心钠素基因多态性与原发性高血压患者左心室肥厚的关系

目的 探讨人类心钠素（ANP）基因多态性与原发性高血压患者左心室肥厚的关系.方法 选择原发性高血压患者106例,根据心脏超声检查结果分为单纯高血压组（对照组）75例和高血压合并左心室肥厚组（观察组）31例,采用PCR技术检测人类ANP基因C664G、G1837A和T2238C位点的多态性,比较两组基因型及等位基因分布差异.结果 观察组患者人类ANP基因C664G位点GG基因型频率为54.8％,高于对照组的33.3％（P＜0.05）.两组患者人类ANP基因G1837A位点和T2238C位点基因型和各等位基因频率差异无统计学意义.结论 人类ANP基因C664G位点的基因变异可能与原发性高血压患者左心室肥厚有关.     

线粒体转运RNA基因突变与原发性高血压的相关研究

目的探究线粒体转运RNA(tRNA)基因突变与母系遗传原发性高血压(EH)的关联性。方法依据EH诊断和母系遗传判别标准,筛选2015年1月至2018年12月解放军总医院心血管内科收治的母系遗传EH患者17例(A组)、非母系遗传EH患者65例(B组)。选取同期来院进行健康体检的正常对照人群33名(C组)。对全线粒体DNA(mtDNA)进行测序并与线粒体基因文库MitoMap的修正剑桥序列进行比对,分析3组受试者线粒体tRNA基因突变率差异及其与母系遗传EH发生的关系。应用SPSS 19.0软件对数据进行分析。结果纳入人群中母系遗传EH占总EH 20.7%(17/82)。mtDNA序列对比分析发现,与C组(0.04%)比较,A组(0.28%,P=0.024)及B组(0.12%,P=0.046)患者线粒体tRNA基因总变异率明显升高,但A与B组间比较差异无统计学意义(P=0.076)。对A组患者进一步分析显示,仅有1个线粒体tRNA基因位点突变的先证者A06、A11和A13所在3个家系分别发生mtDNA A5823G、mtDNA T4386C与mtDNA C15910T突变,三个家系母系成员EH发病率分别为53.8%(7/13)、87.5%(7/8)和75.0%(9/12),发病率均较高,提示这3个位点突变可能与母系遗传EH发生密切关联。另外,mtDNA 5597缺失在A组(4例,23.5%)、B组(14例,21.5%)和C组(1例,3.0%)均出现。与C组比较,A组(P=0.002)与B组(P=0.002)患者mtDNA 5597缺失率均显著升高,但A组与B组间比较差异无统计学意义(P=0.127)。结论 mtDNA A5823G、mtDNA T4386C与mtDNA C15910T突变与母系遗传EH有较好的关联性,但mtDNA 5597缺失与母系遗传EH关系不大。     

同型半胱氨酸相关酶基因多态性与高血压伴周围动脉闭塞性疾病的关系

目的探讨亚甲基四氢叶酸还原酶(MTHFR)基因C677T、胱硫醚B合成酶(CBS)基因844ins68和甲硫氨基合成酶(MS)基因A2756G3种同型半胱氨酸(Hcy)代谢相关酶基因多态性与北京社区汉族老年人群中原发性高血压(EH)、EH伴周围动脉闭塞性疾病(PAOD)易感性的关系。方法PCR扩增老年EH(EH组)、老年EH伴PAOD(EH—PAOD组)患者和老年健康对照组的MTHFR C677T、CBS 844ins68、MS A2756G基因突变点，直接或经限制性内切酶消化后行凝胶电泳，确定基因型并统计基因突变频率。结果EH组100例MTHFR基因3种基因型频率为：C／C29．0％，C／T45．0％，T／T26．0％；EH—PAOD组59例为：C／C15．9％，C／T35．5％，T／T48．6％；对照组100例为：C／C31．0％，C／T50．0％，T／T19．0％。3组MTHFR基因的C677T单核苷酸突变中T突变位点的频率分别为48．5％、64．4％、44．0％。EH—PAOD组与对照组和EH组比较，MTHFR T／T基因型频率和T等位基因频率差异均有统计学意义。而CBS 844ins68、MS A2756G各种基因型频率和等位基因频率在EH组、EH—PAOD组和对照组之间差异无统计学意义。结论MTHFR基因C677T单核苷酸突变可能是北京社区汉族老年人PAOD的遗传性危险因素之一，可能与EH无关。且CBS基因844ins68、MS基因A2756G的突变可能都不足以成为EH和PAOD的遗传危险因子。     

