Echocardiographic and ultrasonographic evaluation of cardiac and vascular hypertrophy in patients with essential hypertension.

High-resolution ultrasonography is a noninvasive technique that allows to investigate the cardiovascular system, in particular the wall thickness and the lumen diameter of the arteries with accuracy and reproducibility. We measured the intima-media thickness of the common carotid artery (CCA) and of its bifurcation (BIF) in 40 patients with essential hypertension, 20 of them with left ventricular hypertrophy (LVH; age 42 +/- 10 years) and 20 without LVH (age 44 +/- 12 years); no other major cardiovascular risk factor was present in all the patients. Both carotid axes have been scanned from different views (anterior, lateral, posterior) on a transversal and longitudinal section using a high-resolution steerable linear array of 5.0 MHz. Carotid diameter and thickness were measured in the longitudinal section. CCA parameters were assessed 20 mm caudally to the flow divider. In patients with LVH, blood pressure (172 +/- 21/108 +/- 9 mm Hg) and left ventricular mass index (156 +/- 38 g/m2) were significantly (p < 0.01) higher than in patients without LVH (blood pressure: 158 +/- 11/99 +/- 12 mm Hg; left ventricular mass index: 98 +/- 10 g/m2), while there was no difference in serum glycemia, triglycerides, total and fractioned cholesterol levels. The intima-media thickness of both the CCA and BIF was significantly higher in the hypertensives with LVH (CCA: 0.85 +/- 0.02 vs. 0.65 +/- 0.02 mm; BIF: 0.93 +/- 0.04 vs. 0.70 +/- 0.03 mm, p < 0.01). There was a statistically significant correlation between the carotid wall thickness and the left ventricular mass index.(ABSTRACT TRUNCATED AT 250 WORDS)     

Presence and severity of carotid atherosclerosis in asymptomatic hypertension patients with left ventricular hypertrophy]

BACKGROUND AND PURPOSE: Arterial hypertension is associated with structural changes in the cardiovascular system. In hypertensives, a relationship has been found between left ventricular hypertrophy and carotid wall thickness, whereas the association with atherosclerotic plaque is less defined. The aim of this study was to evaluate the occurrence and severity of carotid atherosclerosis in hypertensive patients with or without left ventricular hypertrophy (LVH). MATERIALS AND METHODS: We studied 122 hypertensive subjects (62 men and 60 women), aged 60.1 +/- 12.1. Subjects were considered to have left ventricular hypertrophy if their left ventricular mass index (LVMI) at echocardiography exceeded 110 g/m2 in women and 135 g/m2 in men. Carotid intima-media thickness (IMT), external diameter and atherosclerotic plaques were evaluated by high resolution echo-color Doppler. RESULTS: IMT in both common carotid and bifurcation was significantly greater in hypertensives with LVH (p < 0.01), whereas external diameter did not differ significantly in the two groups. Increased presence (73.4 vs 32.8%) and severity (18.7 vs 5.2% for stenosis > 40%) of atherosclerotic plaque were found in the hypertrophic group. A weak but significant association was present among left ventricular mass index, ventricular wall thicknesses and carotid intima-media thickness, and plaque. CONCLUSIONS: In asymptomatic hypertensive subjects, LVH is associated with an increased risk of plaque formation and progression. Vascular hypertrophy may represent a distinct prognostic factor in hypertension and the association of cardiac and vascular hypertrophy may identify a group at high risk of future cardiovascular events.     

Prevalence of left ventricular hypertrophy and carotid thickening in a large selected hypertensive population: impact of different echocardiographic and ultrasonographic diagnostic criteria.

