Neurohumoral profiles in patients with hypertrophic cardiomyopathy: differences to hypertensive left ventricular hypertrophy.

BACKGROUND: Patients with hypertrophic cardiomyopathy (HCM) or hypertensive heart disease (HHD) have increased concentrations of various neurohumoral factors. Thus, the aim of the present study was to evaluate the differences in the neurohumoral profiles of HCM and HHD. METHODS AND RESULTS: Plasma concentrations of epinephrine, norepinephrine, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), angiotensin II and endothelin-1 were measured in 40 patients with HCM, 35 with HHD, and 15 controls. Additionally, the concentrations of these neurohumoral factors in the coronary sinus and aortic root were measured in 12 HCM patients and 10 controls. Plasma concentrations of norepinephrine, ANP and BNP were significantly higher in HCM than HHD and controls. In HCM, there was no significant correlation between the left ventricular mass index and any neurohumoral factor. The plasma BNP concentration significantly correlated with left intraventricular pressure gradient in HCM. There were significant differences in the plasma concentrations of ANP and BNP between HCM with and without left ventricular diastolic dysfunction. Transcardiac production of BNP was significantly higher in patients with obstructive HCM than in those with non-obstructive HCM. CONCLUSIONS: The significant neurohumoral differences between HCM and HHD were the plasma concentrations of norepinephrine, ANP and BNP. In HCM patients, the plasma BNP concentration may reflect the intraventricular pressure gradient and left ventricular diastolic dysfunction whereas the plasma ANP concentration reflects only the left ventricular diastolic dysfunction.     

Decreased adrenergic response in hypertensive patients without left ventricular hypertrophy

To analyze the adrenergic responses and to compare them between hypertensive patients with and without left ventricular hypertrophy (LVH), left ventricular (LV) fractional shortening (FS) and end-systolic wall stress (ESS) were measured by echocardiography and the inotropic response to the infusion of isoproterenol (0.02 μg/kg/min for 5 min) was studied in 25 hypertensive patients without LVH [H(-)] and 30 hypertensive patients with LVH [H(+)]. LVH was determined by echocardiography. Age, gender, heart rate, systolic and diastolic blood pressures, LV end-systolic and end-diastolic diameters, and FS were matched between the groups. The tests were performed before introduction of antihypertensi ve treatment or 4 weeks after its discontinuation. ESS showed a significant inverse linear relation with FS in all the subjects before isoproterenol infusion. The inotropic response to isoproterenol was measured as the increase of FS corrected for the decrease of ESS (ΔFS/-ΔESS), that is, the slope of the change of the relation between FS and ESS. The change in ΔFS/-ΔESS was significantly smaller (0.49 ± 0.15 cm²/g, mean ± SD) in H(?) than in H(+) patients (1.01 ± 0.57 cm²/g) (p < 0.001). It is concluded that, compared with the H(+) group, adrenergic response is depressed in H (?) patients. This depression might be etioloically related to the phenomenon that LVH did not develop in the H(?) group in spite of the same level of pressure load as in the H(+) group.     

Impaired left ventricular functional reserve in hypertensive patients with left ventricular hypertrophy

To determine whether patients with hypertension and especially those with left ventricular hypertrophy have subtle changes in cardiac function, we measured the increase in left ventricular ejection fraction and in systolic blood pressure to end-systolic volume index ratio with exercise in 40 hypertensive patients and 16 age-matched normotensive volunteers. Twenty-two hypertensive patients without hypertrophy had normal end-systolic wall stress at rest and exercise responses. In contrast, the 18 patients with echocardiographic criteria for left ventricular hypertrophy demonstrated a significant increase in end-systolic wall stress at rest compared with normal subjects (69 +/- 16 vs. 55 +/- 15 10(3) x dyne/cm2, p less than 0.05) despite having normal resting left ventricular size and ejection fraction. In patients with left ventricular hypertrophy, the increase in ejection fraction with exercise was less than in the normotensive control subjects (7 +/- 7 vs. 12 +/- 8 units, p less than 0.05), and delta systolic blood pressure to end-systolic volume with exercise was reduced (3.3 +/- 3.8 vs. 8.3 +/- 7.7 mm Hg/ml/m2, p less than 0.05). The hypertensive patients with hypertrophy displayed a shift downward and to the right in the relation between systolic blood pressure to end-systolic volume ratio and end-systolic wall stress compared with control subjects and hypertensive patients without left ventricular hypertrophy. Thus, hypertensive patients with left ventricular hypertrophy by echocardiography and normal resting ejection fraction exhibit abnormal ventricular functional responses to exercise. This finding may have implications in identifying patients at higher risk for developing heart failure.     

