Left ventricular hypertrophy in patients with chronic renal failure treated by hemodialysis

Left ventricular hypertrophy (LVH) is common and important predictor of risk of death in end-stage renal failure. In the present study we have analysed echocardiographically the left ventricular hypertrophy and some possible risk factors continuing to its development in patients with chronic renal failure (crf) treated by hemodialysis (HD). From a cohort of 85 patients with crf we selected for analysis 59 clinically stable patients. Echocardiography (ECHO), body mass index (BMI), serum creatinine, urea, total protein, albumin, hemoglobin, hematocrit, electrolytes and parathyroid hormone (PTH) concentrations were evaluated in all patients at the next hours after HD session. LVH was common in HD patients: concentric LVH was detected by ECHO in 46 patients and in 13 patients eccentric LVH was observed. Mean serum concentrations of urea, creatinine, PTH and phosphate differed from normal values while hemoglobin, total protein, albumin, sodium kalium, calcium serum concentration were in the normal range. Positive correlation was found between PTH serum concentration and LVM r = 0.704 (p < 0.001), between PTH serum concentration and IVS r = 0.267 (p < 0.04), between PTH serum concentration and PW t = 0.238 (p < 0.04), and negative correlation between BMI and LVMI r = -0.451 (p < 0.05). The correlations between serum PTH concentration and LVH and between BMI and LVH confirmed that both hyperparathyroidism and malnutrition are important factors influencing the development of LVH in HD patients.     

Left ventricular hypertrophy in patients with autonomic failure

BACKGROUND: In autonomic failure (AF), supine hypertension may predispose patients to end-organ damage. The pathophysiology of hypertensive heart disease in AF is not known. The aim of the present study was to evaluate the prevalence and predisposing factors of left ventricular hypertrophy (LVH) in patients with AF. METHODS: We studied 25 patients with AF (67 +/- 8 years); 80% were being treated for orthostatic hypotension. Twenty patients with essential hypertension (68 +/- 6 years) were considered as the control group. All subjects underwent echocardiography for measurement of left ventricular mass (LVM). The patients with AF underwent a 24-h BP monitoring and long-term blood pressure (BP) variability was calculated as standard deviation (SD) of the average of the half-hour mean values. RESULTS: The LVM is comparable in patients with AF and hypertensive controls (145 +/- 35 g/m2 v 127 +/- 32 g/m2, P = .07). The proportion of patients with LVH is similar in both populations (AF 80%, hypertensive 70%). The patients with AF were divided into two groups, with and without LVH. The SDs are significantly higher in AF patients with LVH than in those with normal LVM (SD 24-h systolic BP: 22 +/- 4 v 14 +/- 1 mm Hg, P = .001). CONCLUSIONS: A high proportion of patients with AF show LVH. The LVM values are comparable with those of patients with essential hypertension. The development of LVH seems to depend on high BP variability, characteristic of AF patients. Detection of LVH may help in the choice of treatment for orthostatic hypotension and in the prevention of heart failure.     

Regression of left ventricular hypertrophy following stenting of renal artery stenosis.

PURPOSE: To determine if angioplasty of atherosclerotic renal artery stenosis, which reduces the activation of the renin-angiotensin-aldosterone system (RAAS), may lead to regression of left ventricular hypertrophy. METHODS: The study included 102 patients (58 men; mean age 67 years, range 66-69) who underwent stent-supported percutaneous transluminal renal angioplasty (PTRA) and were included in a clinical follow-up program (mean 24+/-14 months, range 6-60). As a control group, 101 contemporaneous patients (68 men; mean age 68 years, range 66-70) with essential hypertension were investigated. The primary endpoint was the change in left ventricular mass index (LVMI) determined by echocardiography. RESULTS: Mean follow-up intervals were 24+/-14 months (range 6-60) in the study group and 27+/-14 months (range 6-60) in the controls (p = 0.09). LVMI decreased significantly by -10+/-26 g/m(2) in the study group, while it increased significantly by 9+/-28 g/m(2) in the control group (p = 0.001 between groups). In the study group, mean arterial blood pressure was significantly reduced from 99+/-11 mmHg to 90+/-11 mmHg (p<0.0001) during follow-up despite a significant reduction in medication, whereas it increased significantly from 102+/-11 mmHg to 105+/-11 mmHg (p = 0.008) in the control group, although medication was significantly increased. After adjustment for various factors and covariables, PTRA prevailed as an independent predictor for regression of LVMI (p = 0.038). CONCLUSION: PTRA induces regression of LVMI that is independent of the reduction in blood pressure induced by this procedure. Reduced activity of the RAAS may account for this regression.     

