Left Ventricular Hypertrophy In Essential Hypertension Research Articles

Circulating MicroRNA-30e Predicts Left Ventricular Hypertrophy In Essential Hypertensive Patients.

The biomarker for left ventricular hypertrophy (LVH) in patients with essential hypertension (EH) remains an unmet clinical need. The microRNA-30 (miR-30) family has been associated with LVH in cellular and animal studies, but not in a clinical setting. The objective of the study was to investigate the clinical significance of circulating levels of miR-30 family as a biomarker for LVH in EH patients. A total of 239 EH patients and 239 healthy controls were enrolled in this study. Circulating levels of miR-30 family members, namely, miR-30a, miR-30b, miR-30c-1, miR-30c-2, miR- 30d, and miR-30e, were evaluated using real-time polymerase chain reaction assays. The circulating miR-30a, miR-30b, and miR-30e were significantly reduced in EH patients in contrast to controls. EH patients with LVH (EH-LVH) had substantially lower circulating miR-30b and miR-30e levels compared to EH patients without LVH (EH-nLVH). Moreover, the expression levels of miR-30b and miR-30e were positively related to LVMI, respectively. Receiver operating curve analysis showed that circulating miR-30e levels distinguished EH patients from controls, and EH-LVH from EH-nLVH patients. Logistic regression analysis identified the circulating miR-30e as a risk factor for LVH in EH patients. Circulating miR-30e level can be used as a biomarker in distinguishing EH-LVH from EH-nLVH. A further prospective study is warranted to validate this finding.

E0583 The intervention role of Valsartan on left ventricular hypertrophy and high-sensitivity C-reactive protein i n hypertension patients

ObjectiveTo explore the relationship between high-sensitivity C-reactive protein (hs-CRP) and left ventricular hypertrophy (LVH) and to examine whether angiotensin receptors antagonist ARB could decrease CRP expression, block or invert the...

Myocardial collagen metabolism in essential hypertension left ventricular hypertrophy before and during antihypertensive treatment

Objectives In patients with hypertensive left ventricular hypertrophy (LVH) antihypertensive treatment leads to reverse ventricular remodelling. We investigated whether myocardial collagen metabolism in patients with hypertensive LVH was implicated in adverse ventricular remodelling and responded to amlodipine combined telmisartan antihypertensive treatment. Design and methods The study was performed in 51 patients with essential hypertensive LVH. After randomization, 25 patients were assigned to amlodipine 2.5mg/day combined telmisartan 40mg/day, and 26 patients to amlodipine 2.5mg/day combined diuretic compound 1 tables/day treatment.

Left ventricular hypertrophy: beyond the image and defining the human cardiac phenotype in hypertension

IntroductionLeft ventricular hypertrophy (LVH) has proven to be a very useful risk marker in hypertension. It indicates a higher risk of cardiovascular events and particularly sudden death [1,2]. It defines the effects of hypertension on an important target organ, the heart, and is one step along th

Pressure Overload and Cardiac Remodelling-A Smoking Gun Points to Uncoupled Nitric Oxide Synthase: Oxidant Stress from Nitric Oxide Synthase-3 Uncoupling Stimulates Cardiac Pathologic Remodeling from Chronic Pressure Load. J Clin Invest 115: 1221-1231, 2005.

Pressure Overload and Cardiac Remodelling-A Smoking Gun Points to Uncoupled Nitric Oxide Synthase: Oxidant Stress from Nitric Oxide Synthase-3 Uncoupling Stimulates Cardiac Pathologic Remodeling from Chronic Pressure Load. J Clin Invest 115: 1221-1231, 2005.

