Left Ventricular Mass In Hypertension Research Articles

118Nt-proBNP combined with R wave in aVL lead predicts mortality better than echocardiographic left ventricular mass in hypertension

118Nt-proBNP combined with R wave in aVL lead predicts mortality better than echocardiographic left ventricular mass in hypertension

NT-proBNP combined with R wave in aVL lead predicts mortality better than echocardiographic left ventricular mass in hypertension

Plasma NT-proBNP and R wave in aVL lead (RaVL) have been associated with mortality in hypertensive patients. The aim of the present study was to test the prognostic value of their combination, in comparison to left ventricular mass index assessed by echocardiography (LVMI). A total of 1104 hypertensive patients having at baseline, an assessment of plasma NT-proBNP, a resting 12-lead ECG, and an echocardiography, were included. LVMI was assessable in 921 patients. After a median follow-up of 8.5 [5.4–13.3] years, 110 deaths occurred, 62 of which were from cardiovascular cause. Optimal thresholds of RaVL and plasma NT-proBNP to predict mortality were 0.7 mV and 150 pg.mL −1 , respectively. A 3-categorical variable based on RaVL and NT-proBNP, was built: 0, when none were above the threshold, 1 or 2 when only one or both were above the threshold. After adjustment for cardiovascular risk factors, previous cardiovascular event and LVMI in Cox regression analysis, we observed a gradual increase risk for patients having 1 marker above the threshold (hazard ratio (HR) 1.76; 95% confidence interval (CI) (1.08–2.86) for all-cause mortality, HR 2.18; 95%CI (1.06–4.46) for cardiovascular mortality) or 2 markers above the threshold (HR 2.76; 95%CI (1.51–5.03) for all-cause mortality, HR 3.90; 95%CI (1.69–9.00) for cardiovascular mortality); the prognostic value of the combination of RaVL and NT-proBNP was greater than that of LVMI, which did not reach statistical significance while included in the same model. Similarly, the combination demonstrated the best accuracy to predict outcome in comparison to LVMI (C-index, ROC curves and likelihood ratio test). Risk stratification in hypertension with the combination of NT-proBNP and RaVL is a simple method that appears more powerful and accurate than LVMI. This approach should be considered as a game changer in hypertension.

A Study of Comparison of Left Ventricular Mass in Hypertensive Patients with Diabetes Mellitus And Without Diabetes

BACKROUND AND OBJECTIVES : Hypertension is a major risk factor for stroke, cardiovascular diseases and aortic dissection and hypertension is associated with significant morbidity and mortality. Hypertension causes 7.1 million premature deaths and the disease burden is 4.5% all over the world. Hypertension is a major public health problem globally. The prevalence of diabetes has raised to 285 million in 2012 when compared to 30 million cases in 1985. The principal morbidity and driver of mortality in patients with diabetes are cardiovascular diseases (CVD). Both hypertension and diabetes increases cardiovascular morbidity and mortality by increasing left ventricular mass. Even though the ECG can identify the findings suggestive of left ventricular hypertrophy, the sensitivity is very less. So echocardiography is preferred for assessment of left ventricular hypertrophy. MATERIALS AND METHODS : This was a prospective cross sectional study conducted in patients attending the hypertension OP of Govt. Kilpauk Medical College Hospital with hypertension and diabetes or hypertension alone of more than 5 years duration without any cardiac disease and healthy individuals of more than 35yrs of age are taken as controls. Echocardiography was done for both study and control groups and left ventricular mass was calculated by using Penn formula and LV mass was compared between the three groups (HT, HT and DM, controls). RESULTS : There is significant statistical correlation between age group and left ventricular mass in hypertension with diabetes group (p =0.039). There is significant statistical correlation between females (p=0.042) with diabetes and hypertension and severity of abnormal left ventricular mass than males (p=0.286). The mean left ventricular mass increases in both males (211.25gm-HT to 224.24gm-HT+DM) and females (169.65gm-HT to 206.06gm-HT+DM) in hypertension and diabetes group and it was statistically significant in females (p=0.015) but not in males (p=0.546). CONCLUSION : The study shows that there is increased left ventricular mass in females with hypertension and diabetes mellitus when compared to females with hypertension alone but not in males. But the mean left ventricular mass was increased in both males and females of diabetes and hypertension group when compared to hypertension only group. Advancing age is also associated with increased left ventricular mass in cases of both hypertension and diabetes group. Increased left ventricular mass is an important cause for increased cardiovascular morbidity and mortality hence, the females with diabetes and hypertension should be managed aggressively for reduction of left ventricular mass.