Left ventricular hypertrophy in hypertensive type 2 diabetic patients according to renal function

AimCardiovascular disease is the main cause of death in diabetic patients undergoing haemodialysis. Dialysis and hypertension increase left ventricular hypertrophy (LVH), a strong predictor of cardiovascular events. This study evaluated left ventricular structure and function in three groups of hypertensive type 2 diabetic patients with different renal function, and assessed the factors associated with LVH, in an Afro-Caribbean population.MethodsLeft ventricular structure and function were measured by ultrasonography. Group 1 consisted of 150 patients with normal renal function, group 2 included 183 patients with renal dysfunction and the third group comprised 75 dialysis patients.ResultsLeft ventricular mass/height^2.7 increased from group 1 to groups 2 and 3 (49.00 g/m^2.7, 57.12 g/m^2.7 and 59.75 g/m^2.7, respectively; P < 0.0001). The prevalences of LVH were 48.3% in group 1, 64.8% in group 2 and 70.3% in the dialysis patients (P = 0.001). LVH was more concentric than eccentric in groups 2 and 3.The factors significantly associated with LVH were obesity in groups 1 and 2, and an increase of 10 mmHg in pulse pressure in groups 2 and 3, according to multivariate logistic-regression analysis.ConclusionOur study confirmed that, in a population of Afro-Caribbean hypertensive type 2 diabetic patients, renal failure was associated to an increased left ventricular mass/height^2.7. The data show that the variables associated with LVH differ according to renal profile. This finding will be of value in the treatment and follow-up of these patients.     

Left ventricular hypertrophy

Opinion statement  

Left ventricular hypertrophy in acute stroke patients with known hypertension

Background: Despite effective treatments, hypertension remains uncontrolled in nearly half of the people with hypertension in the United States. Uncontrolled hypertension leads to end organ damage, such as left ventricular hypertrophy (LVH). To identify reasons for uncontrolled hypertension, we interviewed acute stroke patients with a history of hypertension and evaluated for LVH. Methods: Using a standardized questionnaire, we collected demographic, socioeconomic, and health-care data in 300 acute ischemic and hemorrhagic stroke patients in one hospital. We also collected relevant clinical data from medical records. We analyzed factors associated with echocardiographic LVH as a marker of uncontrolled hypertension in 190 acute stroke patients with a history of hypertension. Results: Overall, 46% (88/190) of patients had LVH. In univariate analysis, lower household income and self-reported poor adherence to hypertension treatment were significantly associated with increased risk of LVH. In multiple logit modeling, only poor adherence to hypertension treatment remained significantly associated with LVH, odds ratio 1.77 (95% CI: 1.01–3.11), p < 0.05. Conclusions: In acute stroke patients, poor adherence to hypertension treatment is a significant independent predictor of LVH. A clear reason for poor adherence to treatment is elusive in a large proportion of these patients in our study. Further research is needed to identify and develop strategies to combat the key factors responsible for poor adherence to hypertension treatment.     

Left ventricular hypertrophy in athletes and hypertensive patients

Systemic hypertension and physical exercise are both associated with cardiac adaptations. The impact is most prominent on the left side of the heart, which hypertrophies leading to left ventricular hypertrophy. This article reviews structural and functional cardiac changes seen in hypertensive and athlete's hearts.     