Impaired left ventricular synchronicity in hypertensive patients with ventricular hypertrophy

OBJECTIVES: The influence of left ventricular hypertrophy (LVH) on left ventricular synchronicity, and the prevalence of left ventricular dyssynchrony in hypertensive patients with LVH are unknown. The purpose of this study was to determine the influence of LVH on left ventricular synchronicity in hypertensive subjects. METHOD: Tissue Doppler imaging (TDI) was performed in 115 hypertensive and 30 control individuals. Hypertensive patients were divided into a LVH group and a non-LVH group according to the left ventricular mass index (LVMI). Diastolic and systolic asynchrony was determined by measuring the maximal differences in time to peak myocardial systolic contraction (Ts-max) and early diastolic relaxation (Te-max) between any two of the left ventricular segments and the standard deviation of time to peak myocardial systolic contraction and early diastolic relaxation of all 12 segments. RESULTS: Ts-max was greater in both the non-LVH and LVH groups than in controls, (96.68 +/- 26.21 versus 79.30 +/- 25.19 versus 53.20 +/- 15.24 ms, both P < 0.001) and in the LVH group than in the non-LVH group (96.68 +/- 26.21 versus 79.30 +/- 25.19 ms, P < 0.01). Te-max was prolonged in both patient groups, being most advance in the LVH group (67.39 +/- 11.01 versus 57.18 +/- 11.42 versus 46.72 +/- 13.24 ms, both P < 0.001 versus control group and P < 0.001 versus non-LVH group). LVH patients had shown a greater prevalence of both systolic and diastolic asynchrony than non-LVH patients. A Ts-max value greater than 88 ms had 68% sensitivity and 71% specificity for detecting hypertensive patients with LVH. CONCLUSION: Left ventricular systolic synchronicity was impaired in hypertensive patients with LVH. TDI was shown to be useful for the detection of myocardial abnormalities in such patients.     

Assessment of coronary reserve in patients with hypertensive disease and without hypertrophy left ventricular

AIM: To study relationship between coronary reserve and left ventricular geometry. METHOD AND MATERIAL: Transesophageal cardiac pacing was carried out in 53 patients with hypertensive disease. Thirty five patients (66%) had left ventricular hypertrophy which was eccentric in 16 and concentric in 19. RESULTS: Myocardial ischemia was induced during pacing in 79.2% of patients; it was painful in 45.2 and painless -- in 54.8% of patients. Test with esophageal pacing was positive in 91.4 and 55.6% of patients with and without left ventricular hypertrophy, respectively. In patients with concentric hypertrophy frequency of positive tests was higher and level of coronary reserve lower than in patients with eccentric left ventricular hypertrophy. There was negative correlation between pacing rate at myocardial ischemia induction and left ventricular myocardial mass index. Painless ischemia was more frequent among patients with left ventricular hypertrophy. Twelve of 42 patients (28.3%) with positive result of pacing had no clinical signs of ischemic heart disease. CONCLUSION: Left ventricular hypertrophy limits coronary reserve, increases prevalence of painless myocardial ischemia. Transesophageal pacing enables detection of preclinical signs of lowered coronary reserve.     

Heart failure in hypertensive patients with left ventricular hypertrophy

Left ventricular hypertrophy (LVH) is supposed to be a useful marker of cardiovascular complications during the course of hypertension. Authors compared the presence of heart failure, left ventricular diastolic dysfunction and chronic atrial fibrillation in hypertensive patients with and without left ventricular hypertrophy defined by echocardiography. Hospital records of 192 hypertensives treated in our medical department during years 1996-1999 were analysed. Left ventricular hypertrophy was defined by echocardiography (Penn convention) as left ventricular mass index > 134 g/m2 in men and > 110 g/m2 in women. Presence of LVH was found in 128 patients (mean age 65.9 years), absence of LVH in 64 patients (mean age 64.8 years). Both groups of hypertensives were matched by demographic parameters, by the presence of hyperlipidemia, by smoking habits. Hypertensive patients with left ventricular hypertrophy were more often treated by ACE inhibitors. There were statistically significant more patients with heart failure, left ventricular diastolic dysfunction and chronic atrial fibrillation in LVH-positive patients than in LVH-negative once. There was also statistically significant lower ejection fraction (50.3 +/- 11.4% vs 56.5 +/- 7.4%) in LVH-positive patients than in LVH-negative once. Left ventricular hypertrophy in patients with hypertension brings usually a complicated course of the disease with a high contribution to the development of chronic heart failure.     

