Blunted sympathetic response to cardiopulmonary receptor unloading in hypertensive patients with left ventricular hypertrophy. A possible compensatory role of atrial natriuretic factor

To investigate whether or not hypertension with left ventricular hypertrophy (LVH) modifies the mechanisms underlying the vascular adjustments to orthostatic stress, we evaluated the hemodynamic and hormonal effects of graded lower-body negative pressure (LBNP) (-10 and -40 mm Hg) before and after sympathetic blockade in 10 hypertensive patients with LVH and in five age- and sex-matched normotensive subjects. In control conditions, LBNP elicited comparable vasoconstrictor responses in the forearm in the two groups. In normotensive subjects, graded increases in plasma norepinephrine and plasma renin activity (PRA) and reductions in plasma immunoreactive atrial natriuretic factor (irANF) were recorded. In hypertensive patients, a significant increase in plasma norepinephrine and plasma renin activity was obtained only with the higher level of LBNP, whereas irANF plasma levels decreased progressively. In both groups, sympathetic blockade abolished the increase in plasma renin activity and did not modify the changes in plasma irANF induced by both levels of LBNP in control conditions. The vascular response to -10 mm Hg LBNP remained unchanged after sympathetic blockade in both groups. However, after sympathetic blockade, the vasoconstrictor response to -40 mm Hg LBNP in normal subjects was no longer different from that elicited by -10 mm Hg LBNP, whereas in hypertensive patients the vasoconstrictor response was still significantly higher than that induced by -10 mm Hg LBNP. Direct correlations between the percent changes in forearm vascular resistance and those in plasma norepinephrine and plasma renin activity were found only in normal subjects in control conditions but were not observed after sympathetic blockade. On the contrary, the inverse correlation between changes in irANF plasma levels and in forearm vascular resistance found in control conditions in both groups was still observed after sympathetic blockade. In a separate group of hypertensive patients with left ventricular hypertrophy, exogenous infusion of ANF induced an increase in venous irANF plasma levels of the same magnitude of the decrease evoked by LBNP and significantly reduced forearm vascular resistance. These data show that in hypertensive patients with left ventricular hypertrophy, sympathetic activation does not contribute to the vascular response to cardiopulmonary receptor unloading (-10 mm Hg LBNP). They also suggest that in these patients inhibition of ANF secretion may play a role in the response to a low level of LBNP so that the peripheral vasoconstriction induced by cardiopulmonary receptor unloading is comparable to that observed in normal subjects despite the lack of appropriate sympathetic reflex vasoconstriction.     

Reversal of inappropriate peripheral vascular responses in hypertrophic cardiomyopathy

OBJECTIVES: We assessed the frequency of abnormal forearm vasodilator responses during lower body negative pressure (LBNP) in 21 non-obstructive hypertrophic cardiomyopathy (HCM) patients (31 +/- 8 [20 to 43] years) with abnormal blood pressure response (ABPR) to exercise and the effects of three drugs used to treat vasovagal syncope (propranolol, clonidine, and paroxetine) in a double-blind crossover study. BACKGROUND: Some HCM patients have an ABPR to exercise, which may be due to paradoxical peripheral vasodilatation. A similar proportion has paradoxical forearm vasodilatation during central volume unloading using LBNP. These abnormal reflexes may be caused by left ventricular mechanoreceptor activation. Similar mechanisms may also contribute to some cases of vasovagal syncope. METHODS: Blood pressure changes were assessed during exercise, and forearm vascular responses and baroreceptor sensitivity were assessed during LBNP using plethysmography. RESULTS: Nine (43%) patients (group A) had paradoxical vasodilator responses (forearm vascular resistance [FVR] fell by 7.5 +/- 4.6 U), and 12 (57%) patients (group B) had normal vasoconstrictor responses during LBNP (FVR increased by 7.7 +/- 4.9 U). Paroxetine augmented systolic blood pressure (SBP) during exercise in group A (21 +/- 6 mm Hg vs. 14 +/- 11 mm Hg at baseline, p = 0.02); no effect was detected in group B. Paroxetine reversed paradoxical vascular responses during LBNP in seven (78%) patients from group A. Propranolol and clonidine had no significant effect on SBP during exercise but reversed paradoxical vascular responses in some patients from group A (n = 5 and n = 3). CONCLUSIONS: Paradoxical vasodilatation during LBNP occurs in 40% of patients with ABPR during exercise and is reversed by propranolol, clonidine, and paroxetine. Paroxetine also improved SBP response to exercise.     

