Regression of left ventricular mass in hypertensive patients treated with perindopril/indapamide as a first-line combination: the REASON echocardiography study

BACKGROUND: Increase in left ventricular mass (LVM) may be linked to morbidity and mortality in hypertensive patients. Arterial stiffness, systolic blood pressure (BP), and pulse pressure (PP) seem to be the main determinants of LVM. The perindopril/indapamide combination normalizes systolic BP, PP, and arterial function to a greater extent than atenolol. The aim of this study was to compare the effects of perindopril (2 mg)/indapamide (0.625 mg) first-line combination with atenolol (50 mg) on LVM reduction in hypertensive patients. METHODS: Two hundred fourteen patients with essential hypertension participating in the PREterax in Regression of Arterial Stiffness in a ContrOlled Double-BliNd (REASON), randomized, double-blind, parallel-group study, underwent M-mode two-dimensional-guided echocardiography. RESULTS: Perindopril/indapamide and atenolol were both effective at brachial BP reduction during the 12-month period. The systolic BP reduction was significantly greater with perindopril/indapamide than with atenolol (-21.2 v -15.3 mm Hg), whereas the reduction in diastolic BP was similar between treatment groups (-12.1 v -11.3 mm Hg). Reduction in LVM was higher with perindopril/indapamide than with atenolol. The between-group difference was significant for LVM (-13.6 v -4.3 g, P = .027), LVM/body surface area (LVMI1, P = .032), and LVM/body height2.7 (LVMI2, P = .013). The 124 patients with LV hypertrophy at baseline showed greatest LVM regression (LVM: -22.5 v -8.9 g, P = .009; LVMI1, P = .031; LVMI2, P = .028). The reduction in LVM adjusted for brachial systolic BP and heart rate was still significantly greater with perindopril/indapamide than with atenolol. CONCLUSIONS: Treatment, based on a first-line perindopril/indapamide combination in hypertensive patients, was more effective than atenolol on regression of echocardiographic indices of LVM and LV hypertrophy.     

Role of arterial hypertension in left ventricle hypertrophy in hemodialysis patients: an echocardiographic study.

To assess the role of arterial hypertension in left ventricle (LV) hypertrophy among hemodialysis patients, echocardiographic evaluation was performed in 10 hypertensive and 13 normotensive hemodialysis subjects matched for age, sex, race, duration of dialysis treatment and degree of interdialytic volume expansion. We excluded from the latter group patients with previous hypertension since hypertensive heart disease may persist after adequate blood pressure control. We also studied 17 normal controls and 10 non-uremic patients with essential hypertension. Comparisons between the two uremic groups showed that the hypertensive patients had a higher mass index (222 +/- 74 x 108 +/- 26, p = 0.0001) and posterior wall thickness (12 +/- 2 x 9 +/- 2, p = 0.0001) and a reduced LV radius/wall thickness ratio (4.4 +/- 0.7 x 5.8 +/- 1, p = 0.0001). There were no significant echocardiographic differences between normal controls and normotensive uremics. In contrast, compared to controls, hypertensive uremic patients showed an increased LV mass index (222 +/- 74 x 83 +/- 21, p = 0.0001) and posterior wall thickness (12 +/- 2 x 7 +/- 1, p = 0.0001) and a reduced LV radius/wall thickness ratio (4.4 +/- 0.7 x 6.5 +/- 1.1, p = 0.001), characterizing concentric hypertrophy. They also had ventricular dilation with larger LV dimensions than in controls (53 +/- 5 x 47 +/- 4, p = 0.004). In patients with essential hypertension, the mass index (135 +/- 22), wall thickness (11 +/- 1) and LV radius/wall thickness ratio (4.3 +/- 0.7) significantly differed (p = 0.0001) from those in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular mass and atrial volume determined by cine magnetic resonance imaging in essential hypertension