老年高血压病患者左心室肥厚危险因素分析

目的　旨在探讨老年高血压病患者伴发左心室肥厚的危险因素。方法　15 5例老年男性高血压病患者分为高血压伴左心室肥厚组(45例)和高血压无左心室肥厚组(110例) ,比较两组患者2 4h血压监测各项指标、纤维蛋白原及血脂等浓度,用多元逐步回归分析,探讨左心室肥厚的可能影响因素。结果　两组患者之间年龄、体重指数、体表面积差异无显著性意义;但高血压病程、2 4h平均脉压、平均收缩压及纤维蛋白原差异有显著性意义;2 4h平均脉压升高可能为左心室肥厚的独立危险因素。结论　高血压伴发左心室肥厚是长期血压控制不良、代谢紊乱等多因素作用的结果,其中,脉压增大者更易出现左心室肥厚。     

Rapid left ventricular filling in untreated hypertensive subjects with or without left ventricular hypertrophy.

In this study, independent contribution of age, HR, BMI, casual and ambulatory blood pressure, LVM and LVEF in evaluating diastolic filling have been investigated in 34 never-treated hypertensive patients and in 15 healthy normotensive subjects. All the subjects were free from coronary artery disease, valvular disease, heart failure, renal disease and psychiatric problems. All the hypertensive subjects (never treated) were subgrouped according to presence or absence of LVH. The PFR decreased significantly and tPFR increased significantly in hypertensive patients in comparison with normotensive subjects and they did not change in the presence vs absence of LVH. The PFR was inversely correlated with BMI, age, 24-h mean SBP and with 24-h DBP. In multiple regression analysis, PFR decreased with BMI, age, 24-h mean SBP and DBP but not with LVMI. These results suggest that BMI, age and 24-h mean blood pressure were the major determinants of PFR abnormalities in hypertensive patients.     

Effect of diuretic therapy on ventricular arrhythmias in hypertensive patients with or without left ventricular hypertrophy

Recent studies have suggested that hypertensive patients with ECG evidence of left ventricular hypertrophy (LVH) may have increased risk of sudden death when treated with diuretics. In the present study echocardiography was used as a more sensitive index for the presence of LVH. Thirty-one patients with uncomplicated hypertension underwent 48-hour ambulatory ECG monitoring both before any treatment and after 4 weeks of hydrochlorothiazide, (HCTZ), 100 mg daily. In 18 patients with left ventricular posterior wall thickness (LVPWT) greater than or equal to 13 mm (average = 14.4 +/- 0.2 mm) on echocardiogram, plasma potassium decreased from 4.1 +/- 0.3 to 3.3 +/- 0.4 mEq/L with HCTZ (p less than 0.01). Premature ventricular contractions (PVCs) averaged 5.7 +/- 9.9/hr at baseline and 7.1 +/- 16.6/hr following HCTZ (p = NS). The total number of couplets was 29 before and 13 after HCTZ, while four brief runs of ventricular tachycardia occurred only before treatment. In the remaining 13 patients with LVPWT less than or equal to 12 mm (average = 11.2 +/- 0.1 mm), plasma potassium decreased from 4.1 +/- 0.3 to 3.4 +/- 0.5 mEq/L with HCTZ (p less than 0.01). The average number of PVCs was 4.3 +/- 8.0/hr after HCTZ (p = NS). One couplet and one 3-beat run of ventricular tachycardia occurred before and one 3-beat run of ventricular tachycardia after HCTZ. Although more complex arrhythmias were noted in the LVH group, the differences were not statistically significant. These results indicate that thiazide therapy does not increase ventricular arrhythmias either in patients with or without LVH.     

