血液透析对终末期肾病患者左心室肥厚的影响

目的探讨血液透析早期对终末期肾病(ESRD)患者心脏结构的影响。方法 32例ESRD患者,分别在进入血液透析前及进入血液透析后半年至1年内行超声心动图检查,比较血液透析前后各参数的变化,同时选取29例慢性肾脏病(CKD)3～4期非透析患者作为对照组。结果与血液透析前比较,ESRD患者血液透析后的干体质量[(60.8±8.8)kg比(64.7±10.3)kg,P=0.004]及体质指数[(22.68±2.35)kg/m~2比(24.08±2.32)kg/m~2,P=0.004]明显下降。收缩压轻度升高,舒张压显著升高[(84.67±11.14)mm Hg比(77.33±9.17)mm Hg,P<0.05]。血白蛋白[(38.73±2.42)g/L比(34.07±3.75)g/L,P<0.05]、血红蛋白[(111.50±12.85)g/L比(83.73±13.65)g/L,P<0.05]均显著上升。对照组左心室肥厚(LVH)发生率37.93%,血液透析前组71.88%,血液透析后组50%。血液透析前ESRD患者的左心室质量指数(LVMI)较对照组显著升高[(152.01±44.37)g/m~2比(120.68±44.60)g/m~2],血液透析后下降为(135.98±34.87)g/m~2,与透析前比较差异有统计学意义(P<0.05)。血液透析前ESRD患者的左心房直径[(40.75±7.11)mm比(34.97±5.80)mm]、室间隔厚度[(11.63±1.48)mm比(10.66±2.02)mm]、左心室后壁厚度[(11.56±1.46)mm比(10.31±1.56)mm]、左心室舒张末直径[(48.28±5.53)mm比(45.62±4.64)mm]和左心室舒张末容积[(110.81±29.45)ml比(96.83±22.74)ml]较对照组明显增大(均为P<0.05),血液透析后与透析前比较,室间隔厚度[(10.84±1.25)mm比(11.63±1.48)mm]和左心室后壁厚度[(10.88±1.18)mm比(11.56±1.46)mm]显著下降(均为P<0.05)。结论 ESRD患者LVH发病率高,部分LVH在血液透析早期可以逆转。     

Course of left ventricular hypertrophy and function in end-stage renal disease after renal transplantation.

Cardiovascular complications are frequent and related to left ventricular (LV) hypertrophy and dysfunction in end-stage renal disease. To examine cardiac changes after renal transplantation, 24 hemodialysis patients (18 men and 6 women, age 47 +/- 12 years) were analyzed in a prospective follow-up study with echocardiography immediately before and 41 +/- 30 months after renal transplantation. Mean systolic blood pressure (hemodialysis vs transplantation: 156 +/- 35 vs 144 +/- 15 mm Hg; p = not significant [NS]), as averages of 6 measurements from 2 weeks, remained constant and elevated. The most frequent echocardiographic findings at both assessments were left atrial dilatation (75 vs 79%; p = NS) and LV hypertrophy (71 vs 67%; p = NS). After transplantation, an increase was found in mean left atrial diameter (41 +/- 5 to 44 +/- 5 mm; p < 0.05) and end-diastolic LV diameter (50 +/- 5 to 53 +/- 5 mm; p < 0.05) at constant LV muscle mass (332 +/- 104 vs 329 +/- 94 g; p = NS). LV ejection fraction (58 +/- 10% to 63 +/- 12%; p < 0.02) and stroke volume (98 +/- 26 to 118 +/- 25 ml; p < 0.02) improved. No influence of blood pressure in sporadic morning determinations or of dialysis fistula patency on alterations of LV mass or function was found. Left atrial diameters increased in patients with patent dialysis fistulas (41 +/- 7 to 45 +/- 5 mm; p < 0.05), but not in those with occluded fistulas (41 +/- 7 vs 42 +/- 4 mm; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Hepatocyte growth factor and left ventricular geometry in end-stage renal disease

