Diminished nocturnal decline in blood pressure in elderly hypertensive patients with left ventricular hypertrophy.

To assess the circadian blood pressure (BP) changes in elderly hypertensive patients with left ventricular hypertrophy (LVH), the ambulatory BP was measured noninvasively every 30 minutes for 24 hours in those patients with LVH (n = 15) and without LVH (n = 23), and in normotensive elderly subjects (n = 11). Although the daytime systolic BP (SBP) was comparable in the two hypertensive groups, the nighttime SBP in patients with LVH tended to be higher than in patients without LVH (149.0 +/- 15.1 versus 138.4 +/- 20.1 mm Hg, p less than 0.10). The LV mass index correlated significantly with the nighttime SBP (r = 0.43, p less than 0.01), but not with the daytime SBP (r = 0.24, ns), with clinic SBP (r = 0.14, p = ns) or the SBP after handgrip exercise (r = 0.31, p = ns). The difference in the systolic BP between daytime and nighttime (D-N SBP) in patients with LVH (2.8 +/- 9.4 mm Hg) was significantly less than that in patients without LVH (12.8 +/- 16.0 mm Hg) (p less than 0.02). In addition, the D-N SBP correlated inversely with the left ventricular mass index (r = -0.33, p less than 0.05). It was concluded that hypertension in the elderly with LVH was associated with a diminished nocturnal decline in blood pressure.     

Morphological and functional characteristics of the heart in untreated hypertension]

To better define the different forms of hypertensive heart disease, we performed 2D guided M mode echo recording of the left ventricle (LV) and Doppler assessment of LV filling in 118 newly recognised (less than 1 year) and untreated hypertensive patients (mean age +/- SD: 49 +/- 10 years, 80 males, 38 females). All recordings were read "blindly". 86 patients underwent also 24 hours BP monitoring during daily routine. MAIN RESULTS: 1) The relative wall thickness (h/r) shows a normal distribution: mean = 0.39; SD = 0.08; 1st quartile = 0.33; 3rd = 0.43; 2) The septal/posterior wall ratio (ST/PWT) shows also a normal distribution: mean = 1.14; SD = 0.24; 1st quartile = 1; 3rd = 1.3; 3) Among patients with LVH (Devereux's criteria, n = 65) the 6 patients with h/r less than or equal to 0.33 are significantly different from the 18 patients with h/r greater than or equal to 0.43 for age (44 +/- 8 vs 51 +/- 10; p less than 0.03), casual (146 +/- 7 vs 166 +/- 13 mmHg; p less than 0.05) and ambulatory SBP (135 +/- 19 vs 146 +/- 16 mmHg; p less than 0.05), peak systolic stress (280 +/- 15 vs 187 +/- 31 Dynes/cm2; p less than 0.001) and E/A ratio (1.17 +/- 0.01 vs 0.94 +/- 0.27; p less than 0.05) but not for ponderal excess. 4) Patients with asymmetric LVH(ST/PWT greater than 1.3 in 22; greater than 1.5 in 10) are significantly different from patients with symmetric LVH for age (54 +/- 10 vs 47 +/- 10; p less than 0.03), diastolic diameter (51 +/- 5 vs 53 +/- 5 mm; p less than 0.02), ST (13.2 +/- 2.9 vs 10 +/- 1.9 mm; p less than 0.001) and PWT (8.9 +/- 1.5 vs 9.7 +/- 1.5 mm; p less than 0.02) but not for BP fractional shortening and LV filling. CONCLUSION: eccentric LVH may be found in young hypertensive patients with normal systolic function and LV filling despite high parietal stress; asymmetric LVH is more frequent in older patients in which LVH seems to develop rather on the septum than on free wall, independently of BP and without consequences on LV function.     

Morning hypertension assessed by home monitoring is a strong predictor of concentric left ventricular hypertrophy in patients with untreated hypertension

This study was performed to test whether morning hypertension defined by the morning-evening difference in home blood pressure (BP) (MEdif) and the average of morning and evening BP (MEave) is a determinant of concentric left ventricular hypertrophy (LVH). The authors enrolled patients with untreated hypertension and performed echocardiography and home BP monitoring for 14 consecutive days. All patients were classified into 4 groups by the MEave and MEdif and morning hypertension was defined by MEave ≥135 mm Hg and MEdif ≥15 mm Hg. Left ventricular (LV) geometry was classified as normal, concentric remodeling, eccentric LVH, or concentric LVH. The morning hypertensive patients had a higher LV mass index and relative wall thickness than the other groups. According to multivariable logistic regression analysis, morning hypertensive patients had a significantly increased risk of the concentric LVH (odds ratio, 6.5; 95% confidence interval, 2.5-17.2; P<.001) compared with home normotensive patients with MEdif <15 mm Hg, after adjusting for confounders. Moreover, even among the home normotensives (white-coat hypertensives), patients with MEdif ≥15 mm Hg had a higher percentage of concentric remodeling than those with MEdif <15 mm Hg (32.5% vs 14.7%, P=.017). Morning hypertension defined by the MEdif and MEave is a strong determinant of concentric LVH, suggesting that this definition could be used to determine the cardiovascular risk of morning hypertension.     