To evaluate the relationship between left atrial volume determined by cine magnetic resonance imaging and progression of left ventricular hypertrophy (LVH), left atrial volume and echocardiographic left ventricular mass (LVM) were measured in 30 hypertensive patients (15 without LVH and 15 with LVH) and 10 normotensive control subjects. We also evaluated the effects of antihypertensive therapy on the cardiac chamber volumes and LVM in hypertensive patients. The cardiac chamber volumes and LVM were indexed by body surface area. Although there were no significant differences in left ventricular chamber volumes among the three groups, both maximum and minimum left atrial volume indexes, and the LVM index were greater in hypertensive patients with LVH than in the other two groups. The LVM index was correlated with maximum left atrial volume index (r = 0.74, P < .0001), and minimum left atrial volume index (r = 0.76, P < .0001), respectively. Furthermore, in multivariate models, the LVM index was significantly correlated with maximum left atrial volume index. In hypertensive patients with LVH, both maximum and minimum left atrial volume indexes, and the LVM index significantly reduced after treatment. The percent of changes in maximum left atrial volume index after treatment was significantly correlated with the percent of changes in LVM index after treatment. In conclusion, our data indicate that LVH is an independent determinant of left atrial enlargement, and both LVH and left atrial enlargement may be reversed by some effective therapeutic interventions.     

Self-reported weight and height: implications for left ventricular hypertrophy detection. An Italian multi-center study

We examined the difference between self-reported and measured body size values and their impact on detection of left ventricular hypertrophy (LVH) by echocardiographic LV mass indexation. A total of 1963 subjects referred by their practitioners for routine echocardiographic examination to nine outpatient echocardiographic laboratories across Italy were included in the study. Left ventricular hypertrophy was defined according to two gender- specific criteria as: A) Left ventricular mass (LVM) index ≥49 g/h(2.7) in men and ≥45 g/h(2.7) in women; B) LVM index ≥125 g/m(2) in men and ≥110 g/m(2) in women. Prevalence of LVH was calculated by indexing LVM to both self-reported and measured anthropometric values. In the whole population, LVH tended to be underestimated by self-reported values by 5.4% according to criterion A (48.5% vs. 53.9%, p < 0.001) and by 1.2% according to criterion B (29.6% vs. 30.8%, p < 0.01); similar findings were observed in the hypertensive subgroup encompassing one-half of the sample. Underestimation of LVH was more pronounced in older patients than in younger patients: 8.6% vs. 3.2% (p < 0.001) by criterion A, 3.1% vs. 0.1% (p < 0.001) by criterion B, in women than in men (8.6% vs. 3.3% (p < 0.001) by criterion A and 1.8% vs. 0.5% (p < 0.01) by criterion B. In a sample of outpatients attending echocardiographic laboratories, LVH is misclassified when left ventricular mass is normalized to self-reported weight and height. The error is related to the clinical characteristics of patients and is more pronounced when LVM is normalized to height(2.7).     

Effects of exercise on coronary circulation in left ventricular hypertrophy caused by hypertension

Exercise is known to promote myocardial vascularity. We therefore studied whether it could prevent coronary abnormalities of hypertensive left ventricular (LV) hypertrophy. Female Sprague-Dawley 1 clip-2 kidneys Goldblatt hypertensive rats (RHR) and their appropriate controls (Sham-SH), were either made to swim (RHR-SW, SH-SW) or kept sedentary (RHR-SED, SH-SED) for 9 weeks. Maximal coronary blood flow (LV CBF, ml/min/gm) and minimal coronary resistance after carbochrome (total LVCR/LV mmHg/ml/min), an index of the functional cross sectional area (CSA) of coronary resistance vessels, were determined in conscious rats by microspheres. Results (m +/- SD) (n = 12 in all groups): (Table: see text). Exercise increased functional coronary CSA in normotensive rats only. This beneficial effect did not occur in hypertension, probably because of functional changes in the coronary vessels of RHR.     

