Left ventricular geometric patterns and QT dispersion in untreated essential hypertension

The spectrum of left ventricular adaptation to hypertension, different types of hypertrophy patterns, and QT dispersion in different types of hypertrophy was investigated in 107 patients with untreated essential hypertension and 30 age- and gender-matched normal adults studied by 12-derivation electrocardiogram (ECG), two-dimensional, and M-mode echocardiography. Left ventricular mass (LVM), body mass index, total peripheral resistance (TPR), relative wall thickness (RWT), and QT dispersion were found to be statistically significantly higher in the hypertension group (P < .001 for all). Among hypertensive patients, 41.1% had both normal LVM and RWT, here called normal left ventricle in hypertension; 10.3% had concentric hypertrophy with increased LVM and RWT; 14.95% had eccentric hypertrophy with increased LVM and normal RWT; and 32.7% had concentric remodeling with normal LVM and increased RWT. Echocardiographically derived cardiac index was higher in the concentric hypertrophy and eccentric hypertrophy patterns (P = .002 and P < .0001, respectively), whereas TPR was higher in the concentric hypertrophy and concentric remodeling patterns (P = .017 and .02, respectively). QT dispersion values were found to be increased in the hypertensive group (P = .001), whereas similar values were calculated for different types of hypertrophy patterns. We conclude that the more common types of ventricular adaptation to essential hypertension are eccentric hypertrophy and concentric remodeling. Concentric hypertrophy is found to be associated with both volume and pressure overload, whereas eccentric hypertrophy is associated with volume overload only and concentric remodeling is associated with pressure overload. But different left ventricular geometric patterns seem to have similar effects on QT dispersion.     

Left ventricular geometry and severe left ventricular hypertrophy in children and adolescents with essential hypertension

BACKGROUND: Left ventricular (LV) hypertrophy has been established as an independent risk factor for cardiovascular disease in adults. Recent research has refined this relationship by determining a cutpoint of 51 g/m(2.7) for LV mass index indicative of increased risk and defining LV geometric patterns that are associated with increased risk. The purpose of this study was to evaluate severe LV hypertrophy and LV geometry in children and adolescents with essential hypertension. METHODS AND RESULTS: A cross-sectional study of young patients (n=130) with persistent blood pressure elevation above the 90th percentile was conducted. Nineteen patients (14%) had LV mass greater than the 99th percentile; 11 of these were also above the adult cutpoint of 51 g/m(2.7). Males, subjects with greater body mass index, and those who had lower heart rate at maximum exercise were at significantly (P<.05) higher risk of severe LV hypertrophy. In addition, 22 patients (17%) had concentric LV hypertrophy, a geometric pattern that is associated with increased risk of cardiovascular disease in adults. Seven patients had LV mass index above the cutpoint and concentric hypertrophy. No consistent significant determinants of LV geometry were identified in these children and adolescents with hypertension. CONCLUSIONS: Severe LV hypertrophy and abnormal LV geometry are relatively prevalent in young patients with essential hypertension. These findings suggest that these patients may be at risk for future cardiovascular disease and underscore the importance of recognition and treatment of blood pressure elevation in children and adolescents. Weight loss is an important component of therapy in young patients with essential hypertension who are overweight.     

Left ventricular geometry as an independent predictor for extracardiac target organ damage in essential hypertension

Left ventricular hypertrophy (LVH) is an independent cardiovascular risk factor. It has not been established, however, whether left ventricular geometry is an independent predictor of extracardiac target organ damage in essential hypertension. Study groups were classified according to relative wall thickness: 27 patients with concentric LVH and 50 patients with eccentric LVH. Age and left ventricular mass indexes of two groups were matched. As indexes of extracardiac target organ damage, retinal funduscopic grade, and serum creatinine level were measured. The severity of hypertensive retinopathy and the renal involvement were more severe in patients with concentric LVH than in patients with eccentric LVH. Extracardiac target organ damage was consistently higher in patients with concentric LVH than in those with eccentric LVH. Systemic hemodynamics paralleled ventricular geometric patterns, with higher peripheral resistance and lower aortic compliance in patients with concentric LVH, whereas end-diastolic volumes and stroke volumes were higher in patients with eccentric LVH than in patients with concentric LVH. In addition, total peripheral resistance was related to retinal fundoscopic grade (r = 0.41, P < .01), and serum creatinine level (r = 0.28, P < .05). Even in the presence of an identical degree of LVH, echocardiographically determined left ventricular geometry may provide a further independent stratification of extracardiac target organ damage in essential hypertension.     

