab Emirates (Emirati)--an ethnic group characterized by an absence of alcohol intake and cigarette smoking--for putative correlations with LVH. Clinical diagnoses of LVH were based on echocardiographic and ECG criteria. ACE I/D and 2350 G>A genotypes were determined by polymerase chain reaction (PCR) and restriction digestion. Univariate and multivariate logistic regression analyses revealed an association between ACE polymorphisms and LVH. Haplotype analysis further supported this finding. The ACE I/D and ACE 2350 G>A polymorphisms were in strong linkage disequilibrium and were independently associated with LVH, suggesting that ACE is likely to be a QTL for LVH. In conclusion, This is the first association study of the ACE 2350 G>A polymorphism with LVH; the results showed that this polymorphism, along with ACE I/D, is associated with LVH.     

Polymorphic markers I/D and G7831A of angiotensin-I-converting enzyme gene and left ventricular hypertrophy in patients with essential hypertension

AIM: To elucidate possible association of angiotensin-I-converting enzyme (ACE) gene polymorphic markers I/D and G7831A with left ventricular hypertrophy (LVH) in patients with essential hypertension. MATERIAL: Patients with essential hypertension (n=123, 37 with and 86 without LVH, mean age 59.15+/-1.19 years). METHODS: Left ventricular (LV) mass was determined echocardiographically by Devereux method. Alleles and genotypes of ACE gene polymorphic markers were identified by polymerase chain reaction. RESULTS AND CONCLUSION: There was no association between I/D marker of ACE gene and LVH. Carriers of A allele compared with carriers of G allele of G7831A marker had significantly higher LV mass (284.1+/-10.20 g, and 248.5+/-14.42 g, respectively, p=0.033) and LV mass index (151.7+/-5.23 g/m2 and 131.0+/-6.74 g/m2, respectively; p=0.02). Among patients with LVH frequency of A allele was significantly higher than among patients without LVH (0.401 and 0.230, respectively; p=0.0065, OR=2.116 [1.197-3.7481]). Using binary logistic regression model we have found that presence of LVH was linked with age, sex and maximal systolic blood pressure (BP). Such factors as smoking, maximal diastolic BP, ordinary systolic and diastolic BP, duration of hypertension, coronary artery disease and diabetes were not related to LV mass index. Using multifactorial logistic regression model we have found that the presence of A allele of G7831A polymorphic marker of ACE gene, age and maximal systolic BP could be considered as independent risk factors of LVH.     

Remodeling of myocardial interstitium in left ventricular hypertrophy and myocardial infarction

Structural and biochemical modifications of the myocardium (remodeling) occur during the development of left ventricular hypertrophy and acute myocardial infarction. An important part of this process of myocardial remodeling occurs in the interstitial compartment. The myocardial interstitium is composed mainly of fibrillar collagen. These changes are associated to modifications in ventricular function that could be deleterious and have clinical manifestations. Some salutory effects of the treatment of both conditions are related to modifications of the process of myocardial interstitial remodeling.     

Angiotensin-converting enzyme gene I/D polymorphism in malignant hypertension

BACKGROUND: The mechanism of the rapid transition of a stable benign hypertensive disease to a severe and devastating malignant hypertension is not fully understood. However, the renin angiotensin system, which is highly activated in malignant hypertension, is established as an important pathogenetic factor in different cardiovascular and renal diseases. Over the last decade, a polymorphism in genes regulating this system has been found. This includes the 287 bp sequence deletion (D)/insertion (I) polymorphism in the angiotensin-converting enzyme (ACE) gene and the methionine (M) to threonine (T) point mutation polymorphism in the angiotensinogen (AGT) gene. These gene polymorphisms have been associated with various cardiovascular and renal diseases and the aim of this study was to investigate whether they were linked to malignant hypertension. METHODS: Forty-two patients with malignant hypertension (mean age 55 years), 42 patients with non-malignant hypertension (mean age 57 years) and 85 normotensive control subjects (mean age 42 years) were investigated with respect to ACE I/D and AGT M/T genotypes. DNA was prepared by standard methods from isolated white blood cells and analysed by the PCR technique. The PCR reaction used in the detection of the ACE I/D polymorphism was optimized for an equal amplification of the I and D alleles. RESULTS: The frequency of the DD genotype was significantly increased in patients with malignant hypertension (43%) compared with patients with non-malignant hypertension (14%) and normotensive control subjects (18%) (p <0.01) for both. The frequency distribution of AGT M/T genotype did not differ between patients with malignant and non-malignant hypertension. CONCLUSION: The DD genotype of the ACE gene occurred more than twice as often in malignant hypertension than in non-malignant hypertension and indicates that ACE gene polymorphism is a significant risk factor for initiation of malignant hypertension.     