环境因素及线粒体基因突变在原发性高血压发病机制中的协同作用

目的:探讨环境因素及线粒体基因突变在原发性高血压(EH)发病机制中的协同作用,为临床诊断和治疗EH提供新的思路.方法:在解放军总医院就诊的990例EH患者接受了详细的病史采集、生化检查及线粒体基因测序分析.结果:多元统计分析显示,EH患者收缩压与线粒体A8343G点突变(β=-22.99±9.00, P=0.01),T8603C点突变(β=26.39±10.39, P=0.01)及性别(β=3.52±1.27,P=0.01)相关;动脉舒张压则与的线粒体基因A8343G点突变(β=-16.31±5.44,P=0.01)、性别(β=-0.34±0.03,P<0.01)、心率(β=0.13±0.03, P=0.01)、家族史(β=1.80±0.78, P=0.02)、入选年龄(β=-0.34±0.03, P<0.01)、发病年龄(β=-0.08±0.03, P=0.01)及空腹血糖(β=-1.96±0.80,P=0.01)相关.结论:线粒体多基因突变与环境因素协同作用影响EH患者的血压.     

内皮素-1基因多态性与海南汉族人原发性高血压的相关性

目的研究内皮素(ET)-1基因K198N、G8002A、+138A/-多态性与海南汉族人群原发性高血压(EH)的相关性。方法采用引物特异性片段长度多态性(PCR-SSP)方法分别检测201名海南籍汉族EH患者及311名海南籍汉族血压正常者ET1基因的+138A/-,K198N,G8002A位点多态性,基因频率采用基因计数法计算。结果海南籍汉族EH组+138A/-位点3A3A基因型的分布频率明显高于正常对照组(P<0.001),EH组3A(+138A/-)分布频率高于正常对照组(70.6 vs 62.2)(P=0.006)。海南籍汉族EH组K198N位点的GG基因型分布频率明显高于正常对照组(50.7%vs 31.8%)(P<0.001)。EH组K198N等位基因G分布频率明显高于正常对照组(74.1%vs 60.1%)(P=0.006)。结论 ET-1基因+138A/-位点的3A3A基因型和3A等位基因、K198N位点的GG基因型和G等位基因与海南汉族人EH相关,3A3A基因型、GG基因型可能是EH发生的危险因素。     

MUTYH基因与结直肠癌发病的关系

目的:检测家族性腺瘤性息肉病(familial adenomatous polyposis,FAP)家族成员MUTYH 基因SNP位点,为结直肠癌易感人群的筛检提供依据.方法:应用PCR-SSCP及基因测序方法检测三个疑似FAP家系患者MUTYH基因SNP位点.PCR-CTPP方法检测中国医科大学附属第一医院结直肠癌组患者283例与对照组307患者血液DNA中MUTYH IVS1-5 A＞C SNP突变位点的情况,分析其多态性与结直肠癌易感性的关系.结果:发现MUTYH基因3个SNP位点,分别为IVS1-5 A＞C(A/C);IVS6 35 A＞G(A/G,G/G)及c.G972C(Q335H)(G/C).结直肠癌患者中发生MUTYH IVS1-5 A/C与MUTYH IVS1-5C/C突变的患者分别为11和2例,对照组中发生MUTYH IVS1-5 A/C突变的患者为4例,但未发现MUTYH IVS1-5 C/C纯合性突变.对照组中MUTYH IVS1-5 A/C等位基因频率与结直肠癌组相比,有显著性差异(X2=7.43,P=0.006).MUTYH IVS1-5 A＞C多态性与结直肠癌易感性有相关性.结论:MUTYH IVS1-5 A＞C位点基因多态性在结直肠癌发生中起着作用,其对了解结直肠癌的发病机制及对高危人群的筛检具有重大意义.     

