Asymmetrical septal hypertrophy in patients with hypertension: A type of hypertensive left ventricular hypertrophy or hypertrophic cardiomyopathy combined with hypertension?

To determine whether asymmetrical septal hypertrophy (ASH) in patients with essential hypertension (HT) is a type of hypertensive left ventricular (LV) hypertrophy or hypertrophic cardiomyopathy (HCM) combined with HT, we investigated a group of 7 hypertensive patients with ASH compared with 12 HCM patients and 10 healthy controls using radionuclide angiography and right ventricular endomyocardial biopsy. The LV time-volume curve and its first and second derivative curves were constructed from cardiac output and time-activity curves constructed by combined forward and reverse-gating from the R wave. The LV wall thickness and ejection fraction were significantly greater in both the HT and HCM groups than in the control group, whereas there were no differences in these indices between the HT and HCM groups. Rapid filling volume index and rapid filling fraction showed significantly lower values in the HCM group than in the control group (p < 0.005). In contrast to the HCM group, these indices in the HT group did not differ from those in the control group. The time to peak filling rate was prolonged in the control, hypertension, and HCM groups in increasing order. Histopathological study revealed a higher incidence of myocardial cell disarray in the HCM than in the HT group. The above results suggest that ASH in hypertensive patients is a type of hypertensive LV hypertrophy.     

Cardiac sympathetic activity in the asymmetrically hypertrophied septum in patients with hypertension or hypertrophic cardiomyopathy

BACKGROUND: In patients with essential hypertension (HT), proportional (symmetric) left ventricular hypertrophy (LVH) is common. In contrast, hypertrophic cardiomyopathy (HCM) is characterized by disproportional LVH and, in particular, asymmetric septal hypertrophy (ASH); however, some hypertensive patients also develop ASH. It has not been determined whether such cases represent a distinct type of hypertensive LVH or HCM combined with hypertension. HYPOTHESIS: The study was undertaken to evaluate sympathetic activity in the interventricular septum in patients with HT and ASH or in patients with HCM. METHODS: The patients were evaluated by I-123 meta-iodobenzylguanidine (MIBG) and thallium-201 (201Tl) single-photon emission computed tomography (SPECT), respectively. They were divided into three groups: patients with essential HT and symmetric septal hypertrophy (Group A), patients with HT and ASH (Group B), and patients with HCM and ASH (Group C). RESULTS: Compared with the lateral wall, early uptake of MIBG in the septum was significantly higher in Group B than in Group A, but not significantly different between Groups A and C. Compared with the lateral wall, early uptake of 201Tl in the septum did not differ among the three groups. No significant difference in the MIBG clearance in the lateral wall was seen among the three groups. By contrast, MIBG clearances in the septum and apex were significantly greater in Group C than in Groups A and B. There was an inverse correlation between systolic thickening and MIBG clearance in the septum. CONCLUSION: These findings suggest that sympathetic activity in the septum differs between patients with HT and ASH and patients with HCM.     

Effect of celiprolol on cardiac hypertrophy in hypertension.

The present study was undertaken to clarify whether celiprolol and atenolol, beta1-selective beta blockers with and without intrinsic sympathomimetic activity (ISA), respectively, might improve ischemic damage in the isolated perfused hearts of spontaneously hypertensive rats (SHR), and whether long-term treatment with celiprolol may reduce left ventricular hypertrophy (LVH) in patients with essential hypertension. Atenolol (50 mg/kg/day) or celiprolol (300 mg/kg/day) for 7 weeks significantly reduced the blood pressure in SHR to the same degree, and both drugs decreased the heart rate, but the magnitude of the fall in heart rate was significantly higher with atenolol treatment than with celiprolol treatment. Both treatments significantly reduced the ratio of LV weight to body weight in SHR and significantly improved the coronary reserve in SHR to the same extent. Both treatments significantly improved the extent of recovery of the pressure-rate product and the extent of percent recovery of the coronary flow after reperfusion following 30 min of ischemia in SHR. Celiprolol treatment in patients with essential hypertension for 12 months significantly decreased interventricular septal thickness (IVST)+LV posterior wall thickness (PWT) and LV mass index (LVMI), but there was no significant correlation between IVST+PWT or LVMI and blood pressure before and after treatment. IVST+PWT and LVMI were significantly decreased after 3 months of treatment and these LVH indices were significantly smaller after 6 and 12 months of treatment than after 3 months of treatment. In conclusion, both celiprolol and atenolol treatment reduced LVH and improved the ischemic damage in SHR. In essential hypertensive patients with LVH, celiprolol treatment effectively reduced blood pressure and achieved LVH regression.     