BACKGROUND: Left ventricular hypertrophy (LVH) and increased carotid intima-media thickness (IMT) represent independent risk factors for cardiovascular disease. OBJECTIVE: To evaluate the prevalence of echocardiographic LVH and common carotid artery (CCA) intima-media (IM) thickening by different criteria in a large sample of hypertensive patients referred to our Hypertension Clinic. METHODS: Echocardiograms and ultrasonographic carotid examinations have been performed in 640 consecutive hypertensives referred to our outpatient's hypertension unit. LVH was diagnosed using six different criteria, when left ventricular mass index (LVMI) exceeded (a) 100 g/m2 in women and 120 g/m2 in men, (b) 110 g/m2 in women and 125 g/m2 in men, (c) 110 g/m2 in women and 134 g/m2 in men, (d) 125 g/m2 in both sexes, (e) 47 g/h2.7 in women and 51 g/h2.7 in men, (f) 105 g/h in women and 126 g/h in men. Thickening of CCA IM was identified using three partition values; when IMT was (a) > or =0.8 mm; (b) >0.9 mm: (c) > or = 1.0 mm in both sexes. RESULTS: Echocardiographic and ultrasonographic examinations of sufficient quality to be analysed were obtained in 611 patients (95.2%). Prevalence of LVH ranged from 18.6% (d) to 42.2% (f) and was significantly higher in men than in women by criteria (d) and (e), but slightly higher in women when using criteria (a) and (c). Eccentric hypertrophy was the most frequent type of LVH independently of the criteria used. Prevalence of IM thickening ranged from 14.7% (c) to 44.2% (a). Significant correlations between left ventricular mass (LVM)/body surface area, LVM/height and LVM/height2.7, and carotid IM thickness were found (r=0.41; p <0.0001; r=0.31; p <0.0001; r = 0.30; p <0.0001, respectively). CONCLUSION: The prevalence of LVH and CCA IM thickening in hypertensive patients is markedly dependent on the partition values used to define these markers of target organ damage. Considering the pivotal role of LVH and CCA IM thickening in assessing the global cardiovascular risk profile in hypertensives, improved standardization in defining LVH and carotid IM thickening is needed.     

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.     

Effects of chronic hypertension and left ventricular hypertrophy on the incidence of sudden cardiac death after coronary artery occlusion in conscious dogs

When acute myocardial infarction occurs in patients with hypertension and left ventricular hypertrophy (LVH), the incidence of sudden cardiac death increases markedly. Possible explanations include increased size of the occluded vascular bed secondary to more extensive atherosclerotic coronary vascular disease in the presence of hypertension, decreased coronary reserve secondary to LVH, and intrinsic electrophysiologic abnormalities in hypertrophied cardiac muscle. To explore these possibilities, we produced acute circumflex coronary occlusion during the resting, conscious state in 32 control dogs and in 28 dogs with hypertensive LVH. Before coronary occlusion, mean arterial pressure was 96 +/- 0.1 mm Hg in control dogs and 125 +/- 5 mm Hg in dogs with hypertensive LVH (p less than 0.01). The control left ventricular/body weight ratio was 4.5 +/- 0.1 g/kg, compared with 6.1 +/- 0.1 g/kg in hypertensive LVH (p less than 0.01). Cumulative mortality at 6, 24 and 48 hours was 9%, 13% and 16% in control dogs and 32%, 43% and 54%, respectively, in dogs with hypertensive LVH (all p less than 0.01 vs control). The perfusion fields of the occluded vessel defined by postmortem coronary angiography were similar in the two groups (31 +/- 2% of left ventricular mass for control vs 29 +/- 2% for hypertensive LVH). Thus, the increased incidence of sudden cardiac death after coronary artery occlusion in hypertensive LVH dogs cannot be explained by increased size of the occluded vascular bed and is probably related to the decreased coronary reserve or intrinsic electrophysiologic abnormalities that characterize pressure-induced hypertrophied cardiac muscle.     

Left ventricular mass in diabetes-hypertension.

BACKGROUND--This study was undertaken to identify whether diabetes mellitus (DM) accelerates the development of left ventricular hypertrophy (LVH) in hypertensive patients. METHODS--Cardiac structure, systolic function, and hemodynamics were evaluated by two-dimensional M-mode echocardiography in diabetic and nondiabetic patients with essential hypertension. RESULTS--Patients with hypertension with and without DM had the same end-systolic and end-diastolic dimensions, cardiac output, total peripheral resistance, and ejection fraction. Diabetic hypertensive patients had greater interventricular septum (1.32 +/- 0.20 vs 1.07 +/- 0.20 cm) and posterior wall (1.20 +/- 0.20 vs 1.00 +/- 0.10 cm) thickness than did nondiabetic hypertensive patients. Consequently, left ventricular mass index was greater in patients with hypertension and DM than in those without DM (158 +/- 45 vs 113 +/- 20 g/m2). With the use of Devereux criteria for recognition of LVH (left ventricular mass index above 134 g/m2 in men and above 110 g/m2 in women), 72% of the diabetic patients had LVH, whereas only 32% of the nondiabetic patients had LVH. Left ventricular contractility, as reflected by the ratio of end-systolic wall stress to end-systolic volume index, was decreased in diabetic compared with nondiabetic hypertensive patients. CONCLUSIONS--The data suggest that DM accelerates the development of LVH in patients with essential hypertension independent of arterial pressure and, therefore, may contribute to the increased cardiovascular morbidity and mortality in patients with hypertension.     