血管紧张素Ⅱ2型受体基因多态性与男性高血压及左心室肥厚的关系

目的探讨血管紧张素Ⅱ2型受体基因的单核苷酸多态性（SNP）与男性原发性高血压（EH）及左心室肥厚之间的关系。方法应用直接测序的方法在211例男性EH患者和187例男性正常对照人群中对血管紧张素Ⅱ2型受体基因作SNP分型,按心脏超声特点将男性EH患者分为左心室肥厚（LVH）组82例及无LVH组129例,评价SNP与EH及LVH的关系。结果男性EH患者A1675G位点中A等位基因频率与正常对照者相比差异有统计学意义（P〈0.05）;有无LVH患者A1675G多态性各基因型构成均无统计学意义（P〉0.05）。结论血管紧张素Ⅱ2型受体基因的A1675G单核苷酸多态性与男性EH发病相关。     

ET-1基因多态性与海南黎族人原发性高血压的相关性

目的研究内皮素1(ET-1)基因K198N、G8002A、+138A/-多态性与海南黎族人群原发性高血压(EH)的相关性。方法采用引物特异性片段长度多态性(PCR-SSP)方法分别检测98名海南籍黎族EH患者及244名海南籍黎族血压正常者组的ET1基因的+138A/-,K198N,G8002A位点多态性,基因频率采用基因计数法计算。研究对象与Hardy-Weinberg平衡的符合程度及组间基因型与等位基因频率比较均用χ2检验。以上统计学处理均采用SPSS16.0软件进行分析。结果海南籍黎族EH组+138A/-位点的4A3A基因型分布频率明显高于正常对照组(53.1 vs37.3)(P<0.001),高血压组中4A(+138/-)等位基因分布频率显著高于正常对照组(28.6 vs 15.78)(P=0.003)。海南籍黎族EH组K198N位点的GT基因型分布频率明显高于在正常对照组(53.1%vs37.3%)(χ2=6.595,P<0.05)。EH组G8002A位点的A等位基因分布频率明显高于正常对照组(34.7%vs 25.0%)(P<0.05)。结论 ET-1基因+138A/-、K198N多态性与海南黎族人EH相关,ET-1基因+138A/-位点的4A3A基因型和4A等位基因、K198N位点的GT基因型、G8002A位点的A等位基因与海南黎族人EH相关,4A3A基因型、GT基因型、A等位基因可能是黎族EH发生的危险因素。     

母系遗传糖尿病线粒体基因突变的观察

采用PCR-RFLP、DNA直接测序技术对14个有明确母系遗传史的糖尿病家系进行线粒体基因筛查。结果14例先证者及对照组均未检出A3243G等3个线粒体基因突变位点。家系成员发现携带G3316A突变，T3394C突变，三例均为健康携带者。结论G3316A突变、T3394C突变不是糖尿病的独立致病因素。     