Hepatocyte growth factor is a pleiotropic cytokine with cardioprotective properties. Its serum concentration is markedly raised in end-stage renal disease. This study assessed the relation of hepatocyte growth factor (HGF) with left ventricular mass and geometry in end-stage renal disease. Serum HGF measurements and echocardiographic studies were performed in 185 patients receiving hemodialysis. Patients with serum HGF above the median (1.85 ng/mL) had more frequent cardiovascular complications. This cytokine was directly related to mean left ventricular wall thickness (r=0.23, P=0.002) and relative wall thickness (r=0.25, P=0.0001); a multivariate analysis showed that this relation was independent of other risk factors. Accordingly, the prevalence of left ventricular concentric geometry (either concentric left ventricular hypertrophy or remodeling) was much higher (n=49, 53%) among patients with HGF values above the median that in those with values < or =1.85 ng/mL (n=31, 34%). Furthermore, the risk for left ventricular concentric geometry was higher in patients with HGF values above the median (odds ratio, 2.57; 95% CI, 1.33 to 4.98; P=0.005), and multiple logistic regression analysis confirmed that this association was independent of other risk factors. In patients receiving hemodialysis, elevated serum HGF is associated with concentric left ventricular geometry. This is consistent with reports that link this cytokine to arterial remodeling and survival in patients with end-stage renal disease and suggests that it is part of a counterregulatory response aimed at attenuating cardiovascular damage in this high-risk population.     

Symmetric and asymmetric left ventricular hypertrophy in patients with end-stage renal failure on long-term hemodialysis

Background: Patients with end-stage renal disease on regular hemodialysis have an increased prevalence of left ventricular (LV) hypertrophy that is associated with morbidity and mortality. Asymmetric septal hypertrophy and impairment of LV outflow can occur in these patients and may contribute to adverse outcomes. More insight into the prevalence, extent, geometry, and promoting factors of LV hypertrophy is important. Methods: An unselected group of 62 patients (31 women), aged 55 ± 14 years, on maintenance hemodialysis was investigated by Doppler echocardiography. Eight patients with valvular heart disease were excluded from further analysis. We assessed prevalence of LV hypertrophy and asymmetric septal hypertrophy, as well as parameters of LV geometry and LV filling and outflow dynamics. Results: Prevalence of LV hypertrophy was 65%. Patients were analyzed according to LV mass and geometry. Mean LV mass index was normal (105 ± 17 g/m²) in Group 1 without LV hypertrophy (n = 19); it was markedly elevated in Group 2 (symmetric hypertrophy, n = 22) and Group 3 (asymmetric hypertrophy with systolic anterior movement of mitral valve, n = 7), and highest (191 ± 54 g/m²) in Group 4 (asymmetric hypertrophy without systolic anterior movement of mitral valve, n = 6, p < 0.001). Age, body mass index, and duration of hypertension were associated with LV hypertrophy and asymmetric septal hypertrophy (p = 0.01). Group 3 with systolic anterior motion of mitral valve had the smallest end-diastolic LV diameters (p = 0.02); increased heart rates, and increased ejection velocities in the LV outflow tract (p = 0.03, and p = 0.005, respectively, vs. Groups 1,2, and 4) which pointed to an impairment of LV outflow. Conclusions: Symmetric LV hypertrophy and asymmetric septal hypertrophy are frequent in patients on maintenance hemodialysis. Predictors for LV hypertrophy were age and body mass index, and, particularly for asymmetric septal hypertrophy, age and hypertension duration. Volume withdrawal during hemodialysis may lead to symptomatic hypotension due to dynamic obstruction in some patients with severe asymmetric septal hypertrophy.     

Cardiac work demands and left ventricular function in end-stage renal disease.

Cardiac hemodynamics were assessed by right and left heart catheterizations in nine patients on hemodialysis. Results showed increased stroke work index and left ventricular work indices. Left ventricular end-diastolic pressure was elevated in all patients (markedly so in five) and did not fall with occlusion of arteriovenous communications. Cardiac output was significantly elevated, but fell to normal postocclusion. Myocardial oxygen consumption, indirectly assessed by tension time and pressure rate indices, appeared increased. Six patients died: four from complications attributed to myocardial failure without infarction, one from transplant-related complications, and one from bacterial meningitis. Five had increased cardiac weights at autopsy, but none showed infarction. This study suggests that increased cardiac work is present in chronic renal failure. Myocardial mass increases result in increased myocardial oxygen demand; however, the increased oxygen requirements may not be met because of reduced erythrocyte mass. Persistance of pressure-volume overload and severe anemia are conducive to myocardial failure.     