肥厚型心肌病的多层螺旋CT诊断研究

目的探讨多层螺旋CT(MSCT)在肥厚型心肌病(HCM)诊断中的价值。方法回顾分析HCM和高血压各30例的MSCT表现。30例HCM患者中,左心室壁局限性肥厚28例,其中室间隔肥厚12例;室间隔合并游离壁肥厚8例;心尖肥厚5例;游离壁肥厚3例,累及前壁、左室顶部和侧壁各1例。全心肥厚2例。结果多数HCM有不同程度的心腔变形。高血压所致室间隔肥厚,多为普遍均匀性肥厚,心腔无明显形态学改变。结论①MSCT能清晰显示心脏的形态结构,可定量评价心室壁肥厚的程度和心腔大小。②MSCT能直观和全面显示HCM的病变部位。③MSCT对HCM与高血压所致左心室壁肥厚的鉴别诊断具有优良价值。     

高血压左心室肥厚的诊断探讨——5437例超声心动图资料分析

回顾性分析 1985～ 1990年 5 437例连续检测的高血压者超声心动图资料 ,以左心室重量指数 (LVMI)作为诊断左心室肥厚 (LVH)的指标 ,男性 >12 5 g/m2 ,女性 >12 0 g/m2 。结果表明 ,LVH检出率为 31.6 % ,男女性之间无显著性差异 ;严重程度分级 ,轻、中、重LVH分别占 6 6 .3 % ,2 1.7%与 12 .0 % ;结构分型 ,不对称性室间隔肥厚、对称性肥厚、扩张性肥厚分别占 2 8.1% ,34.0 %与 37.9% ;如以室间隔与左室后壁厚度实测值为诊断指标 ,虽然阳性符合率很高 (86 .7% ) ,但有较高假阳性率(41.0 % )。     

Four cases of Fabry's disease mimicking hypertrophic cardiomyopathy

Four patients with Fabry's disease diagnosed by right ventricular endomyocardial biopsy had cardiac manifestations simulating hypertrophic cardiomyopathy (HCM). Case 1: A 51-year-old woman, whose elder sister had congestive heart failure, was hospitalized for exertional dyspnea and cardiomegaly. Her electrocardiogram (ECG) showed a short PQ interval (0.10 sec) and left ventricular hypertrophy. Her echocardiogram (Echo) showed moderate symmetrical hypertrophy of the left ventricle (IVST/PWT = 18 mm/17 mm). Case 2: A 32-year-old woman, whose elder sister had an abnormal ECG, was hospitalized for the ECG abnormalities consisting of a short PQ interval (0.10 sec) and ST-T changes in the left precordial leads. The Echo revealed mild symmetrical hypertrophy of the left ventricle (IVST = 13 mm, PWT = 13 mm). Case 3: A 44-year-old man was hospitalized for his ECG suggestive of left ventricular hypertrophy, and his Echo showed asymmetrical septal hypertrophy (ASH; IVST = 22 mm). Case 4: A 51-year-old man was hospitalized for his ECG showing high voltage in the left precordial leads, and his Echo showed ASH (IVST = 20 mm). The cardiac histopathological findings of these cases included cytoplasmic vacuolization by light microscopy, and electron-dense deposits consisting of parallel or concentric lamellae with periodic spacing, suggesting Fabry's disease. The urinary glycolipids of Case 1 were increased biochemically; then the diagnosis of Fabry's disease was confirmed. Cardiac hypertrophy in Fabry's disease has many aspects, because the histopathological changes and clinical manifestations are determined by genetic factors. It was concluded that Fabry's disease may be concealed in some patients with the clinical diagnosis of HCM.     