Impact of left ventricular hypertrophy on blood pressure responses to exercise.

It is claimed that exaggerated blood pressure (BP) responses to exercise are predictive of future hypertension and may also be indicative of left ventricular (LV) hypertrophy. The relation between LV hypertrophy and maximal exercise BP was examined in 35 normal male volunteers and 65 untreated hypertensive male patients. Multiple stepwise regression analysis revealed that preexercise systolic BP was the major determinant of maximal exercise systolic BP (r = 0.52; p less than or equal to 0.0001), indicating that higher baseline BP predicted higher exercise BP. However, hypertensive patients with LV hypertrophy had the smallest increases in systolic BP with exercise. Accordingly, there was an inverse relation between LV muscle mass and systolic BP responses to exercise in these patients (r = -0.34; p = 0.005). When compared with normotensive subjects, hypertensive patients had lower measures of maximal oxygen uptake and exercise heart rates (p = 0.01). This may indicate lower cardiac performance at maximal exercise and explain the reduced capacity of hypertensive patients with LV hypertrophy to increase systolic BP with exercise. Neither baseline nor exercise BPs correlated with LV mass; instead, the model of regression analysis indicated that body weight was the principal determinant of LV mass. Contrary to previous reports, exaggerated exercise BPs were not associated with LV hypertrophy in hypertensive or normotensive patients.     

Concentric left ventricular hypertrophy in patients with aortic regurgitation

Chronic aortic regurgitation (AR) is a disease incorporating volume overload of the left ventricle (LV) which is characterized by hyperactive left ventricular dilatation (LVD). However, we have encountered several patients who had concentric LV hypertrophy (LVH) instead of LVD. We therefore studied 50 consecutive patients with isolated AR but without aortic stenosis and found seven patients with concentric LVH having LV wall thickness (determined by summing ventricular septal and posterior wall thicknesses) exceeding 30 mm and LV diastolic diameters of less than 60 mm. These seven patients with AR and LVH were older (55 +/- 27 vs 42 +/- 11 years) and tended to have milder degree of AR, compared with the remaining 43 patients having AR and LVD. However, patients with AR and LVH did not differ from AR and LVD as to the cardiothoracic ratio, SV1 + RV5, T-waves, ejection fraction, operative findings of valvular morphology and underlying etiologies. In contrast, patients with AR and LVH presented higher systolic (196 +/- 41 vs 149 +/- 26 mmHg, p less than 0.01) and diastolic pressures (74 +/- 14 vs 51 +/- 13 mmHg, p less than 0.01) and higher systemic vascular resistance (1,854 +/- 399 vs 1,388 +/- 352 dyne.sec.cm-5, p less than 0.05) during catheterization than did those with AR and LVD. However, blood pressure at the time of admission was not different in the two groups. These observations indicate that concentric LVH is not rare among patients with AR, and that an association of pressure overload with volume overload of the LV, particularly during exercise or stress, may lead to concentric LVH, even in patients with chronic AR.     

Type 2 diabetes is associated with left ventricular concentric remodeling in hypertensive patients

BACKGROUND: Left ventricular (LV) geometric remodeling is associated with cardiovascular prognosis in hypertensive patients. It is uncertain how LV remodeling is modulated by diabetes in hypertensive patients. In this study, we investigated the impact of diabetes and ambulatory blood pressure (BP) on LV geometric remodeling in hyptensives with/without diabetes. METHODS: Ambulatory BP monitoring and echocardiography were performed to compare 24-h BP levels and LV measurements in 400 uncomplicated hypertensives (mean age, 67 years, 152 men and 248 women) between diabetic (n = 161) and nondiabetic (n = 239) patients. RESULTS: The age (67 v 68 years), percentage of men (43% v 34%), body mass index (24.5 v 24.0 kg/m(2)), 24-h systolic BP (144/80 v 144/82 mm Hg), LV mass index (128 v 130 g/m(2)) were similar between the groups. Diabetic patients had higher relative wall thickness (0.50 v 0.44, P < .001) and higher prevalence of concentric LV hypertrophy (39.4% v 26.8%, P < .001) than nondiabetic patients. The presence of diabetes (odds ratio [OR] = 2.76; 95% confidence interval [CI] = 1.73-4.41, P < .001) and 24-h systolic BP (OR for 10 mm Hg increase = 1.17; 95% CI = 1.01-1.37, P < .05) were independently associated with the higher relative wall thickness (>/=0.45). On the other hand, 24-h systolic BP was independently associated with LV hypertrophy (OR for 10 mm Hg increase = 1.32; 95% CI = 1.14-1.52, P < .05). CONCLUSIONS: Among hypertensive patients, type 2 diabetes was associated with concentric LV geometry independent of ambulatory BP.     