Cardiac mass and function, carotid artery intima-media thickness, and lipoprotein levels in growth hormone-deficient adolescents

The objective of our study was to evaluate whether cardiac mass and function, carotid artery intima-media thickness, and serum lipid and lipoprotein(a) levels are abnormal in adolescents with GH deficiency. Young adults with childhood-onset and adulthood-onset GH deficiency have been found to have a higher cardiovascular risk, as manifested among other factors by reduced left ventricular mass, impaired systolic function, significant increase in arterial intima-media thickness, and dyslipidemia. Twelve adolescents (seven males and five females) with GH deficiency (10 idiopathic and 2 organic), with an age of 14.2 +/- 2.8 yr and a height of 140.6 +/- 17.9 cm (height SD score, -2.6 +/- 0.3), were studied. Six children had received GH in the past but were off therapy for several years, whereas six patients had never been treated with GH. Fasting blood samples were obtained for serum lipids and lipoprotein(a) analysis. Patients underwent transthoracic M-mode and two-dimensional echocardiographic evaluation for measurement of interventricular septal thickness, left ventricular posterior wall thickness, and left ventricular mass, as well as left ventricular ejection fraction at rest and pulmonary venous flow velocities; carotid artery intima-media thickness was measured using high-resolution mode B ultrasound. Seven GH-deficient (GHD) adolescents on GH at the time of the study and 19 healthy adolescents, all comparable for age, pubertal status, height, weight, blood pressure, and pulse, participated in this study as controls. Interventricular septal thickness (6.5 +/- 1.3 vs. 7.0 +/- 1.5 mm), left ventricular posterior wall thickness (7.0 +/- 1.8 vs. 7.5 +/- 2.0 mm), and left ventricular mass after correction for body surface area (71.2 +/- 21.8 vs. 70.7 +/- 18.0 g/m(2)) were similar in untreated GHD patients and healthy controls. Similarly, the left ventricular ejection fraction at rest was similar in untreated GHD subjects and controls (70.0 +/- 0.7 vs. 70.0 +/- 0.6%), as were the pulmonary venous flow velocities (0.54 +/- 0.16 vs. 0.55 +/- 0.10 m/s for diastolic peak velocity; 0.51 +/- 0.16 vs. 0.50 +/- 0.09 m/s for systolic peak velocity; and 0.19 +/- 0.06 vs. 0.19 +/- 0.05 m/s for atrial reversal filling). Carotid artery intima-media thickness (0.60 +/- 0.02 mm and 0.59 +/- 0.02 mm for the right and left carotid arteries, respectively) was also normal in our untreated GHD patients when compared with healthy controls. In addition, all echocardiographic measurements were similar in GHD subjects on or off GH at the time of the study. Low-density lipoprotein cholesterol levels were increased in untreated GHD patients when compared with healthy controls (3.17 +/- 0.70 vs. 2.33 +/- 0.36 mmol/L; P < 0.01), whereas total cholesterol, high-density lipoprotein cholesterol, and triglyceride concentrations were similar to that of controls. Total cholesterol levels were increased in our untreated GHD adolescents when compared with GHD subjects receiving GH therapy at the time of the study, while low-density lipoprotein cholesterol and triglyceride levels were also elevated, although not significantly. Lipoprotein(a) levels were elevated in untreated GHD adolescents when compared with healthy controls, and untreated GHD subjects had higher lipoprotein(a) concentrations than GH-treated patients. GHD adolescents, regardless of whether or not they received GH therapy, do not seem to show alterations in cardiac mass and function or early atherosclerotic changes. They must, however, be followed carefully because they already present cardiovascular risk factors such as dyslipidemia, which may increase their cardiovascular morbidity over time.     