Considerations in Understanding the Coronary Blood Flow- Left Ventricular Mass Relationship in Patients with Hypertension.

: Background: Coronary blood flow (CBF) is essential for optimal cardiac performance and to maintain myocardial viability. There is considerable ambiguity concerning CBF in hypertension.Objective: To investigate the relationship between CBF and left ventricular (LV) mass in persons with hypertension.Methods: OvidSP Medline was systematically searched. Eligible articles assessed CBF, and LV mass in adults with and without hypertension (HTN).Results: Eleven studies met the entry criteria. All 8 studies reported an increase in CBF (ml/min) for persons with hypertension (N=212) compared to individuals without hypertension (N=150). Meta-analysis showed a significant and 2.88 fold higher CBP in hypertension. Six studies adjusted CBF for LV mass; of which 4 studies reported a reduction in CBF. Meta-analysis showed a significant decrease in CBF/g LV mass in hypertension. The two studies that did not show a decrease in CBF, used the argon chromatographic method to measure coronary sinus blood flow suggesting this methodology may have influenced the results. Using the mean CBF in normotensive group to construct the expected CBF according to LV mass, reported CBF in HTN was progressively less than expected In two studies, (N=142), there was a significant inverse correlation between LV mass and CBF/ g LV mass. Multivariate analysis (three studies) consistently found a highly significant independent relationship between LV mass and CBF after considering age, sex, heart rate and several other factors.Conclusion: Hypertension is associated with a reduction in CBF adjusted for LV mass with a highly significant inverse association between CBF and LV mass. Clinicians should be aware that patients with hypertension are at greater risk for myocardial ischemia should develop other factors that limit CBF or myocardial oxygen delivery.

Uricaemia and left ventricular mass in hypertensive patients.

Both hyperuricaemia and left ventricular (LV) hypertrophy are associated with the metabolic syndrome and increased cardiovascular risk. The relationship between uric acid levels and left ventricular mass in hypertension, however, is unclear. In this study, we have investigated this relationship in hypertensive patients without the metabolic syndrome. In a cross-sectional study, 367 nondiabetic, essential hypertensive patients (age 52±14; 194 males and 173 females) free of clinically relevant cardiovascular complications and without the metabolic syndrome were consecutively recruited at a university hypertension clinic. In these patients, we measured plasma levels of uric acid, lipids, glucose and insulin at fast and after an oral glucose load (OGTT), renal function and performed both conventional and tissue Doppler echocardiography. Hypertensive patients with LV hypertrophy had higher uric acid levels and greater prevalence of hyperuricemia than patients with normal left ventricular mass. Uric acid levels were directly related with fasting and post-OGTT plasma insulin and with the HOMA index and inversely with 24-h creatinine clearance. Uric acid was also significantly and directly related with the left ventricular mass and multivariate regression analysis showed that this relationship was independent from components of the metabolic syndrome and renal function in women, but not in men. Elevated uric acid levels are independently related to the left ventricular mass in hypertensive women without the metabolic syndrome. In these patients with a low cardiovascular risk profile, uric acid might contribute to the development of subclinical cardiac damage.