溃疡性结肠炎患者中肿瘤坏死因子相关凋亡诱导配体基因多态性及单倍型分析

目的 探讨肿瘤坏死因子相关凋亡诱导配体(Trail)基因多态性及单倍型与溃疡性结肠炎(UC)的关系.方法 收集UC患者331例,健康对照者832名,PCR扩增Trail目的基因后,直接测序检测Trail基因3非编码区(G1525A/G1588A/C1595T)三种单核苷酸多态性,并分析Trail单倍型与UC的关系.结果 与对照组相比较,Trail G1525A突变等位基因A和基因型GA+ AA的频率在UC组中明显降低(P值均＜0.01);UC组Trail G1588A和C1595T两位点突变等位基因A和T的频率明显低于对照组,且差异有统计学意义(P值均＜0.01).轻和中度UC患者Trail C1595T突变等位基因T和CT+ TT基因型频率为49.15％和64.51％,重度UC患者分别为72.37％和84.21％,两组比较差异均有统计学意义(OR值分别=2.710和2.935,95％CI:1.598～4.596和1.188～7.249,P值均＜0.05).重度UC患者Trail G1525A突变等位基因A的频率为48.69％,较轻和中度UC患者(35.16％)增加(OR=1.750,95％CI:1.082～2.830,P=0.021).UC组中AAT单倍型频率显著低于对照组(43.09％比58.41％,95％CI:1.549～2.229,P＜0.01);GAT单倍型频率在UC组中明显增高(10.15％比0.18％,95％CI:0.005～0.051,P＜0.01).结论 Trail基因多态性及单倍型与UC易感性密切相关.     

Angiotensin inhibition and coronary autoregulation in a canine model of LV hypertrophy

In humans with hypertension and LV hypertrophy, beneficial effects of angiotensin inhibition may be associated with preserved autoregulatory capacity. We studied the effect of acute angiotensin converting enzyme (ACE) inhibition on coronary autoregulatory pressure-flow relations and transmural distribution of blood flow in sham and LV hypertrophy dogs. Heart/body weight ratio increased (p = 0.001) from 5.5 ± 0.7 in sham to 6.9 ± 0.5 in LV hypertrophy dogs. The lower coronary pressure limit (LPL) on the pressure-flow relation was 47 ± 2 mmHg in sham and 57 ± 6 mmHg (p = 0.001) in LV hypertrophy dogs; after acute ACE-inhibition the LPL was reduced to 40 ± 5 mmHg and 49 ± 6 mmHg (p = 0.001), respectively. Transmural distribution of blood flow was preserved at the LPL in both groups before and after acute ACE-inhibition. Concomitant blockade of prostaglandin and nitric oxide release and bradykinin catabolism had no additional effects on the LPL and distribution of blood flow. After acute ACE-inhibition in LV hypertrophy dogs, distribution of blood flow across the LV wall was preserved and subendocardial vascular reserve was maintained even though the LPL was significantly lower. Preservation of autoregulatory capacity by ACE inhibitors contributes to beneficial outcome in patients with hypertension and LV hypertrophy. Received: 2 October 2001, Returned for 1. revision: 17 October 2001, 1. Revision received: 20 December 2001, Returned for 2. revision: 2 January 2002, 2. Revision received: 14 January 2002, Accepted: 17 January 2002     

Time course of differential mitochondrial energy metabolism adaptation to chronic hypoxia in right and left ventricles

OBJECTIVE: The present study was designed to characterize mitochondrial adaptation to chronic hypoxia (CH) in the rat heart. Mitochondrial energy metabolism was differentially examined in both left and right ventricles since CH selectively triggers pulmonary hypertension and right ventricular hypertrophy. METHODS: Rats were exposed to a hypobaric environment for 2 or 3 weeks and compared with rats maintained in a normoxic environment. Oxidative capacity (oxygen consumption and ATP synthesis) was measured in saponin-skinned fibers with glutamate or palmitoyl carnitine as substrates. Enzymatic activities of mitochondrial respiratory chain complexes were measured on tissue homogenates. Morphometric analysis of mitochondria was performed on electron micrographs. Mitochondrial DNA was quantified using Southern blot analysis. RESULTS: Whereas oxidative capacity of both ventricles was decreased following 21 days of CH, oxygen consumption and ATP synthesis was maintained with the glutamate substrate in the right ventricle following 14 days of CH. As for the oxidative capacity, enzyme activities were decreased only in the left ventricle following 14 days of CH and in both ventricles following 21 days of CH. These functional alterations were associated with an increase in numerical density and a decrease in size of mitochondria without a change in volume density in both ventricles. Finally, 21 days of CH also decreased the ratio of mitochondrial DNA to nuclear DNA in both ventricles. CONCLUSIONS: CH alters morphometry and function of mitochondria in the heart, but this effect is delayed in the right compared to the left ventricle, suggesting some adaptive processes at the onset of right ventricular hypertrophy.     

