Comparison of the effects of angiotensin receptor antagonist, angiotensin converting enzyme inhibitor, and their combination on regression of left ventricular hypertrophy of diabetes type 2 patients on recent onset hemodialysis therapy

Left ventricular hypertrophy (LVH) is frequently found at the initiation of dialysis therapy of diabetic and hypertensive patients, and is highly predictive of future cardiac morbidity and mortality. In patients with hypertension and LVH, both an angiotensin converting enzyme (ACE) inhibitor and an angiotensin type 1 receptor (AT1) antagonist regress LVH. However, it remains controversial whether dual blockade of the renin-angiotensin system will regress LVH in these patients using a combination of ACE inhibitor and AT1 antagonist. Thirty-three type II diabetic patients with end-stage renal disease who had just entered into hemodialysis therapy and were diagnosed as having LVH evaluated by echocardiography were selected from three dialysis units staffed by the faculty of Saitama Medical School, Saitama, Japan between 1999 and 2001. The study was carried out for 1 year. All patients were assigned randomly to three groups with equal number: group I, an ACE inhibitor, enalapril 10 mg daily; group II, an AT1 antagonist, losartan 100 mg daily; group III, combination of enalapril 10 mg and losartan 100 mg daily. All antihypertensive drugs were given 30 min after the cessation of dialysis therapy. LVH was evaluated by echocardiography before the start of administration of drugs, at 6 months and 12 months after the start of drug therapy. Systolic blood pressure levels less than 140 mmHg were the target for the three groups. Using repeated measures analysis of variance, applied to those with four echocardiograms, there were progressive decreases over time in left ventricular mass index, posterior wall thickness and interventricular septum thickness. There were no significant differences in regression of LVH as well as blood pressure control between enalapril and losartan groups; however, dual blockade induced an additional 28% reduction in left ventricular mass index compared with any type of monotherapy. Both ACE inhibitors and AT1 antagonists benefit the regression of LVH in diabetic patients who start dialysis therapy. Moreover, combination therapy with ACE inhibitors and AT1 antagonists would provide more beneficial effects on LVH in these patients than monotherapy.     

Evaluation of the Efficacy and Tolerability of a Low-Dose Combination of Isradipine and Spirapril in the First-Line Treatment of Mild to Moderate Essential Hypertension

To investigate the concept of initiating therapy with low doses of a calcium antagonist and an ACE inhibitor, a fixed combination of isradipine 2.5 mg plus the ACE inhibitor spirapril 3 mg was compared with its components, with the full-dose monotherapies (isradipine 5 mg or spirapril 6 mg), and with placebo. After a 2-week wash out phase in pretreated patients and a subsequent 2-week placebo period, 405 patients with a diastolic blood pressure (DBP) between 100 and 114 mmHg were randomly allocated to 12-week once-daily double-blind treatment in one of the six treatment arms. In patients whose blood pressure was not normalized (defined as DBP≤90 mmHg) after 6 weeks of treatment, the dosage of either medication was doubled or, in the placebo group, was switched to the fixed combination. After week 6, the mean reductions from baseline in sitting systolic/diastolic blood pressure 24 hours after dosing (trough) for the fixed combination or the monotherapies isradipine 5 mg, isradipine 2.5 mg, spirapril 6 mg, spirapril 3 mg, and placebo were10.4/8.7, 10.0/9.4, 6.5/6.7, 10.0/8.3, 7.0/5.8, and 2.2/4.7 mmHg, respectively. The blood pressure changes obtained with the low-dose fixed combination were essentially identical to those observed with the full-dose monotherapies, thus showing an additive effect of low-dose isradipine and spirapril. In terms of tolerability, the lowest rate of any adverse events was found in the combination group. In this group, typical adverse events of calcium antagonists, such as headache, flushing, ankle edema, or palpitations, were observed only in 5%, 2%, 1%, and 0%, respectively, dry cough, considered typical for ACE inhibitors, was observed in only 1% of the combination group. In conclusion, the low-dose components isradipine 2.5 mg and spirapril 3 mg were shown to have an additive effect when combined, exerting a blood pressure–lowering effect comparable with the full doses and a trend to a better tolerability profile in comparison with the standard doses. Thus, low-dose combination therapy with these drugs appears to be a rational alternative to conventional monotherapy in the first-line treatment of hypertension. This revised version was published online in July 2006 with corrections to the Cover Date.     