Geometric determinants of electrocardiographic left ventricular hypertrophy

Experimental studies have suggested that electrocardiographic recognition of left ventricular hypertrophy depends on geometric relationships involving wall thickness and chamber size. To determine the clinical significance of these observations, we studied the effects of echocardiographic LV mass (LVM), posterior wall thickness (PWT), interventricular septal thickness (IVST) and internal dimension (LVID) on ECG voltage in 360 patients. Standard voltage and nonvoltage manifestations of LVH correlated modestly with LVM (r = 0.33-0.44, p less than 0.001). Sokolow-Lyon precordial voltage (SLV) (SV1 + RV5 or V6) correlated moderately with LVM (r = 0.41, p less than 0.001), but correlated less well with IVST (r = 0.26), PWT (r = 0.24) or LVID (r = 0.22). Stepwise regression revealed that there was no relation, independent of LVM, between SLV and IVST (r = 0.03), PWT (r = 0.03) or LVID (r = 0.01). The 90 patients with increased LVM (greater than 215 g) but without LVH by SLV (false negatives) were compared with the 48 identified by SLV (true positives). False negatives differed from true positives in LVM (298 +/- 72 vs 339 +/- 98 g, p less than 0.01), age (55 +/- 18 vs 44 +/- 19 years, p less than 0.001), weight (70 +/- 16 vs 63 +/- 14 kg, p less than 0.02), and distance from skin to the interventricular septum (42 +/- 10 vs 38 +/- 8 mm, p less than 0.02). Thus, for a given LVM, ECG voltage criteria of LVH are independent of LV chamber dilatation or other geometric variables, but depend on age, weight and LV depth in the chest, suggesting that stratification of subjects by clinical variables has promise for improved electrocardiographic recognition of LVH.     

Negative U-wave as a predictor of antihypertensive treatment effect on regression of echocardiographic hypertrophy in hypertensive patients.

To clarify the mechanism and the predictors of the reduction in left ventricular mass (LVM) induced by antihypertensive drugs, forty hypertensive patients were classified according to the presence of left ventricular hypertrophy (LVH) as a defined by echocardiographic LVM findings (LVH group: 27 patients, non-LVH group: 13 patients) and according to the presence of negative U-waves (NU) (NU group: 10 patients, non-NU group: 30 patients). Negative U-waves appeared in the LVH group only (10 of 27 patients). The hemodynamic determinants were investigated as a mechanism of LVM reduction in 38 of these patients who were treated for 2 years with antihypertensive drugs. In the LVH group, thickness of interventricular septum (IVST), posterior wall thickness (PWT) and LVM increased significantly compared to the non-LVH group. In the NU group, the left ventricular end-diastolic dimension (LVDD) was significantly larger and the relative wall thickness was significantly smaller compared to the non-NU group in the LVH group, with no difference in LVM between the two groups. Negative U-waves disappeared in all cases after treatment. Significant decreases in LVDD and LV wall thickness were observed in the NU group and significant decrease in LV wall thickness in the non-NU group. LVM index was reduced by 24.0% in the NU group and 9.5% in the non-NU group. The disappearance of negative U-waves was an independent predictor of the reduction of LVH.     