Left ventricular hypertrophy in end-stage renal disease on peritoneal dialysis

Cardiovascular diseases account for the greatest number of deaths among uremic patients.^1,2 Most attention has focused on atherosclerosis, with opinion divided as to whether it is accelerated by uremia.^3,4 Although a “uremic dilated cardiomyopathy” has been reported, its cause and prevalence remain obscure.⁵ In contrast, concentric left ventricular (LV) hypertrophy is known to occur more often in patients treated with dialysis, although apparently little attention has been paid to its possible clinical significance.^6,7 This report was designed to (1) determine the prevalence of LV hypertrophy in patients treated with dialysis, (2) examine the clinical factors that may be responsible for its presence, and (3) determine whether LV hypertrophy was associated with increased mortality. Because blood pressure (BP) is likely to be involved in the pathogenesis of LV hypertrophy, the study was conducted in patients treated with continuous ambulatory peritoneal dialysis because such patients are free of the marked swings in BP that frequently accompany the relatively rapid intravascular volume changes with hemodialysis, and accurate tracking of BP is therefore possible.     

Right ventricular hypertrophy and diastolic dysfunction in arterial switch patients without pulmonary artery stenosis

Objective

To assess pulmonary flow dynamics and right ventricular (RV) function in patients without significant anatomical narrowing of the pulmonary arteries late after the arterial switch operation (ASO) by using magnetic resonance imaging (MRI).

Methods

17 patients (mean (SD), 16.5 (3.6) years after ASO) and 17 matched healthy subjects were included. MRI was used to assess flow across the pulmonary trunk, RV systolic and diastolic function, and RV mass.

Results

Increased peak flow velocity (>1.5 m/s) was found across the pulmonary trunk in 14 of 17 patients. Increased RV mass was found in ASO patients: 14.9 (3.4) vs 10.0 (2.6) g/m² in normal subjects (p<0.01). Delayed RV relaxation was found after ASO: mean tricuspid valve E/A peak flow velocity ratio = 1.60 (0.96) vs 1.92 (0.61) in normal subjects (p = 0.03), and E‐deceleration gradients = −1.69 (0.73) vs −2.66 (0.96) (p<0.01). After ASO, RV mass correlated with pulmonary trunk peak flow velocity (r = 0.49, p<0.01) and tricuspid valve E‐deceleration gradients (r = 0.35, p = 0.04). RV systolic function was well preserved in patients (ejection fraction = 53 (7)% vs 52 (8)% in normal subjects, p = 0.72).

Conclusions

Increased peak flow velocity in the pulmonary trunk was often observed late after ASO, even in the absence of significant pulmonary artery stenosis. Haemodynamic consequences were RV hypertrophy and RV relaxation abnormalities as early markers of disease, while systolic RV function was well preserved.     

Determinants of renal function in patients with renal artery stenosis

Renal artery stenosis (RAS) is an important cause of renal failure; however, the factors associated with loss of kidney function in patients with RAS are poorly described, as are the predictors of an improvement in kidney function after stenting. One hundred patients at seven centers undergoing renal stenting were randomly assigned to an embolic protection device or double-blind use of a platelet glycoprotein IIb/IIIa inhibitor. The glomerular filtration rate (GFR) was measured using the creatinine-derived modified Modification of Diet in Renal Disease (MDRD) equation, cystatin C, and iohexol clearance. In univariate and multivariate models, baseline MDRD and cystatin C GFR were associated with congestive heart failure (CHF) (p = 0.01), lesion length (p = 0.01), and percent stenosis (-0.27, p = 0.01). In multivariate models, MDRD-estimated GFR 1 month after stenting was associated with bilateral stenosis (p < 0.05) and lesion length (p < 0.05), whereas with cystatin C the multivariate model included angiotensin receptor blocker (ARB) (p < 0.05) and minimal luminal diameter (MLD) (p < 0.05). The improvement in GFR from baseline to 1 month, measured as percent change, was related to baseline MDRD (p = 0.009) and cystatin C (p = 0.03) GFR. For MDRD GFR combined treatment with abciximab and Angioguard(?) embolic protection (p = 0.02) remained significant in multivariate analysis as did CHF, which was also significant with cystatin C (p = 0.05). In conclusion, CHF and lesion characteristics (MLD, percent stenosis and lesion length) are determinants of renal function in patients with RAS. In contrast, the acute improvement in renal function after revascularization is most strongly influenced by baseline GFR, and to a lesser degree CHF and combined procedural treatment with abciximab and embolic protection but not lesion characteristics. Clinical Trial Registration - URL:http://www.clinicaltrials.gov. Unique identifier: NCT00234585.     