Partial escape of angiotensin converting enzyme (ACE) inhibition during prolonged ACE inhibitor treatment: does it exist and does it affect the antihypertensive response?

OBJECTIVE: To investigate whether the compensatory rise in renin and plasma angiotensin I in response to repeated angiotensin converting enzyme (ACE) inhibitor treatment results in a partial escape of ACE inhibition over a 24-h dosing interval. DESIGN: A single-blind placebo-controlled study in two parallel groups of eight hypertensive subjects receiving a once-daily dose of the ACE inhibitor, spirapril, of either 12.5 or 25 mg. Detailed 24-h studies were performed at the end of 2 weeks of placebo, and after the first dose and 2 weeks administration of spirapril. METHODS: Twenty-four-hour ambulatory blood pressure was measured invasively. True' angiotensins I and II were measured by radioimmunoassay after high-performance liquid chromatography separation. RESULTS: Both for the lower and higher doses of spirapril, the time-course of changes of spiraprilat, the active metabolite of spirapril, and ACE activity was similar but the maximal rise in angiotensin I was twofold higher after 2 weeks administration than after the first dose. Angiotensin II after the first dose of spirapril fell rapidly, with lowest values 2 to 4 h after dosing. At the end of dosing interval angiotensin II had returned to values seen under placebo with the 12.5-mg dose, but at the end of the 24-h period it was still suppressed with the 25-mg dose. Compared with these first-dose responses the initial maximal degree of angiotensin II suppression after 2 weeks administration of either dose was similar, but during the subsequent hours the degree of angiotensin II suppression tended to be less with the lower and was significantly less with the higher dose of spirapril. With the lower dose of spirapril responses of 24-h ambulatory blood pressure to the first dose and to 2 weeks of administration were almost superimposable, although blood pressures in the second half of the dosing interval tended to be higher during chronic treatment. With the higher dose the response of nocturnal blood pressure after 2 weeks administration was diminished by 8.8 mmHg systolic and 6.8 mmHg diastolic. CONCLUSIONS: Repeated ACE inhibitor treatment with once-daily spirapril leads to a partial escape of ACE inhibition, as reflected by a shorter duration of angiotensin II suppression. This escape also affects the antihypertensive response in the second half of the dosing interval.     

Optimal control of blood pressure can reverse left ventricular hypertrophy in uremic hypertensive hemodialysis patients

We investigated the effects of antihypertensive treatment on left ventricular hypertrophy (LVH) of long-term hemodialysis patients. In uremic patients, it is still controversial in antihypertensive effect to the regression of LVH. The left ventricular size and function of 39 uremic hypertensive long-term hemodialysis patients (27 men, 12 women, mean age 58.3) was evaluated with M-mode, 2-dimensional and Doppler echocardiography before, and 12 months after, the start of combined antihypertensive therapy. This therapy included angiotensin II converting enzyme inhibitors, beta-blockers and calcium antagonists. Patients were classified as responders or nonresponders, depending upon whether their systolic blood pressure (SBP) decreased by more than 10 mmHg after antihypertensive treatment for 12 months. Before treatment, 36 (92%) patients had LVH and diastolic dysfunction and three (8%) had systolic dysfunction. At the end of 12 months, only 25 (64%) patients had LVH, 30 (77%) had diastolic dysfunction and 2 (5%) had systolic dysfunction. Left ventricular mass index (LVMI) also decreased from 203.63 +/- 70.47 g/m2 to 178.57 +/- 67.31 g/m2. LVMI correlated with systolic blood pressure (SBP) but did not correlate with diastolic blood pressure (DBP). There were 26 responders and 13 non-responders. Among responders, both the SBP (153.91 +/- 13.24 mmHg vs 134.43 +/- 14.21 mmHg, p < 0.01) and DBP (90.39 +/- 7.89 mmHg vs 79.98 +/- 7.35 mmHg, p < 0.01) decreased significantly after antihypertensive therapy. Responders also exhibited progressive regression of LVH (LVMI decreased significantly from 208.52 +/- 72.03 g/m2 to 168.52 +/- 55.53 g/m2, p < 0.05). However, LVH regression was not found in nonresponders (LVMI showed 194.84 +/- 64.36 g/m2 vs 193.66 +/- 77.67 g/m2). We conclude that good control of blood pressure can reverse LVH in hypertensive hemodialysis patients.     

