Ventricular Mass In Essential Hypertension Research Articles

Serum Uric Acid and Left Ventricular Mass in Essential Hypertension.

Serum uric acid (sUA) has been associated with cardiovascular risk. Although the recent mechanistic hypothesis poses the basis for the association between sUA and left ventricular mass index (LVMi), the issue remains poorly investigated in a clinical setup. Through a retrospective analysis of the database of the departmental Hypertension Clinic of University Hospital of Salerno Medical School, we identified 177 essential hypertensives (age 60.3 ± 13.3 years; 85 men), free from uric acid-modulating medications and severe chronic kidney disease, and whose sUA values, anthropometric, clinical, and echocardiographic data were available. In the studied cohort, the average duration of hypertension was 8.4 ± 7.1 years. LVMi associated with classical determinants, such as age, blood pressure, and kidney function, although after multivariate correction, only age remained significant. Also, sUA correlated positively with LVMi, as well as body size, metabolism, and kidney function. In a multivariate analysis, sUA confirmed the independent association with LVMi. Also, levels of sUA >5.6 mg/dl are associated with larger cardiac size. We confirmed our data in a replicate analysis performed in a larger population (1,379 hypertensives) from an independent clinic. Our results demonstrate that sUA increases with LVMi, and a cutoff of 5.6 mg/dl predict larger LV sizes. Our data suggest that hyperuricemia might help to stratify the risk of larger cardiac size in hypertensives.

Impact of body fat mass on left ventricular mass in essential hypertension: differences between gender

Impact of body fat mass on left ventricular mass in essential hypertension: differences between gender

Parallel Deterioration of Albuminuria, Arterial Stiffness and Left Ventricular Mass in Essential Hypertension: Integrating Target Organ Damage

Background: Albuminuria, arterial stiffening and left ventricular hypertrophy (LVH) constitute target organ damage. We estimated whether increased urinary albumin excretion, assessed by albumin-to-creatine ratio (ACR), and carotid to femoral pulse wave velocity (c-f PWV) were accompanied by augmented left ventricular (LV) mass index (LVMI) in hypertension. Methods: In 428 non-diabetic untreated hypertensives (257 men, mean age = 52 years, office blood pressure (BP) = 146/93 mm Hg) the distributions of ACR and c-f PWV were split by the median (8 mg/g and 7.8 m/s, respectively). Results: Age, male sex, 24 h systolic BP, ACR and c-f PWV were the independent predictors of LVMI (R² = 0.478, p < 0.0001). Among patients with low ACR (n = 198), those with high c-f PWV (n = 84) compared to those with low c-f PWV (n = 114) were characterized by increased LVMI (by 8.9 g/m², p = 0.012) and prevalence of LVH (30 vs. 14%, p = 0.015). Similarly among patients with high ACR (n = 230), those with high c-f PWV (n = 123) compared to those with low c-f PWV (n = 107) exhibited heightened LVMI (by 13.6 g/m², p = 0.001). Conclusions: Increased ACR in conjunction with pronounced arterial stiffness is accompanied by augmented LV mass and higher LVH rates. Furthermore, the interrelationships between albuminuria, c-f PWV and LVMI suggest parallel target organ damage progression.

Is Smad3 the Key to Inflammation and Fibrosis in Hypertensive Heart Disease?

Hypertensive heart disease (HHD) is characterized by myocardial remodeling not only in the left ventricle but also the left atrium and right ventricle. Clinically it is characterized by intact systolic function and diastolic dysfunction, which make up the major cause of congestive heart failure in the elderly, also termed “heart failure with preserved ejection fraction.” Hypertension is the major determinant for developing heart failure with preserved ejection fraction.1 As reviewed recently by Diez and Frohlich,2 most findings in hypertensive animals and patients demonstrate that HHD also results from pathological structural remodeling of the myocardium in response to a number of hemodynamic and nonhemodynamic factors altered in hypertension. HHD is histologically characterized by left ventricular hypertrophy, cardiac inflammation, and fibrosis. The histological characteristics of inflammation and fibrosis extend from the perivascular space into the intermuscular interstitium. The mismatch of excessive myocyte hypertrophy and disproportionate myocardial fibrosis leads to increased myocardial stiffness and impaired diastolic function in patients with chronic hypertension and heart failure with preserved ejection fraction. The activation of the renin-angiotensin (Ang) system (RAS) plays an important pathophysiological role in HHD and the development of myocardial inflammation and fibrosis. This is supported by the findings that blockade of the RAS, either with Ang-converting enzyme inhibitors or its type 1 receptor blockers, significantly improves cardiac function and regresses cardiac remodeling in patients with hypertension. …