Left ventricular geometry in presenting untreated hypertension

In order to investigate the spectrum of geometry in our patient population, 63 untreated hypertensives underwent two-dimensional echocardiography. Left ventricular (LV) mass index and relative wall thickness, a measure of wall thickness in relation to cavity size, were calculated from the M-mode strip. In addition, to assess the sphericity of the left ventricle the ratio of LV minor to major hemiaxis was calculated. The subjects comprised 41 men (17 Caucasian, 22 Afro-Caribbean and two Oriental), and 21 women (five Caucasian, 12 Afro-Caribbean and two Oriental). Concentric hypertrophy was present in 46% of subjects, concentric remodelling in 32% of subjects, eccentric hypertrophy in only 6% of subjects and a normal left ventricular shape in 16% of subjects. The degree of sphericity of the left ventricle was similar among the four groups, suggesting that it does not change in uncomplicated hypertension. In contrast to the previously published combined series from Sassari and New York we had a low proportion of patients with either eccentric hypertrophy or normal left ventricular geometry. This is probably due to the high proportion of Afro-Caribbean subjects in our clinic population who are more likely to have left ventricular hypertrophy.     

Left ventricular hypertrophy in patients with nephrogenic arterial hypertension

Incidence and geometric peculiarities of hypertrophy of the left ventricle of the heart (HLVH) were studied on the basis of findings from the echocardiographic investigation done in 86 patients with chronic glomerulonephritis (ChGN) with arterial hypertension (AH), with the renal function being preserved and at the early stages of renal insufficiency. HLVH was detected in 30.2% of the patients, in 80.8% of whom it was concentric, and in 19.2% eccentric, in 76%--symmetric and in 23.1%--asymmetric. Incidence of HLVH did not correlate with sex, clinical variant of ChGN, renal function status, and increased with the degree and duration of AH. There was no difference in geometric peculiarities between sexes, clinical variants of ChGN, and no association with degree and duration of AH as well as with functional state of the kidneys.     

Left ventricular repercussion of obesity-induced arterial hypertension in the dog

Obesity and hypertension are frequently associated. The aim of our study was to assess the effects of high fat diet on weight, blood pressure and left ventricule in dogs. We studied 6 male Beagle dogs before and after 7 weeks of hypercaloric hyperlipidic diet. Echocardiography was used to measure left ventricular wall thickness, volumes, ejection fraction and mass. Results are expressed as % of variation of initial values. After 20 weeks, dogs presented abdominal obesity with increased body weight (11.9 +/- 2.3 to 15.2 +/- 2 kg; p < 0.03) associated with an increasing of systolic (196.5 +/- 14.6 to 260.1 +/- 17.5 mmHg; p < 0.03), diastolic (76.6 +/- 9 to 110.6 +/- 10.2; p < 0.004) and mean blood pressure (128.8 +/- 7 to 152.7 +/- 7.6 mmHg; p < 0.004). There were non significant changes concerning diastolic thickness of septum and posterior wall. Left ventricular volumes increased in diastole (41.1 +/- 4.5 to 48.9 +/- 10.3 cm3; p < 0.03) and systole (12.2 +/- 1.7 to 14.9 +/- 3.2 cm3; p < 0.03). So, despite any changes in wall thickness, we observed an increased of ventricular mass (67 +/- 15 to 80 +/- 24.3 g; p < 0.03). Ejection fraction remained unchanged. CONCLUSION: it appears that hight fat diet induces obesity and hypertension in dogs; changes in left ventricule suggest a volodependent hypertension.     