Little Effect of Ordinary Antihypertensive Therapy on Nocturnal High Blood Pressure in Patients with Sleep Disordered Breathing

The antihypertensive effects of four different antihypertensive medications (β-blocking agent, atenolol 50 mg; calcium-antagonist, isradipine SRO [slow release] 2.5 mg; diuretic, hydrochlorothiazide [HCTZ] 25 mg; and angiotension converting enzyme-inhibitor, spirapril 6 mg) on obese patients with sleep disordered breathing and hypertension were compared by the ambulatory blood pressure measurement (ABPM).Eighteen patients were randomized in a double-blind, crossover fashion to receive each of the four different medications for 8 weeks. ABPM was performed at baseline and after an 8-week treatment with these medications. A 2- to 3-week washout period occurred both at baseline and between each of the four medications. Three patients were omitted from statistical analysis because of technical problems of ABPM.Atenolol, isradipine SRO, and spirapril decreased significantly (P < .01) the mean 24-h systolic blood pressure, whereas HCTZ did not. The mean 24-h diastolic blood pressure decreased significantly after all four medications: 12 (SD ± 14) mm Hg with atenolol, 7 (SD ± 10) mm Hg with isradipine SRO, 3 mm Hg (SD ± 14) with HCTZ, and 6 (SD ± 15) mm Hg with spirapril (P < .01). During nighttime none of the medications reduced the mean diastolic or systolic blood pressure significantly. According to the 24-h blood pressure curve the influence of these four medications during the whole measurement period was not similar. Atenolol and spirapril lost their antihypertensive effect during the early morning hours. The antihypertensive effect of HCTZ varied markedly from hour to hour. The trough-to-peak ratio of no medication was >0.50.Negative correlation was observed between the apnea time and the mean systolic 24-h (r = −0.604, P = NS) and the mean systolic nocturnal blood pressure change (r = −0.590, P = NS).Our study revealed that the daytime high blood pressure was quite easily controlled by the ordinary monotherapy in these patients with partial upper airway obstruction and hypertension. Instead none of the medications used decreased nocturnal high blood pressure markedly.     

Regression of echocardiographic left ventricular hypertrophy after 2 years of therapy reduces cardiovascular risk in patients with essential hypertension

BACKGROUND: There is still ambiguity about the prognostic relevance of regression of left ventricular hypertrophy (LVH) (as revealed by echocardiography) in a large population of subjects with hypertension, with and without evidence of LVH in their electrocardiograms (ECGs). This holds true even after adjusting for various confounders including in treatment ambulatory blood pressure (BP). The most suitable time point for a follow-up echocardiography also remains a matter for debate. In this study, we investigated the prognostic relevance of regression of LVH after 2 years of therapy, in a large population of subjects with hypertension, and possessing the aforesaid characteristics. METHODS: The occurrence of adverse cardiovascular events was evaluated in 387 patients with LVH shown by echocardiography at baseline, and these patients were studied again after 2 years of therapy. At the second examination, 245 subjects showed regression of LVH, whereas 142 did not. RESULTS: During the time period before the subsequent follow up (6.2 +/- 3 years, range 1.9-12.9 years), 59 first adverse events (26 cardiac and 33 cerebrovascular) had occurred among these subjects. The event rates per 100 patient-years in patients with and without LVH regression were 1.06 and 4.4, respectively. After adjusting for several covariates at the 2-year visit, including in treatment ambulatory BP, Cox regression analysis showed that cardiovascular risk was significantly lower in patients with LVH regression than in those without (RR 0.36, 95% CI 0.19-0.68, P = 0.002). When left ventricular (LV) mass index reduction was analyzed instead of LVH status, it was found to be significantly associated with reduced risk (RR 0.62 per 1-s.d. decrease, 95% CI 0.44-0.88, P = 0.01). CONCLUSIONS: Regression of LVH, as revealed by echocardiography after 2 years of therapy, is associated with reduced cardiovascular risk in patients with hypertension, whether or not LVH was revealed in their ECGs. This holds true even after adjusting for various confounders including in treatment ambulatory BP.     