Involvement of aldosterone in left ventricular hypertrophy of patients with end-stage renal failure treated with hemodialysis

There is increasing evidence about important cardiovascular effects of aldosterone through classic mineralocorticoid receptors in the heart. It is now clear that aldosterone/excess salt administration has been shown to produce both cardiac hypertrophy and interstitial cardiac fibrosis in rats. In clinical studies, it has been reported that aldosterone seems to play an important role in cardiac hypertrophy. However, it has still not been established whether aldosterone is involved in cardiac hypertrophy in patients with end-stage renal failure treated with hemodialysis. In the present study, we have analyzed the association between cardiac hypertrophy and aldosterone in 29 patients (18 patients with nondiabetic nephropathy and 11 patients with diabetic nephropathy) who developed end-stage renal disease and received hemodialysis. Among the nondiabetic patients, left ventricular mass index correlated significantly with plasma aldosterone concentrations during both before and after hemodialysis, but it did not correlate with plasma renin activity. Furthermore, left ventricular mass index also correlated with mean blood pressure. In contrast, these correlations were not seen in the diabetic patients, despite similar age distribution, duration of hemodialysis, and several echocardiographic parameters between two groups. In conclusion, our study provides new evidence for a relation between left ventricular hypertrophy and plasma aldosterone concentrations that seems to be independent of blood pressure in nondiabetic patients with end-stage renal failure treated with hemodialysis.     

Progression of left ventricular hypertrophy in end-stage renal disease treated by continuous ambulatory peritoneal dialysis depends on hypertension and hypercirculation.

To determine whether obvious hemodynamic advantages of continuous ambulatory peritoneal dialysis (CAPD) over intermittent hemodialysis are reflected in superior cardiac structure and function, 16 of 55 analyzed CAPD patients (CAPD duration: 28 months) were followed over 35 months with echocardiography in a prospective analysis: 26 patients had died. LV dimensions (end-diastolic: 52 +/- 7 vs. 51 +/- 8 mm; control vs. follow-up) and systolic function (ejection fraction: 63 +/- 10 vs. 59 +/- 14%) were normal. Major findings were an increase in the amount of initially observed LV hypertrophy (251 +/- 68 vs. 342 +/- 135 g; p less than 0.03) and a decrease in mean LV volume/mass ratios (0.73 +/- 0.17 vs. 0.54 +/- 0.13; p less than 0.001). Excluding patients with dilated cardiomyopathy and valve disease, the amount of progression in LV hypertrophy was related directly to mean arterial pressure and cardiac output (n = 12; p less than 0.02) despite extensive use of antihypertensive medication (1.9 +/- 1.3 vs. 1.5 +/- 1.4 drugs/patient). No correlation was found with diastolic blood pressure, hemoglobin, serum parathyroid hormone, creatinine, urea, age, or CAPD duration. We conclude that LV hypertrophy is frequent in CAPD patients and further increases during long-term CAPD treatment. Factors contributing to the progression of LV hypertrophy are hypertension and hypercirculation.     

Aging and left ventricular mass and function in people with end-stage renal disease

OBJECTIVES: To identify the main age‐related factors responsible for cardiomyopathy in people with end‐stage renal disease (ESRD). DESIGN: Cross‐sectional. SETTING: Dialysis unit. PARTICIPANTS: Two hundred fifty‐four individuals undergoing chronic dialysis. MEASUREMENTS: Left ventricular (LV) systolic function (assessed according to midwall fractional shortening (mwFS)) and LV mass index (LVMI). RESULTS: At echocardiography, 196 (77%) participants displayed LV hypertrophy (LVH) and 123 (48%) had LV systolic dysfunction. On univariate analysis, age was related directly to LVMI (correlation coefficient (r)=0.33, P<.001) and inversely to mwFS (r=?0.23, P<.001) and a 10‐year increase in age was associated with 4.2‐g/m^2.7 greater LVMI and 0.5% lower mwFS. Albumin, pulse pressure, cardiovascular comorbidities, and C‐reactive protein were age‐related risk factors for LVMI and mwFS, whereas hemoglobin was an age‐dependent risk factor only for LVMI and heart rate and diabetes mellitus only for mwFS. After adjusting for age‐related risk factors, the predictive value of age for cardiomyopathy was substantially less (–67%) and the age‐dependent variability in LVMI and mwFS was much attenuated (?61%), and neither was significant. CONCLUSION: This study suggests that in people with ESRD, the relationship between age and cardiomyopathy is largely dependent on age‐related risk factors and that interventions focused on modifiable risk factors linked to age (e.g., malnutrition and inflammation) could attenuate the detrimental effect of aging on cardiovascular risk in the dialysis population.     

