Hypertensive concentric left ventricular hypertrophy: when is ventricular ectopic activity increased?

The Framingham Study has indicated that patients with left ventricular hypertrophy (LVH) have a greater risk of cardiovascular complications and sudden death than subjects with a normal heart. We have previously demonstrated that ventricular ectopy was more prevalent and complex in hypertensive patients with LVH by electrocardiographic (ECG) criteria than in those without ECG evidence of LVH. The present study was designed to detect and quantify ventricular dysrhythmias in hypertensive patients with early concentric LVH by echocardiography but without LVH by ECG criteria. Continuous ambulatory ECG tracings were recorded for 24 hours in 94 patients with essential hypertension: 37 without LVH, 26 with concentric LVH by echocardiographic but not ECG criteria, and 31 with LVH on both echocardiography and ECG. Patients with LVH by ECG criteria had significantly more premature ventricular contractions (P less than .001) and more complex (higher Lown's class) ventricular ectopy (P less than .001) than hypertensives without LVH or with LVH only by echocardiographic criteria. Prevalence and complexity of ventricular ectopic activity, however, was not affected by mild to moderate concentric cardiac hypertrophy detected echocardiographically. We conclude that unlike LVH shown by ECG, early hypertensive concentric LVH detected echocardiographically is not associated with increased electrical irritability of the myocardium.     

Hypertensive left ventricular hypertrophy is linked to an enhanced catecholamine response to submaximal exercise.

BACKGROUND: The serial plasma catecholamine response to exercise has not been studied fully in relation to left ventricular hypertrophy (LVH) in patients with hypertension (HT). This study determined whether plasma catecholamine responses to exercise are altered in essential HT in the presence or absence of LVH. MATERIALS AND METHODS: Plasma noradrenaline (NA) and plasma adrenaline (A) were measured at rest, during and after treadmill exercise in 59 hypertensive subjects and 22 age-matched control subjects. Patients were divided into LVH(-) (n = 20) and LVH(+) (n = 39) stratified by left ventricular mass index [LVMI: control subjects, LVH(-), LVH(+): 114 +/- 4, 105 +/- 3, 151 +/- 3 g m-2]. RESULTS: Exercise time (9.9 +/- 0.6, 7.6 +/- 0.7, 7.3 +/- 0.6 min) was shorter in patients with HT. Both systolic and diastolic blood pressures were higher in patients with HT, and no difference was observed between LVH(-) and LVH(+) patients. Resting plasma NA was not different (157 +/- 16, 173 +/- 17, 167 +/- 14 pg mL-1), but plasma NA at stage I (300 +/- 30, 342 +/- 40, 469 +/- 40 pg mL-1) was higher in LVH(+) patients than in LVH(-) patients or control subjects. Plasma A response to exercise was similar among the three groups. There was a positive correlation (r = 0.38, P < 0.001) between LVMI and Deltaplasma NA at stage I in all subjects. CONCLUSIONS: Patients with essential HT with LVH had augmented plasma NA response during submaximal exercise, whereas patients without LVH did not exhibit this augmentation. The positive correlation between LVMI and Deltaplasma NA suggested a possible association between the degree of cardiac hypertrophy and sympathetic activation during exercise.     

FGF23 induces left ventricular hypertrophy

Chronic kidney disease (CKD) is a public health epidemic that increases risk of death due to cardiovascular disease. Left ventricular hypertrophy (LVH) is an important mechanism of cardiovascular disease in individuals with CKD. Elevated levels of FGF23 have been linked to greater risks of LVH and mortality in patients with CKD, but whether these risks represent causal effects of FGF23 is unknown. Here, we report that elevated FGF23 levels are independently associated with LVH in a large, racially diverse CKD cohort. FGF23 caused pathological hypertrophy of isolated rat cardiomyocytes via FGF receptor-dependent activation of the calcineurin-NFAT signaling pathway, but this effect was independent of klotho, the coreceptor for FGF23 in the kidney and parathyroid glands. Intramyocardial or intravenous injection of FGF23 in wild-type mice resulted in LVH, and klotho-deficient mice demonstrated elevated FGF23 levels and LVH. In an established animal model of CKD, treatment with an FGF-receptor blocker attenuated LVH, although no change in blood pressure was observed. These results unveil a klotho-independent, causal role for FGF23 in the pathogenesis of LVH and suggest that chronically elevated FGF23 levels contribute directly to high rates of LVH and mortality in individuals with CKD.     