Effects of losartan and atenolol on left ventricular mass and neurohormonal profile in patients with essential hypertension and left ventricular hypertrophy

OBJECTIVE: To compare the effects of the angiotensin II antagonist, losartan, with those of atenolol on left ventricular hypertrophy (LVH), blood pressure and neurohormone concentrations in hypertensive patients with LVH. DESIGN: A multinational, randomized, double-blind trial. SETTING: Hospital. PATIENTS: Hypertensive patients with an echocardiographically documented left ventricular mass index (LVMI) 120 g/m(2) (men) or 105 g/m(2) (women). INTERVENTIONS: Patients allocated randomly to groups received either losartan or atenolol 50 mg/day for 36 weeks, with possible titration to 100 mg/day, and addition of hydrochlorothiazide 12.5 or 25 mg/day. MAIN OUTCOME MEASURES: Changes in LVMI and sitting systolic (SBP) and diastolic (DBP) blood pressures after 36 weeks of treatment (study powered for non-inferiority hypothesis). All echocardiographic data were read in a central laboratory by staff blinded to the treatments and sequence of echocardiographic tapes. RESULTS: The estimated treatment difference between the losartan and atenolol regimens (mean change from baseline at week 36) in LVMI was -2.5 g/m(2) [95% confidence interval (CI) -7.36 to 2.37 g/m(2) ] in favor of losartan, indicating that losartan was significantly non-inferior ( 0.001, non-inferiority limit 8 g/m(2) ) and numerically superior to atenolol in reducing LVMI. The losartan-based regimen significantly reduced LVMI after 36 weeks compared with baseline (-6.56 g/m(2) , 95% CI -10.24 to -2.88 g/m(2) , P<0.001), whereas the atenolol-based regimen had no significant effect (-3.71 g/m, 95% CI -7.75 to 0.32 g/m(2) , P= NS). In a subset of 82 patients, significant changes in serum concentrations of atrial natriuretic peptide, brain natriuretic peptide and immunoreactive amino-terminal pro-brain natriuretic peptide were recorded in losartan-treated ( 0.01) but not atenolol-treated patients. Losartan and atenolol significantly decreased SBP and DBP from baseline after 6, 12, 24 and 36 weeks. The changes from baseline in DBP were greater in the atenolol group at weeks 6 and 36 [difference -2.6 mmHg ( P= 0.016) at week 36]. However, both treatment regimens achieved similar SBP/DBP values at week 36 (141.1 +/- 12.8/86.8 +/- 8.2 mmHg for losartan and 141.4 +/- 17.2/85.0 +/- 10.1 mmHg for atenolol, respectively). Overall, losartan treatment was associated with significantly fewer drug-related clinical adverse events, compared with atenolol (10 and 22%, respectively, P= 0.028). CONCLUSIONS: Both losartan- and atenolol-based regimens effectively decreased blood pressure. Losartan was non-inferior and numerically superior to atenolol in regression of LVH. The reduction in hypertrophy with losartan treatment was accompanied by reductions in circulating concentrations of cardiac natriuretic peptides. Losartan, by specifically blocking angiotensin II, may therefore have effects on the heart beyond those expected from the decrease in blood pressure alone. Losartan was better tolerated than atenolol.     

Effects of enalapril and isradipine alone and in combination on blood pressure, renal function and echocardiographic parameters in mild hypertension

AIMS AND METHODS: A study was carried out to evaluate the influence of antihypertensive treatment with combined low doses of enalapril plus isradipine (5+5 mg daily) compared with those of either drug at a higher dose level (10 mg daily) by double-blind, three-way crossover study (balanced Latin square design) in 102 subjects (mean age 51.9 +/- 7.42 years) with essential hypertension. Left ventricular mass and function were evaluated by M-B mode echocardiography, renal function by glomerular filtration rate (GFR) and by serum and 24-h urinary Na+ and K+ during wash-out period and after 24 weeks of treatment. RESULTS: The supine blood pressure for subjects given placebo was 171/103 mmHg. After 24 weeks of treatment, systolic and diastolic supine blood pressure were significantly lower with 5 mg isradipine plus 5 mg enalapril (134/84 mmHg) than with 10 mg enalapril (137/84 mmHg) or with 10 mg isradipine (144/85 mmHg). Left ventricular posterior wall and septal thickness were significantly and similarly reduced in all groups. Left ventricular systolic and diastolic end diameters were not significantly changed. Left ventricular mass (LVM) was significantly reduced in E plus I group and enalapril group. GFR was not significantly altered. The 24-h urinary Na+ significantly increased with enalapril, more so than isradipine. The combination was tolerated better than either monotherapy. We observed no clinically significant changes in laboratory variables including blood lipoproteins. CONCLUSIONS: The combination of isradipine plus enalapril reduced blood pressure more effectively and was better tolerated than other drug alone. All three groups showed similar changes in echocardiographic indices and no change in renal function.     