Arterial hypertension,left ventricular geometry and QT dispersion in a middle-aged Estonian female population

The aim of the present study was to determine the prevalence of Left ventricular hypertrophy (LVH) and different left ventricular (LV) geometric patterns in the middle-aged women population of Tallinn, to assess the relationship between LV geometry, age, blood pressure and LV repolarization duration and inhomogeneity. A random sample of the population, 482 women aged 35-59, was examined in the framework of a cardiovascular risk factors survey for the WHO/CINDI programme years 1999-2000. Patients with valvular pathology, primary cardiomyopathy, atrial fibrillation, bundle branch blocks and flat T wave on electrocardiography (ECG) were excluded; 398 (82.2%) of the participants underwent echocardiography (Echo) and standard 12-lead ECG at rest and were included in the study. LVH was defined if left ventricular mass (LVM), LVM/height and LVM/BSA were >198 g, >121 g/m and > 120 g/m2, respectively. Arterial hypertension was determined in 23.1% of the women. The prevalence of arterial hypertension was three times higher in those aged 50-59 than in those aged 40-49 (37.4% vs 13.2%; p < 0.05). Different geometric patterns were found as follows: concentric hypertrophy in 9.1%; eccentric hypertrophy 33.9%; concentric remodelling 9.5% and normal geometry 47.5% of the participants. Concentric hypertrophy was found exclusively in hypertensive women and increased with age. No age-related eccentric hypertrophy and concentric remodelling differences were found, either in the normotensive or in the hypertensive group. Prolonged QT dispersion--a marker of increased myocardial electrical instability, was associated with LVH and arterial hypertension and was related mostly to concentric hypertrophy in hypertensives.     

Echocardiographic criteria for left ventricular hypertrophy: the Framingham Heart Study

Of 6,148 original cohort and offspring subjects of the Framingham Heart Study who underwent routine evaluation, a healthy group of 347 men (aged 42 +/- 12 years) and 517 women (aged 43 +/- 12 years) was identified to develop echocardiographic criteria for left ventricular (LV) hypertrophy. Healthy subjects were defined as normotensive, receiving no cardiac or antihypertensive medications, nonobese and free of cardiopulmonary disease. Echocardiographic criteria (in accordance with the American Society of Echocardiography convention) for LV hypertrophy, based on mean plus 2 standard deviations for LV mass, LV mass corrected for body surface area and LV mass corrected for height in this healthy sample are, respectively: 294 g, 150 g/m2 and 163 g/m in men and 198 g, 120 g/m2 and 121 g/m in women. Criteria based on LV mass/height result in higher prevalence rates of LV hypertrophy than LV mass/body surface area while still correcting for body size. The prevalence of LV hypertrophy in the entire study population (using LV mass/height criteria) is 16% in men and 19% in women. Until outcome guided criteria for LV hypertrophy are developed, application of sex-specific criteria based on a healthy population distribution of LV mass offer the best approach to echocardiographic diagnosis of LV hypertrophy.     

Myocardial morphological changes related to sodium intake in normotensive and hypertensive patients never treated before

Several factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of sodium has recently been suggested. In the present study, we assessed the influence of dietary sodium on the degree of left ventricular hypertrophy (LVH) and LV structure in 30 normotensive (NT) subjects aged 34 +/- 11 years (mean +/- SD) and 50 patients (39 +/- 10 years) with mild essential hypertension EH (canal blood pressure 154 +/- 16/96 +/- 11 mmHg), who had never received antihypertensive drugs. Posterior wall thickness (PWT) and left ventricular mass (LVM) were measured by M-mode echocardiography and urinary sodium excretion (UNa, mmol/24h) was taken as an index of sodium intake. In NT and EH, LVM was directly correlated with UNa (r = 0.48 and 0.49; p less than 0.006 and 0.002, respectively). A stepwise multiple regression analysis confirmed that UNa was a determinant of LVM independently of sex, age, and body weight in the two groups. In NT the correlation with UNaV was the result of an increase of the end-diastolic diameter without change in PWT whilst in EH it was the consequence of an increase in wall thickness (R = 0.49, p less than 0.0001) without a modification of LV diameter. These results suggest that salt intake may be an important determinant of cardiac structural adaptation in both NT and EH subjects; however, only EH have a salt sensitive LV wall hypertrophy.     