基于心腔内超声造影测量左心室肥厚患者室壁厚度

目的 采用左心室腔内超声造影(LVO)改善心内膜显影,评价LVO诊断左心室心肌肥厚的价值。方法 选择经常规超声心动图检查不能清晰显示并测量左心室壁厚度的患者66例,测量造影前后室间隔、左心室侧壁基底段、中间段及心尖段的室壁厚度,并用Bland-Altman法分析观察者内和观察者间的一致性。结果 LVO后,65例(98.48%,65/66)心内膜边缘的清晰程度明显改善,易于测量室壁厚度。LVO测定的室壁厚度与常规超声心动图所测厚度的差异有统计学意义(P<0.05)。常规超声与LVO测量的室壁厚度相符仅31个节段。Bland-Altman法分析显示,左心室壁厚度测LVO值的观察者内和观察者间的一致性较好。结论 LVO能够通过增进左心室腔的显影,改善心内膜边缘的清晰度,有利于准确测定心肌厚度。     

厄贝沙坦对左室肥厚及左室舒张功能影响的观察

目的采用超声心动图技术观察厄贝沙坦对左室肥厚及左室舒张功能的影响,以期为临床寻找能逆转左室肥厚、改善左室舒张功能的有效药物。方法选择经超声心动图检查确诊为左室肥厚的高血压患者50例,在停用其他降压药1周后,服用厄贝沙坦,维持用药20周,每天测血压2次;治疗前后由专人进行超声心动图检查。结果 50例患者治疗后血压平均下降(14.2±7.2)mmHg/(7.9±3.8)mmHg(P<0.01);治疗后与治疗前比较,左室舒张功能改善,差异有统计学意义(P<0.01)。结论厄贝沙坦不仅24h平稳降压,且可逆转左室肥厚、改善左室舒张功能,副作用少,是临床可取的降压药。     

Statins: a perspective for left ventricular hypertrophy treatment

Left ventricular hypertrophy (LVH), despite its adaptive nature, is associated with an increased risk of cardiovascular morbidity and mortality. Achievement of LVH regression is thus considered a principal therapeutic aim. However, regression of LVH induced by various therapeutic means may exhibit differing patterns, with variable biological implications. Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (statins) have been shown to induce prevention or regression of LVH in different models of pathological myocardial growth. In addition to reduction of LV mass, statins were shown to reduce myocardial fibrosis, increase capillary density network and attenuate electrical instability of the hypertrophied heart. Most importantly, statins improved systolic and diastolic LV function and even decreased mortality. The inhibition of hypertrophic growth was only partly achieved by reduction of haemodynamic overload. Direct mechanisms, such as inhibition of neurohumoral activation in the myocardial tissue, attenuated production of growth factors and markers of inflammation and reduction of oxidative stress also seem to participate. The protective effect of statins was associated with the inhibition of expression and activation of small guanosintriphosphate-binding proteins such as Ras and Rho, which control the intensity of oxidative stress, the production and availability of nitric oxide, and the expression of genes involved in myocardial growth. In addition to reduction of LV mass, statins may also improve the prognosis of LVH independently of their lipid-lowering effect.     

Relevance of echocardiographic left ventricular hypertrophy in mild hypertension

The current diagnostic criteria for uncomplicated mild hypertension inadequately distinguish the subgroup actually at increased risk for cardiovascular sequelae, from the large group not at increased risk, and therefore unlikely to benefit from current pharmacological intervention. Although finding of electrocardiographic left ventricular hypertrophy indicates increased risk, the ECG lacks sufficient sensitivity to be diagnostically useful in mild hypertension. It can be argued that echocardiographic screening for LV hypertrophy may better detect the subpopulation of mildly hypertensive patients at increased risk. The known relationships between ambulatory BP, LV hypertrophy and prognosis support this hypothesis. Further study is required, however, before echocardiography can be advocated for routine application to the diagnosis and management of mild hypertension.     

Bioenergetic abnormalities associated with severe left ventricular hypertrophy.

Transmurally localized 31P-nuclear magnetic resonance spectroscopy (NMR) was used to study the effect of severe pressure overload left ventricular hypertrophy (LVH) on myocardial high energy phosphate content. Studies were performed on 8 normal dogs and 12 dogs with severe left ventricular hypertrophy produced by banding the ascending aorta at 8 wk of age. Spatially localized 31P-NMR spectroscopy provided measurements of the transmural distribution of myocardial ATP, phosphocreatine (CP), and inorganic phosphate (Pi); spectra were calibrated from measurements of ATP content in myocardial biopsies using HPLC. Blood flow was measured with microspheres. In hypertrophied hearts during basal conditions, ATP was decreased by 42%, CP by 58%, and the CP/ATP ratio by 32% in comparison with normal. Increasing myocardial blood flow with adenosine did not correct these abnormalities, indicating that they were not the result of persistent hypoperfusion. Atrial pacing at 200 and 240 beats per min caused no change in high energy phosphate content in normal hearts but resulted in further CP depletion with Pi accumulation in the inner left ventricular layers of the hypertrophied hearts. These changes were correlated with redistribution of blood flow away from the subendocardium in LVH hearts. These findings demonstrate that high energy phosphate levels and the CP/ATP ratio are significantly decreased in severe LVH. These abnormalities are proportional to the degree of hypertrophy but are not the result of persistent abnormalities of myocardial perfusion. In contrast, depletion of CP and accumulation of Pi during tachycardia in LVH are closely related to the pacing-induced perfusion abnormalities and likely reflect subendocardial ischemia.     

