High levels of plasma atrial natriuretic factor and impaired left ventricular diastolic function in hypertensives without left ventricular hypertrophy.

OBJECTIVE: To seek possible correlations between plasma atrial natriuretic factor (ANF) and left ventricular diastolic function (LVDF) in hypertensive patients. DESIGN: Since LVDF abnormalities can be detected in patients with normal left ventricular mass, we studied a group of hypertensive patients without left ventricular hypertrophy. METHODS: Untreated hypertensive patients (n = 23) and normotensive control subjects (n = 19) were studied. LVDF indices were obtained by M-mode and pulsed Doppler echocardiography. Blood samples for plasma ANF were taken in the recumbent position from subjects on normal-sodium intake. RESULTS: Plasma ANF levels were significantly higher in hypertensive patients than in normotensive subjects. All indices for systolic function were normal in both normotensive subjects and hypertensive patients. Left atrial diameter was significantly higher for hypertensive patients than for normotensive subjects. Considering LVDF, all indices for ventricular filling were found to be altered, on average, in hypertensive patients, the only exception being peak early velocity. In addition, significant correlations were found between plasma ANF and the pulsed Doppler parameters of left ventricular filling, peak atrial velocity and the peak early:peak atrial velocity ratio. Overall correlations between plasma ANF and left atrial diameter, and between left atrial diameter and left ventricular mass index were also observed. CONCLUSIONS: The high levels of plasma ANF observed in our hypertensive patients and their correlation with the LVDF indices (which mainly reflect the atrial contribution to ventricular filling) could be the result of an increased atrial stretch due to diastolic ventricular dysfunction. This may exist in hypertensive patients before the development of ventricular hypertrophy.     

Arrhythmogenicity in left ventricular hypertrophy in mild to moderate arterial hypertension]

BACKGROUND. Several studies have evidenced that hypertensive patients (pts) with left ventricular hypertrophy (LVH) have an increased incidence of malignant ventricular arrhythmias and sudden death. The purpose of our study was to investigate the prevalence of risky ventricular arrhythmias in uncomplicated hypertensive pts (untreated during last 10 days) in comparison with normotensive ones. In this context, not only the value of left ventricular mass index (LVMI) was taken into account, but also the type of LVH and the related functional behaviour. PATIENTS AND METHODS. 59 untreated mild to moderate essential hypertensives (EH), without symptoms or signs of coronary artery disease, were classified in 3 groups: normal (i.e. without hypertrophy) EH (NEH: 12 pts, 6 M and 6 F, mean age +/- SD 52 +/- 10 yrs), concentric hypertrophic EH (CEH: 30 pts, 15 M and 15 F, mean age +/- SD 59 +/- 10 yrs), and eccentric hypertrophic EH (EEH: 17 pts, 7 M and 10F, mean age +/- SD 60 +/- 10 yrs), according to echocardiographic measurements. Values and duration of arterial hypertension were comparable among the groups. A normotensive, age-matched group was studied as control (C: 21 pts, 11 M and 10 F, mean age +/- SD, 57 +/- 10 yrs). 24-hour Holter electrocardiographic monitoring (ECG-H) and Signal-Averaged electrocardiography (SAECG) were performed seeking to identify the arrhythmogenic risk. Echocardiographic analysis was accomplished by means of a computerized system: LVMI, ratio of LV wall thickness to LV internal radius (relative wall thickness = RWTh), systolic velocity of circumferential fractioning (VCFs), peak of LV relaxation rate (pLVRr) and peak-systolic stress (pSS) were evaluated. RESULTS. Normal LV systolic function was generally found, but both NEH and EEH groups showed a significant reduction in pLVRr in comparison with C and CEH groups (mean values +/- SD: 3.52 +/- 1,3 and 3.40 +/- 0.9 vs 4.92 +/- 0.4 and 4.27 +/- 1.4 sec-1, respectively, p < .05 for both). pSS was significantly higher in EEH and NEH than in CEH and C (mean values +/- SD: 149 +/- 42 and 157 +/- 66 vs 116 +/- 28 and 122 +/- 15 10(3) dynes/cm2, respectively; p < .05 for both). At ECG-H, EEH had a prevalence of potentially malignant ventricular arrhythmias (PMVA: ventricular extrasystoles > or = 30/h; ventricular couplets, > or = 2 episodes/24h, or triplets, > or = 1 episode/24h; R on T), significantly larger than in C (35.3% vs 4.8%, p < .05) and almost significantly larger than in NEH and CEH (8.3% and 10%, respectively). No differences in LVMI were found between EEH with or without PMVA. In respect of functional LV behaviour, the former group showed lower values of VCFs (2.33 +/- 0.6 vs 3.71 +/- 1.32 sec-1, (p < .005) than the latter group. At SAECG, the EEH exhibited again a greater prevalence of abnormal findings than C (35.3% vs 0%, p < 0.5). No correlations were found between ECG-H and SAECG abnormalities, nor between the latter group and LVMI or LV functional indexes. Among pts showing a more pronounced impairment of diastolic function (pLVRr < 4 sec-1), EEH exhibited the highest prevalence of both PMVA (50%) and late potentials (41%). CONCLUSIONS. Our data suggest that uncomplicated mild to moderate essential hypertension may be associated with higher risk of ventricular arrhythmias, particularly when cardiac involvement is characterized by eccentric LVH. On the contrary, in this stage of hypertensive disease, LVMI as well as LV function do not seem to influence the ventricular arrhythmogenesis. The clinical importance of these findings is uncertain, and further studies are needed.     