Technetium-99m sestamibi cavity/myocardium count ratio in the detection of left ventricular hypertrophy

BACKGROUND AND HYPOTHESIS: Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular mortality and morbidity. This study was designed to assess whether technetium-99m (99mTc) sestamibi cavity-to-myocardium count (c/m) ratio would differentiate LVH from normal geometry, and discriminate between the two patterns-concentric and eccentric--of LVH. METHODS: In all, 72 patients including 32 hypertensive patients with both normal 99mTc sestamibi single-photon emission computed tomography imaging and good-quality echocardiographic recordings were studied retrospectively. Four different patterns of left ventricular (LV) geometry were defined: normal (n = 47), concentric remodeling (n = 3), eccentric LVH (n = 13), and concentric LVH (n = 9). RESULTS: Left ventricular hypertrophy was detected in 22 of 32 hypertensive patients. The c/m ratio calculated on midventricular short-axis slices of dipyridamole-stress 99mTc sestamibi images was significantly decreased in patients with LVH compared with subjects with normal geometry (0.05 +/- 0.02 vs. 0.17 +/- 0.08, p = 0.001). A c/m ratio of <0.124 yielded a sensitivity of 86%, a specificity of 64%, and an overall diagnostic accuracy of 68% for detecting LVH. Negative correlations of c/m ratio were found to LV mass-index (r = -0.44, p = 0.004), septal width (r = -0.42, p = 0.008), posterior wall thickness (r = -0.39, p = 0.001), and relative wall thickness (r = -0.40, p = 0.001). Multiple linear regression analysis revealed that LV mass index was the single independent predictor of c/m ratio. Although both groups with concentric and eccentric LVH had a significantly lower mean c/m ratio than those with normal geometry (p = 0.01 and p = 0.01, respectively), no significant difference of c/m ratio was found between the two patterns of LVH. CONCLUSION: A new index, c/m ratio on 99mTc sestamibi images, has a potential to discriminate between LVH and normal geometry in subjects free of myocardial ischemia.     

Epicardial coronary artery size in hypertensive and physiologic left ventricular hypertrophy

BACKGROUND: In the hypertensive heart, epicardial arteries are not enlarged, despite increased total coronary flow related to augmented cardiac workload, wall stress, and left ventricular (LV) mass. The aims of this study were to assess the impact of different hemodynamic factors and LV mass on baseline left main coronary artery (LMA) size in hypertensive LV hypertrophy (LVH) and physiologic LVH, used as a pressure-independent model of hypertrophy. METHODS: In 104 subjects without coronary disease (26 normotensive subjects without LVH, 15 athletes with physiologic LVH, and 63 untreated hypertensive subjects [28 without and 35 with LVH]), LMA size and coronary flow reserve (CFR) were measured by transesophageal echocardiography, and LV mass, volumes, stroke work, and wall stress were measured by transthoracic echocardiography. RESULTS: The LMA area in normotensive control subjects, athletes, and hypertensive subjects without and with LVH was 13.2 +/- 4.2, 17.5 +/- 2.9, 10.1 +/- 3.2 and 13.1 +/- 3.9 mm(2). In normotensive control subjects, LMA size increased with body surface area, rate-pressure product, stroke work, and LV mass or wall thickness (r = 0.39, 0.39, 0.47 and 0.67 or 0.62, P < .05-0.01). In athletes with physiologic LVH, LMA area increased with CFR (0.65, P < .01). In the whole hypertensive population, LMA lumen increased with LV mass (r = 0.40, P < .01), and decreased with office systolic blood pressure (r = -0.48, P < .01). CONCLUSIONS: In the hypertensive LVH, baseline LMA area is not increased and is inversely related to office systolic blood pressure. In the physiologic LVH, increase in baseline LMA size seems to reflect effect of high-flow stimuli.     