Fosinopril improves left ventricular diastolic function in young mildly hypertensive patients without hypertrophy

To clarify whether fosinopril monotherapy can improve left ventricular diastolic function (LVDF) in young mildly hypertensives without hypertrophy, we studied 66 patients (pts) with diastolic blood pressure 90–100 mmHg, aged <45 years, with normal 2-dimensional echocardiography (2-D echo), and impaired DF. Impaired DF was defined as a Doppler transmitral early (E) to atrial (A) filling velocity ratio (E/A ratio) <1. Thirty-eight pts were selected for fosinopril monotherapy. Mean age was 36 years. Duration of documented hypertension was 5.4 years. Mean daily dose of fosinopril was 20 mg. Twenty-eight controls were treated with hydrochlorothiazide and hydralazine combination. Sixty-six age- and sex-matched healthy subjects served to establish normal reference values of 2-D and Doppler echo measurements. All hypertensives were treated for 30 months and re-examined 4 weeks after cessation of treatment. The fosinopril-treated group showed improvements in transmitral E (52 ± 8 cm/s, vs. 61 ± 9 cm/s, p < 0.01), A (56 ± 9 cm/s, vs. 47 ± 6 cm/s, p < 0.05), and E/A ratio (0.93 ± 0.16, vs. 1.29 ± 0.18, p < 0.01). Moreover, the early to atrial velocity-time integral ratio (1.31 ± 0.10, vs. 2.24 ± 0.10, p < 0.001) improved. The pulmonary venous flow pattern normalized after fosinopril therapy. LV mass index, relative wall thickness, LV dimension, left atrial dimension, fractional shortening, heart rate, and body mass index did not change. The hydrochlorothiazide-hydralazine combination-treated group did not show an improved diastolic function. It is concluded that long-term fosinopril monotherapy leads to an improvement of impaired LVDF in young mildly hypertensives without hypertrophy.     

Tumor necrosis factor and interleukin-6 levels in hypertensive patients with and without left ventricular hypertrophy

The objective of this prospective study was to examine the association between serum levels of TNF (tumor-necrosis factor) and IL-6 (interleukin-6) and left ventricular mass in hypertensive patients. Hypertensive patients currently receiving medical therapy were eligible. All subjects underwent echocardiography with measurements of left ventricular (LV) mass and ejection fraction (EF) and had serum levels of TNF and IL-6 measured by ELISA immunoassay. 35 subjects (20F, 15M; mean age 56.4 +/- 10.5 yrs) were studied. 19 patients (54%) had elevated LV mass. Of these patients, 6 (32%) had detectable serum TNF levels and 1 (7%) had detectable IL-6 levels, (p = NS). Hypertensive patients with elevated LV mass do not consistently exhibit elevated cytokine levels when compared to those with normal LV mass.     

伊贝沙坦对高血压左室肥厚患者的左室结构的影响

目的 研究伊贝沙坦对高血压左室肥厚（LVH）患者的左室结构的影响。方法 60例原发性高血压左室肥厚患者随机分为2组：治疗组每天口服伊贝沙坦150mg，对照组每天口服氨氯地平5mg。平均12个月，观察用药后血压、左室结构的变化。结果 用药后2组收缩压（SBP）和舒张压（DBP）均显著降低（P〈0．01）；室间隔厚度（IVST）及左室后壁厚度（LYPWT）均变薄（P〈0．01），左室重量指数（LYMI）明显减少（P〈0．01），对照组各项指标无明显变化（P〈0．05）。结论 对原发性高血压左室肥厚的患者，长期应用伊贝沙坦具有良好降压效果，同时还可逆转LVH，改善患者预后。     

斑点追踪技术评价无左心室肥厚高血压患者左心室扭转与解旋运动

目的探讨无左心室肥厚高血压患者左心室扭转与解旋运动的特点。方法入选无左心室肥厚的高血压患者85例及健康对照者40名,应用超声二维斑点追踪技术(2D-STI)测量并计算短轴心尖部旋转峰值(PAR)及达峰时间、基底部旋转角度峰值(PBR)及达峰时间、左心室整体扭转角度峰值(Ptw)及达峰时间,收缩末期扭转角度(AVCtw)、等容舒张末期扭转角度(MVOtw)、解旋减半时间(HTU)、解旋率。结果高血压组PAR、Ptw、AVCtw、MVOtw高于对照组[(10.55±4.14)°比(8.95±3.46)°,(18.18±4.58)°比(16.33±4.50)°,(17.11±4.82)°比(14.95±4.61)°,(14.33±4.43)°比(12.40±4.86)°,均P<0.05],解旋率低于对照组[(36.06±15.98)%/ms比(48.96±21.16)%/ms,P<0.05]。Ptw与PAR呈正相关,与PBR呈负相关(分别r=0.825,-0.474,均P<0.05);Ptw与LVMI呈正相关(r=0.208,P<0.05),解旋率与左心室质量指数(LVMI)呈负相关(r=-0.231,P<0.05)。结论高血压患者左心室扭转及解旋运动的异常早于室壁厚度的增加,2D-STI技术可定量检测左心室扭转与解旋运动,有可能作为评价高血压患者左心室收缩及舒张功能的早期指标。     