Myocardial hypertrophy and left ventricular diastolic function in hypertensive patients: an echo Doppler evaluation

The presence and the characteristics of left ventricular diastolic dysfunction in mild to moderate systemic hypertension were evaluated in 13 normotensive subjects (Group I), in 12 hypertensive subjects without (Group II) and 28 with (Group III) LV hypertrophy who underwent two-dimensional Doppler echocardiographic study. Among Group III patients, a subset (n = 12) with a dilated left ventricle was identified. Diastolic filling parameters were impaired in Group III patients while, in Group II, they were intermediate between Groups I and III. In all Group III patients normalized peak filling rate (nPFR) correlated directly with mean velocity of circumferential fibre shortening (mVCF) (r = 0.55; P less than 0.001) and inversely with left ventricular mass index (LVM) (r = -0.60; P less than 0.001), left ventricular end-diastolic diameter (LVIDd) (r = -0.63; P less than 0.001), LV peak systolic stress (LVWST) (r = -0.64; P less than 0.01). A separate analysis showed that these correlations were also present in patients without left ventricular dilation; in the subset with left ventricular dilation nPFR correlated only with LVWST (r = -0.73; P less than 0.01), but not with LVM, mVCF, LVIDd. Thus, left ventricular hypertrophy is one of the major determinants of diastolic dysfunction in hypertensives; other factors influence nPFR values in hypertensive patients when the left ventricle dilates.     

Diastolic dysfunction precedes myocardial hypertrophy in the development of hypertension

BACKGROUND: Left ventricular (LV) hypertrophy and impaired diastolic function may occur early in systemic hypertension, but longitudinal studies are missing. METHODS: We performed an echocardiographic follow-up study in young initially normotensive male offspring of hypertensive (OHyp) (n = 25) and normotensive (ONorm) (n = 17) parents. Blood pressure (BP), LV mass, and mitral inflow were determined at baseline and after 5 years. Pulmonary vein flow pattern assessment and septal myocardial Doppler imaging were additionally performed at follow-up. RESULTS: At follow-up, BP was not significantly different between the two groups (128 +/- 11/84 +/- 10 v 123 +/- 11/81 +/- 5 mm Hg, OHyp v ONorm) but five OHyp had developed mild hypertension. LV mass index remained unchanged and was not different between the two groups at follow-up (92 +/- 17 v 92 +/- 14 g/m2). Diastolic echocardiographic properties were similar at baseline, but, at follow-up, the following differences were found: mitral E deceleration time (209 +/- 32 v 185 +/- 36 msec, P < .05) and pulmonary vein reverse A wave duration (121 +/- 15 v 107 +/- 12 msec, P < .05) were prolonged in the OHyp as compared to the ONorm. Compared to the normotensive subjects, the five OHyp who developed hypertension had more pronounced alterations of LV diastolic function, that is, significantly higher mitral A (54 +/- 7 v 44 +/- 9 cm/sec, hypertensives v normotensives, P < .05), lower E/A ratio (1.31 +/- 0.14 v 1.82 +/- 0.48, P < .05), increased systolic-to-diastolic pulmonary vein flow ratio (1.11 +/- 0.3 v 0.81 +/- 0.16, P < .005), longer myocardial isovolumic relaxation time (57 +/- 7 v 46 +/- 12 msec, P < .05) as well as smaller myocardial E (10 +/- 1 v 13 +/- 2 cm/sec, P < .05) and E/A ratio (1.29 +/- 0.25 v 1.78 +/- 0.43, P < .05), despite similar LV mass (91 +/- 16 v 93 +/- 18 g/m2). CONCLUSIONS: Over a 5-year follow-up, initially lean, normotensive, young men with a moderate genetic risk for hypertension, developed Doppler echocardiographic alterations of LV diastolic function compared to matched offspring of normotensive parents. These alterations were more pronounced in the OHyp who developed mild hypertension and occurred without a distinct rise in LV mass.     