Angiotensin-converting enzyme polymorphisms and their potential impact on left ventricular myocardial geometry after aortic valve surgery

BACKGROUND AND AIM OF THE STUDY: Genetic variants of the angiotensin-converting enzyme (ACE) cascade may influence left ventricular myocardial mass (LVMM) regression after aortic valve surgery. Postoperative long-term changes in LV indices were investigated in patients with asymptomatic aortic regurgitation (AR) and symptomatic aortic stenosis (AS) and related to alleles of ACE polymorphisms. METHODS: A total of 96 patients was included in the study, 21 with class IIa AR (22%) and 75 with class I AS (78%) recommendations for surgery. Patients were evaluated for demographic risk factors and underwent a thorough clinical examination including 3-D cardiac imaging by ultrafast-computed tomography. Genomic DNA was isolated for genotyping. RESULTS: AR patients were younger (55.8 +/- 8.9 versus 64 +/- 9.1 years, p = 0.0014), had a larger body surface area (1.92 +/- 0.21 versus 1.82 +/- 0.19 m2, p = 0.039), and were more likely to be asymptomatic (myocardial infarction, p = 0.04; syncope, p = 0.0099; thromboembolism, p = 0.03; NYHA class IV, p = 0.04). Postoperatively, the reduction in absolute LVMM (from 297.1 +/- 52.6 to 190.1 +/- 57.1 g versus 214.4 +/- 55.7 to 143.8 +/- 40.0 g; pT = 0.0000001) and indexed LVMM (from 156.0 +/- 31.7 to 99.3 +/- 28.4 g/m2 versus 118.7 +/- 28.3 to 79.3 +/- 20.6 g/m; pT = 0.0000001) over time was more significant in AR patients, but never reached normal values. Enforced ACE inhibitor medication resulted in significantly higher postoperative indexed LVMM differences in homozygote DD patients compared to AR patients with II/ID alleles of ACE 16 ins/del polymorphism. CONCLUSION: AR patients showed a statistically significant decrease in absolute/indexed LVMM during follow up, but never achieved LV mass recovery compared to standard values or to values in patients undergoing aortic valve replacement for AS. The benefits of ACE inhibitors were observed among AR patients with homozygote DD alleles of ACE 16 ins/del polymorphism.     

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 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.     

Angiotensin-converting enzyme gene 2350 G/A polymorphism is associated with left ventricular hypertrophy but not essential hypertension.

The angiotensin-converting enzyme (ACE) gene (ACE) is one of the most studied candidate genes related to essential hypertension (EH) and left ventricular hypertrophy (LVH). ACE rs4343 synonymous coding polymorphism (2350 G/A) is known among the polymorphisms of this gene to have the most significant effect on plasma ACE concentrations. The aim of the present study was to investigate the association of this polymorphism with EH and LVH in 440 subjects (246 EH patients and 194 controls) from a Chinese Han population. In this study, 2350 G/A genotypes were identified by polymerase chain reaction and restriction digestion in all study participants, and left ventricular mass was assessed by 2-mode echocardiography in 178 untreated EH patients. There was no significant difference in either genotype distribution (p=0.3659) or allele frequency (p=0.1453) between EH and control groups. In addition, the 2350 G/A polymorphism had no effect on blood pressure in either controls or untreated EH patients. The distribution of genotypes differed significantly when patients with LVH were examined, i.e., 14.71% GG, 54.41% GA, and 30.88% AA patients had this complication, and 36.36% GG, 42.73% GA, and 20.91% AA patients did not (p=0.0070). The LVH patients had a higher A allele frequency (58.09%) than patients without LVH (42.27%) (p=0.0037). Logistic regression analysis revealed that the association between the A allele and LVH was independent of age, blood pressure, and body mass index. The relative risk of LVH in patients bearing the A allele (GA+AA group) compared with that of GG hypertensive patients was 3.31 (95% confidence interval [CI]: 1.43 to 7.68). These findings suggest an association between LVH and the 2350A allele in hypertensive patients.     