Echocardiographic left ventricular hypertrophy

Echocardiographic left ventricular hypertrophy

Blood pressure-independent association between aortic characteristic impedance and left ventricular mass in hypertension

A. A. Argyris , G. Kollias , T. G. Papaioannou , E. Nasothimiou , J. Blacher , M. E. Safar , A. Achimastos , P. P. Sfikakis , A. D. Protogerou 1 Hypertension Center and Cardiovascular Research Laboratory, 1st Dpt of Propaedeutic Medicine, “Laiko” Hospital, Athens, Greece Biomedical Engineering Unit, 1st Dpt of Cardiology, “Hippokration” Hospital, Athens, Greece Hypertension Center, 3rd University Dpt of Medicine, “Sotiria” Hospital, Athens, Greece Paris Descartes University, AP-HP, Diagnosis and Therapeutic Center, Hotel-Dieu, Paris, France

Variant on chromosome 9p is associated with left ventricular mass

It is well known that among hypertensive patients, an increased left ventricular mass (LVM) is a powerful predictor of cardiovascular morbidity and mortality. However, the mechanisms underlying LVM in hypertension are not completely understood, as the absolute value of blood pressure and other risk factors associated do not predict alone a definite LVM progression. Recently, the 9p21 chromosomal region has been consistently associated with coronary heart disease. We examined the association of 384 single nucleotide polymorphisms (SNPs) in the short arm of chromosome 9 with LVM in 821 hypertensive individuals from northern Italy. We identified a SNP (rs894379) in the intronic region of the centlein, centrosomal protein (CNTLN) gene on chromosome 9p22, whose minor allele G is associated with an increased LVM. We performed a follow-up validation analysis for the top SNP in 1038 hypertensive individuals from southern Italy. We then combined the results and found a nominal association for rs894379 (β = 2.46, P = 0.0026). We describe a new variant associated with echocardiography LVM. This result, though it needs to be further investigated, may improve our understanding of the genetic determination of this prognostically relevant trait.

Endothelial dysfunction predicts regression of hypertensive cardiac mass

BackgroundSubclinical organ damage is a condition with an increased risk for fatal and nonfatal cardiovascular events. Particularly, endothelial dysfunction and left ventricular mass (LVM) are recognized as independent predictors of cardiovascular events in hypertensive patients. Besides, LVM in hypertensives is inversely related to forearm blood flow (FBF) responses to the endothelium-dependent vasodilating agent. We evaluated the role of endothelium-dependent vasodilation in the progression/regression of LVM in a group of hypertensive subjects. MethodsWe enrolled 170 hypertensive outpatients (88 men, 92 women; age 47±11years). LVM was calculated with the Devereux formula and indexed by surface area (LVMI). Endothelium-dependent vasodilation was investigated by intra-arterial infusions of acetylcholine (ACh). ResultsDuring the follow-up blood pressure (BP) decreased from 150/91±17/11 to 135/80±14/9mm Hg (P=0.0001), and LVMI from 120±28 to 118±28g/m2 (P=0.194). The mean annual rate of variation of LVMI was −0.38±3.9g/m2, which was not statistically different in men and women. It was correlated with baseline ACh-stimulated FBF (r=−0.272, P=0.0001) and BMI (r=0.164, P=0.016). At multivariate analysis, FBF was the only baseline covariate that remained significantly associated with LVMI variation, also after correction for antihypertensive treatment and BP reduction. The interaction between baseline LVM and ACh-stimulated FBF was investigated in a multiple linear regression model showing that a fixed reduction in ACh-stimulated FBF (100%) induces different variation of annual rate of LVMI at different levels of baseline LVM. ConclusionsOur data demonstrate, for the first time, the role of endothelial function in the progression/regression of LVMI, independently of traditional cardiovascular risk factors and antihypertensive therapy.

A prediction model for left ventricular mass in patients at high cardiovascular risk

Left ventricular (LV) mass has a continuous relation with cardiovascular risk, and regression of LV mass induced by pharmacological treatment is associated with improved prognosis. Therefore, early identification of patients with a large LV mass is desired. We developed a model to predict LV mass in individual hypertensives at high cardiovascular risk. We analyzed data of 536 hypertensives with symptomatic extracardiac atherosclerotic disease or marked risk factors for atherosclerosis from a cross-sectional study in a tertiary referral center. LV mass was measured by cardiac MRI. We developed the prediction rule with multivariable linear regression analysis and stepwise backward elimination. Internal validation was assessed with bootstrap sampling to obtain an estimate of model performance (R²) that may be expected for new patients. Important predictors for LV mass included sex, height, body mass index, systolic blood pressure, and previous aneurysm of the abdominal aorta. R² of the prediction model was 45% after internal validation, which was considerably higher than the R² of previously reported models (range 1-38%). Addition of electrocardiography data showed limited improvement of the model performance (R²=47%). We present a prediction model for LV mass in hypertensives at high cardiovascular risk. After external validation, this model may be used in clinical practice to estimate LV mass for early identification of large LV mass. The predictions of the model may support appropriate medical care in the prevention of cardiovascular disease.