Left ventricular performance, ventriculo-arterial coupling and mechanical output in hypertensive patients with and without left ventricular hypertrophy]

Left ventricular hypertrophy (LVH) is a physiological process of adaptation of the heart to mechanical load increase. Despite depression of left ventricular (LV) contractile performance, work efficiency is preserved and ventriculoarterial coupling is almost normal in hypertensive patients with LVH. To assess the differences between patients with and without LVH, LV contractile performance, the ventriculoarterial coupling and mechanical efficiency were compared in 2 groups of hypertensive patients with similar body surface area and arterial pressures, 23 without LVH (group 1) and 30 with LVH (group 2) and compared to data of 20 normotensive subjects. Left ventricular angiography coupled with simultaneous recording of pressures with micromanometer were used to determine end-systolic stress-to-volume ratio (ESSVR), end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW) and pressure-volume area (PVA). Left ventricular contractile performance assessed by Ees/100 g myocardial mass and EESVR were lower in group 2 than in group 1 (1.23 +/- 0.28 vs 1.89 +/- 0.48 mmHg/mL/100 g and 6.22 +/- 1.07 vs 9.56 +/- 0.97 g/cm2/mL/m2, respectively, both p < 0.0001, control subjects: 1.47 +/- 0.41 and 6.97 +/- 1.22, respectively). Ventriculoarterial coupling evaluated through Ea/Ees ratio (0.51 +/- 0.05 in group 1 vs 0.53 +/- 0.08 in group 2, 0.49 +/- 0.09 in control subjects), and work efficiency evaluated through EW/PVA ratio (0.80 +/- 0.02 in group 1 vs 0.78 +/- 0.03 in group 2, 0.80 +/- 0.03 in control subjects), were similar in the 2 groups and were comparable to control subject values. In conclusion, this study shows that ventriculoarterial coupling and work efficiency are comparable in hypertensive patients with and without LVH. These results suggest that in patients without LVH the matching between left ventricle and arterial receptor is preserved through an enhancement of myocardial contractility which is energetically costly. Conversely, LVH seems to be a useful adaptation which minimizes the energetical cost of high pressure generation.     

Relationship between hypertensive left ventricular hypertrophy, neurohormonal factors and ventricular arrhythmias in very old patients

OBJECTIVE: To study the relationship between hypertensive left ventricular hypertrophy (LVH) in very old patients (> or = 80 years) with neuro-hormonal factors and ventricular arrhythmias. METHODS: Heart rate variation, plasma renin (Ren), angiotensin-II (AT-II), aldosterone (Ald), insulin (Ins), Holter and ambulatory blood pressure monitoring were measured in 60 cases (> or = 80 years) which were divided into 2 groups: 30 with primary hypertension accompanied LVH in very old patients (group A); 30 with simple primary hypertension (group B). RESULTS: There was no significant difference of AT-II and Ren between group A and B (P > 0.05); Ins and Ald values in group A was much higher than in group B (P all < 0.01); the data of heart rate variability, including very low frequency (VLF) and low frequency (LF) and LF/HF (high frequency) in group A were significantly higher than in group B (P < 0.01, < 0.05, < 0.05, respectively); incidence of premature ventricular contractions (PVC) and myocardial ischaemia in group A were higher than in group B patients. CONCLUSIONS: Sympathetic nerve excitability in group A was greatly increased; hypertensive LVH was closely associated with Ald and Ins level, but not with AT-II and Ren. Group A is characterized by a significantly greater frequency of premature ventricular contractions and ischaemia.     

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。     

高血压病左室肥大Q-T离散度异常与室性心律失常的关系

观察180例高血压病患者的Q-T离散度(Q-Td),左室肥大组及左室正常组Q-Td分别为67.31±13.57和38.8±8.55ms(P<0.001),左室肥大组室性心律失常检出率为92.5%,其中复杂性者为64.2%,室速为23.9%,该组中Q-Td>60ms 3项检出率均高于<60ms及左室正常组中Q-Td>60ms者,复杂性室性心律失常及室速有显著性差异(P<0.001).提示高血压左室肥大Q-Td增加与室性心律失常尤其是复杂性室性心律失常及室速有一定关系,结合左室重量指数(LVMI)和Q-Td可作为评估高血压病患者预后的参考指标.     