Left ventricular hypertrophy: a potent cardiovascular risk factor and its relationship to office and ambulatory blood pressure

Left ventricular hypertrophy (LVH) is an important cardiovascular risk factor. The presence of LVH carries risk independent of hypertension. LVH can be detected non-invasively using electrocardiography or echocardiography. Clinical studies have consistently shown that ambulatory blood pressure is a stronger correlate of left ventricular mass than office blood pressure. Furthermore, treatment-induced decreases in left ventricular mass index are also more tightly related to reductions in ambulatory blood pressure than reductions in office blood pressure. The primary intervention for subjects with hypertension and LVH is optimal blood pressure control. Several small studies now suggest that therapeutic changes resulting in regression of left ventricular mass also confer a reduction in cardiovascular risk. Therefore, LVH is a serious negative risk factor that is more closely related ambulatory rather than office blood pressure. Fortunately, current evidence suggests that optimal antihypertensive therapy resulting in regression of hypertrophy will reduce at least short-term cardiovascular events. Physicians need to be more aware of LVH as a cardiovascular risk factor.     

Circadian blood pressure pattern in patients with treated hypertension and left ventricular hypertrophy

Left ventricular hypertrophy in hypertensives is an important determinant of prognosis. In the present study 45 patients with treated essential hypertension were divided into two groups: 23 patients had normal left ventricular dimension and 22 patients had echocardiographic signs of left ventricular hypertrophy (LVH). All patients were adequately treated during daytime, but ambulatory blood pressure monitoring showed a distinct abnormal pattern in the LVH group characterized by a lack of blood pressure reduction during the night; 16 of 22 patients with LVH had no blood pressure decline during the night, whereas 17 of 23 patients without hypertrophy showed this reduction (P less than 0.01). In conclusion, patients with hypertension and LVH often reveal a lack of blood pressure decline during the night, which may be the reason for the development of left ventricular hypertrophy (and thus should be managed by a different circadian blood pressure therapy) or which may be the consequence of progressive structural changes in the resistance vessels, along with the development of left ventricular hypertrophy. It is suggested that patients with hypertension and left ventricular hypertrophy should have ambulatory twenty-four hour blood pressure monitoring.     

Mild left ventricular hypertrophy in essential hypertension: is it really arrhythmogenic?

Left ventricular hypertrophy (LVH) has been associated with an increased incidence of ventricular arrhythmias and sudden cardiac death in hypertensive patients. However, it is not known whether this relationship exists in early asymptomatic hypertensives with mild LVH. We prospectively examined 100 consecutive patients with essential hypertension, 35 without and 65 with mild LVH on echocardiography. All underwent a detailed noninvasive arrhythmia work-up and were subsequently followed-up for 3 ± 1 years in an ambulatory hypertension clinic. None of the 12-lead electrocardiographic parameters examined differed between the two hypertensive groups. A similarly low incidence of simple forms of ventricular ectopy was present in both groups, whereas complex forms of ventricular ectopy were extremely rare in either group. The signal-averaged electrocardiographic parameters examined were also not significantly affected by the presence of mild LVH. Arrhythmia-related symptoms or malignant ventricular arrhythmia events were not observed in either group of patients during follow-up with antihypertensive treatment. The latter resulted in LVH regression in the 65 patients with mild LVH at baseline. It appears that mild LVH among ambulatory hypertensive patients does not carry an additive arrhythmogenic risk and can be successfully reversed with the appropriate antihypertensive therapy, with no need of additional antiarrhythmic management.     

The effect of valsartan on regression of left ventricular hypertrophy in type 2 diabetic patients

AIM: The aim of the present study was to examine the effects of an angiotensin II receptor antagonist, valsartan, on echocardiographically proven left ventricular hypertrophy (LVH) in patients with type 2 diabetes. METHODS: Outpatients with type 2 diabetes mellitus were recruited at Niigata University Hospital. The left ventricular mass index (LVMI) was calculated by echocardiography. LVH was considered to be present if the LVMI was > 131 g/m(2) in males and > 100 g/m(2) in females. Patients with LVH received a low dose (40 mg/day) of valsartan for 12 months. This low dose had no clinical effect on blood pressure. RESULTS: Of the 38 patients who entered the study, 14 (36.8%) had LVH. After only 6 months of valsartan therapy, the mean LVMI decreased significantly, from 126.5 +/- 27.8 to 119.0 +/- 23.5 g/m(2) (p < 0.01 vs. baseline). Also, a significant decrease was observed after 12 months (116.5 +/- 30.9 g/m(2), p < 0.05 vs. baseline). Compared to baseline, there were no significant differences after treatment in body mass index, glycosylated haemoglobin (HbA(1c)), systolic blood pressure and diastolic blood pressure. CONCLUSIONS: In type 2 diabetic patients with LVH, treatment with a low dose of valsartan, an angiotensin II receptor antagonist, for 12 months, reduced LVMI, with no reduction in systemic blood pressure. This drug may be safely administered to type 2 diabetic patients with LVH. The long-term risk-reduction effects will have to be evaluated in further trials.     