Amlodipine: effective for treatment of mild to moderate essential hypertension and left ventricular hypertrophy

This was a 20-week, open-label, uncontrolled clinical investigation of the long-acting calcium antagonist amlodipine in 33 male or female patients with essential hypertension and left ventricular hypertrophy (LVH). A once-daily dose (5-10 mg/day) of amlodipine provided a consistent antihypertensive effect, reducing the sitting diastolic (-13.8% change) and systolic (-13.0% change) blood pressures by clinically meaningful and statistically significant (p = 0.0001, n = 33) amounts. Amlodipine had no effect on heart rate. A significant regression in LVH was seen (left ventricular mass index reduced from 169.0 [SD 30.7] g/m(2) to 140.6 [SD 19.6] g/m(2), p < 0.01, n = 12). There was also a significant reduction in total peripheral resistance and improvement in left ventricular diastolic filling (E/A ratio increased from 0.86 pre-treatment to 1.03 post-treatment, p = 0.038, n = 12). These results are consistent with other studies in showing that a relatively short treatment regimen with amlodipine is associated with a significant reduction in left ventricular mass index.     

Responses of atrial natriuretic factor to long-term sodium restriction in mild to moderate hypertension.

The effects of long-term sodium restriction on plasma atrial natriuretic factor (ANF) concentrations, and the role of baseline plasma ANF concentration as an indicator of changes in haemodynamics and left ventricular hypertrophy during this treatment were studied in 40 middle-aged previously untreated mildly to moderately hypertensive men and women in a 6-month controlled randomized study. The main emphasis of the treatment programme was to reduce daily sodium intake to less than 70 mmol. Mean sodium excretion decreased from 148 +/- 74 mmol 24 h-1 to 79 +/- 71 mmol 24 h-1 in the treatment group, but remained unchanged in the control group (173 +/- 68 mmol 24 h-1 vs. 186 +/- 62 mmol 24 h-1; P less than 0.01 for the difference in changes between the groups). Mean plasma ANF concentrations in the treatment group were 52.4 +/- 20.7 (median 50) pg ml-1 at baseline and 38.7 +/- 26.3 (median 42) pg ml-1 at 6 months, and the corresponding values in the control group were 55.5 +/- 20.5 (median 50) pg ml-1 and 46.1 +/- 32.4 (median 50) pg ml-1, respectively (P = NS for the difference in changes). The ANF concentration decreased from 70 +/- 14 pg ml-1 to 32 +/- 26 pg ml-1 in treated subjects with a high baseline plasma ANF concentration (greater than 50 pg ml-1), but increased from 37 +/- 11 pg ml-1 to 45 +/- 27 pg ml-1 in subjects with a low baseline plasma ANF concentration (less than or equal to 50 pg ml-1) (difference in changes P less than 0.001). Compared with treated subjects with low baseline plasma ANF levels and with controls, treated subjects with high baseline plasma ANF levels showed a decrease (P less than 0.05) in interventricular septal and left posterior wall thicknesses, in relative wall thickness, and in peripheral resistance. These results suggest that in mildly to moderately hypertensive subjects long-term sodium restriction decreases high plasma ANF concentrations concomitantly with regression of concentric left ventricular hypertrophy, probably as a result of changes in haemodynamics.     