Angiotensin-converting enzyme gene polymorphism interacts with left ventricular ejection fraction and brain natriuretic peptide levels to predict mortality after myocardial infarction

OBJECTIVES: The goal of this study was the exploration of the associations between the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and post-myocardial infarction (MI) outcomes, especially any interaction with the accepted clinical prognostic markers brain natriuretic peptide (BNP) and left ventricular ejection fraction (LVEF). BACKGROUND: The ACE gene I/D polymorphism has been implicated in the development of MI, hypertension, and left ventricular hypertrophy. We examined the association of ACE I/D and prognosis after acute MI. METHODS: Patients incurring acute MI were genotyped for the ACE I/D polymorphism. Clinical data included assays of neurohormones, radionuclide ventriculography, and mortality over a mean 2.6 years of follow-up. RESULTS: Patients (n = 978) had a mean age of 62.1 years, and 78% were male. Overall genotype frequencies were II 23.2%, ID 49.5%, and DD 27.3%. Chi-square analysis revealed an association between the ACE D allele and death after MI (88 of 103 who died were DD or ID; p < 0.05), with an odds ratio for mortality of 8.03 (95% confidence interval, 2.16 to 29.88). Patients with the DD genotype had higher (p < 0.05) plasma BNP, N-terminal BNP (N-BNP), and endothelin-1 levels within 96 h after MI than grouped ID/II patients. Multivariate analysis indicated ACE genotype, age, and previous MI were independent predictors of death (p < 0.05). Patients with an ACE D allele in combination with either a lower than median LVEF or greater than median BNP had a higher mortality (p < 0.001 and p < 0.025, respectively) than the risk associated with the D allele itself. CONCLUSIONS: Angiotensin-converting enzyme genotyping may provide additional prognostic information in patients after MI in combination with the proven utility of LVEF, plasma BNP, and N-BNP measurements.     

QT dispersion and left ventricular hypertrophy in athletes: relationship with angiotensin-converting enzyme I/D polymorphism

BACKGROUND: QT dispersion (QTd) is a measure of inhomogeneous repolarization of myocardium and is used as an indicator of arrhythmogenicity. QTd is increased in myocardial hypertrophy secondary to systemic hypertension. The relation between left ventricular (LV) enlargement in endurance trained subjects and QTd is unknown. The cloning of the angiotensin-converting enzyme (ACE) gene has made it possible to identify a deletion (D)-insertion (I) polymorphism that appears to affect the level of serum ACE activity. The aim of this study was to assess whether physiologic left ventricular hypertrophy as a result of physical training is associated with an increased QT length or dispersion depending on ACE I/D polymorphism. METHODS: 56 endurance athletes and 46 sedentary subjects were included in this study, and they underwent both complete echocardiographic and electrocardiographic examination, the QT interval was measured manually as an average based on a 12-lead ECG. We also analysed ACE I and D allele frequencies in all patients. RESULTS: Athletes had a significantly increased LV mass (235.1 +/- 68.5 g vs. 144.9 +/- 44.5 g, p < 0.001) and corrected QTd (QTcd) (55.5 +/- 18.1 ms vs. 42.9 +/- 17.2 ms, p < 0.001) in comparison to control subjects. There was a positive correlation between left ventricular mass index and QTcd in athletes (r = 0.3, p = 0.024). Left ventricular mass and mass index in ACE DD, DI and II genotypes were significantly different (p < 0.001). QTcd was significantly different between ACE DD (63.2 +/- 12.8 ms) and ACE II (44.9 +/- 17.6 ms) genotypes in athletes (p < 0.05). CONCLUSION: These data show that myocardial hypertrophy induced by exercise training might be associated with increased QTd as observed in systemic hypertension and might be affected by ACE I/D polymorphism.     