Lowering Left Ventricular Mass in Hypertension: A Way to Improve Cardiovascular Prognosis?

Lowering Left Ventricular Mass in Hypertension: A Way to Improve Cardiovascular Prognosis?

Arterial pulsatile hemodynamic load induced by isometric exercise strongly predicts left ventricular mass in hypertension

Although resting hemodynamic load has been extensively investigated as a determinant of left ventricular (LV) hypertrophy, little is known about the relationship between provoked hemodynamic load and the risk of LV hypertrophy. We studied central pressure-flow relations among 40 hypertensive and 19 normotensive adults using carotid applanation tonometry and Doppler echocardiography at rest and during a 40% maximal voluntary forearm contraction (handgrip) maneuver. Carotid-femoral pulse wave velocity (CF-PWV) was measured at rest. Hypertensive subjects demonstrated various abnormalities in resting and induced pulsatile load. Isometric exercise significantly increased systemic vascular resistance, aortic characteristic impedance (Zc), induced earlier wave reflections, increased augmentation index, and decreased total arterial compliance (TAC; all P < or = 0.01). In hypertensive subjects, CF-PWV was the strongest resting predictor of LV mass index (LVMI) and remained an independent predictor after adjustment for age, gender, systemic vascular resistance, reflection magnitude, aortic Zc, and TAC (beta = 2.52 m/s; P < 0.0001). Age, sex, CF-PWV, and resting hemodynamic indexes explained 48% of the interindividual variability in LVMI. In stepwise regression, TAC (beta = -17.85; P < 0.0001) during handgrip, Zc during handgrip (beta = -150; P < 0.0001), and the change in the timing of wave reflections during handgrip (beta = -0.63; P = 0.03) were independent predictors of LVMI. A model that included indexes of provoked hemodynamic load explained 68% of the interindividual variability in LVMI. Hemodynamic load provoked by isometric exercise strongly predicts LVMI in hypertension. The magnitude of this association is far greater than for resting hemodynamic load, suggesting that provoked testing captures important arterial properties that are not apparent at rest and is advantageous to assess dynamic arterial load in hypertension.

Hypoadiponectinemia

Hypertension is a public health challenge of increasing importance because of its high frequency and concomitant risk of cardiovascular and renal disease. It has been estimated that the worldwide prevalence of hypertension was 972 million in 2000, and this number will increase by 60% by the year 2025.1 A large body of evidence indicates that the increasing prevalence of hypertension is sustained by the escalation of overweight and obesity. Actually, most hypertensive patients are also overweight or obese,2 and this may contribute to further deteriorate their cardiovascular risk profile. Similar to hypertension, obesity is independently associated with numerous adverse cardiovascular outcomes, and, most importantly, adipose tissue expansion and hypertension have a synergistic negative impact on cardiovascular prognosis. Hence, the hypertension–obesity pandemic imposes today a considerable burden on societies and healthcare systems that one can reasonably expect to increase further in the next years. The importance of preventing hypertension underscores the critical role of a better understanding of the most common mechanisms underlying its development. The association between obesity and hypertension has been recognized for many decades,2 and an almost linear relation appears between body mass index and systolic and diastolic blood pressures, at least over a body mass index range from 16 to 31 kg/m2.3 Also, risk estimates from the Framingham Heart Study suggest that ≈78% of the hypertension cases in men and 65% in women can be directly attributed to obesity.4 Further evidence for a consistent link between adiposity and hypertension comes from studies showing that weight gain is almost invariably associated with an increase in blood pressure. The increase in blood pressure is closely related to the magnitude of weight gain, and even moderate weight gain is associated with an increased risk of developing hypertension.5 In addition, even modest weight …