Antioxidant changes in the hypertrophied heart due to energy metabolic disorder

Oxidative stress has been implicated in the pathogenesis of both heart hypertrophy and heart failure. Hypertrophied heart, in response to pressure overload, is associated with an increase in antioxidant capacity and a decrease in oxidative stress. However, in the hypertrophied heart due to energy metabolic disorder, antioxidant capacity has not been investigated. Antioxidant changes in juvenile visceral steatosis (JVS) mice, a model of heart hypertrophy due to disorder of fatty-acid oxidation, were examined at 4 weeks (developing hypertrophy stage) and 8 weeks of age (established hypertrophy stage). Superoxide dismutase activity in the JVS mice was higher than that in control mice at 4 weeks of age and was not different from that in the control mice at 8 weeks of age. Glutathione peroxidase activity in the JVS mice at 8 weeks of age was lower than that in the control mice. Catalase activity showed no significant differences between the control and the JVS mice. Lipid peroxidation in the JVS mice was significantly reduced at 4 weeks of age and increased toward control levels at 8 weeks of age. The levels of vitamin E in the heart were increased in the JVS mice at 8 weeks of age. To determine whether antioxidants affect the pathogenesis of hypertrophy in this model, long-term treatments of vitamin E and 2-mercaptopropionyl glycine were performed. Vitamin E treatment partially reduced the heart hypertrophy in these mice. The present study shows that heart hypertrophy in the JVS mice is accompanied with increased antioxidant capacity as indicated in other animal models of heart hypertrophy. The precise mechanism of heart hypertrophy in JVS mice is still unknown, but oxidative stress may play a role in the pathogenesis of heart hypertrophy. Received: 21 August 2000, Returned for 1. revision: 4 September 2000, 1. Revision received: 16 January 2001, Returned for 2. revision: 19 January 2001, 2. Revision received: 30 January 2001, Accepted: 31 January 2001     

The effects of long-term pressure-overload and aging on the myocardium

The effects and interactions of aging and hypertension on the myocardium were studied in spontaneously hypertensive (SHR) and normotensive (WKY) rats. Cardiac hypertrophy developed in SHR during the first 7 months of life and was initially more marked in the subendocardium than in the subepicardium. Capillary density decreased in proportion to cellular enlargement but became normalized between 7 and 15 months when cell size no longer increased, suggesting a proliferation of capillaries during this time period. Between 15 and 22 to 23 months significant cellular enlargement occurred in both SHR and WKY despite the fact that blood pressure levels were not changed.Stereological analysis showed that mitochondria/myofibrils volume ratio in SHR decreased during the development of hypertrophy, continued to decrease as hypertrophy stabilized, but normalized during senescence. Residual bodies (lipofuscin granules), characteristic of aging in myocardial cells, accumulated more markedly in SHR than in WKY. Certain other focal alterations which also are associated with aging, i.e. cell membrane invaginations and increased numbers of caveolae, appeared earlier and became more widespread in SHR. In addition, long-term hypertension elicited alterations which were not associated with aging (honey-combed t-tubules, and mitochondrial and myofibril degeneration).These data provide evidence for three conclusions regarding cardiac hypertrophy and hypertension, and aging in SHR. First, changes which are inevitable with aging are accentuated. Second, certain ultrastructural changes appear to be related to long-term hypertension rather than to the natural aging process. Finally, the relationship between the volumes of contractile and energy producing organelles is modified by factors which are not clearly related to either aging or hypertrophy and hypertension.     