Glucose intolerance exaggerates left ventricular hypertrophy and dysfunction in essential hypertension

The influence of glucose intolerance, the preclinical stage of diabetes mellitus, on the progression of left ventricular hypertrophy and left ventricular dysfunction in essential hypertension, was assessed with two-dimensional M-mode echocardiography in age- and sex-matched essential hypertensive patients with (n = 28) or without (n = 44) glucose intolerance, and normotensive control subjects (n = 29). Left ventricular mass index in hypertensive patients with glucose intolerance was significantly higher than that in hypertensive patients without glucose intolerance (mean +/- SD, 115.6 +/- 28.2 v 102.1 +/- 22.1 g/m2; P < .05). Left ventricular diastolic function as reflected by peak lengthening rate was reduced in glucose-intolerant hypertensive patients than in hypertensive patients without glucose intolerance (2.68 +/- 0.71 v 3.16 +/- 0.82/sec; P < .05). End-systolic wall stress/left ventricular end-systolic volume index, an index of left ventricular contractility, was reduced more in glucose-intolerant hypertensive patients than in hypertensive patients without glucose intolerance (2.75 +/- 0.55 v 3.13 +/- 0.55 10(3) dyn.m2/cm2.mL-1; P < .01). These findings suggest that glucose intolerance accelerates progression of left ventricular hypertrophy and deteriorates left ventricular diastolic function and contractility in essential hypertension.     

Left ventricular hypertrophy, blood pressure and ACE genotype in untreated hypertension

It has been suggested that the deletion polymorphism of the angiotensin-converting enzyme (ACE) genotype may be important in the development of left ventricular hypertrophy (LVH). In order to test this hypothesis we investigated the interaction between blood pressure (BP), LVH and ACE genotype in 86 previously untreated hypertensive patients. Each underwent two-dimensional and Doppler echocardiography and ACE genotyping. There were no significant differences in BP, the parameters of left ventricular structure (including left ventricular mass index) or diastolic function between the three genotype groups. Additionally, there were no significant differences in the relationship between systolic BP and left ventricular mass index among the three genotype groups (II genotype, r = 0.46, P = 0.02; ID genotype, r = 0.42, P = 0.01; DD genotype, r = 0.34, P = 0.10; F = 0.38). In contrast to some previous studies, we have found in this group of previously untreated hypertensive subjects no evidence to suggest that the deletion polymorphism of the ACE genotype is important in the development of LVH.     

Parallel increase in carotid, brachial and left ventricular cross-sectional areas in arterial hypertension

Few data have been published about the relation between the vessels geometry and development of left ventricular (LV) hypertrophy in patients with arterial hypertension. The aim of this study is to describe arterial and LV geometry changes due to mild-to-moderate arterial hypertension in an untreated hypertensive population. In 95 untreated patients with mild-to-moderate hypertension and 23 age- and sex-matched healthy normotensives, we measured the end-diastolic diameter and wall thickness of the left ventricle and the internal diameter and intimal-medial thickness (IMT) of carotid and brachial arteries. From these data, the cross-sectional areas (CSAs) of arterial and myocardial walls were calculated. Hypertensive patients were further subdivided on the basis of the presence of LV hypertrophy defined according to Devereux et al as anatomical LV mass >125 g/m. In hypertensive patients with hypertrophy, carotid and brachial CSAs increased, without significant changes in thickness/diameter ratio (arterial 'enlargement'), while the left ventricle developed 'concentric' hypertrophy. Arterial and LV CSAs showed a significant direct correlation with systolic blood pressure (BP). However, when data were corrected for BP, the correlation between the increase in arterial and LV CSAs became much improved than for the raw data. In conclusion patients with untreated mild-to-moderate hypertension, both carotid and brachial arterial walls showed an enlargement that was proportional to the development of LV hypertrophy. These results suggest that the effects of arterial hypertension on carotid, brachial and LV wall geometry have a common modulation.     

QT dispersion as a marker of left ventricular mass in essential hypertension

Resting L1210 cells were treated with nimustine (ACNU), a bifunctional alkylating anticancer agent, for 2 h in a nutrient-depleted medium. The cells were then transferred to a fresh medium and incubated for a further 48 h. Functions of the cells thus prepared were examined in terms of the dye-exclusion of the membrane, 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino)carbonyl] -2H-tetrazolium hydroxide, inner salt, sodium salt (XTT)-reducing ability of the mitochondria, and heat generation due to vital metabolism as the measure of cell viability. The cells treated with ACNU were functioning normally in all the cell functions examined but were completely devoid of proliferating capacity. These results suggest the possibility that ACNU might impair the proliferative capacity of the resting cell population inside a solid tumor without causing such impairment to the cells of normal organs and tissues composed of intrinsically non-proliferative cells.     