Evaluation of the left ventricular anatomy in hypertrophic cardiomyopathy: comparison between echocardiography and cardiac magnetic resonance imaging

AIM: The aim of this study was to assess the relationship between echocardiographic indexes of left ventricular (LV) hypertrophy with LV mass (LVM) obtained at cardiac magnetic resonance (CMR) in a population of patients with hypertrophic cardiomiopathy (HCM). METHODS: Thirty-nine patients with HCM underwent echocardiography and CMR. By echocardiography maximal wall thickness (MWT), Spirito' and Maron's hypertrophy index and the Wigle's score were obtained. Absolute LVM was measured through CMR and indexed to body surface area (LVMi). Data were analysed using linear regression analysis. RESULTS: In 31% of patients there was an incomplete echocardiographic LV anatomic characterization. However, there was a good correlation between MWT measured at echocardiography and at CMR (P<0.001; r=0.755). Overall echocardiographic indexes of LV hypertrophy correlate with either LVM and LVMi: MWT (P=0.008, r=0.420 and P=0.003, r=0.467, respectively); Spirito' and Maron's hypertrophy index (P=0.003, r=0.551 and P=0.001, r=0.606, respectively) and Wigle's score (P=0.004, r=0.522 and P=0.004, r=0.522, respectively). CONCLUSION: In our HCM population, although a complete anatomic LV anatomic characterization was not obtained by echocardiography in all patients, echocardiographic hypertrophic indexes showed a good correlation with LVM obtained by CMR.     

Effect of Comorbidities and Medications on Left Ventricular Mass Regression After Bariatric Surgery

J Clin Hypertens (Greenwich). 2010;12:223–227. ^©2010 Wiley Periodicals, Inc. Hypertension, diabetes, and obesity frequently coexist and significantly contribute to cardiovascular morbidity and mortality. Weight loss in obese individuals has been associated with improved blood pressure control and regression in left ventricular (LV) hypertrophy. The authors investigated the impact of comorbidity and medication on clinical and echocardiographic parameters after weight loss in obese patients. Serial echocardiography and clinical data were collected in 62 patients before bariatric surgery and after 6 months or 10% weight loss. Obese patients with diabetes or hypertension had higher baseline LV mass (LVM) (334±73 g in hypertension and diabetes vs 252±97 g in hypertension and 219±75 g in disease-free patients, P=.003; P=.089for differences in LVM indexed by height), despite the lack of significant differences in body mass index or systolic blood pressure. There were no significant differences in baseline LVM or LVM index related to the medication used to treat hypertension. After weight loss, patients on β-blocker therapy experienced the most significant LV hypertrophy regression (−76.5±79.1 g with β-blockers, −17.8±43.7 g with diuretics, −4.5±46.6 g with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, and −23.1±50.9 g in not treated patients, overall P=.538; β-blockers vs no therapy P<.005; P=.145 for differences in LVM index). Bariatric surgery, combined with a weight loss program, provide substantial weight and LVM reduction regardless of comorbidities or blood pressure changes. β-Blocker therapy appears to be associated with the greatest LVM regression after weight loss.     