高血压伴左心室肥厚与T波顶峰后宽度的关系

目的探讨高血压左心室肥厚(LVH)患者T波顶峰后宽度(TpTe间期)的改变及其临床意义。方法随机抽取2010-10-2011-06桂林医学院附属医院心内科住院的原发性高血压(EH)患者313例,根据超声心动图(UCG)测定的左心室质量指数(LVMI)分为LVH组和非LVH(NLVH)组。比较两组TpTe间期、校正TpTe间期(TpTec)、QT间期、校正QT间期(QTc)、QRS时限、LVMI、左心室舒张末期内径(LVEDD)、室间隔厚度(IVST)、左心室后壁厚度(LVPWT)的改变及其相互关系;比较不同血压水平对TpTe间期的影响;EH患者左心室不同构型TpTe间期改变的特点。结果与NLVH组比较,LVH组TpTe间期[(100.0±23.3)比(85.3±14.1)ms]、TpTec[(108.6±26.7)比(91.4±15.4)ms]、QTc[(435.0±23.6)比(420.0±23.5)ms]、QRS时限[(105.3±22.3)比(95.6±16.1)ms]均延长(均P<0.01),LVMI[(142.8±29.3)比(82.5±19.0)g/m2],LVEDD[(58.9±7.5)比(47.6±6.5)cm],IVST[(9.7±1.0)比(8.8±1.2)cm],LVPWT[(9.4±1.1)比(8.5±1.1)cm]明显增大(均P<0.01),QT间期延长,但差异无统计学意义。TpTe间期在不同左心室构型间的改变为:离心型肥厚>向心性肥厚>左心室游离壁肥厚>正常心室形态。Pearson相关分析表明,TpTe间期、TpTec与LVMI(r=0.43,0.44)、LVEDD(r=0.41,0.43)呈正相关(P<0.05)。多元线性回归分析显示,LVMI、LVEDD是TpTe间期重要的影响因素(β=0.026、0.280)。结论 TpTe间期可作为评价高血压伴左心室肥厚靶器官损害程度的心电学指标之一。     

Clinical evaluation of biventriculo-cineangiographic findings in hypertensive left ventricular hypertrophy

In the present study, we demonstrated that hypertensive left ventricular hypertrophy can be divided angiographically into symmetrical (SH) and asymmetrical septal hypertrophy (ASH) groups. In the SH group, the dynamics of the septal wall and the free wall were almost the same as those of the control group. On the other hand, the ASH group rather resembled the HCM group in the thickness and dynamics of the septal wall and the free wall as well as in the septal configuration. The most characteristic difference of the ASH and HCM groups from the SH group was in the significantly greater thickness of the septal wall at end diastole. However, in view of the developmental mechanism of hypertensive heart, it is interesting to note that the more the septal-free wall ratio increases, the more the thickness of the septal wall increases in the SH group.     

原发性高血压患者是否伴有心房颤动左心重塑对比

探讨伴发心房颤动 (简称房颤 )的高血压患者左室肥厚性重塑 ,左室、左房几何形状重塑与未发生房颤的高血压病患者之间的异同。顺序门诊或住院的原发性高血压患者 ,排除对心脏几何结构有影响的疾病及其他原因导致的房颤。将患者分为两组 :原发性高血压无房颤组 (EH组 )和原发性高血压伴房颤组 (EHAF组 )。行超声心动图检测左室舒张末期长径、心尖四腔横径、左房横径和左房面积、左室室间隔厚度 (IVST)、左室后壁厚度 (PWT)、左室舒张末期内径 (EDD)、左房前后径和左房长径。计算 :IVST/PWT比值、左室横 /长径比值、左房平均横 /长径比、左房室平均横径比和左房室长径比。同时测量身高和体重 ,计算体重指数和左室质量指数 (LVMI)。结果 :EH组入选患者 4 4 6例 ,EHAF组 78例 ,EHAF组比EH组年龄大 (P <0 .0 1)。EHAF组IVST、LVMI明显大于EH组(P <0 .0 5和 0 .0 1) ,EHAF组左室心尖四腔横径大于EH组 (P <0 .0 5 ) ,左室长径和EDD两组间无明显差异 ,E HAF组左室横 /长径比值大于EH组 (P <0 .0 5 )。EHAF组左房各内径和面积均明显大于EH组 (P <0 .0 1) ,左房平均横 /长径比EHAF组小于EH组 (P <0 .0 1)。左房室平均横径比及左房室长径比EHAF组均明显大于EH组(P <0 .0 1)。结论 :高血压伴房颤者左室肥厚性重塑严?     