Neurohumoral and hemodynamic effects of lower body negative pressure in patients with congestive heart failure

Baroreflex modulation of forearm vascular resistance (FVR) has been reported to be abnormal in patients with congestive heart failure (CHF). However, the neurohumoral mechanisms for this impairment are not defined. We assessed the responses of arterial pressure, FVR, plasma norepinephrine, and plasma renin activity to lower body negative pressure in 29 patients with compensated CHF (New York Heart Association class III and IV) and in 11 normal age-matched control subjects. Baseline mean arterial pressure (83 +/- 2 vs 84 +/- 2 mm Hg) and mean arterial pressure during LBNP (-10, -20, and -40 mm Hg) were not significantly different in the two groups. Basal FVR (43.7 +/- 4 vs 27 +/- 2 units), plasma norepinephrine (605 +/- 81 vs 155 +/- 8 pg/ml), and plasma renin activity (8.3 +/- 1.7 vs 1.2 +/- 0.2 ng/ml/hr) were significantly (p less than 0.01) higher in patients with CHF. The relative increases in FVR responses during LBNP of -10, -20, and -40 mm Hg (10 +/- 4% vs 70 +/- 12%, 17 +/- 6% vs 106 +/- 21%, and 24 +/- 9% vs 152 +/- 28%) were markedly attenuated in patients with CHF compared to control subjects. Plasma norepinephrine and plasma renin activity responses during LBNP were also attenuated in patients with heart failure. Our results suggest that baroreflex control of FVR and plasma norepinephrine and plasma renin activity is impaired in CHF because of the inability of the cardiopulmonary baroreceptors to alter sympathetic outflow.     

The effect of chronic pulmonary hypertension on left ventricular size, function, and interventricular septal motion

The effect of right ventricular pressure overload secondary to chronic pulmonary arterial hypertension on left ventricular size and function and on interventricular septal motion was studied in 13 patients in whom coronary artery disease, hypertension, and hypoxemia were excluded. Regional and global left ventricular function were assessed by computer-assisted analysis of two-dimensional directed M-mode echocardiograms obtained within 24 hours of a hemodynamic study. Septal position and motion were further analyzed by delineating seven points along the right and left sides of the septum during a single cardiac cycle. All echocardiographic data were compared to those of 10 normal subjects. Mean values for right ventricular systolic, mean pulmonary artery and pulmonary capillary wedge pressures were: 71 +/- 26 mm Hg, 46 +/- 16 mm Hg, and 7 +/- 1 mm Hg, respectively. Septal motion was interpreted from the M-mode echocardiograms as normal in seven patients (group I) and abnormal in the remaining six patients (group II). The only hemodynamic parameter which distinguished these two patterns was delta P, the transseptal systolic pressure gradient across the interventricular septum, which was significantly different (p less than 0.02) in group I (delta P = 65 +/- 16 mm Hg) from that of group II (delta P = 21 +/- 24 mm Hg). As a result of abnormal septal position, the septal-free wall dimensions of the left ventricle were reduced, but there was no evidence of depressed left ventricular performance in these patients. We conclude that resting left ventricular function is well preserved in patients with pulmonary hypertension, despite significant alterations in septal position and left ventricular size.(ABSTRACT TRUNCATED AT 250 WORDS)     

老年高血压患者动脉僵硬度与左心室肥厚关系

目的探讨老年高血压患者动脉僵硬度与左心室肥厚的关系。方法选择原发性老年高血压患者68例,以左心室重量指数(LVMI)作为评价左心室肥厚指标,将患者分为左心室肥厚组(32例)和非左心室肥厚组(36例)。以颈动脉-股动脉肢体动脉搏动波(cfPWV)和脉压作为评价动脉僵硬度指标,进行24 h动态血压监测、cfPWV及超声心动图检测,并进行多因素相关分析。结果左心室肥厚组较非左心室肥厚组患者cfPWV高[(14.45±1.83)m/s vs(10.89±1.94)m/s]、脉压大[(78.66±9.05)mm Hg(1 mm Hg=0.133 kPa)vs(60.39±7.74)mm Hg],两组比较,差异有统计学意义(P<0.01),logistic回归分析显示,LVMI与cfPWV、脉压呈正相关。结论动脉僵硬度增加是老年高血压患者左心室肥厚的重要危险因素。     