Optimal control of blood pressure can reverse left ventricular hypertrophy in uremic hypertensive hemodialysis patients

We investigated the effects of antihypertensive treatment on left ventricular hypertrophy (LVH) of long-term hemodialysis patients. In uremic patients, it is still controversial in antihypertensive effect to the regression of LVH. The left ventricular size and function of 39 uremic hypertensive long-term hemodialysis patients (27 men, 12 women, mean age 58.3) was evaluated with M-mode, 2-dimensional and Doppler echocardiography before, and 12 months after, the start of combined antihypertensive therapy. This therapy included angiotensin II converting enzyme inhibitors, beta-blockers and calcium antagonists. Patients were classified as responders or nonresponders, depending upon whether their systolic blood pressure (SBP) decreased by more than 10 mmHg after antihypertensive treatment for 12 months. Before treatment, 36 (92%) patients had LVH and diastolic dysfunction and three (8%) had systolic dysfunction. At the end of 12 months, only 25 (64%) patients had LVH, 30 (77%) had diastolic dysfunction and 2 (5%) had systolic dysfunction. Left ventricular mass index (LVMI) also decreased from 203.63 +/- 70.47 g/m2 to 178.57 +/- 67.31 g/m2. LVMI correlated with systolic blood pressure (SBP) but did not correlate with diastolic blood pressure (DBP). There were 26 responders and 13 non-responders. Among responders, both the SBP (153.91 +/- 13.24 mmHg vs 134.43 +/- 14.21 mmHg, p < 0.01) and DBP (90.39 +/- 7.89 mmHg vs 79.98 +/- 7.35 mmHg, p < 0.01) decreased significantly after antihypertensive therapy. Responders also exhibited progressive regression of LVH (LVMI decreased significantly from 208.52 +/- 72.03 g/m2 to 168.52 +/- 55.53 g/m2, p < 0.05). However, LVH regression was not found in nonresponders (LVMI showed 194.84 +/- 64.36 g/m2 vs 193.66 +/- 77.67 g/m2). We conclude that good control of blood pressure can reverse LVH in hypertensive hemodialysis patients.     

Irbesartan reduces common carotid artery intima-media thickness in hypertensive patients when compared with atenolol: the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) study

BACKGROUND AND PURPOSE: Angiotensin II promotes cell growth and has been implicated in the development and maintenance of left ventricular (LV) hypertrophy and of structural vascular changes. We wished to examine whether an angiotensin receptor blocker (ARB) would influence structural vascular changes beyond the effects of blood pressure reduction. METHODS: Hypertensive patients with LV hypertrophy (age 55 +/- 9 years, blood pressure 162 +/- 19/104 +/- 8 mmHg, LV mass index 148 +/- 31 g m(-2); mean +/- SD) were randomized double-blind to the ARB irbesartan (n=52) or the beta(1) receptor blocker atenolol (n=56) for 48 weeks. Ultrasonography of the left and right common carotid artery (CCA) and echocardiography were performed at week 0 and 48. RESULTS: With similar reductions in blood pressure, CCA intima-media thickness (IMT) was reduced by irbesartan (from 0.92 +/- 0.14 by 0.01 +/- 0.10 mm, NS), whereas it was increased by atenolol (from 0.94 +/- 0.21 by 0.03 +/- 0.12 mm, P=0.018; P=0.002 between groups). CCA lumen diameter was less reduced by irbesartan than by atenolol. Thus, CCA intima-media area was reduced by irbesartan (from 21.3 +/- 5.0 by 0.90 +/- 2.45 mm(2), P=0.034) but not by atenolol (from 21.3 +/- 6.1 by 0.18 +/- 2.71 mm(2), NS; P=0.037 between groups). Changes in CCA IMT or area did not relate to changes in LV mass. CONCLUSIONS: The favourable effects by irbesartan on CCA IMT with an outward vascular remodelling suggest that angiotensin II mediates structural vascular changes, beyond the effects of blood pressure. This may be important in the prevention of cerebrovascular events.     

Biochemical endothelial markers and cardiovascular remodeling in refractory arterial hypertension