Left ventricular and carotid structure in untreated, uncomplicated essential hypertension: results from the Assessment Prognostic Risk Observational Survey (APROS)

The impact of hypertension on left ventricular (LV) and vascular structure and the relation of left ventricular hypertrophy (LVH) with vascular changes in untreated essential hypertensives has not been fully explored. This study investigated the prevalence of structural abnormalities of LV and carotid arteries and their determinants in a large population of untreated, uncomplicated essential hypertensive patients. The Assessment of Prognostic Risk Observational Survey was a multicentre (44 centres) prospective study including 1142 untreated hypertensives classified as low or medium cardiovascular risk on the basis of the routine diagnostic work-up recommended by the 1999 World Health Organization/International Society of Hypertension guidelines. All patients underwent ultrasound examinations of the heart and carotid arteries. LVH and carotid structural changes were diagnosed when: (1) LV mass index exceeded 125 g/m(2) in men and 110 g/m(2) in women; (2) there was at least one plaque (focal thickening>1.3 mm) in any segment of either carotid artery or a diffuse common carotid intima-media thickness (IMT) (average of IMT>/=0.8 mm) was present. Overall, 1074 patients (504 women, mean age 48.1+/-11.4 years) completed the study with ultrasonographic examinations of good technical quality. The prevalences of LVH and LV concentric remodelling in the total population were 26.8 and 10.7%, respectively. Eccentric hypertrophy was more prevalent than concentric hypertrophy (15.2 vs 11.6%). One or more carotid plaques or thickening were present in 27.4% of the patients. A stepwise increase in IM thickness occurred from the lowest values in patients with normal cardiac mass and geometry (0.68 mm) to intermediate in those with LV remodelling (0.76 mm) and eccentric LVH (0.81 mm) and to the highest level in patients with concentric LVH (0.87 mm). Patients with LV concentric remodelling and concentric LVH had a significantly greater relative carotid wall thickness than those with normal geometry and eccentric LVH (0.25 and 0.26 vs 0.18 and 0.19, respectively, P<0.01). According to a multivariate analysis age, blood glucose, systolic BP and pulse pressure were the main independent predictors of LVH, while age, systolic BP and total cholesterol were the variables with the greatest impact on IM thickening. To conclude, this study shows that: (1) altered patterns of LV structure and geometry and carotid structural changes occur in a large fraction of patients with untreated essential hypertension; (2) there is a significant association between carotid wall thickening and LVH; (3) the probability of LVH or carotid thickening is significantly greater in elderly, in patients with higher systolic BP and in patients with associated metabolic risk factors.     

Patients with type 2 diabetes have exaggerated brachial and central exercise blood pressure: relation to left ventricular relative wall thickness

BACKGROUND: A hypertensive response to exercise has prognostic significance. Patients with type 2 diabetes have vascular abnormalities which may predispose to exaggerated brachial and central blood pressure (BP) during exercise. This study aimed to test this hypothesis and to determine the clinical significance of high exercise BP by examining its relation to left ventricular (LV) mass. METHODS: Brachial and central BP were recorded at rest and in response to maximal exercise in 73 diabetic patients (aged 54 +/- 10 years) and 73 controls (aged 53 +/- 12 years). Brachial BP was recorded using mercury sphygmomanometry and LV mass using 2D-echocardiography. Central BP was estimated by radial tonometry using an exercise-validated generalized transfer function. RESULTS: At rest there were no significant (P > 0.05) differences between groups in brachial or central BP. The diabetic patients had significantly increased exercise brachial systolic BP (SBP: 199 +/- 25 mm Hg vs. 185 +/- 21 mm Hg; P = 0.002) and central SBP (158 +/- 17 mm Hg vs. 149 +/- 15 mm Hg; P = 0.002). There was a significantly higher prevalence of an exaggerated exercise BP response (> or =210/105 mm Hg; men and > or =190/105 mm Hg; women) in the diabetic patients (51% vs. 22%; P < 0.01). Compared with those with normal exercise BP, LV relative wall thickness (RWT) was significantly higher (0.41 +/- 0.09 vs. 0.36 +/- 0.08; P < 0.05) and LV hypertrophy was more prevalent (35% vs. 16%; P < 0.05) in those with a hypertensive response. After accounting for other confounding variables, exercise central SBP remained independently associated with LV RWT (beta = 0.22; P = 0.006). CONCLUSION: Diabetic patients are more likely to exhibit exaggerated exercise BP. Regardless of disease status, high exercise central SBP may contribute to cardiovascular risk via adverse cardiac remodeling.     