Late ventricular potentials in left ventricular hypertrophy in patients with stage-II hypertension

AIM: To evaluate diagnostic significance of high-resolution ECG in patients with blood hypertension (BH) stage II with left ventricular hypertrophy (LVH) in the presence or absence of angiographically verified atherosclerosis of the coronary arteries. MATERIALS AND METHODS: ECG (registration of late ventricular potentials by M. Simson and R. Haberl), echo-CG and coronaroventriculography were performed in 63 males with BH stage II. RESULTS: Late ventricular potentials (LVP) were detected according to M. Simson in 6.3% of the examinees, while according to R. Haberl in none of them. Duration of filtered complex QRS was normal in all the patients. LVP characteristics were not significantly different in the presence or absence of coronary atherosclerosis. Severe and moderate LVH patients differed significantly by duration of low-amplitude high-frequency signals. An inverse correlation existed between duration of low-amplitude signals in the end of filtered complex QRS and parameters of echo-CG. CONCLUSION: LVP registration both by M. Simson and R. Haberl failed to provide additional information on substrate of the arrhythmia in hypertension stage II patients with LVH free of clinical symptoms of tachyarrhythmia. However, there is an inverse correlation between duration of low-amplitude signals in the end of filtered complex QRS and thickness of interventricular septum, asymmetry index, left ventricular myocardial mass.     

Cardiac troponins and left ventricular hypertrophy in hemodialysis patients

BACKGROUND: Cardiovascular diseases are the leading cause of death in hemodialysis patients. Left ventricular (LV) hypertrophy is an important predictor of cardiovascular morbidity and mortality in these patients. Cardiac troponins (cTnT and cTnI) are indicators of myocardial cell damage. AIM: The aim of this study was to determine prevalence of LV hypertrophy, prevalence of elevated serum cTnT and cTnI in hemodialysis patients, and identify the correlation between cardiac troponins and LV hypertrophy. METHODS: The study included 115 hemodialysis patients (71 men and 44 women), mean age 53.30 +/- 12.17 years, mean time on dialysis 4.51 +/- 4.01 years and average Kt/Vsp 1.17 +/- 0.23. Mean serum cTnT was 0.14 +/- 0.23 ng/ml, mean serum troponin I 0.20 +/- 0.48 ng/ml. Mean LV posterior wall thickness in diastole (LVPWd) was 11.44 +/- 2.09 mm, mean LV interventricular septal wall thickness in diastole (IVSd) 11.21 +/- 2.12 mm, mean LV end diastolic volume index (iLVEDV) 100.80 +/- 34.62 mL/m2 and mean LV mass index (LVMi) 143.85 +/- 41.21 g/m2. RESULTS: We found statistically significant positive correlations (p <0.05) between serum troponin T concentration, IVSd, LVPWd and iLVEDV. A highly significant positive correlation (p < 0.01) was found between serum troponin T and LVMi. One-year follow-up showed that patients with cardiac troponin T > 0.10 ng/ml and cardiac troponin I > 0.15 ng/ml had significantly lower (p < 0.01) survival rate than patients with troponin T < or = 0.10 ng/ml and troponin I < or = 0.15 ng/ml. CONCLUSION: A significant positive correlation exists between serum troponin T concentration and echocardiographic indicators of LV hypertrophy in hemodialysis patients. Patients with higher serum levels of cardiac troponins have lower survival rates during one year follow up.     

左室肥厚与左心室舒张功能不全相关性的研究

目的 探讨心脏左室壁肥厚,评价左室舒张功能不全的可行性。方法 对15例非左心室肥厚（对照组：室壁厚度≤11mm）和15例左心室肥厚（LVH组：室壁厚度≥12mm）高血压病人,采用胸骨旁长轴切面测量室间隔（IVSd）及左室后壁厚度（LVPWd）;在心尖四腔切面,常规测量二尖瓣血流频谱E峰、A峰及E／A比值。选取室间隔、左室侧壁的二尖瓣瓣环水平为取样点,使用组织多普勒（DTI）测量心肌舒张早期峰值速度（Ve）、舒张晚期峰值速度（Va）及Ve/Va比值。30例受试者均行冠脉造影,测量左室舒张末压（LVEDP）。结果 与对照组比较,LVH组的IVSd、LVPWd、LVEDP明显增大,P〈0．01;而E／A、Ve／Va明显减小（P〈0．01）。IVSd和LVPWd与LVEDP呈直线正相关（r分别为0．79和0．77,P〈0．001）。IVSd与V e/Va和E／A呈直线负相关（r分别为-0．77和-0．70,P〈0．001）;LVPWd与Ve/Va和E／A亦呈直线负相关（r分别为-0．66和-0．56,P〈0．001）。结论 左室肥厚可以作为评价左室舒张功能的简便、可靠指标。     

Clinical applications of multiparametric CMR in left ventricular hypertrophy

There are a number of diseases which can increase left ventricular myocardial wall thickness through a number of different mechanisms. Multi-parametric mapping techniques are a new addition to the cardiovascular magnetic resonance (CMR) armoury with a number of potential clinical roles. In this review article, we will explore the role of imaging in left ventricular hypertrophy, and particularly developments in CMR. We focus on ability of CMR to characterize myocardial tissue using multiparametric mapping (native T1, T2 and extracellular volume mapping), to bridge from the microscopic histological domain and into the clinical domain of non-invasive imaging.