Plasma B-type natriuretic peptide reflects left ventricular hypertrophy and diastolic function in hypertension

BACKGROUND: Hypertension is associated with changes in concentrations of vasoactive peptides and procollagen propeptides, but their relationships with left ventricular hypertrophy and cardiac function are unclear. METHODS: We measured plasma levels of atrial natriuretic peptide (ANP), its amino terminal propeptide (NT-proANP), B-type natriuretic peptide (BNP), endothelin-1 (ET-1), and serum levels of the aminoterminal propeptide of type I procollagen (PINP) and the aminoterminal propeptide of type III procollagen (PIIINP) and echocardiographic parameters in 97 patients with hypertension in the Anglo-Scandinavian Cardiac Outcomes Trial. RESULTS: Median values (reference values) of the peptides were: ANP 11.2 (6.9-14.9) pmol/l, NT-proANP 351 (143-311) pmol/l, BNP 1.1 (0.4-7.2) pmol/l, ET-1 8.7 (1.2-5.0) pmol/l, PIIINP 2.8 (1.7-4.2) microg/l and PINP 29 (19-84) microg/l. Plasma BNP levels in patients with left ventricular hypertrophy (1.2 pmol/l) and patients with echocardiographic signs of diastolic dysfunction (1.5 pmol/l) were greater than those in patients without hypertrophy (0.7 pmol/l) and normal diastolic parameters (0.9 pmol/l) (p<0.05). BNP was the only biochemical parameter that independently predicted interventricular septal diastolic diameter (p<0.05), left ventricular mass index (p<0.01) and ratio of the velocity-time integrals of the E and A waves of the mitral inflow in a stepwise logistic regression analysis (p<0.05). CONCLUSIONS: The results show that BNP reflects the remodelling process in hypertension.     

Silent myocardial ischaemia in treated hypertensives with and without left ventricular hypertrophy

BACKGROUND: Silent ischaemia has been reported to be associated with an increased risk of myocardial infarction and sudden death in a wide range of patient groups. The aim of this study was to examine the prevalence of silent ischaemia in hypertensive patients with and without left ventricular hypertrophy (LVH). METHODS: Twenty hypertensive patients participating in the Anglo-Scandinavian Cardiac Outcomes Trial with echocardiographic LVH (11 males, nine females), and 20 age, sex, blood pressure, and drug treatment-matched hypertensive patients without LVH underwent 24-h combined ambulatory blood pressure and electrocardiographic (ECG) monitoring. Ischaemic events were defined by the 'rule of 3 x 1'-asymptomatic ST-depression >/= 1 mm (0.1 mV), lasting at least 1 min, and with a duration of at least 1 min between two events. RESULTS: Thirteen patients with LVH had ischaemic events, whilst only four without LVH demonstrated ischaemia. Median numbers of events (seven versus zero; P < 0.01) and median total ischaemic area (0.25 versus 0 mV*min/day; P < 0.01) were significantly increased amongst hypertensive patients with LVH by comparison to those without LVH. CONCLUSION: Despite similar levels of established risk factors for atherosclerotic coronary artery disease, the prevalence of silent ischaemia was markedly increased amongst hypertensive patients with LVH by comparison to those with normal left ventricular dimensions. Ambulatory ECG monitoring may have a use in the identification of those at greatest risk of cardiovascular complications and sudden death, amongst hypertensive patients with persistent cardiac hypertrophy despite anti-hypertensive therapy.     