Insertion/deletion polymorphism of angiotensin I converting enzyme gene and left ventricular hypertrophy in patients with type 2 diabetes mellitus

INTRODUCTION: Left ventricular hypertrophy (LVH) is a well known risk factor of death from cardiovascular causes. Patients with type 2 diabetes mellitus are at particularly high risk of developing cardiovascular disease, which accounts for 80% of deaths in this group. Type 2 diabetes mellitus is probably related to increased left ventricular mass (LVM). Existing data show that the renin-angiotensin-aldosterone (RAA) system may play a role in the development of LVH. Since the I/D polymorphism of angiotensin-converting enzyme (ACE) gene influences the activity of RAA, it is likely that it could also have an impact on LVH. AIM: To assess the relationship between I/D polymorphism of the ACE gene and the severity of LVH assessed by echocardiography (Echo) in patients with type 2 diabetes mellitus. METHODS: The study group consisted of 103 patients (37 women and 66 men; mean age 60.1+/-9.1 years) suffering from type 2 diabetes mellitus with a mean duration of 9.0+/-6.5 years. BMI, waist-to-hip ratio (WHR), arterial blood pressure, LVM and LVM index (LVM indexed for body surface area [g/m(2)] or height raised to the power 2.7 [g/m(2.7)]) were evaluated. I/D polymorphism of the ACE gene was determined using polymerase chain reaction (PCR). RESULTS: Distribution of I/D polymorphism of the ACE gene in the study group was as follows: genotype II--32.0%, ID--42.7%, DD--25.2% of patients. LVH was diagnosed in 43-71% of patients (depending on criteria used). Distribution of individual genotypes was similar in patients with and without LVH. Genotypes II, ID and DD were observed in 37.3%, 31.4% and 31.4% of patients without LVH (according to the Levy criteria) and in 26.9%, 53.9%, 19.2% in the LVH group, respectively. In persons with DD genotype, when compared to group II, significantly higher values of systolic and diastolic blood pressure were noted (147.7+/-20.2 vs 138.2+/-16.7 mmHg, p=0.03 and 89.4+/-9.7 vs 81.9+/-8.7 mmHg, p=0.004, respectively). CONCLUSIONS: In patients with type 2 diabetes mellitus there is no relationship between I/D polymorphism of the ACE gene and LVH.     

Influence of angiotensin-converting enzyme I/D gene polymorphism on the right ventricular myocardial performance index in patients with a first acute anterior myocardial infarction.

BACKGROUND: The genetic influence on the myocardial performance index is uncertain, so the aim of the present study was to determine the effects of polymorphism of the angiotensin-converting enzyme (ACE) gene on the right ventricular myocardial performance index (RVMPI) after a first acute anterior myocardial infarction (MI). METHODS AND RESULTS: The subjects were 116 patients with a first acute anterior MI. Based on the polymorphism of the ACE gene, they were classified into 3 groups: deletion/deletion (DD) genotype (group 1, n=45), insertion/deletion (ID) genotype (group 2, n=58), insertion/insertion (II) genotype (group 3, n=13). Echocardiograms were used to determine the RVMPI, left ventricular myocardial performance index (LVMPI), tricuspid E/A, tricuspid deceleration time and the left ventricular diameter diastolic and diameter systolic (LVDd and LVDs). RVMPI and LVMPI were significantly higher in the ACE DD group. Tricuspid E/A, DT, LVDd and LVDs showed no differences among the 3 groups. CONCLUSION: The ID polymorphism of the ACE gene may affect RVMPI and LVMPI after a first acute anterior MI.     