Exercise systolic blood pressure: a powerful determinant of increased left ventricular mass in patients with hypertension

This study examines the relation between left ventricular mass determined by two-dimensional echocardiography and exercise blood pressure in patients with hypertension. Sixty-seven patients with hypertension and 19 normal subjects underwent treadmill exercise testing and two-dimensional echocardiography. The left ventricular mass index in the normal subjects was 80 +/- 10 g/m2 (mean +/- SD). Patients with hypertension were classified into two groups according to left ventricular mass: Group I (n = 42) had normal mass and Group II (n = 25) had increased mass (greater than 2 SD above the mean value in 19 normal subjects). There was a poor correlation between left ventricular mass and blood pressure at rest. However, a better correlation was found between left ventricular mass and exercise systolic blood pressure (r = 0.58, p less than 0.001) or the change in systolic blood pressure from rest to exercise (r = 0.48, p less than 0.001). Twenty-two (76%) of 29 patients with an exercise systolic blood pressure of 190 mm Hg or greater had an increased left ventricular mass index, whereas only 3 (8%) of 38 patients with an exercise systolic blood pressure of less than 190 mm Hg had an increased left ventricular mass index (p less than 0.0001). Thus, in patients with hypertension, left ventricular mass index is poorly related to blood pressure at rest, but is related to exercise systolic blood pressure. Patients with an exercise systolic blood pressure of 190 mm Hg or greater usually have an increased left ventricular mass. These findings may have therapeutic implications.     

Attenuation of reflex forearm vasoconstriction by alpha-human atrial natriuretic peptide in men

This study examined whether atrial natriuretic peptide (ANP) modulates reflex forearm vasoconstriction in humans. Synthetic alpha-human ANP (alpha-hANP) was infused at a rate of 0.03 microgram/kg/min in 8 healthy men (mean age 23 +/- 0.7 years, mean +/- SEM). The alpha-hANP decreased systolic blood pressure and central venous pressure (CVP) but did not significantly alter resting heart rate and forearm vascular resistance (FVR). The magnitudes of reflex increases in FVR during lower body negative pressure (LBNP) at -110, -20, and -40 mm Hg were less during infusion of alpha-ANP than those magnitudes during infusion of saline solution. The slope of the regression line relating changes in CVP and those in FVR was less during infusion of alpha-hANP than the slope during infusion of saline solution. Forearm vascular responses to intra-arterial infusion of norepinephrine at doses of 100, 200, and 500 ng/min did not significantly differ during infusion of alpha-hANP and saline solution. These results suggest that alpha-hANP attenuates cardiopulmonary baroreflex control of FVR in normal men.     

Left ventricular hypertrophy in patients with autonomic failure

BACKGROUND: In autonomic failure (AF), supine hypertension may predispose patients to end-organ damage. The pathophysiology of hypertensive heart disease in AF is not known. The aim of the present study was to evaluate the prevalence and predisposing factors of left ventricular hypertrophy (LVH) in patients with AF. METHODS: We studied 25 patients with AF (67 +/- 8 years); 80% were being treated for orthostatic hypotension. Twenty patients with essential hypertension (68 +/- 6 years) were considered as the control group. All subjects underwent echocardiography for measurement of left ventricular mass (LVM). The patients with AF underwent a 24-h BP monitoring and long-term blood pressure (BP) variability was calculated as standard deviation (SD) of the average of the half-hour mean values. RESULTS: The LVM is comparable in patients with AF and hypertensive controls (145 +/- 35 g/m2 v 127 +/- 32 g/m2, P = .07). The proportion of patients with LVH is similar in both populations (AF 80%, hypertensive 70%). The patients with AF were divided into two groups, with and without LVH. The SDs are significantly higher in AF patients with LVH than in those with normal LVM (SD 24-h systolic BP: 22 +/- 4 v 14 +/- 1 mm Hg, P = .001). CONCLUSIONS: A high proportion of patients with AF show LVH. The LVM values are comparable with those of patients with essential hypertension. The development of LVH seems to depend on high BP variability, characteristic of AF patients. Detection of LVH may help in the choice of treatment for orthostatic hypotension and in the prevention of heart failure.     