Influence of regression of left ventricular hypertrophy on left atrial size and function in patients with moderate hypertension

OBJECTIVES: The aim of the study was to evaluate the effect of regression of left ventricular (LV) hypertrophy on left atrial (LA) size and function in patients treated with telmisartan, an angiotensin II receptor blocker. METHODS: Patients population included 80 patients with mild-moderate LV hypertrophy treated with telmisartan. Patients were followed over a period of 12 months from the start of telmisartan treatment. LA size was measured during systole from the parasternal long-axis view from M-mode. Atrial function was assessed by Doppler-echocardiography and the following parameters were measured: transmitral peak A velocity, atrial filling fraction, atrial ejection force (AEF), peak E velocity, deceleration time and isovolumic relaxation time, LA maximal and minimal volume, and LV cardiac mass index (LVMI). RESULTS: All patients had an increased LVMI and decrease during follow-up. LA dimensions were greater at baseline and reduced after 1 year of treatment. LA volume indexes maximal volume, minimal volume and P volume were reduced compared with baseline value (maximal volume from 35+/-5 to 32+/-5, p<0.05; minimal volumes from 14+/-2 to 10+/-4, p<0.05). AEF, a parameter of atrial systolic function, increased from 12+/-3 to 15+/-2.4 (p<0.01). The reduction of LA volumes correlate with reduction of LVMI (LA maximal volume and LVMI r = 0.45; p<0.01; LA minimal volume and LVMI r = 0.34; p<0.05). A positive correlation was also found between LV mass index and P volume (r = 0.41; p<0.01), LV mass index and LA active emptying volume (r = 0.39; p<0.01), and LV mass index and LA total emptying volume (r = 0.38; p<0.05). CONCLUSIONS: The present study suggests that regression of LV hypertrophy due to telmisartan is associated with reduction of LA volumes that expresses variation of LV end-diastolic pressure. The reduction of LV end-diastolic pressure is associated with an increase in diastolic filling and with a significant reduction of active and passive emptying contribution of left atrium to LV stroke volume.     

Plasma insulin levels do not change during atrial natriuretic factor infusion in human essential hypertensives

In order to evaluate the effects of atrial natriuretic factor (ANF) infusion on plasma insulin (IRI) in hypertension, 32 essential hypertensives (aged 40 to 62 years) were studied. After 1 week of pharmacologic washout under normal sodium intake (120 mEq of Na+/day), patients were randomly assigned to receive either ANF (0.04 micrograms/kg/min) or its vehicle (50 mL of isotonic saline) over a 60-min period in supine position. Plasma IRI and glucose were measured at -60, 0, 20, 40, 60, 120, 180, and 240 min (infusion time: from 0 to 60 min). Plasma levels of IRI and glucose did not change significantly during ANF infusion. On the contrary, after ANF discontinuation plasma IRI rose from levels of 13.5 +/- 6.4 microU/mL at 60 min to values of 20.1 +/- 11.3 microU/mL at 240 min (P less than .0001 v time 0). Plasma glucose showed a similar behavior, increasing from values of 100.4 +/- 5.0 mg/dL at 60 min to values of 120.0 +/- 5.1 mg/dL at 240 min (P less than .02 v time 0). Our findings suggest that ANF did not influence insulin release in hypertensives. The increase of plasma glucose and IRI observed after ANF discontinuation could be due to the relapse of sympathetic activity, suppressed during ANF infusion.     