左心室肥厚的鉴别诊断——表现为左心室肥厚的遗传性疾病

心肌肥厚是一种非特异性的表现,在许多心脏疾病发展的后期都可能出现,其本身并不能揭示根本的病理生理机制和病因。根据发病机制心肌肥厚可以分为获得性和遗传性。获得性左心室心肌肥厚,多继发于血液动力学障碍和内分泌疾病等,如高血压、主动脉瓣狭窄、生长激素分泌过多;遗传性左心室心肌肥厚,     

Role of aldosterone in left ventricular hypertrophy in hypertension

BACKGROUND: Aldosterone induces cardiac fibrosis in experimental animal models, but only limited information is available on the association between aldosterone and left ventricular (LV) hypertrophy in human beings. The aim of the present study was to determine the role of aldosterone in LV geometry and to investigate other types of target organ damage in hypertensive patients. METHODS: A total of 25 patients with primary aldosteronism caused by Conn's adenoma, 29 patients with renovascular hypertension, and 29 patients with essential hypertension (EHT) were included in the present study. Echocardiographic examinations and 24-h ambulatory blood pressure (BP) monitoring were conducted in all subjects. RESULTS: The mean 24-h systolic and diastolic BP in primary aldosteronism and renovascular hypertension were found to be comparable to those in EHT. However, LV mass index adjusted by age, sex, mean 24-h systolic BP, mean 24-h pulse rate, body mass index, and duration of hypertension was significantly increased in the patients with primary aldosteronism and renovascular hypertension compared with values in patients with EHT (150.2 +/- 7.7, 142.3 +/- 7.2, and 115.2 +/- 7.2 g/m(2), respectively). Hypertensive organ damages, such as proteinuria and hypertensive retinopathy, were more pronounced in the patients with renovascular hypertension; however, LV hypertrophy was especially exaggerated in patients with primary aldosteronism. CONCLUSIONS: These results indicate that aldosterone may induce LV hypertrophy in human beings as well as in experimental animals, and that angiotensin II and aldosterone may differentially participate in causing hypertensive target organ damage.     

Relation between heart rate and left ventricular mechanical dyssynchrony in patients with end-stage renal disease

The effect of heart rate (HR) on left ventricular (LV) mechanical dyssynchrony has not been studied by phase analysis of myocardial perfusion imaging and has yielded conflicting results by echocardiography. We measured indexes of LV dyssynchrony by automated analysis of gated single-photon emission computed tomography in 140 patients with end-stage renal disease (ESRD) and 133 subjects with normal renal function (control group). Patients with abnormal perfusion pattern or QRS duration >120 ms were excluded. HR at time of acquisition of gated images was recorded. LV ejection fraction (EF), volumes, mass, and 2 indexes of dyssynchrony, phase SD and bandwidth, were derived. Almost 50% of patients in each group had an abnormal LVEF (<50%). HR at rest ranged from 48 to 113 beats/min (75 ± 13). Patients with abnormal LVEF had a higher phase SD (30 ± 13° vs 22 ± 11° and 28 ± 16° vs 15 ± 6° for the ESRD and control groups, respectively, p <0.001 each) and higher histographic bandwidth (88 ± 44° vs 62 ± 33° and 80 ± 49° vs 43 ± 14° for the ESRD and control groups, p <0.001 each). Patients with ESRD and normal LVEF had higher SD and bandwidth than the control group (22 ± 11° vs 15 ± 6° and 62 ± 33° vs 43 ± 14°, respectively, p <0.001 each). The control and ESRD groups were divided into tertiles based on HR. The phase SD and bandwidth were similar in the first (slowest HR) and third (highest HR) tertiles in every group (p = NS). There were no significant correlations between phase SD or bandwidth and HR in either group. In conclusion, within the HR range examined in this cross-sectional study, there was no relation between HR at rest and LV dyssynchrony.     

Norepinephrine and concentric hypertrophy in patients with end-stage renal disease

We have recently observed that in patients with end-stage renal disease (ESRD) raised plasma norepinephrine (NE) is an independent predictor of incident cardiovascular events but that its prognostic power is reduced when this sympathetic marker is tested in statistical models including also left ventricular mass. Because left ventricular hypertrophy (LVH) may be a mechanism whereby NE contributes to the high rate of cardiovascular events in ESRD, we examined the relationship between plasma NE and echocardiographic parameters of left ventricle mass in a large group of ESRD patients. Mean wall thickness (MWT) was higher in patients in the third NE tertile than in the other 2 tertiles (P=0.001), and such an increase was paralleled by a rise in relative wall thickness (RWT) (P=0.006). Concentric LVH was more prevalent in patients in the third NE tertile (46%) than in the second (38%) and first (25%) NE tertiles. Multivariate regression analysis confirmed that the association of plasma NE with the muscular component of left ventricle (MWT) and with RWT was independent (P< or =0.001) of other cardiovascular risk factors, and in these models, plasma NE ranked as the second correlate of MWT and RWT. Similarly, multiple logistic regression analysis showed that the association of plasma NE with concentric LVH was strong and again independent of other risk factors (P=0.003). Plasma NE is associated to concentric LVH in ESRD patients. These observations constitute a sound basis for testing the effect of anti-adrenergic drugs on left ventricle mass and on cardiovascular outcomes in patients with ESRD.     