ACE and AGTR1 Polymorphisms in Pathogenesis of Human Left Ventricular Hypertrophy

The A2350G polymorphism of exon 17 of the angiotensin I-converting enzyme gene (ACE) and the A1166C polymorphism of the 3′-untranslated region (3′-UTR) of the angiotensin II type 1 receptor gene (AGTR1) were tested for association with left ventricular hypertrophy (LVH) in patients with essential hypertension (EH) or arterial hypertension (AH) combined with diabetes mellitus type 2 (DM2). The patients with EH or AH + DM2 did not differ significantly in ACE or AGTR1 allele or genotype frequencies from healthy subjects. Both polymorphisms were associated with LVH in EH. AGTR1 allele 1166C was more frequent in patients with LVH than without (33.6 vs. 20.7%) and affected the left ventricular mass index (LVMI) in patients with EH (p = 0.007). The frequency of ACE allele 2350G in EH patients with LVH was 1.5 times higher, and that of genotype GG was 3.5 times higher, than in patients without LVH. LVMI differed significantly (p = 0.002) between patients with different ACE genotypes, being maximum in homozygotes GG and minimum in homozygotes AA. Thus, AGTR1 allele 1166C and ACE allele 2350G were identified as predisposing to LVH in EH. The two polymorphisms were not associated with the incidence or severity of LVH in patients with AH and DM2.

Plasma tissue inhibitor of metalloproteinase-1 and pro-collagen III N peptide are elevated in left ventricular hypertrophy

Essential hypertension (EH) aortic stenosis (AS) and hypertrophic obstructive cardiomyopathy (HOCM) can cause left ventricular hypertrophy (LVH). LVH is associated with increased collagen concentrations in the heart but the mechanisms causing LVH in EH, AS and HOCM are different. Collagen synthesis (fibrogenesis) can be monitored by measurement of pro-collagen III N peptide (PIIINP) which measures synthesis of mature collagen III. Inhibition of degradation was assessed by plasma tissue inhibitor of metalloproteinase -1 (TIMP-1) which inhibits the activity of metalloproteinases. We investigated levels of TIMP-1 and PIIINP in patients with the three types of LVH. Patients with EH had never been treated or had been off treatment for one month and patients with AS had blood samples taken preoperatively for PIIINP and TIMP-1. The results for the EH, AS and HOCM groups were compared with seventeen normotensive controls. Heparinised plasma was used in the assays for TIMP-1 and PIIINP which were measured by ELISA and RIA respectively. (See Table) p<0.05 in comparison to controls p<0.05 in comparison to controls Elevated levels of collagen in the left ventricule in EH arise from both increased collagen synthesis as well as decreased collagen degradation whereas in AO and HOCM the increased heart collagen is associated with increased collagen III synthesis. This suggests that LVH can arise by different biochemical mechanisms.

MYOCARDIAL IMAGING WITH 123I-METAIODOBENZYLGUANIDINE IN ESSENTIAL HYPERTENSION AND RENOVASCULAR HYPERTENSION

Iodine-123 metaiodobenzylguanidine (MIBG) myocardial imaging is considered to reflect cardiac sympathetic function. We performed myocardial MIBG scintigraphy and echocardiography in 27 patients with essential hypertension (EHT), 7 patients with renovascular hypertension (RVHT), and 8 normotensive subjects (NT) to investigate alterations in MIBG myocardial imaging in the presence of hypertension and left ventricular hypertrophy (LVH). EHT were divided into two groups based on LV wall thickness; EHT with LVH group (≥13 mm, n = 15) and EHT without LVH group (<13 mm, n = 12). The delayed uptake of MIBG was decreased, and the washout rate of MIBG was greater in the EHT with LVH group than EHT without LVH group or NT group. The washout rate was correlated with LV mass and LV diastolic function (as assessed by mitral flow). In RVHT group, the MIBG washout rate increased even without LVH, compared with NT and EHT without LVH groups. In summary, the washout rate of MIBG increased in parallel with the development of LVH in EHT and increased independently of the LV mass in RVHT. Cardiac sympathetic function could be altered in hypertensive LVH and in renovascular hypertension.

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.