Angiotensin-converting enzyme gene I/D polymorphism and carotid artery disease in renovascular hypertension

There is evidence linking the activation of the renin-angiotensin system (RAS) with target organ damage in renovascular hypertension (RVH). A genetic association of the DD genotype of the angiotensin-converting enzyme (ACE) gene with cardiovascular complications has been found in various clinical conditions. The aim of our study was to determine whether the insertion/deletion (I/D) polymorphism of the ACE gene is associated with the high prevalence of target organ damage reported in RVH. A total of 65 atherosclerotic patients (age 68.2 +/- 5.2 years) with RVH and 49 atherosclerotic patients (age 68.0 +/- 6.3 years) with essential hypertension (EH) were sequentially enrolled when attending the outpatient clinic for specialist assessment of their vascular disorder. Cardiac, renal, and vascular involvement were assessed in both groups and blood was taken for genetic analysis. Patients with RVH had a higher prevalence of left ventricular hypertrophy (LVH), carotid artery disease, and albuminuria than those with EH. In RVH, but not in EH, the DD genotype was significantly associated with severe arterial disease. In RVH, carotid disease (lumen narrowing >60%) was present in 62% of DD patients versus 25% of the other genotypes (OR = 4.90, 95% CI: 1.70-14.13). Such an association was also present in peripheral vascular disease: 72.4% in DD patients versus 41.6% in the other genotypes (OR = 3.67, 95% CI = 1.29-10.36). Logistic regression analysis showed that the DD genotype was the strongest predictor of risk of severe carotid disease. We conclude that, in atherosclerotic RVH, there is an association of the severity of vascular disease with the DD genotype of the ACE gene.     

Angiotensin-converting enzyme gene polymorphism and microvascular complications in Turkish type 2 diabetic patients

The aim of this study was to investigate whether an association exists between the angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphism and microvascular complications of type 2 diabetes mellitus in Turkish patients. A total of 239 type 2 diabetic patients and 138 sex and age matched control subjects were included into the study. The I/D polymorphism was determined by polymerase chain reaction (PCR). Nephropathy status was determined according to urinary albumin/creatinine ratio (microg/mg) (<30 normoalbuminuria, 30-300 microalbuminuria, >300 macroalbuminuria) and retinopathy was evaluated by fundoscopic examination and by flourescein fundus angiography. The distribution of ACE I/D polymorphism and allele frequencies in diabetic patients were not significantly different from controls, DD genotype 32.2 versus 37.2%; ID genotype 50.6 versus 47.1%; and II 17.2 versus 15.2%; D allele 57.5 versus 61.2%; I allele 42.5 versus 38.8%. Genotype distribution between normo-, micro- and macroalbuminuric patients did not differ significantly (DD:ID:II (%), normoalbuminuria, 35:46:19; microalbuminuria, 28:55:17; macroalbuminuria, 31:55:14). There was also no difference in genotype distribution between patients with and without retinopathy (DD:ID:II (%), retinopathy positive, 32:51:17; retinopathy negative, 33:49:18). In conclusion, the ACE I/D polymorphism does not seem to be associated with diabetic nephropathy and retinopathy in Turkish type 2 diabetic patients.     

A dangerous bridge: myocardial infarction due to myocardial bridging in left ventricular hypertrophy

A 63-year-old woman with a history of hypertension presentedto the coronary care unit with a subacute anterior wall myocardialinfarction (MI). She reported of initial left-sided chest pain,dyspnoea, and weakness 18 h before hospital admission, duringa long-distance     

醛固酮合成酶基因多态性与原发性高血压及左心室肥厚关系的研究进展

醛固酮是人体内最重要、作用最强的盐皮质激素。醛固酮合成酶的基因多态性与原发性高血压以及左心室肥厚有着密切的关系,这些关系的阐明对于在临床中治疗个体化,减轻避免药物的不良反应,研制新的抗高血压药物等起着极大的作用。