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.

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

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.

Prognostic value of different indexizations of left ventricular mass in hypertension

We assessed the prognostic value of different indexations of left ventricular (LV) mass in a large cohort of patients with essential hypertension. In a 2-center study, 2180 patients with essential hypertension [mean age 50, 47% women, baseline blood pressure (BP) 160/98 mmHg (SD 13/6)], good-quality echo tracings before treatment and no previous events were followed for an average of 4.6 years (range 0-14). Treatment was tailored to the single patient. During follow-up there were 250 major cardiovascular morbid events, at a rate of 2.47 events per 100 person-years. At entry, LV mass was 107.9 (SD 28) g/body surface area (m2), 118.9 (SD 34) g/height (m) and 49.8 g/height (m2.7). In a Cox analysis stratified by center, after adjustment for age (p<0.0001), 24-hour ambulatory pulse pressure (p=0.0002), current smoking (p<0.0001), total cholesterol (p=0.05) and diabetes (p<0.0001), LV mass provided the best improvement in the model fitting when indexed by body surface area (-2L=2942.2) and by height (-2L=2946.9), while indexation by height2.7 was less efficient (-2L=2949.3; p < 0.05) than the one by body surface area. In a ROC curve analysis, the best efficiency of LV mass for identification of subjects with future events (sens/spec = 1 on the ROC curve) was achieved by the following cut-off points: 111.8 g/body surface area (m2), 122.8 g/height (m) and 51.0 g/height (m2.7). The corresponding prevalence of LV hypertrophy was 37.8%, 39.4% and 40.3%, and the ROC areas were 0.67, 0.66 and 0.67 (p=n.s.), respectively.

Use of ambulatory blood pressure monitoring data to predict left ventricular mass in hypertension.

Many studies have shown definite but weak correlations between 24h blood pressure and left ventricular mass in hypertension. The present study applied an original multivariate analysis of parameters from ambulatory blood pressure monitoring to predict left ventricular mass in hypertension. Two hundred untreated hypertensive subjects (age=51+/-13 years, clinic blood pressure=163/98mmHg) had echocardiography and 24h recording of blood pressure. Data from 102 subjects were used to construct a mathematical model for prediction of left ventricular mass. The remaining 98 subjects were used to validate the model. The model included age, weight, height, 24h systolic blood pressure, heart rate over 24h, standard deviations of systolic blood pressure and of heart rate over 24h. Using this model, we explained 63% of the variance of left ventricular mass. Moreover, the model was validated for the correlation (r=0.70) between measured and the estimated left ventricular mass. Systolic blood pressure, heart rate and their standard deviations over 24h contribute to left ventricular mass in hypertensive subjects. Thus, it is important to take into account not only blood pressure but also heart rate in clinical studies.

Reverse remodeling of cardiac myocyte hypertrophy in hypertension and failure by targeting of the renin-angiotensin system.

ACE inhibitors (ACEIs) and angiotensin II type 1 (AT(1)) receptor blockers are effective in reducing left ventricular mass in hypertension and heart failure. However, the ability of these drugs to reverse excessive myocyte lengthening and transverse growth in heart failure is unknown. L-158,809 (an AT(1) blocker; AT(1)), enalapril (an ACEI), and hydralazine (a vasodilator) were administered to spontaneously hypertensive heart failure rats between 6 and 10 months of age (early treatment) and between 18 and 22 months of age (late treatment). After 4 months of treatment, hemodynamics and chamber dimensions were collected before left ventricular myocyte isolation and subsequent analysis of myocyte shape. Each drug reduced systolic blood pressures to normal values. In the early and late studies, the ACEI reduced myocyte volume. Myocyte length was also reduced in the late study. However, the AT(1) was most effective in reversing myocyte dimensions to near-normal values in both studies. Hydralazine was ineffective in reducing cell size but arrested progression of myocyte lengthening in the late study. Changes in myocyte shape reflected alterations in chamber dimensions and wall thickness. Reversal of myocyte hypertrophy was produced in hypertensive/heart failure rats with an AT(1). The ACEI was effective but to a lesser extent. Results indicate that it is possible to significantly reverse myocyte remodeling pharmacologically even if therapy is initiated near the onset of failure. Further work is needed to determine whether similar results can be obtained in humans.