Evaluation of Docosahexaenoic Acid in a Dog Model of Hypertension Induced Left Ventricular Hypertrophy

Marine n-3 polyunsaturated fatty acids alter cardiac phospholipids and prevent cardiac pathology in rodents subjected to pressure overload. This approach has not been evaluated in humans or large animals with hypertension-induced pathological hypertrophy. We evaluated docosahexaenoic acid (DHA) in old female dogs with hypertension caused by 16 weeks of aldosterone infusion. Aldosterone-induced hypertension resulted in concentric left ventricular (LV) hypertrophy and impaired diastolic function in placebo-treated dogs. DHA supplementation increased DHA and depleted arachidonic acid in cardiac phospholipids, but did not improve LV parameters compared to placebo. Surprisingly, DHA significantly increased serum aldosterone concentration and blood pressure compared to placebo. Cardiac mitochondrial yield was decreased in placebo-treated hypertensive dogs compared to normal animals, which was prevented by DHA. Extensive analysis of mitochondrial function found no differences between DHA and placebo groups. In conclusion, DHA did not favorably impact mitochondrial or LV function in aldosterone hypertensive dogs.     

Long-term risk of diabetes, hypertension and left ventricular hypertrophy associated with the metabolic syndrome in a general population

OBJECTIVES: Metabolic syndrome is accompanied by an increased risk of developing diabetes mellitus. Limited or no evidence exists on whether and to what extent metabolic syndrome increases the risk of developing office hypertension, daily-life hypertension and left ventricular hypertrophy. METHODS: In 1412 individuals representative of the population of Monza, plasma glucose, office, home and ambulatory blood pressure, and echocardiographic left ventricular mass index were measured between 1990 and 1992 and 10 years later. New onset diabetes mellitus, new onset office, home and ambulatory hypertension as well as new onset left ventricular hypertrophy were assessed in individuals with and without metabolic syndrome (Adult Treatment Panel criteria) at the first examination. RESULTS: New onset diabetes mellitus, hypertension and left ventricular hypertrophy were all much more frequent in individuals with metabolic syndrome than in those without. In patients with metabolic syndrome, the adjusted risk of new onset diabetes mellitus was five to six times greater (P < 0.001), that of new onset office, home or ambulatory hypertension 3.5, 2.9 and 3.2 times greater (P < 0.001), respectively, and that of new onset left ventricular hypertrophy 2.6 times greater (P < 0.001). The most important predictors of new onset diabetes mellitus, hypertension and left ventricular hypertrophy were the baseline blood glucose, blood pressure and left ventricular mass index, respectively, with an independent contribution, in each condition, from other metabolic syndrome components. The metabolic syndrome as such did not have an additional predictive value. CONCLUSION: In the general population, metabolic syndrome is associated with a marked increase in the risk not only of new onset diabetes mellitus but also of new onset office and daily-life hypertension, and left ventricular hypertrophy. This may account for the increased rate of cardiovascular morbidity and mortality exhibited with this condition in long-term studies.     

Comparative study of sinoaortic denervated rats and spontaneously hypertensive rats

BACKGROUND: Both hypertension and high blood pressure variability (BPV) are involved in cardiovascular damage. This comparative study was designed to explore the possible effects of both of these phenomena on the cardiovascular system. METHODS: The high BPV model of 16-week sinoaortic denervated (SAD) rats and the hypertension model of spontaneously hypertensive rats (SHR) were used for comparison at the same age of 26 weeks. The comparison was focus on hemodynamics, cardiovascular hypertrophy, and hemodynamic responses to ketanserin. Linear regression analysis was performed to study the role of hemodynamics in cardiovascular hypertrophy. RESULTS: In SHR, hypertension was accompanied by a moderately high BPV, whereas in SAD rats, substantially high BPV existed alone, without hypertension. Left ventricular hypertrophy was severe in SHR but was mild in SAD rats. Aortic hypertrophy was present in SAD rats but was absent in SHR. In SAD rats, the hypertrophy was correlated with BPV but not with blood pressure (BP) level. However, in SHR, hypertrophy was correlated with both BP and BPV level. The BP-lowering effect of ketanserin was comparable in both models, whereas its BPV-lowering effect was greater in SAD rats than in SHR. This hypersensitivity was associated with basal BPV level in SAD rats. CONCLUSIONS: These results indicate that hypertension may be more important than high BPV in causing left ventricular hypertrophy, and that the aorta may be more sensitive to substantially high BPV.     