The cardiovascular risk factor, left ventricular hypertrophy, is highly prevalent in stable, treated angina pectoris

BACKGROUND: In coronary artery disease (CAD), a potentially reversible factor leading to cardiac death is left ventricular hypertrophy (LVH). However, LVH will only have a large impact overall in CAD if it is highly prevalent. Therefore we aimed to assess the prevalence of LVH in patients with stable, treated angina and its relationship with blood pressure (BP). METHODS: Three hundred twenty-two consecutive patients with angiographically confirmed coronary artery disease were recruited. Echocardiographic LV mass was performed and correlated with both office and 24-h ambulatory BP. RESULTS: Of the 267 patients with LV mass measurements, 195 (73%) had LVH. The mean 24-h ambulatory BP reading was systolic 125 +/- 12 mm Hg and diastolic 68 +/- 8 mm Hg in the LVH group. Of the LVH patients 62% had a nonhypertensive 24-h BP reading. On multivariate logistic regression analysis, factors independently related to LVH were history of hypertension (odds ratio [OR] 1.848, 95% confidence interval [CI] 1.051-3.248), body mass index (OR 1.085, 95% CI 1.011-1.165), and age (OR 1.039, 95% CI 1.004-1.076). CONCLUSIONS: We conclude that echo LVH is very common in patients with stable, treated angina and the majority of these patients had a nonhypertensive BP at the time of study. Studies are now required to determine whether identifying and vigorously treating LVH in CAD would reduce the risk of premature death in these patients.     

ACE inhibitors and regression of left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a common condition and a powerful independent risk factor for coronary heart disease, congestive heart failure, and other cardiac morbidity. It is associated with the male sex and advancing age. Its most common cause is hypertension, and many antihypertensive agents induce regression of LVH. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reverse LVH by a mechanism as yet unknown. Reduction in afterload and other hemodynamic abnormalities by reduction of blood pressure is clearly a factor, but ACE inhibitors also block adrenergic action and other sympathetic nervous system influences, and the reduction in angiotensin II produces many effects. By inhibiting this potent vasoconstrictor and suppressing its degradation of the powerful vasodilator bradykinin, and by promoting sodium and water excretion, ACE inhibitors contribute to the restoration of normal ventricular function. Angiotensin II promotes protein synthesis in myocardial myocytes, and blocking this action may arrest the hypertrophic process. To determine the effect of angiotensin II on LVH and normalization of LV function, a study is now underway evaluating the effects of lisinopril, a new lysine analog of enalapril, and a diuretic agent in the treatment of hypertension LVH.     

地尔硫卓逆转高血压左室肥厚的研究

目的 比较地尔硫卓与卡托普利对高血压左室肥厚的消退作用。方法 观察32例高血压患者口服地尔硫卓12周后左室形态结构和左室功能变化,并与34例卡托普利治疗对比。结果 地尔硫卓组与卡托普利组治疗后LVMI分别降低6.3％和17.9％(P<0.05,P<0.01),E/A比值分别升高22.3％和22.1％(P<0.01)。结论 提示两药均能逆转左室肥厚和改善左室舒张功能。卡托普利对逆转左室肥厚更具优点,并探讨其作用机制。     

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。     

Left ventricular hypertrophy and renin-angiotensin system blockade

The renin-angiotensin system (RAS), an important control system for blood pressure and intravascular volume, also causes left ventricular hypertrophy (LVH) and fibrosis. The main causal mechanism is the increase in blood pressure, which leads to increased left ventricular wall stress; however, aldosterone release from the adrenals and (more controversially) the direct action of angiotensin II on the cardiomyocytes also play a role. Large clinical trials evaluating the blockade of the RAS with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers have demonstrated an ability to prevent progression and induce regression of left ventricular mass, thereby reducing the significant and independent cardiovascular risk conferred by LVH. Regression of left ventricular mass is also achieved by other medication classes, but the RAS blockers have an additional beneficial effect for the same blood pressure reduction, for which the mechanism is not entirely clear. Studies comparing the efficacy of angiotensin-converting enzyme inhibitors versus angiotensin receptor blockers to achieve LVH regression have not demonstrated any clear benefit of one class over the other.     