Inflammatory Activation and Left Ventricular Mass in Essential Hypertension

Inflammation is an independent risk factor for high blood pressure, and as a consequence inflammatory cytokines could be related with left ventricular hypertrophy (LVH). We sought to assess the association and predictive role of different cytokine levels with LVH in a group of patients with essential hypertension (HT). We studied 251 asymptomatic hypertensive patients (142 with LVH and 109 without LVH), referred from 11 hospitals. A routine physical examination, laboratory analyses, and echo-Doppler study were performed. Plasma soluble tumor necrosis factor (TNF) receptors (sTNF-R1 and sTNF-R2), interleukin-6 (IL-6), and interleukin-1 receptor antagonist (IL-1ra) were centrally determined. Hypertensive patients with LVH had higher inflammatory cytokine levels than the group without hypertrophy (P < 0.001). Multivariate linear regression reported that sTNF-R1 (P < 0.01) was an independent predictor of left ventricular mass index (LVMI). All cytokines had significant area under the curves for detection of LVH, but sTNF-R1 has the highest area, 0.71 +/- 0.03 (P < 0.001). Finally, prevalence of LVH was increased in the group of patients with higher cytokine levels, and logistic regression analysis showed that sTNF-R1 (odds ratio = 2.59, 95% CI of 1.14-5.87) was an independent predictor of LVH. Cytokine levels were significantly correlated with LVMI in hypertensive patients. The sTNF-R1 was an independent predictor of LVMI. Plasma sTNF-R1 concentrations could be a predictive factor of LVH in patients with essential HT.

Association of Increased Plasma Cardiotrophin-1 With Inappropriate Left Ventricular Mass in Essential Hypertension

Association of Increased Plasma Cardiotrophin-1 With Inappropriate Left Ventricular Mass in Essential Hypertension

9.11 Association between Plasma Aldosterone, Metabolic Syndrome and Left Ventricular Mass in Essential Hypertension

9.11 Association between Plasma Aldosterone, Metabolic Syndrome and Left Ventricular Mass in Essential Hypertension

Association of Increased Plasma Cardiotrophin-1 With Left Ventricular Mass Indexes in Normotensive Morbid Obesity

To the Editor: We read with great interest the article by Lopez et al,1 who hypothesize that cardiotrophin-1 (CT-1), a cytokine that induces cardiomyocyte growth, may be abnormally upregulated in hypertensive patients with inappropriate left ventricular mass (LVM), suggesting that an excess of CT-1 may contribute to inappropriate left ventricular growth. This possibility is supported by the finding of a correlation between CT-1 levels and the observed LVM/predicted LVM ratio, independent from concentric left ventricular hypertrophy (LVH). de Simone et al2 suggested that, other than hemodynamic load, the process that yields to inappropriate LVH can also depend on the protracted activity over time of cytokines, among other nonhemodynamic factors. The observation by Lopez et al1 that CT-1 levels were high in treated patients in whom inappropriate LVM persisted …

Response to Letter Regarding Article, “Relationship Between Central Sympathetic Drive and Magnetic Resonance Imaging–Determined Left Ventricular Mass in Essential Hypertension”

We thank Dr Schlaich and colleagues for their letter finding that our publication1 has provided further information about the relationship between sympathetic activity and left ventricular hypertrophy, and particularly that it raises the need for future studies involving cardiac sympathetic activity. Their letter also raises concerns about the potential confounding effect of blood pressure (BP) and the heterogeneous nature of regional sympathetic output. We agree that ambulatory BP …

Letter by Schlaich et al Regarding Article, “Relationship Between Central Sympathetic Drive and Magnetic Resonance Imaging–Determined Left Ventricular Mass in Essential Hypertension”

To the Editor: The demonstration of a relation between left ventricular (LV) hypertrophy and the risk of cardiovascular morbidity and mortality both in hypertensive patients and in the general population1 evoked a large series of investigations into the mechanisms underlying the development of LV hypertrophy. Clearly, hemodynamic factors, in particular systolic blood pressure, play a crucial role.2 Convincing evidence also exists of a close relation between cardiac norepinephrine release and LV hypertrophy.3 A recent report by Burns and colleagues …

Association of Increased Plasma Cardiotrophin-1 With Inappropriate Left Ventricular Mass in Essential Hypertension