Regression of left ventricular hypertrophy in hypertensive heart transplant recipients treated with enalapril, furosemide, and verapamil.

BACKGROUND. This prospective study was designed to examine whether left ventricular (LV) hypertrophy of the denervated transplanted heart may be reversed by medical therapy and, if so, to investigate the time course of this process and its effect on exercise capacity, myocardial function, and cardiac hemodynamics. METHODS AND RESULTS. Ten hypertensive heart transplant recipients with LV hypertrophy were evaluated before therapy with enalapril plus furosemide alone or combined with verapamil, at initial blood pressure (BP) control and after 3, 6, 9, and 12 months, using 24-hour noninvasive ambulatory BP monitoring, M-mode and two-dimensional echocardiography, and supine bicycle ergometry. Average 24-hour systolic and diastolic BP declined from 158 +/- 10 and 104 +/- 7 mm Hg to 129 +/- 9 and 84 +/- 10 mm Hg at initial BP control (p less than 0.005 and p less than 0.025, respectively) and total peripheral resistance from 1,687 +/- 177 to 1,376 +/- 122 dyne.sec.cm-5 (p less than 0.025), remaining normal thereafter. Exercise capacity remained unchanged during the study. LV mass, mass-to-volume ratio, and end-diastolic septal plus posterior wall thickness decreased progressively from 211 +/- 30 g, 2.49 +/- 0.62 g/ml, and 25.7 +/- 2.6 mm to 184 +/- 26 g, 2.22 +/- 0.46 g/ml, and 22.5 +/- 1.9 mm after 3 months (all p less than 0.025) and to 174 +/- 25 g, 2.07 +/- 0.38 g/ml, and 21.5 +/- 1.5 mm after 6 months (all p less than 0.005), remaining unaltered at 9 and 12 months. A correlation was found between the decrease in average 24-hour mean BP and LV mass after 3 months of antihypertensive therapy (r = 0.71, p less than 0.05). Systolic meridional wall stress, LV end-diastolic and stroke volume, ejection fraction, and cardiac output remained unchanged throughout the observation period. CONCLUSIONS. The results indicate that regression of LV hypertrophy is induced by effective antihypertensive therapy in the denervated transplanted heart. The extent of decrease in average 24-hour BP appears to be the main determinant for the extent of reduction in LV mass. LV afterload as characterized by systolic meridional wall stress, LV size and pump function, and physical exercise capacity of the transplant patients are not influenced by the therapeutic regimen chosen in this study.     

Subclinical left ventricular dysfunction in systemic hypertension and the role of 24-hour blood pressure

The relation between blood pressure (BP) and left ventricular (LV) systolic function in systemic hypertension is controversial. We assessed the relation of LV midwall fractional shortening (FS) to 24-hour BP in 1,702 never-treated hypertensive subjects (age 48 +/- 12 years), who underwent 24-hour BP monitoring and echocardiography. Stress-corrected endocardial and midwall FS (the latter calculated taking into account the epicardial migration of midwall during systole) were predicted in hypertensives on the basis of the values observed in 130 healthy normotensives (age 43 +/- 13 years, office BP 126/78 mm Hg). Subjects below the fifth percentile of observed-to-predicted FS had depressed LV function. The use of midwall FS resulted in an increase from 3.5% to 17.5% in the proportion of patients with depressed chamber function. Compared with the group with normal function, subjects with low midwall LV function had similar office systolic BP (155 +/- 21 vs 154 +/- 17 mm Hg), but increased 24-hour systolic BP (140 +/- 17 vs 133 +/- 12 mm Hg, p <0.001). Midwall FS had a closer negative relation to 24-hour systolic BP than to office systolic BP (r = -0.27 vs -0.08, p <0.001), whereas this difference was not apparent for diastolic BP (r = -0.23 vs -0.20). Compared with endocardial FS, midwall FS had a stronger inverse association to LV mass (r = -0.45 vs -0.16, p <0.001). Thus, an increased 24-hour BP load may chronically lead to depressed myocardial function in systemic hypertension in the absence of clinically overt heart disease.     