Specific features of left ventricular hypertrophy in hypertensive obese women. An echocardiographic study

The echocardiographic features of the left ventricle of 37 obese women (body mass index above 30) and 37 lean controls, matched for sex, age, height and blood pressure levels, were studied. Twenty-six patients in each group were hypertensive. The normotensive obese patients did not show any differences, comparing to the normotensive controls; on the contrary, the hypertensive obese patients had higher left ventricular mass (LVM), stroke volume and cardiac output (CO), and lower total peripheral resistance (TPR) than the hypertensive controls. A positive correlation was found between the LVM and the CO (r = 0.57, P less than 0.01) in hypertensive obese patients, and between the relative wall thickenss (h/r, that is the ratio between the left ventricular wall thickness and the left ventricular radius) and TPR (r = 0.64, P less than 0.01) in the hypertensive controls. It is concluded that obesity per se does not determine left ventricular hypertrophy in women; however, when obesity is associated with arterial hypertension, a distinct pattern of hypertrophy, characterized by high CO and low TPR, develops.     

Prolonged QT interval is associated with blood pressure rather than left ventricular mass in spontaneously hypertensive rats

QT interval is prolonged in hypertensive individuals, although the factors responsible for this increase are not completely understood. We questioned whether enhanced left ventricular mass (LVM) or increased systemic blood pressure represents the principal factor determining QT prolongation in the period of development of hypertension and left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHR). In 12-and 20-week-old SHR (SHR12 and SHR20) and age-matched normotensive Wistar-Kyoto rats (WKY12 and WKY20), arterial systolic blood pressure (sBP) was measured using tail-cuff technique. Orthogonal Frank ECG was registered in anaesthetized animals in vivo, and bipolar ECG was measured in spontaneously beating isolated hearts in vitro. Progressive increase of sBP and LVM resulted in significant QT prolongation in SHR20 as compared to WKY12, WKY20, and also to SHR12 in vivo (WKY12: 82 +/- 9 ms, WKY20: 81 +/- 9 ms, SHR12: 88 +/- 15 and SHR20: 100 +/- 10, respectively; p < 0.05) but not in isolated hearts (WKY20: 196 +/- 39 ms and SHR20: 220 +/- 55, respectively; NS). In whole animals, QT duration was positively related to sBP (r = 0.6842; p < 0.001) but not to LVM (r = 0.1632, NS) in SHR20. The results suggest that QT prolongation in SHR developing hypertension and LVH depends on blood pressure rather than increase in LVM. In this period, myocardial hypertrophy is probably the predisposition for QT prolongation, but the significant change manifests only in the presence of elevated systemic factors.     

The limited value of plasma B-type natriuretic peptide for screening for left ventricular hypertrophy among hypertensive patients

BACKGROUND: Several reports have suggested that plasma B-type natriuretic peptide (BNP) levels are elevated in hypertensive patients especially with left ventricular (LV) hypertrophy. However, few data have been available concerning the utility of plasma BNP measurement to identify LV hypertrophy in hypertensive patients in a general population screening context. METHODS: We measured plasma BNP concentrations in 1112 volunteers in a health screening program (mean age, 57 years). All subjects underwent electrocardiography, chest X-ray, and echocardiography. Among the sample, 284 subjects were designated as hypertensive because they were on antihypertensive drugs or showed elevated systemic blood pressure. By echocardiography, 36 of the hypertensive patients showed significant LV hypertrophy. RESULTS: There were no significant differences in age and sex between the LV hypertrophy and non-LV hypertrophy groups. Plasma BNP levels in the LV hypertrophy group were significantly higher than in the non-LV hypertrophy group (19.4 +/- 18.9 v 28.2 +/- 28.2 pg/mL; P <.05). However, the ability of plasma BNP levels to discriminate between LV hypertrophy and non-LV hypertrophy patients was not sufficient as the area under the receiver operating characteristic curve was 0.588 (95% CI: 0.528-0.646) with sensitivity of 50.0% and specificity of 69.0%. Positive and negative predictive values for detecting LV hypertrophy among hypertensive patients were 18.9% and 90.5%, respectively. This ability did not improve significantly when the screening was limited to patients with untreated LV hypertrophy or concentric LV hypertrophy. CONCLUSIONS: Plasma BNP testing in a mass screening setting is of limited use for the identification of LV hypertrophy patients among hypertensive patients with heterogeneous etiology.     