Improved electrocardiographic diagnosis of left ventricular hypertrophy

This study was aimed at improving the performance of standard electrocardiographic criteria of left ventricular hypertrophy (LVH) in essential hypertension using echocardiographic left ventricular mass as reference. In 923 white, untreated hypertensive subjects (mean age 51, prevalence of echocardiographic LVH 34%), sensitivity of electrocardiographic criteria of LVH varied between 9% and 33% and specificity was generally ≥90%. The sum of S V3 + RaVL (Cornell voltage) showed the closest association with echocardiographic left ventricular mass (r = 0.48, p < 0.001), and its performance was superior to that of Sokolow-Lyon voltage in a receiver-operating characteristic curve analysis. A modified partition value of the Cornell voltage was tested (>2.4 mV in men and >2.0 mV in women), that yielded a good combination between sensitivity (26% in men and 19% in women, overall 22%) and specificity (96% in men and 95% in women, overall 95%). When LVH at electrocardiography was defined as the positivity of at least 1 of the following 3 criteria—SV3 + RaVL >2.4 mV in men or >2.0 mV in women, a typical strain pattern, or a Romhitt-Estes point score ≥5—sensitivity increased to 39% in men and 29% in women (overall 34%) and specificity decreased to 94% in men and 93% in women (overall 93%). Sensitivity of electrocardiography progressively increased from the first to the fourth quartile of left ventricular mass in subjects with echocardiographic LVH. In conclusion, the performance of standard electrocardiography for the diagnosis of LVH in essential hypertension can be improved using a modified sex-specific partition value of the Cornell voltage (2.4 mV in men and 2.0 mV in women). The combination of 3 highly specific criteria (Cornell voltage, Romhitt-Estes score, left ventricular strain) allows a further increase in sensitivity without compromising specificity.

Evaluation of the Cardiac Effects of Antihypertensive Agents

Left ventricular hypertrophy (LVH) in hypertension is initially a useful compensatory process, but it can also represent the first step toward a pathologic process that leads to the development of congestive heart failure. In fact, epidemiologic studies have documented that LVH in essential hypertension represents an independent risk factor for cardiovascular morbidity and mortality. Reversing or even preventing LVH, through a reduction of elevated blood pressure values and modification of some other pathogenetic factors, should represent a major therapeutic goal for the treatment of hypertensive patients. It has been demonstrated that different classes of antihypertensive drugs do not have the same effect in reducing left ventricular mass, probably because, beyond the control of blood pressure, their pharmacologic interference with the adrenergic system, the renin-angiotensin-aldosterone system, or other growth factors can influence the development and the reduction of cardiac hypertrophy. Two recent meta-analyses of the principal regression studies have indicated that angiotensin-converting enzyme (ACE) inhibitors and calcium antagonists, followed by drugs capable of reducing sympathetic nervous system activity, are most effective in decreasing LV mass. The results of experimental and clinical studies have demonstrated that the reversal of cardiac hypertrophy is associated with an improvement of the functional consequences of increased LV mass. Further studies are needed to verify whether the reversal of LVH per se increases survival rate in patients with essential hypertension.

Influence of the arterial blood pressure and nonhemodynamic factors on left ventricular hypertrophy in moderate essential hypertension

In a group of 36 untreated patients with mild to moderate essential hypertension (office systolic and diastolic blood pressures (BPs) 160 ± 3.4 and 102 ± 1.5 mm Hg, respectively), a 24-hour ambulatory BP monitoring and determination of left ventricular (LV) mass index according to the formula of Devereux were performed. After an overnight fast, blood samples were taken for the determination of serum aldosterone, plasma renin activity and serum parathyroid hormone. Urinary catecholamines were sampled for 24 hours. LV mass index (143.7 ± 8 g/m 2) did not correlate significantly either with office systolic or diastolic BP. The correlation of LV mass index with mean 24-hour systolic BP (145 ± 3 mm Hg) was statistically significant: r = 0.395, p = 0.026. However, the best correlation was obtained with mean 24-hour diastolic BP (90 ± 3 mm Hg) with r = 0.500 (p = 0.004). Urinary catecholamines were not correlated with LV mass index. LV mass index correlated significantly with plasma renin activity (r = 0.346, p = 0.050), and aldosterone (r = 0.559, p = 0.001). There was a very significant correlation between LV mass index and parathyroid hormone (r = 0.719, p = 0.00001) even after adjustment for mean 24-hour systolic and diastolic BPs. These results clearly demonstrate that ambulatory BP determinants but not office BP parameters are well correlated with LV hypertrophy in essential hypertension. Nonhemodynamic factors are important determinants of LV mass as well. Besides the renin-angiotensin-aldosterone system, parathyroid hormone appears to play an important role in cardiac hypertrophy.