BACKGROUND: Hypertension is the most important and well established risk factor for atherosclerosis. The vascular and cardiac remodeling present in refractory hypertensive patients are related to endothelial dysfunction, a key factor in early atherogenesis and cardiovascular disease. However the mechanistic relationship among biochemical endothelial function markers, cardiovascular remodeling, and refractory hypertension is unknown. METHODS: We evaluated the left ventricular mass and function, carotid thickness, and plasma nitrate/nitrite (NO2/NO3), cyclic 3'-5'-guanosine monophosphate (cGMP), and thromboxane B2 (TXB2) levels in refractory hypertensive (RH; n = 20) and healthy (CONTROL; n = 20) subjects 22-65 years old. Carotid thickness, left ventricular mass index (LVMI), and left ventricular fraction ejection (LVFE) were estimated by duplex scan ultrasound. Nitrates/nitrites were assayed using the Griess reaction, and plasma cGMP and thromboxane B2 were determined by enzymatic immunoassay (EIA). RESULTS: Left ventricular mass index was higher in the RH group (138 +/- 20 vs. 108 +/-17 g/m2, p < 0.001) but there was no significant difference in the ejection fraction (67 +/- 5% vs. 69 +/- 4%). Pulse pressure (61 +/- 9 mmHg vs. 46 +/- 10 mmHg) and carotid thickness (1.59 +/- 0.22m vs. 1.04 +/- 0.14mm) were significantly higher (p < 0.001) in RH patients whereas NO2/NO3, cGMP, and thromboxane B2 plasma concentrations were similar in bot groups. CONCLUSION: There was no association between cardiovascular remodeling and the particular biochemical markers of endothelial function we assessed in refractory hypertensive patients.     

绝经后高血压患者左心室肥厚与颈动脉弹性功能的超声观察

目的探讨绝经后高血压患者左心室肥厚(LVH)与颈动脉弹性功能的相关性。方法采用超声心动图检测85例绝经后高血压患者和40名年龄匹配绝经后健康女性(对照组)。按是否存在LVH,又将绝经后高血压患者分为LVH组45例和NLVH组40例。采用高频超声检测颈动脉扩张性(DC)、顺应性(CC)和僵硬度(β)作为评价弹性功能的指标。结果与对照组比较,NLVH组和LVH组的左心室质量指数(LVMI)和β升高[LVMI:(81.00±11.07)g/m2和(115.00±4.41)g/m2比(62.37±9.14)g/m2;β:7.29±2.75和11.34±4.24比5.96±2.50,均为P<0.05],DC和CC降低[DC:(1.95±0.68)×10-3/k Pa和(1.33±0.81)×10-3/k Pa比(3.04±1.27)×10-3/k Pa;CC:(0.44±0.11)mm2/k Pa和(0.35±0.19)mm2/k Pa比(0.67±0.19)mm2/k Pa,均为P<0.01]。与NLVH组比较,LVH组的LVMI和β进一步升高(均为P<0.01),DC和CC进一步降低(均为P<0.05)。LVH组患者的LVMI与雌二醇、DC和CC呈负相关(r=-0.374、-0.440、-0.382,均为P<0.05),与β呈正相关(r=0.554,P<0.01)。结论随着雌激素水平的降低,绝经后高血压患者LVH与颈动脉弹性功能受损存在相关性。     

Early carotid atherosclerosis and cardiac diastolic abnormalities in hypertensive subjects

Despite the fact that it is known that hypertension may be associated to early atherosclerosis manifestations, few data are to date available on the relationship between early carotid abnormalities and left ventricular diastolic dysfunction. To address this issue, 142 hypertensive patients (64 females and 78 males) younger than 55 years, at the first diagnosis of mild-to-moderate essential hypertension (WHO/ISH criteria), were selected from a database consisting of 3541 subjects referred to ultrasound cardiovascular laboratory in the last 5 years. Carotid intima-media thickness (IMT) was detected by high-resolution vascular ultrasound and left ventricular structure and function by the use of Doppler echocardiography. According to carotid IMT values, all patients were subgrouped into two groups consisting of 89 (62.6%) pts with IMT > or = 1 mm (A) and 53 (37.4%) pts with IMT < 1 mm (B). Our results show that isovolumic relaxation time (IVRT), deceleration time of E velocity (EDT) and left ventricular relative wall thickness (LV-RWT) were significantly (P < 0.05) higher in group A (IVRT 112 +/- 8.9 ms; EDT 288 +/- 21.8 ms; LV-RWT 0.40 +/- 0.08) than in group B (IVRT 92.3 +/- 4.6 ms; EDT 203.3 +/- 27.01 ms; LV- RWT 0.37 +/- 0.06). Moreover, the prevalence of left ventricular hypertrophy (LVH) was significantly (P < 0.01) higher in group A (30/89; 33.7%) than in group B (8/53; 15%). A positive correlation (P < 0.001) between IMT, EDT and IVRT was found only in hypertensives without LVH. These results are consistent with the indication that IMT evaluation has to be recommended both in hypertensive patients with LVH and in those without LVH, but with left ventricular diastolic dysfunction. This approach might improve the prognostic stratification of hypertensive subjects and it might be suitable to recognize the subset of patients at a higher risk of cardiovascular disease or events early.     