Inappropriate left ventricular mass is present when the value of left ventricular mass exceeds individual needs to compensate hemodynamic load imposed by increased blood pressure. The goal of this study was to investigate whether plasma concentration of cardiotrophin-1, a cytokine that induces exaggerated hypertrophy in cardiomyocytes with hypertensive phenotype, is related to inappropriate left ventricular mass in patients with essential hypertension. The study was performed in 118 patients with never-treated hypertension and without prevalent cardiac disease. The left ventricular mass prediction from stroke work (systolic blood pressurexDoppler stroke volume), sex, and height (in meters(2.7)) was derived. An observed left ventricular mass/predicted left ventricular mass value >128% defined inappropriate left ventricular mass. Plasma cardiotrophin-1 was measured by an enzyme-linked immunosorbent assay. The studies were repeated in a group of 45 patients after 1 year of antihypertensive treatment. At baseline 67 and 51 patients presented with appropriate and inappropriate left ventricular mass, respectively. Plasma cardiotrophin-1 was higher (P<0.001) in patients with inappropriate mass than in patients with appropriate mass and normotensive controls. A direct correlation was found between cardiotrophin-1 and observed left ventricular mass/predicted left ventricular mass ratio (r=0.330, P<0.001) in all hypertensive patients. After treatment, plasma cardiotrophin-1 decreased and increased in patients in which inappropriate left ventricular mass regressed and persisted, respectively, despite a similar reduction of blood pressure in the 2 subgroups of patients. Albeit descriptive in nature, these results suggest the hypothesis that an excess of cardiotrophin-1 may contribute to inappropriate left ventricular growth in hypertensive patients.

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). …

Relationship Between Central Sympathetic Drive and Magnetic Resonance Imaging–Determined Left Ventricular Mass in Essential Hypertension

Sympathetic activation has been implicated in the development of left ventricular hypertrophy (LVH). However, the relationship between sympathetic activation and LV mass (LVM) has not been clearly defined across a range of arterial pressure measurements. The present study was planned to determine that relationship, using cardiac magnetic resonance imaging to accurately quantify LVM, in hypertensive patients with and without LVH and in normal subjects. Twenty-four patients with uncomplicated and untreated essential hypertension (LVH[-]) were compared with 25 patients with essential hypertension and left ventricular hypertrophy (LVH[+]) and 24 normal control subjects. Resting muscle sympathetic nerve activity was quantified as multiunit bursts and single units. Cardiac magnetic resonance imaging-determined LVM was indexed to body surface area (LVM index); in the LVH[-] group, LVM index was 67+/-2.1 g/m2, a value between those of the LVH[+] (91+/-3.4 g/m2) and normal control (57+/-2.2 g/m2) groups, respectively. The sympathetic activity in the LVH[-] group (53+/-1.3 bursts per 100 cardiac beats and 63+/-1.6 impulses per 100 cardiac beats) was between (at least P<0.001) those of the LVH[+] (66+/-1.7 bursts per 100 cardiac beats and 77+/-2.2 impulses per 100 cardiac beats) and normal control (39+/-3.0 bursts per 100 cardiac beats and 45+/-3.4 impulses per 100 cardiac beats) groups. Significant positive correlation existed between sympathetic activity and LVM index in the LVH[-] and LVH[+] groups (at least r=0.76, P<0.0001) but not in the normal control group. However, no consistent relationship existed between arterial blood pressure and sympathetic activity or LVM index. These findings further support the hypothesis that central sympathetic activation is associated with the development of LVH in human hypertension.

Sleep and Hypertension

Even though sleep is widely considered to be a restorative and refreshing process, it is characterized by complex activity of the cardiovascular autonomic mechanisms and by relevant changes of arterial pressure and heart rate. It has been widely reported that fluctuations and variability of cortical and visceral activities involve a differential autonomic regulation of the cardiovascular system in relationship to different sleep cycles. During non–rapid eye movement (REM) sleep, arterial pressure and heart rate tend to decrease, whereas periods of relative hypertension and tachycardia characterize REM periods. With regard to the cardiovascular autonomic modulation, non-REM sleep is characterized by a vagal predominance, whereas during REM sleep, a relative increase in sympathetic activity is demonstrated by an increased sympathetic outflow to muscle blood vessels.1–3 See p 849 Therefore, this continuous cycling of non-REM and REM phases, with the consequent cardiovascular autonomic changes, makes sleep a period of considerable physiological turbulence characterized by sudden and abrupt blood pressure and heart rate changes. This cardiovascular instability has stimulated the investigation of the neural mechanisms involved in maintaining the cardiovascular homeostasis during the different sleep phases. The first pivotal study conducted with the Oxford technique in normotensive and hypertensive subjects4 clearly showed that changes in baroreflex function investigated by quantifying the reflex RR interval lengthening in response to a pharmacologically induced increase in systolic blood pressure (obtained through intravenous injection of phenylephrine), occurred ongoing from wakefulness to sleep. These changes consisted of an increase in the reflex sensitivity and of a resetting, moving the operating point of the reflex toward lower blood pressure values.4 In the past few years, this issue has been further investigated because it is now possible to investigate the arterial baroreflex function by analyzing the correlated blood pressure and spontaneous heart rate …

Renin-Angiotensin-Aldosterone System and Salt-Sensitivity Genes are Not Associated with Left Ventricular Mass in Essential Hypertension