Impaired adaptation of cardiopulmonary receptors to western diet in normotensive black immigrants

A blood pressure increase was reported in black immigrants from Africa to Western countries. The present study was undertaken to evaluate whether an impairment of the cardiopulmonary reflex might make blacks unable to adapt peripheral vascular resistance to increased sodium intake.Ten normotensive clinically healthy blacks (aged 38 ± 6 years) who had recently migrated from Mogadishu, Somalia to Florence and 10 age- and gender-matched healthy white subjects were investigated. Cardiopulmonary baroreceptor reflex was studied after 7 days of normal (108 mEq) and low (30 mEq) sodium intake by assessing forearm vascular resistance (FVR) and central venous pressure (CVP) during the application of lower body negative pressure (LBNP) at −10 and −20 mm Hg.With a normal sodium diet the gain in cardiopulmonary baroreceptor reflex, expressed as the FVR increase per mm Hg of CVP reduction, was significantly lower in blacks than in white subjects (2.6 ± 1.1 v 5.1 ± 1.1 U per mm Hg of CVP, P < .001). Differences between the groups disappeared with a low-sodium diet because the reduction of the efficiency of the cardiopulmonary baroreceptor reflex was lower in blacks than in whites (2.4 ± 0.7 v 3.3 ± 0.7 U per mm Hg of CVP, P = .09).In conclusion, the efficiency of the cardiopulmonary reflex is lower in normotensive black immigrants than in whites. The lower adaptation of the cardiovascular system to the Western sodium diet could contribute to reported long-term blood pressure increase.     

Iodine-123 phenylpentadecanoic acid myocardial scintigraphy in patients with left ventricular hypertrophy: alterations in left ventricular distribution and utilization

Regional alterations in myocardial substrate uptake and/or utilization have been demonstrated in rats with hypertension. To determine whether alterations in left ventricular fatty acid uptake and/or utilization are present in patients with left ventricular hypertrophy (LVH), we compared the results of rest and exercise iodine-123 phenylpentadecanoic acid (IPPA) myocardial scintigraphy in 10 patients with hypertension who had concentric LVH without evidence of coronary artery disease and in 15 normal subjects. Patients with LVH had more heterogeneous left ventricular activity of IPPA compared to normal subjects after exercise but not at rest (23 +/- 8% versus 13 +/- 5% difference in maximum segmental activity at 4 minutes after exercise; p = 0.005). Although IPPA clearance was similar in both patients with LVH and normal subjects, postexercise washout in segments showing decreased initial IPPA uptake was reduced compared to washout at rest in patients with LVH (11.7 +/- 7.5% versus 21.5 +/- 8.4% at 20 minutes after injection, n = 15; p = 0.005). Exercise thallium-201 (TI-201) scintigraphy was normal in all seven patients with LVH tested. Patients with LVH showed significantly greater heterogeneity in IPPA uptake compared to TI-201 uptake immediately after exercise (25 +/- 5% versus 16 +/- 6%; p = 0.013). We conclude that (1) compared to normal subjects, patients with LVH show heterogeneous myocardial IPPA activity after exercise but not at rest; (2) postexercise washout of IPPA was decreased in segments with reduced uptake after exercise in patients with LVH; and (3) the distribution of IPPA is more heterogeneous than that of TI-201 immediately after exercise in patients with concentric LVH. The postexercise heterogeneity in IPPA uptake and delayed washout in segments with reduced initial uptake is consistent with exercise-induced myocardial ischemia in patients with LVH.     

Left ventricular hypertrophy in men with normal blood pressure: relation to exaggerated blood pressure response to exercise

OBJECTIVE: To determine whether normal, nonhypertensive subjects who have unusually large increases of systolic blood pressure with exercise have left ventricular hypertrophy (LVH). DESIGN: Case-comparison using echocardiography as a criterion standard for measurement of left ventricular mass and the diagnosis of LVH. SETTING: Population-based health fitness screening program and referral Veterans Affairs Hospital. SUBJECTS: Thirty-nine men (average age, 44.6 +/- 8.5 years; range, 34 to 71 years) were studied, including 25 participants in a health fitness screening program and an additional 14 normal men with atypical chest pain. Twenty-two subjects with a systolic blood pressure during peak exercise of 210 mm Hg or greater were compared with 17 others with systolic pressure less than 210 mm Hg during exercise. MEASUREMENTS AND MAIN RESULTS: Left ventricular hypertrophy (left ventricular mass index greater than 134 g/m2) was found in 14 of 22 men with a systolic blood pressure of 210 mm Hg or greater (present in 6.3% of normotensive healthy male volunteers in a health screening program) but in only 1 person with a lower exercise blood pressure. Left ventricular mass index was linearly correlated (r = 0.65, n = 39, P less than 0.001) with maximum exercise blood pressure. Whereas LVH was mild in about 50%, substantial LVH was present in the others. The presence of LVH was not related to superior physical conditioning and was accompanied by increased left atrial size suggesting impaired left ventricular filling. CONCLUSIONS: Even in the absence of hypertension, exaggerated blood pressure responses during exercise testing suggest a probability of 0.64 (95% CI, 0.41 to 0.83) of LVH, a finding associated with the cardiac "end-organ" manifestations of hypertension.     