原发性高血压左室肥厚患者冠状动脉粥样硬化狭窄特点

目的:探讨原发性高血压(EH)伴左室肥厚(LVH)患者冠状动脉粥样硬化狭窄特点。方法:选择经过冠状动脉造影的EH患者566例,伴LVH者140例(LVH组),与单纯EH患者426例(对照组)对比分析冠状动脉粥样硬化狭窄的部位、狭窄的程度、狭窄的范围等的差异。结果:LVH组与对照组比较,LVH组患者发生冠状动脉粥样硬化狭窄的概率明显升高(P<0.01),其危险性增加5.09倍。同时,LVH组发生左前降支冠状动脉粥样硬化狭窄概率显著高于对照组(P<0.01),在其他部位冠状动脉粥样硬化狭窄程度2组比较差异无统计学意义(P>0.05)。LVH组冠状动脉狭窄患者运动平板试验的心肌缺血检出率为33.1%(42/127),而对照组冠状动脉狭窄患者的心肌缺血检出率为12.5%(35/280),P<0.05。在传统冠状动脉粥样硬化危险因素中,只有血压与LVH存在协同效应(P<0.05)。结论:EH伴LVH患者冠状动脉粥样硬化狭窄发生率显著升高,左前降支是主要狭窄部位,而且更易于发生心肌缺血。     

The relationship between fragmented QRS and non-dipper status in hypertensive patients without left ventricular hypertrophy

Background: Fragmented QRS (fQRS) has been shown to be associated with poor outcome in various cardiovascular diseases. Non-dipper hypertension is also associated with increased cardiovascular mortality. The aim of our study is to investigate the relationship between fQRS and non-dipper status in hypertensive patients without left ventricular hypertrophy (LVH). Methods: This study included 106 hypertensive patients without LVH. Patients were divided into two groups: dipper hypertension and non-dipper hypertension. The presence of fQRS was analyzed from surface electrocardiography. Results: Frequency of fQRS (56% vs. 19.6%, p < 0.001) and mean number of leads with fQRS (1.9 ± 1.7 vs. 0.6 ± 1.0, p < 0.001) were significantly higher in patients with non-dipper hypertension compared to dipper hypertension. In addition, the number of leads with fQRS was positively correlated with systolic (r = 0.334, p < 0.001) and diastolic (r = 0.280, p = 0.004) blood pressures (BP). By a multivariate regression analysis, fQRS (OR: 5.207, 95% CI: 2.195–12.353, p < 0.001) was found to be independent predictor of non-dipper status. Conclusion: fQRS is independent predictor of non-dipper status in hypertensive patients without LVH. Also, the higher number of leads with fQRS is associated with higher sleep systolic and diastolic BPs.     

Regression of left ventricular hypertrophy in hypertensive elderly patients with carvedilol

In hypertensive patients, the development of left ventricular hypertrophy seems to increase the risk of cardiovascular death although some antihypertensive agents have been associated with regression in left ventricular hypertrophy. A few studies have evaluated the carvedilol, a new drug having a balanced pharmacology of vasodilatation and beta-receptor blockade, particularly in elderly hypertensive patients. To test its effects on left ventricular hypertrophy, patients with essential hypertension and left ventricular hypertrophy were studied before and at the end of 6 months of therapy with 25 mg of carvedilol daily. Candidates had to have moderate, uncontrolled essential hypertension with echocardiographically documented left ventricular hypertrophy (left ventricular mass index > 130 g/m2 for men and > 110 g/m2 for women). Of 26 patients selected, 4 dropped out. The remaining 22 patients successfully completed 6 months of therapy. The average age was 69 +/- 8 years. Carvedilol caused a significant reduction of mean systolic blood pressure from 175 to 145 mmHg (p < 0.001), of diastolic blood pressure from 102 to 82 mmHg (p < 0.001), of left ventricular mass index from 148 +/- 24 g/m2 (p < 0.003), and a non significant change of the mean heart rate from 78 to 72 beats/min. In our study, carvedilol was well tolerated in patients with essential hypertension and left ventricular hypertrophy.