Impact of the time rate of blood pressure variation on left ventricular mass

OBJECTIVES: Blood pressure (BP) changes are steeper in hypertensive than in normotensive individuals, whereas an increased rate of BP fluctuations is associated with medial hypertrophy of the carotid arteries. We evaluated the association between the rate of BP variation derived from ambulatory blood pressure monitoring (ABPM) data analysis and left ventricular mass (LVM). METHODS: ABPM and echocardiographic measurements of LVM were performed in 365 normotensive, 185 white-coat hypertensive (WCH) and 448 uncomplicated hypertensive individuals. RESULTS: The daytime and night-time rate of systolic blood pressure (SBP) and diastolic BP variation were significantly higher in hypertensive than in normotensive (P < 0.001) and WCH (P < 0.05) individuals. In the entire study population multiple linear regression models revealed independent determinants of LVM in the following rank order: body mass index (beta + 0.266, P < 0.001), daytime SBP (beta + 0.264, P < 0.001), male sex (beta +0.220, P < 0.001), age (beta + 0.203, P < 0.001), daytime heart rate (HR; beta - 0.191, P < 0.001), daytime rate of SBP variation (beta + 0.167, P < 0.001), and SBP dipping (beta - 0.132, P < 0.001). A 0.1 mmHg/min increase in the daytime rate of SBP variation correlated with an increment of 7.087 g (95% confidence interval 4.775-9.399) in the LVM. The addition of the daytime rate of SBP variation in the multiple regression model for the prediction of LVM significantly increased the adjusted model R [R change 0.024 (2.4%); P for change < 0.001]. CONCLUSION: Steeper BP variations may produce a greater stress on the left ventricular wall and may have an additive role to body habitus, BP and HR levels in the detection of cardiac hypertrophy. Target-organ damage in hypertensive patients, in addition to BP levels, dipping status and BP variability, may also be related to a steeper rate of BP oscillations.     

Relationship Between Left Ventricular Geometry and Soluble ST2 in a Cohort of Hypertensive Patients

Left ventricular (LV) hypertrophy (LVH) is classified according to geometric pattern into 4 types: concentric hypertrophy, eccentric hypertrophy, concentric remodeling, and normal geometry. Prevalence of death and cardiovascular complications associated with hypertension depend on the geometric pattern. Although soluble ST2 levels, a novel cardiac biomarker of mechanical strain is increased in hypertension, the relationship with hypertensive LV geometric patterns has not been studied. The authors investigated the relationship between soluble ST2 levels and LV geometric patterns in a cohort of hypertensive patients. LVH was considered present when echocardiographic LV mass index exceeded 49.2 g/m^2.7 in men and 46.2 g/m^2.7 in women. Patients with concentric hypertrophy had higher soluble ST2 levels compared with patients with normal geometry (20.4±8.4 ng/mL vs 14.3±5.4 ng/mL, P<.002). Therefore, soluble ST2 level is not only affected by hypertensive LV, but may be a future biomarker in differentiating concentric hypertrophy from normal geometry in hypertension.     

Usefulness of B-type natriuretic peptide and C-reactive protein in predicting the presence or absence of left ventricular hypertrophy in patients with systemic hypertension

The diagnosis of left ventricular (LV) hypertrophy, an independent predictor of death and cardiovascular events, is difficult without using echocardiography. This study tested the hypothesis whether C-reactive protein (CRP) and B-type natriuretic peptide (BNP) would be useful to exclude echocardiographic LV hypertrophy. Consecutive hypertensive outpatients were asked to participate. Exclusion criteria were overt heart failure, severe renal insufficiency or any other severe concomitant illness. A venous blood sample was taken to measure plasma CRP and BNP concentrations. Echocardiographic LV hypertrophy was defined as LV mass > or =125 g/m2 for men and > or =110 g/m2 for women. In total, 320 patients were studied, and 37 patients (12%) had echocardiographic LV hypertrophy. Patients with LV hypertrophy were significantly older and had higher CRP and BNP concentrations and higher systolic blood pressure than those without LV hypertrophy. The optimal cut-off points for the diagnosis of LV hypertrophy were 35 pg/ml for BNP (sensitivity 73%, specificity 72%) and 2.5 mg/L for CRP (sensitivity 68%, specificity 59%). Only 1 of 123 patients with values of BNP and CRP less than the optimal cut-off point had echocardiographic LV hypertrophy, resulting in a high negative predictive value of 99% for the 2 blood tests combined to exclude LV hypertrophy. In conclusion, in hypertensive patients, echocardiographic LV hypertrophy can be excluded on the basis of a single blood sample for the determination of BNP and CRP.     