不同类型钙拮抗剂对高血压病患者左心室肥厚的逆转作用

以单盲法观察钙拮抗剂地尔硫(艹卓)(硫氮(艹卓)酮)、硝苯地平(硝苯吡啶)及尼群地平对高血压病患者左心室肥厚的逆转作用。服药8～10个月,三种药物均使患者的平均室间隔、左室后壁厚度及左室重量指教下降。其中地尔硫(艹卓)的作用最强,硝苯地平和尼群地平的作用相似,但不及地尔硫(艹卓)明显。三种药物均不影响左心收缩功能,但均能使舒张功能改善。     

高血压病左室结构功能变化与血浆内皮素的相关性

目的 :探讨高血压病患者左室结构 ,功能变化与血浆内皮素 （ET）的关系。方法 :原发性高血压不伴左室肥厚（L VH）组 （EH） 35例 ,伴 L VH组 （EH+ L VH） 2 8例 ,正常对照组 30例。放射免疫法测定血浆 ET水平 ,超声心动图检测心脏结构与功能。计算左室重量指数 （L VMI） ,平均室壁厚度 （MWT） ,相对室壁厚度 （RWT）。结果 :EH组及 EH+ L VH组血浆 ET高于正常对照组 （P<0 .0 1） ,EH + L VH组 ET高于 EH组 （P<0 .0 1） ,ET与 L VMI,MWT室间隔厚度 ,左室后壁厚度呈正相关 （r分别为 0 .42 4,0 .316 ,0 .2 6 8和 0 .317,均 P<0 .0 1） ,ET与 E/ A呈负相关 （r=-0 .30 4,P<0 .0 1）。结论 :ET与高血压和 L VH相关。     

经胸超声心动图评价高血压心脏病与左心室流出道梗阻的应用价值

目的:应用经胸超声心动图(transthoracic echocardiography,TTE),评价高血压心脏病与肥厚型心肌病(HCM)左心室流出道梗阻的二维及血流动力学特征,为临床鉴别诊断提供影像学依据。方法:左心室流出道梗阻患者31例,其中高血压性左心室流出道梗阻12例,肥厚型梗阻性心肌病19例,二维图像下测量两组患者的室间隔厚度及左心室后壁厚度,在静息状态和激发试验后测量两组患者的左心室流出道流速及最大压差,分别进行组间及组内比较。结果:室间隔厚度肥厚型心肌病组(19.6±1.8)mm明显高于高血压组(12.4±0.6)mm,差异有统计学意义(P<0.05)。左心室后壁厚度:肥厚型心肌病组(11.5±0.5)mm,高血压组(11.3±0.6)mm,两组间比较差异无统计学意义(P>0.05)。高血压组组内比较激发试验后左心室流出道流速(398.6±36.7)cm/s及压差[(68.4±12.9)mmHg,1 mmHg=0.133kPa],均高于静息状态下流速178.2±23.4)cm/s,压差(13.5±6.2)mmHg,差异有统计学意义(P<0.05)。结论:经胸超声心动图能准确评价左心室流出道梗阻的解剖结构与血流动力学特征,可准确鉴别梗阻类型及梗阻程度。     

Left ventricular systolic and diastolic function in the hypertrophied ventricle

To investigate left ventricular (LV) systolic and diastolic function in cardiac hypertrophy, we analysed LV pressure (catheter tip-manometer) and simultaneously performed cineangiography in 24 patients with systemic hypertension (HT), 25 patients with hypertrophic cardiomyopathy (HCM) and 25 normal subjects. We digitized LV cineangiograms frame by frame and computed volume and its derivatives, wall thickness and circumferential wall stress. LV systolic pump function was normal or supernormal in HT and HCM. However, myocardial contractility assessed by end-systolic wall stress-volume relation was depressed in HCM whereas it is normally maintained in HT. LV diastolic function was also impaired in HCM and even in HT despite normal systolic function. The LV hypertrophy group showed significantly prolonged time constant of isovolumic relaxation, increased time from end-systole to the peak filling rate, and upward shift of the diastolic pressure-volume relationship. The characteristic findings of LV diastolic function in LV hypertrophy, therefore, can be summarized as impaired isovolumic relaxation, delayed early diastolic filling and decreased diastolic distensibility. The mechanisms of abnormal systolic and diastolic function may include myocardial ischemia and/or calcium overload in hypertrophied myocardium, but further study will be needed to clarify these problems.     