高血压左室肥厚及心功能与血浆脑钠肽浓度变化的关系探讨

目的 探讨高血压患者左室肥厚及左室舒张功能与血浆脑钠肽（BNP）浓度的关系.方法 高血压患者62例,其中伴左心室肥厚组患者32例,不伴左心室肥厚组患者30例;健康对照组30名.高血压患者给予厄贝沙坦片75～150 mg/d,治疗6个月.所有对象行超声心动图测定左心室重量指数（LVMI）、E/A（二尖瓣舒张期E峰/A峰）比值.采用美国博适Triage及其试剂盒快速测定血浆BNP水平,对BNP与LVMI、E/A比值作相关分析.结果 高血压左心室肥厚患者组的血浆BNP水平（ng/L）明显高于高血压不伴左心室肥厚患者组和健康对照组（54.8±16.9比36.7±15.4,P＜0.05;54.8±16.9比16.4±12.7,P＜0.05）.经厄贝沙坦治疗后,高血压左心室肥厚患者组血浆BNP水平（ng/L）明显下降（54.8±16.9比36.8±12.6,P＜0.05）,E/A比值明显上升（0.86±0.57比1.09±0.65,P＜0.05）,差异有统计学意义,且与LVMI呈显著正相关 （r＝0.57,P＝0.028）,与E/A比值呈显著负相关（r＝-0.68,P＝0.009）.结论 血浆BNP浓度能较好地反映高血压患者左心室肥厚及左室舒张功能状态.     

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.     

QT dispersion intervals in hypertensives with left ventricular hypertrophy

Left ventricular hypertrophy is an important risk factor of cardiovascular complications during the course of hypertension. Increased QT dispersion is associated with sudden cardiac death in congestive heart failure and in other cardiovascular diseases. Our aim was to compare QT dispersion from routine ECG in hypertensive patients with and without left ventricular hypertrophy defined by echocardiography. Authors examined 71 hypertensives treated in our medical department. 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. QT dispersion was defined from routine ECG (QTmax - QTmin). Presence of LVH was found in 26 patients (mean age 59.3 years), absence of LVH in 45 patients (mean age 57.8 years). Hypertensives with secondary hypertension, hypertrophic cardiomyopathy, sings of ischemia in ECG, arrhythmias, myocardial infarction, heart failure, diabetes mellitus and patients treated by antiarrhythmic drugs of the Ic and III groups were excluded. Both groups of hypertensives were matched by demographic parameters, and by the presence of hypertension, obesity, hyperlipidemia and smoking habites. There were statistically significant longer QT dispersion and QTc dispersion (59.0 +/- 20.1 ms, 64.0 +/- 23.7 ms) in LVH-positive patients than in LVH-negative once (43.2 +/- 9.5 ms, 48.4 +/- 11.1 ms). Left ventricular hypertrophy in patients with hypertension brings usually a complicated course of the disease. Authors recommend to look after left ventricular hypertrophy presence in hypertensives as it carries much more complicated course of the disease. Measurment of QT dispersion adds farther stratificational information to these patients.     

Plasma atrial natriuretic peptide levels in elderly hypertensives: effects of blood pressure reduction with amlodipine

Atrial natriuretic peptide (ANP) is a hormone of relatively recent discovery concerned with sodium homeostasis. Increased levels of ANP are found in the elderly and in hypertensives, but the mechanisms for this are unclear. This study determined the effect of amlodipine, a calcium antagonist, which is the only class of antihypertensive agent that has little or no influence on the renin-angiotensin system (Bauer and Reams, 1988) on plasma ANP in a group of 18 elderly hypertensives and a placebo (vit B complex) on a further group of 6 elderly hypertensives. The mean pre-treatment plasma ANP was 62.7 pg/ml (range 18-148.7 pg/ml) and 52.0 pg/ml (range 15.0-148.4 pg/ml) after treatment with amlodipine (not statistically significant). However, systolic blood pressure fell from a mean of 181.6 mmHg to 151.1 mmHg and diastolic blood pressure fell from a mean of 101.6 mmHg to 83.6 mmHg after treatment with amlodipine (statistically significant, P < 0.001). In the group treated with vit B complex, the mean plasma ANP level was 68.4 pg/ml (range 31.4-119.5 pg/ml) before treatment and 63.6 pg/ml (range 29.2-127.3 pg/ml) after treatment. This was not statistically significant and there was no significant change in blood pressure. These findings reinforce the theory that raised plasma ANP levels found in elderly hypertensives are a function of the aging process itself or of age-related physiological changes rather than the result of hypertension.     