Role of adrenergic receptor system in canine left ventricular hypertrophy

Although sympathetic nervous system and catecholamines have been postulated to play an important role in the development of myocardial hypertrophy, the precise mechanism is still ill-defined. We then developed two experimental canine models; 12 dogs with surgical cardiac denervation by the method of Geis et al, inducing up-regulation of myocardial adrenergic receptors, and 12 dogs with chronic infusion of subhypertensive dose of norepinephrine (NE) at a rate of 0.04 mg/kg/day. After two months, both models induced myocardial hypertrophy, as indicated by significant increases in left ventricular (LV) wall thickness and cell diameter as compared with 14 sham-operated control dogs. Cardiac denervation remarkably depleted myocardial NE contents, while plasma NE remained unchanged. Both alpha-1 and beta receptors were unregulated, Bmax increasing by 90% and 50% respectively. Decrease in myocardial cyclic-AMP content was relatively small as compared with the marked reduction in myocardial NE, probably by the compensatory augmentation of beta receptor system activity. Chronic NE infusion also reduced myocardial NE content possibly due to stimulation of presynaptic alpha-2 receptor inhibiting NE synthesis and release. Number of alpha-1 and beta receptors also increased by 90% and 30% respectively, while myocardial cyclic-AMP content remained unchanged. These observations indicate that neither direct stimulation of NE on the myocardial cell nor increased in cyclic-AMP is the mechanism for cardiac hypertrophy in both models.(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of the vectorcardiogram-derived spatial QRS-T angle in diagnosing left ventricular hypertrophy

IntroductionCurrent criteria for electrocardiographic (ECG) diagnosis of left ventricular hypertrophy (LVH) have a low diagnostic accuracy. Addition of demographic, anthropomorphic, and additional ECG variables may improve accuracy. As hypertrophy affects action potential morphology and intraventricular conduction, QRS prolongation and T-wave morphology may occur and become manifest in the vectorcardiographic variables spatial QRS-T angle (SA) and spatial ventricular gradient. In this study, we attempted to improve the diagnostic accuracy for LVH by using a combination of demographic, anthropomorphic, ECG, and vectorcardiographic variables.MethodsThe study group (n = 196) was divided in 4 subgroups with, on one hand, echocardiographically diagnosed LVH or a normal echocardiogram and, on the other hand, with any of the conventional ECG signs for LVH or with normal ECGs. Each subgroup was randomly split into halves, yielding 2 equally-sized (n = 98) data sets A and B. Age, sex, height, weight, body mass index, body surface area (BSA), frontal QRS axis, QRS duration, QT duration, maximal QRS vector magnitude, SA, and ventricular gradient magnitude and orientation were univariate studied by receiver operating characteristic analysis and were used to build a stepwise linear discriminant model using P < .05 as entry and P > .10 as removal criterion. The discriminant model was built in set A (model A) and tested on set B. Stability checks were done by building a discriminant model on set B and testing on set A and by cross-validation analysis in the complete study group.ResultsThe discriminant model equation was D = 5.130 × BSA ? 0.014 × SA ? 8.74, wherein D greater than or equal to 0 predicts a normal echocardiogram and D less than 0 predicts LVH. The diagnostic accuracy (79%) was better than the diagnostic accuracy of conventional ECG criteria for LVH (57%).ConclusionThe combination of BSA and SA yields a diagnostic accuracy of LVH that is superior to that of the conventional ECG criteria.     

高血压脑梗死患者左心室肥厚与胰岛素抵抗

目的探讨胰岛素抵抗在高血压并发脑梗死患者的左心室肥厚形成中的作用.方法测定21例脑梗死,13例脑梗死合并左心室肥厚患者口服葡萄糖耐量试验后血糖、血胰岛素变化和左心室质量,并作相关分析.结果合并左心室肥厚的脑梗死患者血糖、血胰岛素升高,胰岛素敏感指数降低,其餐后1h血糖、空腹胰岛素和左心室质量呈正相关(r=0.01,0.83,P<0. 05).结论脑梗死患者的胰岛素抵抗与其左心室肥厚呈正相关,提示胰岛素抵抗参与了脑梗死左心室肥厚形成,其机制有待进一步研究.