Ethnic differences in carotid and left ventricular hypertrophy

OBJECTIVES : Afro-Caribbean subjects have a higher prevalence of hypertension, a lower prevalence of ischaemic heart disease and a higher premature mortality compared to White Europeans. Left ventricular hypertrophy (LVH) is also more prevalent in Afro-Caribbeans even at similar levels of blood pressure. It is widely believed that carotid artery intima-media thickening (IMT) represents an early marker for the development of atheroma, and carotid IMT and LVH are associated in White populations. Whether the relationship between carotid IMT and LVH is similar in Black subjects is unknown. METHODS : Thirty-eight subjects were studied using carotid and femoral ultrasonography and echocardiography; 19 Afro-Caribbean and 19 White European subjects were matched for age, sex and mean 24 h systolic blood pressure. RESULTS : The Afro-Caribbean group had a significantly greater left ventricular mass index (LVMI) compared to the White European: 136.4 +/- 6.1 versus 112.4 +/- 6.2 g/m2, P < 0.01. However, carotid IMT, carotid diameter, femoral IMT and femoral diameter were similar between the groups: 0.75 +/- 0.02 versus 0.77 +/- 0.04 mm, 6.54 +/- 0.15 versus 6.56 +/- 0.16 mm, 0.66 +/- 0.03 versus 0.68 +/- 0.03 mm and 8.40 +/- 0.33 versus 8.25 +/- 0.23 mm, respectively. CONCLUSIONS : Afro-Caribbean subjects with similar blood pressures have similar mean carotid and femoral IMTs compared to White Europeans, in spite of marked differences in LVMI. Whether this reflects a discrepancy in the degree of cardiovascular risk for similar levels of LVMI or whether this is a reflection of an altered pattern of target organ damage associated with hypertension in Afro-Caribbean subjects is unclear.     

Cardiovascular effects of type 1 diabetes mellitus in children

Previous studies have shown that type 1 diabetes mellitus (DM) is associated with cardiovascular abnormalities. Early detection and treatment of these abnormalities may help to prevent the natural progression of the disease. The present study was undertaken to define early cardiovascular abnormalities in children with type 1 DM. Simultaneous evaluation of multiple cardiovascular parameters was performed in 14 children with type 1 DM and 14 age-and gender-matched normal subjects. Measurements of carotid artery intima-media thickness (cIMT, echocardiography), carotid and aortic (ascending and abdominal) distensibility (echocardiography, brachial artery blood pressure), aortic pulse wave velocity (carotid to femoral artery, Doppler), and left ventricular dimensions, mass, and function (echocardiography) were performed. Diabetic children demonstrated a greater cIMT (0.36 +/- 0.04 mm vs 0.31 +/- 0.03 mm, p = 0.002) and decreased carotid artery distensibility (4.4 +/- 1.6 cm(2) . dynes(-1) . 10(-6) vs 6.0 +/- 1.9 cm(2) . dynes(-1) .10(-6), p < 0.01) compared to control. Aortic pulse wave velocity was increased in DM (6.70 +/- 0.39 vs 6.30 +/- 0.31, p = 0.02) compared to control. Left ventricular diameters, mass, and systolic and diastolic function did not differ between the 2 groups. Simultaneous assessment of multiple cardiovascular parameters in children with type 1 DM revealed impaired carotid artery structure and function, and decreased elastic properties of the aorta, before demonstrable changes in left ventricular structure and function could be detected.     

Cardiovascular impact of end-stage renal insufficiency in children undergoing hemodialysis