Plasma norepinephrine and left ventricular hypertrophy in systemic hypertension

The relations between some pressure and humoral factors, and some echocardiographic indexes of left ventricular (LV) hypertrophy were studied in 64 patients with essential hypertension. Fifty-seven percent of these patients showed echocardiographic evidence of LV hypertrophy (LV mass greater than 215 g). Multivariate stepwise regression analysis showed that only mean blood pressure (BP) and circulating norepinephrine (NE) levels were significantly related to LV mass index in the group of patients with LV hypertrophy. However, mean BP was the only factor related to LV mass index in the subgroup of patients with LV hypertrophy and plasma NE within the normal laboratory range, whereas NE was the sole factor related to LV mass index in the subgroup with LV hypertrophy and abnormally elevated NE levels (greater than mean + 2 standard deviations of the normal laboratory range). Correlation of LV mass index vs NE was -0.35 (not significant) in the former group of patients and 0.89 (p less than 0.01) in the latter group. NE showed no relation with the echocardiographic variables in the hypertensive patients without LV hypertrophy; in this group, diastolic BP was the only factor related to LV mass index. Circulating NE levels were slightly higher in patients with LV hypertrophy (213 +/- 68 ng/liter) than in those without LV hypertrophy (187 +/- 46 ng/liter), but differences were not significant when adjusting NE for age. Plasma renin activity was not dissimilar in the absence or presence of hypertrophy. In conclusion, our findings suggest that NE might be associated with pressure factors in regulating LV hypertrophy development only in a subgroup of hypertensive patients characterized by echocardiographic LV hypertrophy and abnormally elevated circulating NE levels.     

Low-dose infusion of atrial natriuretic factor in mild essential hypertension

Intra-arterial blood pressure, cardiac output, heart rate, right heart indexes, urinary electrolytes, and urinary volume were monitored in eight patients with untreated (WHO Class I) essential hypertension. The patients were given synthetic atrial natriuretic factor (ANF) (99-126 alpha-hANP) at 1 and 2 pmol/kg/min in series (phases 1 and 2, 2 hours each dose) or vehicle (hemaccel) in random order on two separate occasions while on their usual diet. Arterial plasma ANF levels increased significantly from basal and time-matched placebo values from 25 +/- 2 and 28 +/- 3 pmol/l to 50 +/- 4 and 83 +/- 9 pmol/l at the end of phases 1 and 2, respectively (p less than 0.001). After 30 minutes during phase 2, systolic blood pressure decreased significantly by 20 +/- 4 mm Hg (p less than 0.001) from basal and time-matched placebo values and remained significantly reduced (-17 +/- 4 mm Hg, p less than 0.001) by the end of the recovery period (2 hours after infusions were completed). Pulmonary systolic blood pressure decreased by 5 +/- 1 mm Hg (phase 2, p less than 0.05). Cardiac output decreased by 0.5 +/- 0.1 l/min below baseline at the end of phase 2 of ANF infusion, whereas it increased significantly (p less than 0.02) by 0.6 +/- 0.1 l/min during vehicle infusion. Systemic diastolic, pulmonary diastolic, right atrial, and wedge pressures were not significantly changed during ANF or vehicle infusions, nor were pulmonary vascular resistance or heart rate altered. Systemic vascular resistance did not change significantly during both infusions, whereas during recovery, systemic vascular resistance decreased significantly after ANF infusion was discontinued (p less than 0.05). Microhematocrit levels increased dose dependently during ANF. The maximum increase was observed at the end of phase 2 (+4.7 +/- 1.7%), whereas the microhematocrit level decreased to -2.4 +/- 0.6% with vehicle (p less than 0.001) at the end of phase 2. Urinary sodium excretion increased significantly (p less than 0.02) by the end of phase 2 under ANF infusion (+38 +/- 15%), whereas it decreased (-10 +/- 6%) under placebo infusion by the end of phase 2. Urinary magnesium excretion was significantly increased during ANF infusion from phase 1 (p less than 0.02), whereas urinary potassium levels, calcium levels, creatinine levels, volume, and glomerular filtration rate did not differ significantly between the two infusions. Plasma renin, angiotensin II, aldosterone, and catecholamine concentrations did not change significantly during ANF or vehicle infusions.(ABSTRACT TRUNCATED AT 400 WORDS)     