The effect of left ventricular geometry on myocardial performance index in hypertensive patients]

OBJECTIVE: The aim of this study was to investigate the relationship between the myocardial performance index (MPI) and left ventricular (LV) geometry in hypertensive patients. METHODS: The MPI, which is a marker of systolic and diastolic ventricular function, was measured in 64 hypertensive patients and in 15 healthy persons (Control). According to the value of relative wall thickness (RWT) and LV mass index (LVMI), hypertensive patients were subdivided into four groups: normal (N), 17 patients (26.6%); concentric remodeling (CR), 21 patients (32.8%); concentric hypertrophy (CH), 16 patients (25%); and eccentric hypertrophy (EH), 10 patients (15.6%). RESULTS: A higher MPI was found in all patient groups (N, 0.56+/-0.11; CR, 0.59+/-0.11; CH, 0.68+/-0.19; EH, 0.57+/-0.10) compared with the controls (0.44+/-0.09) (p=0.004, p<0.001, p<0.001 and p = 0.002, respectively). In the CH group, the MPI was also higher than in N, CR and EH groups (p=0.006, p<0.03 and p=0.009, respectively). No significant difference was found among N, CR and EH groups. The MPI was correlated with LVMI (r=0.28, p=0.014), RWT (r=0.24, p=0.035) and interventricular septum diastolic thickness (r=0.32, p=0.004). CONCLUSION: The systolic and diastolic LV functions are impaired in all subgroups of hypertensive patients according to their LV geometry compared to control group. This impairment is more advanced in patients with concentric hypertrophy than in those with the other LV geometric patterns.     

Echocardiographic assessment of myocardial fibrosis in young men with arterial hypertension and different types of left ventricular remodeling

In order to study structural functional characteristics of myocardium including parameters of myocardial fibrosis according echocardiography data in men with various levels of arterial pressure (AP) we examined 215 men aged 18-25 (mean 21.1+/-0,1) years with history of elevated AP at casual measurement. AP phenotype (normotension, stable arterial hypertension [AH], unstable AH) was determined on the basis of multiple measurements of clinical AP and 24 hour AP monitoring. At echocardiography we assessed presence of left ventricular (LV) hypertrophy (LVH), type of LV geometry, proportionality of LV myocardial mass (LVMM), diastolic function. Myocardial fibrosis was assessed by pixel density distribution range (PDDR) with the use of analysis of reflected signal. There were no manifestations of LV remodeling in subjects with normal AP. Concentric LV remodeling was found in 27.5 and 60.5% of patients with unstable and stable AH, respectively. Concentric LVH was found only in patients with stable AH (4.8%). Disproportionally high LVMM was found in 16.1% of subjects with stable AH. In a combined group with concentric LV remodeling and LVH rate of disproportionally high LVMM was 20.8%. We noted significant (p<0.001) increase of PDDR in stable AH (181.4+/-2.2) compared with PDDR in normal AP (164.6+/-4.6) and unstable AH (160.1+/-2.7). In stable I degree AH PDDR (177.3+/-2.2) was insignificantly lower than in II degree AH (185.7+/-3.9). PDDR in concentric LV remodeling was 180.5+/-2.3, in concentric LVH- 166.8+/-13.2, in normal LV geometry - 168.4+/-2.5. PDDR in disproportionally high LVMM was higher than in proportional LVMM. Independent interrelationship was found between PDDR and body mass index (r=0.17; p=0.03), duration of AH (r=0.17; p=0.03), isovolumic relaxation time (r= 0.15; p=0.04). In young men LV remodeling can be detected at the stage of unstable AH. In stable AH degree of myocardial fibrosis was associated with higher AP level, concentric LV geometry, disproportionally high LVMM, lowering of diastolic function.     

Association between exercise capacity and left ventricular geometry in overweight patients with mild systemic hypertension

The purpose of this study was to determine the relation between left ventricular (LV) geometry and exercise capacity in unmedicated, hypertensive patients. Analysis of the data revealed peak oxygen consumption (ml kg(-1) min(-1)) for concentric hypertrophy (corrected mean +/- SE 23.5 +/- 1.2) was significantly less (F = 3.68, p <0.02) than the concentric remodeling (28.1 +/- 1.2) and normal (27.3 +/- 0.6) geometries. The LV geometric pattern was found to be associated with exercise capacity in unmedicated, hypertensive patients, such that patients with concentric hypertrophy showed reduced capacity.     