Night-time blood pressure is more important than daytime blood pressure for left ventricular mass in hypertension

Night-time blood pressure is more important than daytime blood pressure for left ventricular mass in hypertension

Relation between coronary blood flow and left ventricular mass in hypertension: noninvasive quantification of coronary blood flow by thallium-201 myocardial scintigraphy.

This study was conducted to quantify coronary blood flow (CBF) noninvasively according to the fractionation principle and to elucidate the relation between CBF and left ventricular hypertrophy. CBF/cardiac output (CO), estimated on the basis of the ratio of myocardial uptake/total injected dose of thallium-201 (% cardiac uptake), was determined in 14 control subjects and 40 patients with essential hypertension. CBF and CBF per 100 g of myocardium (unit CBF) were calculated according to the following formulas: CBF= % cardiac uptake x CO, and unit CBF = (CBF/LVM) X 100, where CO and left ventricular mass (LVM) are echocardiographically determined. There was good reproducibility of % cardiac uptake (r = 0.983, p < 0.0001). Percent cardiac uptake was greater in hypertensive patients (4.65+/-1.44%) than in control subjects (3.64+/-0.64%), and there was a positive correlation between % cardiac uptake and LVM. CBF (ml/min) was greater in hypertensive patients (240.7+/-80.5) than in control subjects (194.9+/-36.9), but unit CBF (ml/min/100 g) was less in hypertensive patients (102.2+/-26.7) than in control subjects (150.3+/-30.5). Multiple regression analyses showed that LVM was the most potent independent predictor of resting CBF in hypertension. Our results indicate that CBF, determined by thallium-201 myocardial scintigraphy, increases parallel to the increase in LVM, but unit CBF decreases even in the resting condition in patients with essential hypertension.

B28 - Lack of correlation between insulin and left ventricular mass in hypertension

B28 - Lack of correlation between insulin and left ventricular mass in hypertension

729-3 Left Ventricular Hypertrophy in Essential Hypertension Depends on ACE Genotype

A deletion/insertion polymorphism in the ACE gene accounts for approximately 50% of the variance in plasma angiotensin converting enzyme (ACE) concentration, and may be linked to tissue ACE activity. The deletion allele (D) occurs with increased frequency in patients with hypertrophic and dilated cardiomyopathy. Left ventricular hypertrophy (LVH) is a recognised complication of essential hypertension, and is associated with increased morbidity and mortality. Angiotensin II, which is produced by ACE, promotes myocyte growth and collagen deposition, and has been causally linked with the development of LVH. To examine the contribution of ACE genotype to the development of left ventricular hypertrophy in patients with essential hypertension. Eighty-five consecutive patients (58 males, [59.5%]; mean age 53.8 years) attending the out-patient hypertension clinic were studied. Blood pressure was measured using a semi-automatic sphygmomanometer. Echocardiography was performed and left ventricular mass (indexed for height and weight) was calculated from M-mode measurements according to the Penn convention. DNA was extracted from peripheral blood leucocytes by a commercially available method, and ACE genotype determined by the polymerase chain reaction using standard primers and conditions. DD (n = 25) ID (n = 41) II (n = 19) LVMI (g/M 2 ) † (27.5) 116.1 (42.9) 116.5 (48.2) 108.0 SBP (mmHg) † 149.2 (22.4) 159.1 (28.6) 156.3 (26.5) Relationship of LVMI to SBP p &lt; 0.001 P = 0.002 P = 0.729 D = ACE gene deletion allele; I = ACE gene insertion allele. † Results expressed as mean ± standard deviation There is a significant correlation between LVM and SBP in patients with the deletion allele, but not in homozygotes for the insertion allele. The deletion homozygotes have a similar left ventricular mass to the heterozygotes, but for a lower mean SBP. These data suggest that systolic blood pressure is a major determinant of left ventricular mass in hypertension, but the relationship is expressed only in the presence of the deletion allele.