Cardiac hypertrophy and arterial dysfunction have been described in end-stage renal disease (ESDR) in adults. The incremental elastic modulus (Einc), is a marker of vascular wall material stiffness and an independant predictor of cardiovascular mortality in adults with ESRD on hemodialysis. The relationship between arterial changes and the heart is unknown in the children with ESRD in the same conditions. Using a high-resolution vascular ultrasound and a computerized system of measurement (Iotec), we assessed noninvasively 10 ESRD patients (mean +/- SD, age, 11.5 +/- 4 years; blood pressure [BP], 120 +/- 10/63 +/- 4 mmHg) and 10 age-, sex-, and BP-matched controls (mean +/- SD, age, 11 +/- 4 years; BP, 114 +/- 8/58 +/- 8 mmHg). The systolic and diastolic diameter of the common carotid artery (CCA), the thickness of the wall (intima-media thickness, IMT), the cross sectional compliance (CSC), the cross sectional distensibility (CSD) and the (Einc) were determined. CSC and CSD were evaluated at the same level of pressure. The CCA pressure waveform was obtained by applanation tonometry to assess the reflected wave by the augmentation index (AI). Further the left ventricular mass index was assessed. The flow mediated dilation (FMD) (endothelium-dependent function) and the vasodilation induced by glyceryl-trinitrate (GTNMD) (GTN, an endothelium-independent dilator) were evaluated at the brachial artery site. Compared to control subjects, ESRD patients have mechanical artery dysfunction with lower CSC and CSD (0.11 +/- 0.04 vs 0.18 +/- 0.05 mm2.mmHg-1; p < 0.01; 0.43 +/- 0.10 vs 0.82 +/- 0.20 mmHg-1.10(-2); p < 0.001) and higher Einc (2.60 +/- 1.00 vs 1.40 +/- 0.30 mmHg.10(3); p < 0.001). Furthermore an earlier return of the reflected pulse wave (AI -0.24 +/- 0.08 vs -0.58 +/- 0.06; p < 0.005) is correlated to LV mass index (r = 0.55, P < 0.01) that is significantly increased (134 +/- 63 vs 69 +/- 25 g/m2; p < 0.005). These patients have an impaired FMD (4 +/- 2 vs 7 +/- 1%; p = 0.02) with a normal GTNMD. This study shows that early arterial dysfunction can occur in children with ESRD.     

Association of left bundle branch block with left ventricular structure and function in hypertensive patients with left ventricular hypertrophy: the LIFE study

Electrocardiographic (ECG) left bundle branch block (LBBB) is associated with left ventricular hypertrophy (LVH), but its relation to left ventricular (LV) geometry and function in hypertensive patients with ECG LVH is unknown. Echocardiograms were performed in 933 patients (548 women, mean age 66+/-7 years) with essential hypertension and LVH by baseline ECG in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. LBBB, defined by Minnesota code 7.1, was present in 47 patients and absent in 886 patients. Patients with and without LBBB were similar in age, gender, body mass index, blood pressure, prevalence of diabetes, and history of myocardial infarction. Despite similarly elevated mean LV mass (126+/-25 vs 124+/-26 g/m(2)) and relative wall thickness (0.41+/-0.07 vs 0.41+/-0.07, P=NS), patients with LBBB had lower LV fractional shortening (30+/-6 vs 34+/-6%), ejection fraction (56+/-10 vs 61+/-8%), midwall shortening (14+/-2 vs 16+/-2%), stress-corrected midwall shortening (90+/-13 vs 97+/-13%) (all P<0.001), and lower LV stroke index (38+/-7 vs 42+/-9 ml/m(2)) (P<0.05). Patients with LBBB also had reduced LV inferior wall and lower mitral E/A ratio (0.75+/-0.18 vs 0.87+/-0.38) (all P<0.05). The above univariate results were confirmed by multivariate analyses adjusted for gender, age, blood pressures, height, weight, body mass index, heart rate, and LV mass index. Among hypertensive patients at high risk because of ECG LVH, the presence of LBBB identifies individuals with worse global and regional LV systolic function and impaired LV relaxation without more severe LVH by echocardiography.     

Assessment of regional myocardial systolic function in hypertensive left ventricular hypertrophy using harmonic myocardial strain imaging

OBJECTIVES: Regional myocardial systolic function in hypertensive left ventricular hypertrophy was assessed using the newly developed myocardial strain imaging. METHODS: This study included 17 patients with hypertensive left ventricular hypertrophy (LVH group) and 22 normal subjects (N group). The transmural location of the strain peak value (StPP), and the strain peak value (StPV) in the end-systolic phase were measured at the posterior wall by myocardial strain imaging. Left ventricular mass index was simultaneously measured in both groups. RESULTS: StPV was significantly lower in the LVH group than the N group (1.00 +/- 0.36 vs 1.38 +/- 0.42, p < 0.01) and StPP was significantly moved to the epicardium side compared with the N group (31 +/- 10% vs 11 +/- 5%, p < 0.0001). StPV decreased and StPP increased with greater left ventricular mass index (r = -0.61, p < 0.0001; r = 0.72, p < 0.0001, respectively). CONCLUSIONS: Myocardial systolic impairment in hypertensive left ventricular hypertrophy may occur from the endocardium side, and the impairment may progress with increased left ventricular hypertrophy.     