Effects of angiotensin II receptor blockade-based therapy with losartan on left ventricular hypertrophy and geometry in previously treated hypertensive patients

BACKGROUND: The 2003 European Society of Hypertension/European Society of Cardiology (ESH/ESC) guidelines recommend angiotensin II receptor antagonists (AIIRAs) as a first-line therapy in hypertensives with left ventricular hypertrophy (LVH). AIM: We investigated the long-term effects of an AIIRA-based therapy on left ventricular (LV) structure and geometry in previously, unsatisfactorily treated essential hypertensive patients. METHODS: Sixty-eight consecutive patients referred to our hypertension hospital outpatient clinic with: (i) LVH (LV mass index, LVMI 51 g/m(2.7) in men and 47 g/m(2.7) in women), (ii) uncontrolled clinic blood pressure (BP140 and/or 90 mmHg) and (iii) antihypertensive therapy not including angiotensin-converting enzyme (ACE) inhibitors or AIIRAs were selected for this study. Two-dimensionally guided M-mode echocardiograms were carried out at baseline and after 6, 12, 18 and 24 months of follow-up. In all patients, losartan (50-100 mg/day, mean dose 82 mg/day) was added as first step to the previous therapy. Additional drugs, tailored to the single patient, were added, if necessary, to achieve target BP values (<140/90 mmHg). RESULTS: Overall, 59 patients completed the study with the primary efficacy measurements (LVMI) at all appropriate times. A significant reduction in both clinic systolic BP and diastolic BP was found across the entire period of study respect to baseline (-17/10, -22/12, -24/13 and -26/14 mmHg at 6, 12, 18 and 24 months, p < 0.001 respectively), leading to target clinic BP in 75.6% of cases. LVMI was significantly lower after 1 year of treatment (-11 +/- 12%, p < 0.05) with a further significant reduction at the end of treatment (-22 +/- 18%, p < 0.01). The proportion of patients achieving normalization of LVMI was 47.4% and more importantly, the prevalence of concentric LVH fell from 38.9% to 6.7% (p < 0.01). CONCLUSIONS: Our findings indicate that long-term intensive treatment based on the AIIRA losartan induced a normalization of LVH in about 50% of patients and more importantly caused an almost complete regression of concentric LVH, the most dangerous adaptive pattern. The transition from concentric to normal or eccentric LV geometry may have in these high-risk patients a favourable prognostic implication in addition to the recognized positive effect of reducing LVMI.     

Polymorphic markers I/D and G7831A of angiotensin-I-converting enzyme gene and left ventricular hypertrophy in patients with essential hypertension

AIM: To elucidate possible association of angiotensin-I-converting enzyme (ACE) gene polymorphic markers I/D and G7831A with left ventricular hypertrophy (LVH) in patients with essential hypertension. MATERIAL: Patients with essential hypertension (n=123, 37 with and 86 without LVH, mean age 59.15+/-1.19 years). METHODS: Left ventricular (LV) mass was determined echocardiographically by Devereux method. Alleles and genotypes of ACE gene polymorphic markers were identified by polymerase chain reaction. RESULTS AND CONCLUSION: There was no association between I/D marker of ACE gene and LVH. Carriers of A allele compared with carriers of G allele of G7831A marker had significantly higher LV mass (284.1+/-10.20 g, and 248.5+/-14.42 g, respectively, p=0.033) and LV mass index (151.7+/-5.23 g/m2 and 131.0+/-6.74 g/m2, respectively; p=0.02). Among patients with LVH frequency of A allele was significantly higher than among patients without LVH (0.401 and 0.230, respectively; p=0.0065, OR=2.116 [1.197-3.7481]). Using binary logistic regression model we have found that presence of LVH was linked with age, sex and maximal systolic blood pressure (BP). Such factors as smoking, maximal diastolic BP, ordinary systolic and diastolic BP, duration of hypertension, coronary artery disease and diabetes were not related to LV mass index. Using multifactorial logistic regression model we have found that the presence of A allele of G7831A polymorphic marker of ACE gene, age and maximal systolic BP could be considered as independent risk factors of LVH.     

Progressive hypertrophy regression with sustained pressure reduction in hypertension: the Losartan Intervention For Endpoint Reduction study