Renin-Angiotensin-Aldosterone System and Salt-Sensitivity Genes are Not Associated with Left Ventricular Mass in Essential Hypertension

11β-Hydroxysteroid dehydrogenase type 2 activity is associated with left ventricular mass in essential hypertension

Left ventricular mass (LVM) is under the control of aldosterone and angiotensin II in experimental hypertension, but the effect of aldosterone on LVM is controversial in essential hypertension (EH). Some EH patients show a mild impairment of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) activity without clinical features of the syndrome of apparent mineralocorticoid excess, where the incomplete cortisol-to-cortisone conversion leads to glucocorticoid-mediated mineralocorticoid effects. The mineralocorticoid receptor and 11beta-HSD2 are co-expressed in human heart. We investigated whether LVM may be regulated by glucocorticoids in EH patients. The ratio between 24 h urinary tetrahydro derivatives of cortisol and cortisone (THFs/THE), plasma renin activity, 24 h urinary aldosterone, blood pressure, and LVM indexed for height(2.7) (LVMh(2.7)) were analysed in 493 never-treated hypertensives and 98 normotensives. THFs/THE was associated with LVMh(2.7) in hypertensives and normotensives (r=0.32, P<0.001, and r=0.17, P=0.04, respectively) and persisted after adjusting for confounders (multiple regression analysis). Body mass index, sex, recumbent plasma renin activity, and THFs/THE accounted for 26.1% of LVMh(2.7) variation. Urinary aldosterone was not correlated with LVMh(2.7). We suggest that glucocorticoids may take part in the regulation of LVM in EH patients as a function of 11beta-HSD2 activity, and contribute to the target organ damage associated with essential hypertension.

Aortic calcification is associated with age and sex but not left ventricular mass in essential hypertension.

The aim of this study was to investigate the prevalence of aortic calcification in patients with essential hypertension and its relationship with age, sex, and left ventricular hypertrophy. Two hundred ninety consecutive patients with essential hypertension were studied. A chest radiograph and an echocardiograph were performed. Aortic calcification was observed in 74/290 (25.5%) patients. Patients with calcification were mostly female (67.6%) and older (71.8+1.9 years), whereas patients without calcification were younger (59.0+0.79) and of both sexes (51.85% female). Left ventricular mass index in male patients with aortic calcification was 147.3+4.32 g/m(2) and without calcification was 132.7+2.28 g/(2) (p=0.023). Female patients' values were 131.9+4.32 g/m(2) with calcification and 121.2+2.85 g/m(2) without calcification (p=0.025). Left ventricular mass was independently associated with age and sex but not with aortic calcification. The prevalence of aortic calcification in essential hypertension is considerably higher compared to the general population. Essential hypertension and age seem to contribute to the concurrent appearance of aortic calcification and increased left ventricular mass.

P137 Diurnal variations of blood pressure and left ventricular mass in essential hypertension

P137 Diurnal variations of blood pressure and left ventricular mass in essential hypertension

A meta-analysis of the effects of treatment on left ventricular mass in essential hypertension

Purpose Antihypertensive medications have different effects on left ventricular mass. We conducted a meta-analysis of double-blind trials that measured the effects of antihypertensive therapy on left ventricular mass. Methods Medical databases and review articles were screened for double-blind, randomized controlled trials (through September 2002) that reported the effects of diuretics, beta-blockers, calcium antagonists, angiotensin-converting enzyme (ACE) inhibitors, or angiotensin II receptor antagonists on echocardiographic left ventricular mass in essential hypertension. Treatment arms of the same drug class, weighted for the number of patients, were combined. Analysis of covariance was performed to detect differences among drug classes in effects on left ventricular structure. Results Eighty trials with 146 active treatment arms (n = 3767 patients) and 17 placebo arms (n = 346 patients) were identified. Adjusted for treatment duration and change in diastolic blood pressure, there was a significant difference ( P = 0.004) among medication classes: left ventricular mass index decreased by 13% with angiotensin II receptor antagonists (95% confidence interval [CI]: 8% to 18%), by 11% with calcium antagonists (95% CI: 9% to 13%), by 10% with ACE inhibitors (95% CI: 8% to 12%), by 8% with diuretics (95% CI: 5% to 10%), and by 6% with beta-blockers (95% CI: 3% to 8%). In pairwise comparisons, angiotensin II receptor antagonists, calcium antagonists, and ACE inhibitors were more effective at reducing left ventricular mass than were beta-blockers (all P <0.05 with Bonferroni correction). Conclusion Antihypertensive drug classes have different effects on left ventricular mass reduction. Whether a greater reduction of left ventricular mass results in better clinical outcomes remains to be determined.

Effects of amlodipine and fosinopril on heart rate variability and left ventricular mass in essential hypertension

Effects of amlodipine and fosinopril on heart rate variability and left ventricular mass in essential hypertension