Mechanism(s) of Systolic Blood Pressure Reduction and Drug Therapy in Hypertension

Antihypertensive drug therapy is a major modality of cardiovascular (CV) disease prevention, especially for stroke, congestive heart failure, and renal insufficiency. Coronary risk is also consistently prevented by antihypertensive treatment, but to a lesser extent.1–4 The Prime Study2 has shown that drug-induced blood pressure (BP) reduction in hypertensive subjects is associated with a significant decrease of coronary risk. However, when treated and untreated subjects are compared, at any given value of systolic BP (SBP), this risk remains higher in treated than in untreated subjects, suggesting the persistence of residual coronary complications. Results of therapeutic trials also indicate that coronary risk is associated with a particular hemodynamic pattern in treated hypertensive subjects.3 Although diastolic BP (DBP) is significantly lowered by drug treatment to <90 mm Hg (80% of the patients), SBP remains above 140 mm Hg in 60%, indicating an increase of pulse pressure (PP), which is the difference between SBP and DBP.4 It is widely accepted that SBP and PP rise sharply with age and that this increase is a major manifestation of vascular aging and stiffening, which are now considered major predictors of CV risk, independent of the mean BP (MBP) level.4 The purpose of this review is to analyze the mechanism(s) of SBP in untreated and chronically treated hypertensive subjects and to determine which pathophysiological factors are susceptible to attenuating consistently coronary and CV complications in hypertensive populations. Ventricular ejection in humans is associated with 2 principal events. First, the coronary circulation is transiently interrupted, as the principal consequence of cardiac contraction, and, second, an acute shock of stroke volume against the aortic wall is observed (Figure 1). Then, the BP curve may be considered as a wave, which travels along the arterial tree at a given speed, the pulse wave velocity (PWV). …

Albuminuria predicts cardiovascular events independently of left ventricular mass in hypertension: a LIFE substudy.

We wanted to investigate whether urine albumin/creatinine ratio (UACR) and left ventricular (LV) mass, both being associated with diabetes and increased blood pressure, predicted cardiovascular events in patients with hypertension independently. After 2 weeks of placebo treatment, clinical, laboratory and echocardiographic variables were assessed in 960 hypertensive patients from the LIFE Echo substudy with electrocardiographic LV hypertrophy. Morning urine albumin and creatinine were measured to calculate UACR. The patients were followed for 60+/-4 months and the composite end point (CEP) of cardiovascular (CV) death, nonfatal stroke or nonfatal myocardial infarction was recorded. The incidence of CEP increased with increasing LV mass (below the lower quartile of 194 g to above the upper quartile of 263 g) in patients with UACR below (6.7, 5.0, 9.1%) and above the median value of 1.406 mg/mmol (9.7, 17.0, 19.0%(***)). Also the incidence of CV death increased with LV mass in patients with UACR below (0, 1.4, 1.3%) and above 1.406 mg/mmol (2.2, 6.4, 8.0%(**)). The incidence of CEP was predicted by logUACR (hazard ratio (HR)=1.44(**) for every 10-fold increase in UACR) after adjustment for Framingham risk score (HR=1.05(***)), history of peripheral vascular disease (HR=2.3(*)) and cerebrovascular disease (HR=2.1(*)). LV mass did not enter the model. LogUACR predicted CV death (HR=2.4(**)) independently of LV mass (HR=1.01(*) per gram) after adjustment for Framingham risk score (HR=1.05(*)), history of diabetes mellitus (HR=2.4(*)) and cerebrovascular disease (HR=3.2(*)). (*)P<0.05, (**)P<0.01, (***)P<0.001. In conclusion, UACR predicted CEP and CV death independently of LV mass. CV death was predicted by UACR and LV mass in an additive manner after adjustment for Framingham risk score and history of CV disease.