Association between elevated brain natriuretic peptide levels and the development of left ventricular hypertrophy in patients with hypertension

PURPOSE: To examine whether plasma levels of brain natriuretic peptide identify hypertensive patients at risk for progressive cardiac hypertrophy. SUBJECTS AND METHODS: We examined the association between plasma brain natriuretic peptide levels and left ventricular structural changes in 54 hypertensive patients and 28 normotensive control subjects. Patients were divided into those with elevated (n = 14) or normal (n = 40) levels of brain natriuretic peptide, based on a cutoff level of 41 pg/mL (2 SD above the mean in the control subjects). Left ventricular function and geometry were assessed echocardiographically at baseline and follow-up. RESULTS: At baseline, initial left ventricular chamber size, wall thickness, and systolic function did not differ between the hypertensive patients and normotensive subjects. After a mean (+/- SD) follow-up of 9 +/- 3 months, blood pressure was relatively unchanged in the hypertensive patients with normal brain natriuretic peptide levels, whereas there were significant increases in systolic blood pressure and pulse pressure (both P <0.05 versus baseline) in patients with elevated brain natriuretic peptide levels. Moreover, left ventricular midwall systolic function had decreased significantly at follow-up in those with elevated levels (P <0.05 versus baseline). At follow-up, the hypertensive patients with elevated brain natriuretic peptide levels had a significantly greater left ventricular mass index and relative wall thickness than those with normal levels. Multiple regression analyses determined that only initial plasma brain natriuretic peptide was significantly (P <0.01) associated with subsequent left ventricular hypertrophy. CONCLUSION: Plasma brain natriuretic peptide levels may identify hypertensive patients who are likely to have progressive cardiac hypertrophy.     

Left ventricular systolic response to exercise in patients with systemic hypertension without left ventricular hypertrophy

Supine exercise radionuclide angiography was performed in 367 men to assess left ventricular (LV) systolic response to exercise; 58 had systemic hypertension without LV hypertrophy on a resting electrocardiogram and 309 were normotensive. All patients met the following criteria defining a low pretest likelihood of coronary artery disease: age less than 50 years; normal electrocardiographic response to exercise; absence of typical or atypical chest pain; and exercise heart rate greater than 120 beats/min. Patients taking beta-receptor blockers were excluded. There were no significant differences between hypertensive and normotensive groups in peak exercise heart rate, workload or exercise duration. However, hypertensive patients had significantly higher peak exercise systolic blood pressures and peak exercise rate-pressure products. There were no differences between patients with and without hypertension in resting ejection fraction, peak exercise ejection fraction (hypertensive patients 0.71 +/- 0.01, normotensive patients 0.70 +/- 0.05) or change in ejection fraction at peak exercise (hypertensive patients 0.07 +/- 0.01, normotensive patients 0.07 +/- 0.04). Diastolic and systolic ventricular volumes tended to be smaller in the hypertensive patients, but the difference was not statistically significant. The change in systolic volume with exercise was similar in the 2 groups (hypertensive -10 +/- 3 ml/m2, normotensive -10 +/- 1 ml/m2). In the absence of electrocardiographic evidence of LV hypertrophy, systemic hypertension does not influence LV systolic response to exercise.     