Familial cardiomyopathy with different clinical features in individual members

The mother and three children of a family whose parents were consanguineous, each had cardiomyopathy with various patterns of hypertrophy and dilatation. All members had asymmetrical septal hypertrophy (ASH), and three of them were characterized as hypertrophic cardiomyopathy (HCM). Another one had ventricular dilatation mimicking dilated cardiomyopathy (DCM). Case 1: The 57-year-old mother had a typical ASH pattern; her septal/posterior wall thickness ratio (IVST/LVPWT) was 2.5. Case 2: The 37-year-old daughter had basal septal hypertrophy. Case 3: The 32-year-old elder son had typical concentric hypertrophy. Case 4: The 30-year-old younger son had an episode of congestive heart failure, and showed DCM-like features with considerable dilatation and impaired wall motion of the left ventricle. The hypertrophic pattern in cardiomyopathies is thought to depend partially on the ages of the onset, or its evolution with aging.     

血浆内皮素和降钙素基因相关肽与高血压左室肥厚的关系研究

目的检测高血压左室肥厚（LVH）患者血浆内皮素和降钙素基因相关肽的浓度，期望进一步揭示高血压左室肥厚的发病机制。方法选择健康成年人30名为正常对照组，严格按照2005年《中国高血压防治指南》标准选取1、2级原发性高血压（EH）患者90例，其中非左室肥厚组30例，左室肥厚组60例，测量血压、左室室间隔厚度（IVST）、左室后壁厚度（PWT）及采取肘静脉血3ml，分离血浆，测量血浆内皮素和降钙素基因相关肽的浓度。所得数据用x±s表示，采用t检验和直线相关检验。结果①高血压组血浆内皮素的浓度均高于正常对照组（P〈0．01），左室肥厚组高于非左室肥厚组（P〈0．05），左室肥厚组左室室间隔厚度、左室后壁厚度与血浆内皮素的浓度呈正相关。②高血压组患者血浆降钙素基因相关肽的浓度均低于正常对照组（P〈0．01），左室肥厚组低于非左室肥厚组（P〈0．01），左室肥厚组左室室间隔厚度、左室后壁厚度与血浆降钙素基因相关肽的浓度呈负相关。③内皮素／降钙素基因相关肽比值在正常对照组接近于1，在高血压组大于1，其中左室肥厚组大于非左室肥厚组。结论血浆内皮素、降钙素基因相关肽的浓度比例失衡参与了高血压及左室肥厚的发生，二者在高血压及左室肥厚的发生、发展中具有不可忽视的作用，所以通过检测血浆内皮素、降钙素基因相关肽的浓度可能对高血压的诊断及临床治疗评价都起着重要作用。     

Hypertrophic cardiomyopathy with left ventricular dilatation

There is increasing interest in the notion that some patients with hypertrophic cardiomyopathy (HCM) progress to morphological and functional manifestations similar to those of dilated cardiomyopathy (DCM). From 165 consecutive patients with HCM, 20 patients with left ventricular dilatation (left ventricular end-diastolic diameter greater than or equal to 50 mm) were selected and designated as dilated HCM. The diagnosis of HCM was established in these patients either by detection of the classical form of HCM in family members, with 2-dimensional echocardiographic evidence of asymmetric septal hypertrophy (ASH; septal thickness greater than or equal to 15 mm and a ratio of septal to posterior wall thickness greater than or equal to 1.3); or by demonstrating myocardial fiber disarray in autopsy or biopsy samples. The clinical manifestations of these patients with dilated HCM were then compared with those of other forms of HCM without left ventricular dilatation; 1) 40 patients with hypertrophic obstructive cardiomyopathy (HOCM) who had resting intraventricular pressure gradients of 20 mmHg or more, 2) 80 patients with non-obstructive HCM, each of whom had ASH of the entire ventricular septum (typical ASH), and 3) 25 non-obstructive patients whose hypertrophy was localized to the apical region of the ventricular septum (apical ASH). Patients having apical hypertrophy with a spade-like configuration on the left ventriculogram were excluded from the study. Compared with HOCM and typical ASH groups, the patients with dilated HCM had family histories of significantly more frequent HCM and less frequent hypertension. The patients with dilated HCM also had significantly less fractional shortening (FS), decreased interventricular septal thickness, greater left ventricular end-diastolic pressure (LVEDP), and left ventricular dilatation. During the follow-up period (average: 3.5 years), seven patients (35%) with dilated HCM died; five from congestive heart failure (CHF), one suddenly, and one three days following mitral valve replacement. The other five patients had CHF at the time of their follow-up examination. The patients with apical ASH had clinical features similar to those of dilated HCM; a higher familial frequency, less marked septal hypertrophy, and higher LVEDP. They tended to develop left ventricular dilatation, associated with reduced fractional shortening, although left ventricular diameter at end-diastole did not exceed 50 mm. These findings suggested that dilated HCM is not a rare condition. It is observed in 12% of consecutive patients with HCM.(ABSTRACT TRUNCATED AT 400 WORDS)     