Left ventricular hypertrophy and endothelial functions in patients with essential hypertension

OBJECTIVE: In this study, we used a non-invasive method in patients with essential hypertension and without any overt clinical evidence of atherosclerosis to investigate the role of left ventricular hypertrophy (LVH) in endothelial functions. METHODS: We assessed endothelial function in 32 hypertensive patients with LVH (group 1), 28 hypertensive patients without LVH (group 2) and 29 normotensive subjects (control group). Flow-mediated (endothelium-dependent) and nitrate induced (endothelium-independent) dilatation of the brachial artery was evaluated in all groups. RESULTS: Flow-mediated dilatation was considerably higher in the control group than in group 1 and 2 (13.98 +/- 2.92%, 4.67 +/- 1.09% and 7.02 +/- 1.79% respectively, p < 0.001). In addition, endothelium-dependent dilatation was significantly lower in group 1 than in group 2 (p < 0.001), whereas nitrate induced changes were similar in all groups. CONCLUSION: Vascular endothelial functions are impaired in hypertensive patients. There may be heterogeneity of endothelial dysfunction among patients with hypertension. Presence of LVH has an additional negative effect on endothelial function in hypertensive patients.     

高血压患者左心室肥厚与QT离散度增大

目的　进一步探讨高血压左心室肥厚及左心室质量增大与 QT离散度 (QTdispersion,QTd)改变的关系。方法　采用 12导联心电图同步描记及心脏超声检查等方法对 94例原发性高血压患者 [男性 40例 ,女性 5 4例 ,年龄 (5 9.9± 11.2 )岁 ]和 11例正常人 [男性 4例 ,女性 7例 ,年龄 (5 2 .8±16 .9)岁 ]作 QTd及左心室肥厚、左心室质量检测分析。结果　高血压左心室肥厚组 ( 组 ,n=6 2 ) QTd较非肥厚组 ( 组 ,n=32 )以及正常对照组 ( 组 ,n=11)均明显增大 (P<0 .0 1～ 0 .5 0 ) ,QTd与左心室质量呈正相关 (r=0 .47,P<0 .0 1)。结论　原发性高血压左心室肥厚、左心室质量增大可使 QTd明显增大 ,具有心室肌复极不均一、有形成折返性室性心动过速及心脏性猝死的潜在危险     

Left ventricular hypertrophy.

OBJECTIVE: To review the pathophysiology, epidemiology, patterns, diagnosis, and treatment of left ventricular hypertrophy with emphasis on the elderly. DATA SOURCES: A computer-assisted search of the English-language literature (MEDLINE database) followed by a manual search of the bibliographies of pertinent articles. STUDY SELECTION: Studies on the pathophysiology, epidemiology, patterns, diagnosis, and treatment of left ventricular hypertrophy were screened for review. Studies on left ventricular hypertrophy in the elderly and recent studies were emphasized. DATA EXTRACTION: Pertinent data were extracted from the reviewed articles. Emphasis was on studies involving the elderly. Relevant articles were reviewed in depth. DATA SYNTHESIS: Available data about the pathophysiology, epidemiology, patterns, diagnosis, and treatment of left ventricular hypertrophy with emphasis on studies involving the elderly were summarized. CONCLUSIONS: Left ventricular hypertrophy caused by hypertension or other cardiovascular disease is not only a marker for but also a contributor to cardiovascular morbidity and mortality in elderly and young patients. The question of whether regression of left ventricular mass in patients with hypertension will decrease cardiovascular morbidity and mortality needs to be answered by prospective studies using different types of antihypertensive drugs. Future studies on the efficacy of antihypertensive drugs and on stratification of therapy should include echocardiographic estimates of left ventricular mass index.     