Changes in cardiovascular risk by reduction of left ventricular mass in hypertension: a meta-analysis

Background Some studies have suggested that serial changes in left ventricular (LV) mass in hypertensive subjects predict the subsequent risk of cardiovascular disease. The aim of this meta-analysis was to evaluate the prognostic impact of LV hypertrophy regression in hypertension. Methods We undertook a meta-analysis of studies that reported echocardiographic LV mass before and during antihypertensive therapy, with subsequent assessment of cardiovascular events. The aims of this meta-analysis were: 1) to compare subjects with LV hypertrophy (LVH) during treatment (persistence or new development of LVH) with those with LVH at baseline, but not during treatment (regression of LVH); and 2) to compare subjects with LVH at baseline, but not during treatment with those without LVH both before and during treatment (regression of LVH versus persistently normal LV mass). Results The four eligible studies included 1064 hypertensive subjects (41% women) aged 45 to 51 years who repeated the echocardiographic study 3 to 10 years after the initial examination. The definition of LVH was based on a LV mass corrected by body surface area >125 g/m 2 in two studies and >110 g/m 2 (for women) and 124 g/m 2 (for men) in two studies. Compared with subjects with lack of regression or new development of LVH, those with LVH regression showed a reduced risk of subsequent cardiovascular disease (odds ratio 0.41, 95% CI 0.21 to 0.78, P = .007). Compared with subjects with regression of LVH, those with persistently normal LV mass showed a similar risk of subsequent events (odds ratio 0.64, 95% CI = 0.31 to 1.30, P = .21). Conclusion Compared with persistence or new development of LV hypertrophy, regression of LV hypertrophy during antihypertensive treatment is associated with a marked reduction in risk for subsequent cardiovascular disease.

Effect of body weight changes on 24-hour blood pressure and left ventricular mass in hypertension: a 4-year follow-up

Background Few data are available on the long-term effects of weight loss on 24-h blood pressure (BP) and left ventricular mass in overweight hypertensive patients. Methods A total of 181 never-treated overweight hypertensive subjects (body mass index, 25 to 39 kg/m 2, office BP 145/94 ± 12/7 mm Hg) had 24-h BP monitoring and echocardiography twice, at baseline and after 3.8 ± 2 years (minimum 1 year). None of the subjects received antihypertensive drugs during the follow-up. Main outcome measures were changes in 24-h BP and in left ventricular mass. Results Percent change in body weight had a direct relationship with 24-h BP changes ( r = 0.35 and 0.31 for systolic and diastolic BP, respectively; both P < .001). The associations with office BP changes ( r = 0.13, P = .10 for systolic BP; r = 0.15, P = .06 for diastolic BP) were significantly weaker (both P < .01, z test). The patients who lost weight during follow-up ( n = 106) had a significantly lower increase in 24-h BP (+0.6 ± 9/ +0.2 ± 6 v +4.9 ± 9/ +2.7 ± 7 mm Hg for systolic/diastolic BP, both P < .01) and in left ventricular mass (−3 ± 30 g v +9 ± 32 g, P < .02) than the remaining subjects. In a multiple linear regression, a 10% weight loss independently predicted a 4.3/3.8 mm Hg decrease in 24-h systolic/diastolic BP. Conclusions Long-term weight loss determines a sustained BP reduction during the 24 h and a decrease in left ventricular mass in overweight hypertensive subjects. The relation of weight loss with ambulatory BP changes is closer than that with office BP.

Left ventricular mass and systolic dysfunction in essential hypertension.

A relation between left ventricular (LV) hypertrophy and depressed midwall systolic function has been described in hypertensive subjects. However, a strong confounding factor in this relation is concentric geometry, which is both a powerful determinant of depressed midwall systolic function and a correlate of LV mass in hypertension. To evaluate the independent contribution of LV mass to depressed systolic function, 1827 patients with never-treated essential hypertension (age 48 +/- 12 years, men 58%) underwent M-mode echocardiography under two-dimensional guidance. Relative wall thickness was the strongest determinant of low midwall fractional shortening (r = -0.63, P < 0.0001). The significant inverse relation observed between LV mass and midwall fractional shortening (r = -0.43, P < 0.0001) persisted after taking into account the effect of relative wall thickness (partial r = -0.27, P < 0.0001). Within each sex-specific quintile of relative wall thickness, prevalence of subnormal afterload-corrected midwall systolic function was greater in subjects with, than in subjects without, LV hypertrophy (P < 0.05 for the first, third, fourth and fifth quintile). In a multiple linear regression analysis, both LV mass (P < 0.0001) and relative wall thickness (P < 0.0001) were independent predictors of a reduced midwall fractional shortening. In conclusion, the inverse association between LV mass and midwall systolic function is partly independent from the effect of relative wall thickness. LV hypertrophy is a determinant of subclinical LV dysfunction independently of the concomitant changes in chamber geometry.