Association of atrial natriuretic peptide and type a natriuretic peptide receptor gene polymorphisms with left ventricular mass in human essential hypertension.

OBJECTIVES: The goal of our study was to investigate the relationships between atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and type A natriuretic peptide receptor (NPRA) gene polymorphisms and left ventricular structure in human essential hypertension. BACKGROUND: Experimental evidence supports a key role for natriuretic peptides in the modulation of cardiac mass. This relationship has not yet been described in human disease. METHODS: A total of 203 hypertensive patients were studied by mono-bidimensional echocardiography. Three markers of the ANP gene (-C664G, G1837A, and T2238C polymorphisms) and a microsatellite marker of both NPRA and BNP genes were characterized. RESULTS: Patients carrying the ANP gene promoter allelic variant had increased left ventricular mass index (117.4 +/- 1.7 g vs. 95.7 +/- 1.7 g, p = 0.005), left ventricular posterior wall thickness (1.14 +/- 0.07 cm vs. 0.96 +/- 0.01 cm, p < 0.0001), left ventricular septal thickness (1.12 +/- 0.10 cm vs. 1.04 +/- 0.01 cm, p = 0.01), and relative wall thickening (47.5 +/- 4.1% vs. 39.4 +/- 5.3%, p = 0.001) as compared with the wild-type genotype. These associations were independent from anthropometric factors and major clinical features and were confirmed in a large subgroup of never-treated hypertensive patients (n = 148). Carrier status of the ANP gene promoter allelic variant was associated with significantly lower plasma proANP levels: 1,395 +/- 104 fmol/ml versus 3,110 +/- 141 fmol/ml in hypertensive patients carrying the wild-type genotype (p < 0.05). A significant association for NPRA gene variants with left ventricular mass index and left ventricular septal thickness was found. The analysis of BNP did not reveal any effect on cardiac phenotypes. CONCLUSIONS: Our findings show that the ANP/NPRA system significantly contributes to ventricular remodeling in human essential hypertension.     

Effect of endurance exercise training on left ventricular size and remodeling in older adults with hypertension

BACKGROUND: It is not known whether exercise training can induce a reduction of blood pressure (BP) and a regression of left ventricular hypertrophy (LVH) in older hypertensive subjects. This study was designed to determine whether endurance exercise training, by lowering BP, can induce regression of LVH and left ventricular (LV) concentric remodeling in older hypertensive adults. METHODS: We studied 11 older adults with mild to moderate hypertension (BP 152.0 +/- 2.5/91.3 +/- 1.5 mm Hg, mean +/- SE), 65.5 +/- 1.2 years old, who exercised for 6.8 +/- 3.8 months. Seven sedentary hypertensive (BP 153 +/- 3/89 +/- 2 mm Hg) subjects, 68.5 +/- 1 years old, served as controls. LV size and geometry and function were assessed with the use of two-dimensional echocardiography. RESULTS: Exercise training increased aerobic power by 16% (p < .001), and it decreased systolic (p < .05) and diastolic (p < .05) BP, LV wall thickness (from 12.8 +/- 0.4 mm to 11.3 +/- 0.3 mm; p < .05), and the wall thickness-to-radius (h/r) ratio (from 0.48 +/- 0.02 to 0.41 +/- 0.01; p < .05). There were no significant changes in the controls. The changes in LV mass index (deltaLVMI) were different between the two groups. LV mass index decreased in the exercise group (deltaLVMI - 14.3 +/- 3.3 g) but not in the controls (deltaLVMI 1.4 +/- 4.1 g; p = .009). A multiple stepwise regression analysis showed that among clinical and physiological variables including changes in resting systolic BP, aerobic power, body mass index, and systolic BP during submaximal and maximal exercise, only the reduction in resting systolic BP correlated significantly with a regression of concentric remodeling (delta h/r ratio r = .80; p = .003). The other variables did not add to the ability of the model to predict changes in the h/r ratio. CONCLUSIONS: The data suggest that exercise training can reduce BP and induce partial regression of LVH and LV concentric remodeling in older adults with mild or moderate hypertension.     

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.