OBJECTIVE : To examine the time course of left ventricular (LV) geometric response to blood pressure (BP) control during 2 years of systematic antihypertensive treatment. DESIGN : A total of 754 hypertensive patients with left ventricular hypertrophy (LVH) by Cornell voltage-duration product or Sokolow-Lyon voltage criteria on a screening electrocardiogram had their LV mass measured by echocardiogram at enrolment in the Losartan Intervention For Endpoint Reduction (LIFE) trial, and after 12 and 24 months of blinded therapy with losartan-based or atenolol-based regimens. SETTING : The LIFE trial, in which hypertensive patients with electrocardiographic LVH (Cornell voltage-duration product > 2440 mm x ms and/or Sokolow-Lyon voltage criteria SV1 + RV5-6 > 38 mm) were randomized to >or= 4 years double-blinded treatment with losartan or atenolol. PARTICIPANTS : A total of 754 LIFE participants with serial echocardiographic measurements of LV geometry. INTERVENTIONS : None. MAIN OUTCOME MEASURES : LV wall thicknesses, diameter and mass, and its indices. RESULTS : Mean systolic/diastolic BP fell from 173/95 to 150/84 mmHg after 1 year (P < 0.001) and to 148/83 mmHg at year 2 (P = not significant). Mean echocardiographic LV mass fell from 233 g at baseline to 206 g after 1 year (P < 0.001, adjusted for change in systolic BP) and to 195 g at year 2 (P < 0.001 versus year 1), with a parallel decrease in indexed LV mass [from 56.1 to 49.7 g/m2.7 (P < 0.001), to 47.1 g/m2.7 (P < 0.001 versus year 1)]. Relative wall thickness decreased from 0.41 at baseline to 0.37 at year 1 (P < 0.001), to 0.36 at year 2 (P < 0.001 versus year 1). As a result, there were serial decreases in prevalences of eccentric LVH [44 to 38%, and to 30% (P < 0.001 versus year 1)] and concentric LVH [24 to 7% (P < 0.001), to 2% (P < 0.05 versus year 1)], and increases in the proportion with normal LV geometry [22 to 50% (P < 0.001), and to 64% (P < 0.01 versus year 1)]. CONCLUSIONS : Sustained BP reduction in hypertensive patients with target organ damage causes continued decrease in echocardiographic LV mass and prevalence of anatomic LVH for at least 2 years despite only small BP decreases after the first year of blinded therapy. These data document cardiac benefit of sustained BP control and suggest that maximum LVH regression with effective antihypertensive treatment requires at least 2 years.     

Effects of training on systolic time intervals at rest and during isometric exercise in men and women 61 to 64 years old

To determine whether regular exercise improves left ventricular (LV) contractile function in persons 60 years and older, systolic time intervals (STIs) were measured in 10 healthy men and women (mean age 62 +/- 1 year [+/- standard deviation]) before and after 6 months of intense endurance training. STIs, systolic and diastolic blood pressure (BP) and heart rate (HR) were determined at rest and in response to isometric handgrip exercise. Systolic BP, diastolic BP and HR increased acutely from rest in response to handgrip (p less than 0.002). The indexes of total electromechanical systole and LV ejection time (ET) index increased (p less than 0.01), preejection period (PEP) index increased (p less than 0.05) or remained unchanged and PEP/LVET did not change from values at rest in response to handgrip. Training resulted in an 18% increase in maximal oxygen uptake (p less than 0.01). After training, systolic and diastolic BP were reduced at rest (p less than 0.002) and, along with HR, were lower in response to handgrip (p less than 0.002). However, training did not alter STIs at rest or during handgrip. These findings indicate that healthy persons in their 60s have a normal LV response to isometric exercise. Prolonged, intense endurance training does not alter LV contractile function at rest or in response to isometric exercise. However, training can significantly reduce BP at rest, and markedly lower the HR-systolic BP product attained during acute isometric stress, even in normotensive older subjects.     

Left ventricular ejection fraction response during exercise in asymptomatic systemic hypertension

To study the effect of mild-to-moderate elevations in diastolic blood pressure (BP) on systolic left ventricular (LV) function, 28 hypertensive patients and 20 normal subjects underwent upright exercise first-pass radionuclide angiography. All were asymptomatic, had normal rest and exercise electrocardiographic findings and no evidence of LV hypertrophy or coronary artery disease. LV function at rest was similar in the 2 groups, but with exercise hypertensive patients had a greater end-systolic volume (69 +/- 19 vs 51 +/- 19 ml, p less than 0.002) and lower ejection fraction (EF) (0.59 +/- 0.09 vs 0.72 +/- 0.07, p less than 0.0001), stroke volume (101 +/- 28 vs 130 +/- 36 ml, p less than 0.005) and peak oxygen uptake (23 +/- 7 vs 33 +/- 9 ml/kl/min, p less than 0.05). Hypertensive patients were separated into 3 groups: group 1-12 patients with an increase in EF with exercise greater than or equal to 0.05; group 2-7 patients with a change in EF with exercise less than 0.05; and group 3-9 patients with a decrease in EF with exercise greater than or equal to 0.05. Group 3 hypertensive patients were older, had a higher heart rate at rest and lower peak oxygen uptake. Rest LV function was similar in the 3 hypertensive subgroups, but exercise end-systolic volumes were higher in groups 2 and 3. Exercise thallium-201 images was normal in all but 1 of 14 hypertensive group 2 or 3 patients.(ABSTRACT TRUNCATED AT 250 WORDS)