G protein β 3 subunit gene 825T allele is associated with increased left ventricular mass in young subjects with mild hypertension

Background A nucleotide substitution (C→T) at position 825 of the gene GNB3 encoding the β 3 subunit of heterotrimeric G proteins is associated with alternative splicing and enhanced signal transduction. There is accumulating evidence from different populations that the 825T allele is associated with increased prevalence of hypertension, obesity, and left ventricular hypertrophy. However, it is unclear to what extent the 825T allele has a direct influence on left ventricular structure, independently of the effects of pressure and body mass index. Therefore we explored whether the GNB3 825T allele is associated with increased left ventricular mass index in a selected and homogeneous group of young, never treated, mild hypertensives. Procedures Young subjects (n = 207, aged 18 to 45 years) were genotyped at the GNB3 825 locus. In each patient, 24-h ambulatory blood pressure (BP) measurement and two-dimensional guided M-mode echocardiography combined with Doppler sonography were performed. Results: The genotype distribution among patients was in Hardy-Weinberg equilibrium. Patients carrying the 825T allele had an increased left ventricular mass index (95.1 ± 1.5 v 89.7 ± 1.5 g/m 2; P = .01) in comparison to those with CC genotype. The association between left ventricular mass index and 825T allele was independent of gender, age, BP, heart rate, alcohol intake, and physical activity. Conclusions: In young patients with mild hypertension without heart disease the 825T allele is associated with an increased left ventricular mass index. These hypothesis-generating data suggest that GNB3 825T allele may be considered as one genetic marker predisposing to an increase in left ventricular mass in hypertensives, and justifies larger studies.

Left ventricular mass and cardiovascular morbidity in essential hypertension: the MAVI study

OBJECTIVESThis study investigated the prognostic value of left ventricular (LV) mass at echocardiography in uncomplicated subjects with essential hypertension.BACKGROUNDOnly a few single-center studies support the prognostic value of LV mass in uncomplicated hypertension.METHODSThe MAssa Ventricolare sinistra nell’Ipertensione study was a multicenter (45 centers) prospective study. The prespecified aim was to explore the prognostic value of LV mass in hypertension. Admission criteria included essential hypertension, no previous cardiovascular events, and age ≥50. There was central reading of echocardiographic tracings. Treatment was tailored to the single subject.RESULTSOverall, 1,033 subjects (396 men) were followed for 0 to 4 years (median, 3 years). Mean age at entry was 60 years, and systolic/diastolic blood pressure was 154/92 mm Hg. The rate of cardiovascular events (×100 patient-years) was 1.3 in the group with normal LV mass and 3.2 in the group (28.5% of total sample) with LV mass ≥125 g/body surface area (p = 0.005). After adjustment for age (p < 0.01), diabetes (p < 0.01), cigarette smoking (p < 0.01) and serum creatinine (p = 0.03), LV hypertrophy was associated with an increased risk of events (RR [relative risk] 2.08; 95% CI [confidence interval]: 1.22 to 3.57). For each 39 g/m2(1 SD) increase in LV mass there was an independent 40% rise in the risk of major cardiovascular events (95% CI: 14 to 72; p = 0.0013).CONCLUSIONSOur findings show a strong, continuous and independent relationship of LV mass to subsequent cardiovascular morbidity. This is the first study to extend such demonstration to a large nationwide multicenter sample of uncomplicated subjects with essential hypertension.