Assessment of hypertensive heart by 2-dimensional echocardiography in mass screening

Two-dimensional echocardiography (2DE) was used in the mass screening of 3,017 participants (1,195 males, 1,822 females, mean age 59) living in 13 areas in Japan. The 2DE findings of left ventricular hypertrophy (LVH) and LV function were compared with the presence and severity of hypertension (Ht). Out of 1,100 patients who had an evident history of Ht above 160/95 mmHg (Ht group), 298 patients (27.4%) were complicated by LVH. In contrast, LVH was also recognized in 60 (11.2%) of 535 borderline Ht cases and in 87 (6.3%) of 1,382 normotension cases. LVH cases in the Ht group were divided into 3 groups: mild (220: 73.8%), moderate (63: 21.2) and severe (15: 5.0). Asymmetric septal hypertrophy (ASH) was recognized in 111 patients (37.2%) of the 298 LVH cases. The prevalence of ASH in these LVH patients was higher according to the severity of the LVH: mild LVH = 31%, moderate LVH = 51% and severe LVH = 67%. The prevalence of LVH was higher in males than in females. This was especially apparent in the moderate to severe LVH groups and also noted to be higher according to the increase of mean blood pressure. The prevalence of mild to moderate LVH was significantly higher in the poorly-controlled group than in the well-controlled group. In contrast, no significant difference in prevalence of severe LVH was noted between the well-controlled and poorly-controlled groups. The prevalence of LV dysfunction was significantly greater in moderate or severe LVH groups than in non or mild LVH groups. It tended to be higher in the poorly-controlled group compared with the well-controlled group. The regression of LVH was frequently detected in the well-controlled group by the follow-up study. We conclude that 2DE observation of LV performance in mass screening will be extremely valuable in the long term follow-up of Ht patients.     

Number and size of myocytes, amount of interstitial space and extent of disarray of the hearts in patients with systemic hypertension and asymmetric septal hypertrophy

Wall thickness, the extent of disarray, the number and the size of myocytes and the amount of interstitial space were measured in the ventricular septum (VS) and left ventricular (LV) free wall in hearts of 6 patients with chronic systemic hypertension and asymmetric septal hypertrophy (ASH). Twenty-five subjects (15 with no cardiac disease, and 10 with systemic hypertension) without ASH served as the controls. In the six patients with ASH, the degree of ASH ranged from 1.3 to 1.6. The extent of disarray in VS was 20% in one heart and within normal limits (mean +/- SD = 3 +/- 3%) in the other 5. The size of myocytes increased both in the VS and LV free wall and the VS/LV ratio ranged from 0.9 to 1.0. There was no significant difference in the % area of interstitial space between hearts with ASH and controls, and the VS/LV ratio ranged from 0.9 to 1.1. The number of transmural muscle layers (number of myocytes) was 680 +/- 90 in the VS and 440 +/- 40 in the LV free wall of these with ASH, and 500 +/- 60 in the VS and 490 +/- 60 in the LV free wall of control subjects. The VS/LV ratio of the number of myocytes ranged from 1.3 to 1.7 and was correlated with the VS/LV ratio of wall thickness. Although the sample is small, our findings suggest that most hearts from patients with chronic systemic hypertension and ASH have no diffuse disarray in the VS and that ASH probably occurs secondary to pressure overload.(ABSTRACT TRUNCATED AT 250 WORDS)