氯沙坦对高血压左心室肥厚的逆转作用

目的 :评价氯沙坦对高血压左心室肥厚的逆转作用。方法 :对 5 2例高血压左心室肥厚的患者用氯沙坦 5 0～ 10 0 mg治疗 8～ 10周后进行观察。结果 :氯沙坦治疗后血压平均下降 2 9/12 mm Hg± 5 /3mm Hg,治疗后室间隔厚度 (IVST)、心室后壁厚度 (PWT)、左室重量指数 (L VMI)均有明显减少 (均为 P<0 .0 1) ,说明左室肥厚减轻 ,左室舒张功能得到改善。结论 :氯沙坦能有确切降压效果 ,并有逆转左室肥厚的作用     

高血压左室肥厚与脑卒中的相关性分析

目的：探讨高血压病引起的左心室肥厚、左心室重量增加对房室传导、心肌细胞复极离散度及脑卒中的影响。方法：临床确诊的高血压病人188例，采用超声心动图测量室间隔厚度及左心室重量，心电图测量P—Rd、Q—Td、J—Td。结果：合并左室肥厚者108例，不合并左室肥厚者80例。左室肥厚组患者P—Rd、Q—Td、J—Td及脑卒中发生率明显高于不合并左室肥厚者。结论：高血压左室肥厚与房室传导时限、心室肌复极的一致性及脑卒中发生率密切相关，可能成为预测脑卒中发生的危险因素之一。     

Time-Frequency Analysis of Heart Rate Variability in Hypertension: Clinical and Echocardiographic Associations

Background: Autonomic regulation of heart rate is impaired in hypertensive patients. The aim of this study is to elucidate the relation between HRV measures as assessed in time-frequency and frequency domains and clinical and echocardiographic features of hypertension with and without left ventricular hypertrophy. Methods: Forty patients with hypertension were divided into two groups according to gender adjusted echocardiographic signs of left ventricular hypertrophy: group 1–20 patients with hypertension and normal LVMI; group 11–20 patients with hypertension and echocardiographic signs of left ventricular hypertrophy. The control group consists of 20 age-matched healthy subjects. HRV analysis was accomplished using frequency-domain analysis (fast Fourier transform) and time-frequency analysis (smoothed pseudo-Wigner distribution). Results: HRV components, very low frequency power (VLFP), low frequency power (LFP), high frequency power (HFP), and total power (TP) were attenuated (P > 0.05) in hypertensive patients with and without left ventricular hypertrophy. LFP/HFP and low frequency related power (LFRP) were markedly higher in group I patients than of group II and controls (P > 0.01, P > 0.0001, and P > 0.001, P > 0.05, respectively). While patients of group II had significantly lower values of VLFP, LFP, LFP/HFP ratio and LFRP as compared with group I patients (P > 0.04, P > 0.0001, P > 0.01, and P > 0.0001, respectively). The burst activity at 0.1 Hz was increased in group I patients while in group II patients it was attenuated. HRV indices associated significantly with cardiac output and systolic blood pressure in patients without signs of left ventricular hypertrophy. In patients with signs of left ventricular hypertrophy, HRV indices correlated with LVMI, related wall thickness, age, and body surface area. Conclusion: HRV responds differently in different stages of hypertension, with increase response of sinus node to sympathetic influences in hypertension without left ventricular hypertrophy and withdrawal of sympathetic and parasympathetic influences in presence of left ventricular hypertrophy.