Supernormal contractility in primary hypertension without left ventricular hypertrophy

Forty-three subjects with uncomplicated primary hypertension and without echocardiographic left ventricular hypertrophy and 54 normotensive volunteers were studied by two-dimensional targeted M-mode echocardiography to evaluate systolic function and contractility before the development of compensatory hypertrophy. The ratio of peak systolic pressure to end-systolic dimension was used to assess left ventricular performance and was divided for either posterior wall thickness or cross-sectional area to generate hypertrophy-independent indices of inotropic state. Fractional shortening was normal in the hypertensive group, despite the increase in end-systolic stress. Systolic pressure/dimension ratio was higher in hypertensive subjects (p less than 0.001), as were hypertrophy-independent indices of inotropic state (p less than 0.005), which were inversely correlated to left ventricular mass (p less than 0.001). Values in 11 hypertensive subjects were above the upper confidence limit of the normal shortening/stress relation, which provides a load-independent measure of inotropic state. They showed high hypertrophy-independent indices of inotropic state (p less than 0.01), while the other hypertensive subjects did not. High fractional shortening, wall stress, and systolic pressure (p less than 0.01) were found in the subgroup with supernormal performance, while left ventricular mass was not different from that of other subgroups, depicting inadequate left ventricular hypertrophy. The duration of hypertension was the same in the subgroups. Supernormal inotropic state could be considered one form of primary adaptation to high wall stress that serves to maintain systolic ventricular performance.     

Relationship of atrial natriuretic factor to left ventricular volume and mass

Although atrial natriuretic factor is primarily of atrial origin, recent observations indicate that the hormone is also synthesized by hypertrophied left ventricular myocardium. To assess the separate influences of left ventricular and left atrial dilatation and left ventricular hypertrophy on human atrial natriuretic factor levels, left atrial dimension and volume and left ventricular dimension and mass were compared in 49 normal subjects, in 33 patients with chronic aortic regurgitation, and in 15 patients with chronic mitral regurgitation. When compared with normal subjects, patients with chronic aortic and mitral regurgitation had similarly dilated and hypertrophied left ventricles (p less than 0.0005), while only mitral regurgitation patients had significantly enlarged (p less than 0.0005) mean left atrial dimension and volume. Likewise, plasma atrial natriuretic factor was elevated among patients with mitral regurgitation (60.3 +/- 47.0 fmol/ml) but was normal in patients with aortic regurgitation (19.0 +/- 11.0 fmol/ml versus 12.4 +/- 5.2 fmol/ml in normals; both p less than 0.0005 versus mitral regurgitation). Among all 97 subjects, atrial natriuretic factor levels correlated more closely with left atrial dimension and volume (r = 0.62 and 0.64, p less than 0.0005) than with left ventricular dimension (r = 0.44, p less than 0.0005) or mass (r = 0.40, p less than 0.0005). In addition, multivariate analysis indicated that left atrial volume bore a stronger independent relationship to plasma atrial natriuretic factor levels than either age or left ventricular variables.(ABSTRACT TRUNCATED AT 250 WORDS)     

应用多普勒组织成像技术评价原发性高血压左室舒张功能及其相关因素

目的:应用多普勒组织成像技术(DTI)探讨原发性高血压(EH)左室舒张功能的特点,同时检测血中心钠素(ANP)、脑钠素(BNP)的变化,分析两者与左室舒张功能的关系。方法:对照组20例,EH患者(EH组)61例,均行常规超声及DTI检查,EH患者根据左室质量指数(LVMI)分为左室心肌肥厚(LVH)亚组和无 LVH(NLVH )亚组。DTI测量二尖瓣侧环心肌舒张早期峰值运动速度(e)、晚期峰值运动速度(a)及其比值(e/a),测量二尖瓣瓣尖水平舒张早期的最大流速(E0)、舒张晚期的最大流速(A)及 E0 与A流速的比值E0/A。入选病例均测定血浆ANP、BNP浓度。结果:与对照组相比,EH患者E0/A、e/a减小,LVH亚组减小更明显;与对照组相比,EH血浆 ANP、BNP浓度升高, LVH升高更明显; E0/A、e/a比值与 ANP 呈负相关( r = - 0.56和 r = -0.60, 均P<0.01),与BNP呈负相关( r=-0.62和 r=-0.65,均 P<0.01)。结论:血浆 ANP、BNP与应用DTI技术评价的EH左室舒张功能均有较好相关性。