Left ventricular hypertrophy and clinical outcomes in hypertensive patients

The prevalence of left ventricular hypertrophy (LVH) rises with severity of hypertension (HT), age, and obesity. Its prevalence ranges from 20% in mildly hypertensive patients to almost 100% in those with severe or complicated HT. However, the diagnosis of LVH is not straightforward, and the definitions and criteria used in clinical studies lack consistency. While many factors play a role in the onset and progression of LVH, blood pressure (BP) is recognized as a central factor. Twenty-four-hour BP measurements are more closely related to LVH than conventional BP readings taken in the clinician's office. Increased renin-angiotensin system (RAS) activity also plays an important role in the development of LVH, and various studies show a correlation between plasma renin activity and left ventricular mass (LVM). LVH is a recognized marker of HT-related target organ damage, and a strong and independent risk factor for adverse cardiovascular (CV) outcomes. CV risk increases with increasing LVM, and decreases with regression of LVH in response to antihypertensive treatment. Therefore the detection, prevention, and reversal of LVH are important goals in HT management. Most antihypertensive drugs can attenuate BP and LVH. However, each drug class may induce LVH regression to a different extent and these extents seldom correlate with the degree of BP reduction achieved. Data from the few large comparative studies in this area suggest that certain classes of antihypertensive drugs and/or their combinations are more effective than others. In particular, calcium channel blockers and drugs that target the RAS, such as angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), appear to have a specific effect on LVH, independent of BP reduction. Guidelines, therefore, have recommended these drug classes for the treatment of hypertensive patients with LVH.     

经皮肾动脉介入治疗肾动脉狭窄的远期临床疗效

目的观察肾动脉狭窄患者经皮肾动脉介入治疗对血压及肾功能的远期疗效。方法选取1998年1月至2006年6月在沈阳军区总医院心内科住院诊治的肾动脉狭窄患者120例为研究对象,观察术后72h及随访5年的血压及肾功能的变化,评价肾动脉介入治疗对肾性高血压、肾功能不全的影响。结果120例行经皮肾动脉介入治疗的患者肾动脉病变狭窄程度76．1％±19．4％,支架直径（5．8±1．2）mm,支架长（17．1±4．2）mm,支架残余狭窄2．1％±0．5％,介人手术成功率达100％。术前血压（178．7±28．4／100．2±17．6mm）Hg,术后72h血压（128．1±14．5／75．1±10．1）mmHg,随访5年时血压（140．2±18．7／84．4±13．2）mmHg;术后72h及5年随访血压值较术前显著下降,差异均有统计学意义（P〈0．05）。术后人均服用降压药物比术前明显减少,差异有统计学意义[（2．7±1．0）种m（3．5±1．0）种,P〈O．05]。术前估算肾小球率过滤（estimated glomerular filtration rate,eGFR）（65．50±24．41）mL／（min·1．73m^2）,术后72heGFR（61．16±23．36）mL／（min·1．73m^2）,术后5年eGFR（64．12±23．30）mL／（min·1．73m^2）;术后72h及术后5年与术前eGFR比较,均差异无统计学意义（P〉O．05）。27例肾动脉狭窄合并肾功能异常的患者术前eGFR（35．43±11．66）mL／（min·1．73m^2）,术后72heGFR（33．86±12．51）mL／（min．1．73m^2）,术后5年eGFR（39．10±12．69）mL／（min·1．73mz）;术后5年eGFR较术前呈上升趋势,但与术前比较,差异无统计学意义（P〉0．05）。结论肾动脉介入治疗可显著降低肾性高血压患者术后血压,减少应用降压药物种类．对术前肾功能正常者无影响;5年随访观察经皮肾动脉介入治疗对术前肾功能异常者无明显改善。