高血压患者动态脉搏波速度与左室肥厚和左心功能的关系

目的 探讨高血压患者动态脉搏波速度（pulse wave velocity, PWV）与左心室重构和左室舒张功能的关系。方法 本研究回顾性收集在2011年5月-2013年1月期间,于卫生部北京医院门诊或住院的≥18岁的原发性高血压患者,采用Mobil-O-Graph PWA无创动态血压监测仪测量动态血压和动态PWV。同期进行超声心动图检查,评估左心室结构和功能。采用Pearson相关分析,比较动态PWV和左室结构功能参数之间的相关性。采用二元Logistics回归分析,分析动态PWV、年龄、性别、体重指数、糖尿病、吸烟、血脂异常和是否服用降压药物对左室肥厚（LVH）的影响。结果 总共有136患者纳入此研究。平均年龄55.4±14.1岁,72.1%为男性。动态PWV平均值为8.10±1.97ms-1,动态PWV与左心室质量指数（LVMI）（r=0.257,p=0.003）和左心房前后径（r=0.431,p<0.001）呈显著正相关,与E/A比值呈显著负相关（r=-0.337,p<0.001）。二元logistic回归分析显示,高血压患者动态PWV是LVH的独立危险因素。结论：高血压患者中,动态PWV与LVMI相关,可能是LVH的独立危险因素。     

Antihypertensive effect of isradipine administered once or twice daily on ambulatory blood pressure

The antihypertensive efficacy of sustained-release isradipine administered once daily compared to the immediate-release formulation administered twice daily was assessed by ambulatory blood pressure (BP) monitoring in a double-blind randomized crossover study in 76 mild-to-moderate hypertensive patients. Conventional BP and heart rate parameters were evaluated after a 4-week placebo period and patients qualified for entry if sitting diastolic BP was between 95 and 114 mm Hg. Ambulatory BP monitoring was measured at baseline and after active treatment with both formulations. The 2 regimens induced a significant and almost identical reduction (p less than 0.001) in the mean 24-hour BP without affecting heart rate. Isradipine was more effective in patients whose clinical hypertension was confirmed by ambulatory BP monitoring (35) than in patients who remained normotensive by ambulatory BP monitoring criteria (41). The isradipine-treated ambulatory hypertensive group experienced significantly greater decreases in BP during 24-hour, work, awake and sleep periods than did the ambulatory normotensive group. These data suggest that sustained-release isradipine has a sustained antihypertensive effect throughout 24 hours comparable to that of isradipine given twice daily and may improve compliance with long-term treatment. In addition, the results confirm the usefulness of ambulatory BP monitoring in determining truly hypertensive patients likely to respond to drug administration.     

Comparison of ambulatory and clinical blood pressures, and their correlation with organic heart damage, in the elderly

Casual blood pressure (BP) measurements may sometimes indicate the presence of cardiovascular morbidity and mortality, but the correlations between BP values and the subsequent occurrence of such complications are low. This may depend on the known inability of casual BP measurements to reflect accurately the 24-hour mean and overall profile of the BP. In this study, electrocardiography (ECG) of left ventricular muscle mass was related to various measures of BP during circadian ambulatory BP monitoring in 156 hypertensive and non-hypertensive elderly patients. Multiple regression analysis performed to establish the presence of left ventricular hypertrophy (LVH) revealed that the product of ambulatory systolic BP x diastolic BP (p = 0.027) and ambulatory diastolic BP were significant variables. Clinical pressure variables were not significant. Multiple linear regression analysis to establish the degree of LVH in function of the pressure variables generated a model where the variables included are the product of ambulatory systolic BP x diastolic BP (p = 2.7 x 10(-8)), ambulatory systolic BP (p = 7.8 x 10(-6)) and ambulatory diastolic BP (p = 2.4 x 10(-6)). Results obtained agree with the literature and revealed that LVH evaluated using ECG-Romhilt-Estes score was correlated in terms of presence/absence of organ damage and in terms of score to ambulatory monitoring values.