Pulmonary artery structural changes in pulmonary hypertension complicating congenital diaphragmatic hernia

Primary pulmonary hypertension is characterized by the presence of smooth muscle cells in nonmuscular compartments or segments of the vessel and the abnormal deposition of collagen in both the small muscular arteries and arterioles and the large elastic arteries. Victorian blue van Gieson staining and Immunostaining with anti-alpha smooth muscle actin (ASMA) were performed on lung tissues obtained during autopsy from 21 patients who had congenital diaphragmatic hernia (CDH) complicated by persistent pulmonary hypertension (PPH) and 10 control patients who died of sudden infant death syndrome (SIDS). The degree of medial thickening and adventitial thickening was measured in pulmonary arteries by image analysis and compared statistically. There was a significant increase in adventitial as well as medial thickness in arteries of all sizes in CDH patients compared with control patients (P < .001). The most striking increase occurred in arteries with an external diameter (ED) of less than 75 microns. Calculation of the areas of the various components in the wall of each vessel showed that for smaller vessels (< 75 microns ED), the area of the lumen was smaller and the area of the media and adventitia was larger in CDH patients compared with control patients (P < < .001). In vessels greater than 75 microns ED, the areas of media in CDH was the same as in controls and the area of adventitia in CDH was significantly larger than controls (P < .001). The present study provides evidence that an increase in adventitial thickness and adventitial area occurs in pulmonary arteries in CDH patients complicated by PPH. The structural changes in the adventitia of the pulmonary arteries may be an important factor in the development of PPH in patients with CDH.     

Microalbuminuria in essential hypertension

The prevalence of microalbuminuria in patients with essential hypertension ranges between 10 and 25%. The level of albuminuria is highly correlated with arterial pressure and more closely ambulatory arterial pressure. The interaction between albuminuria and arterial pressure is enhanced by overweight and smoking. The renal mechanisms of microalbuminuria are not well elucidated; however, an increase in filtration fraction suggestive of intraglomerular hypertension was observed in patients with hyperfiltration. The significance of microalbuminuria as a marker of cardiovascular risk or hypertensive renal damage needs to be confirmed through long-term follow-up studies. Antihypertensive treatment has variable influence on albuminuria; and angiotensin-converting enzyme inhibitors and to a lesser extent other agents, tend to partially correct this abnormality.     

The changes in plasma arginine-vasopressin in patients with essential hypertension and the correlation with patient's condition

The levels of plasma arginine-vasopressin (AVP) in 80 patients with essential hypertension were measured, and its impact on the disease and its clinical significance were studied. The results showed that: (1) The levels of plasma AVP in patients with essential hypertension were significantly higher than that in normotensive subjects (P < 0.001). It dropped to normal level after antihypertensive drugs. (2) The concentrations of plasma AVP in both hypertensive subjects and normotensive subjects were not correlated with age and sex (P < 0.05). (3) The concentration of plasma AVP in patients with essential hypertension was the highest in stage III, the lowest in stage I, and middle in stage II. (4) The levels of plasma AVP in patients with malignant hypertension were significantly higher than that in patients with benign hypertension (P < 0.05). A positive correlation was found between the levels of plasma AVP and blood pressure (r = 0.3398, P < 0.01). (5) The concentrations of plasma AVP in hypertensive subjects with ventricular hypertrophy were higher than that in hypertensive subjects with out ventricular hypertrophy (P < 0.05). (6) The concentrations of plasma AVP in hypertensive subjects with heart failure were significantly higher than that in hypertensive subjects with out heart failure (P < 0.001). The results suggest that AVP has a role in the pathogenesis of hypertension, hypertension complicated with ventricular hypertrophy and hypertension complicated with heart failure. The levels of plasma AVP may be viewed as an index of the patient's condition in hypertensive subjects.