Multivariate associates of QT interval parameters in diabetic patients with arterial hypertension: importance of left ventricular mass and geometric patterns

The aim of the study was to assess the determinants of increased QT interval parameters in diabetic patients with arterial hypertension and, in particular, the strength of their relationships to echocardiographically derived left ventricular mass (LVM) and geometric patterns. In a cross-sectional study with 289 hypertensive type 2 diabetic outpatients, maximal QT and QTc (heart rate-corrected) intervals, and QT, QTc, and number-of-leads-adjusted QT interval dispersions were manually measured from standard baseline 12-lead ECGs. Electrocardiographic criteria for left ventricular hypertrophy (LVH) were either Sokolow-Lyon or Cornell sex-specific voltages. LVM and geometric patterns were determined by 2D echocardiography. Statistical analyses involved bivariate tests (Mann-Whitney, chi2, Spearman's correlation coefficients, ANOVA and receiver-operating-characteristic (ROC) curve analyses) and multivariate tests (multiple linear and logistic regressions). QT dispersion measurements showed significant correlations with echocardiographic LVM (r=0.26-0.27). ROC curves demonstrated a poor isolated predictive performance of all QT parameters for detection of LVH (areas under curve: 0.58-0.59), comparable to that of electrocardiographic voltage criteria. Only patients with concentric hypertrophy had significantly increased QT dispersion (QTd) when compared to those with normal geometries (64.24+/-21.09 vs 53.20+/-15.35, P<0.05). In multivariate analyses, both electrocardiographic and echocardiographic LVH were independent predictors of increased QTd, as well as only QTd and gender were determinants of LVM. In conclusion, increased QT interval dispersion is associated with LVM and concentric hypertrophy geometric pattern in diabetic hypertensive patients, although in isolation neither QTd nor any QT parameter presents enough predictive performance to be recommended as screening procedures for detection of LVH.     

Exercise-induced myocardial capillary growth in the spontaneously hypertensive rat

Spontaneously hypertensive rats (SHR) were studied to test the hypothesis that endurance exercise training can stimulate capillary growth and offset the decrement associated with the development of myocardial hypertrophy. The exercise group (SHR-T) was trained on a treadmill for 10 weeks at 70-90% maximum VO2 and compared to nontrained SHR and normotensive Wistar-Kyoto (WKY) at 16 weeks of age. Thus, the training program coincided with the development of hypertension and hypertrophy in SHR. Image analysis was used to study capillaries in one micron thick left ventricular tissue samples from perfuse-fixed hearts. Training did not affect left ventricular mass or blood pressure, but reversed the characteristic decrements in capillary surface area (CSA), volume (CV), and numerical density (CD). CSA and CV were most markedly affected by exercise, as mean values for these parameters increased by 31 and 40%, respectively, compared to SHR. The magnitude of these changes approximated the magnitude of hypertrophy as evidenced by left ventricular weight/body weight ratios (42% in SHR and 37% in SHR-T). Anatomical intercapillary distance was also normalized by training (means +/- SEM): SHR-T, 11.65 +/- 0.31; SHR, 13.97 +/- 0.37; WKY, 11.19 +/- 0.37. These data indicate that exercise stimulates capillary growth in the face of developing hypertension and its related left ventricular hypertrophy.