Evaluation of a noninvasive system for determining left ventricular filling pressure

BACKGROUND: Measurement of left ventricular filling pressure (LVFP) provides an accurate assessment of left ventricular failure. Clinical and radiographic methods of estimating LVFP are unreliable. The noninvasive method of analyzing the decline in the arterial pressure during the strain phase of the Valsalva maneuver may be used to directly measure LVFP. OBJECTIVE: To examine the relationship and the level of accuracy of a noninvasive system (VeriCor) in directly determining left ventricular end diastolic pressure (LVEDP) using simultaneously recorded VeriCor and LVEDP measurements obtained during left heart catheterization. METHODS: During elective right and left heart catheterization, LVFP was assessed by measuring pulmonary capillary wedge pressure (PCWP) and LVEDP in 57 patients followed immediately by a Valsalva maneuver using the VeriCor assembly to estimate these pressures noninvasively. RESULTS: VeriCor measurements had a significant correlation with the catheter-measured LVEDP (r = 0.86), comparable to the correlation of the catheter-measured PCWP with LVEDP (r = 0.81). The predictive accuracy of VeriCor for LVEDP, however, appeared to be superior to that of catheter-measured PCWP for LVEDP: 84% of VeriCor measurements compared with only 41% of PCWP measurements were within 4 mm Hg of catheter-measured LVEDP, and 93% of VeriCor measurements compared with only 67% of PCWP measurements were within 6 mm Hg of catheter-measured LVEDP. CONCLUSION: VeriCor is a reliable noninvasive tool for measuring LVFP.     

Improvement in midwall myocardial shortening with regression of left ventricular hypertrophy

Despite normal indices of left ventricular (LV) chamber function, patients with LV hypertrophy (LVH) due to hypertension are thought to have depressed midwall systolic shortening compared with normotensives. The aims of the present study were (1) to confirm this observation and (2) to assess the effects of antihypertensive therapy that cause regression of LVH on LV systolic function assessed at both the midwall and endocardium. Thirty-eight previously untreated hypertensive subjects with LVH underwent echocardiography and were compared with 38 normotensive control subjects. Comparisons between the group with LVH and the control group revealed no significant differences in cardiac output (4. 32+/-0.23 versus 4.55+/-0.21 L/min), ejection fraction (62.5+/-2% versus 66.4+/-1.07%), or endocardial fractional shortening (34.5+/-1.45% versus 37.0+/-0.82%), but shortening assessed at the midwall was significantly less in the group with LVH (17.9+/-1.11% versus 21.6+/-0.63%, P<0.01). Subsequently, 32 patients with uncontrolled hypertension (24 previously untreated and 8 on existing antihypertensive therapy) underwent treatment with ramipril, with the addition of felodipine and bendrofluazide if required, to reduce blood pressure to <140/90 mm Hg. These 32 patients underwent echocardiography at baseline, after blood pressure control, and after an additional 6 months of tight blood pressure control. Good blood pressure control was achieved after 6 months compared with baseline (143/86+/-2.8/1.4 versus 174/103+/-4.1/1.9 mm Hg; P<0.01) with significant regression of LV mass index (124+/-3.4 versus 145+/-3.8 g/m(2), P<0.01). LV fractional shortening assessed at the midwall improved with regression of LVH (21.9+/-0.84 and 18.7+/-1. 19%, P<0.05), with posttreatment midwall shortening being similar to that of the normal control subjects evaluated in the first study. Hypertensive patients with LVH have depressed midwall systolic shortening despite normal indices of LV chamber function. Regression of LVH after good blood pressure control improved midwall shortening to normal levels.     

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.     

Increased right ventricular wall thickness in left ventricular pressure overload: echocardiographic determination of hypertrophic response of the "nonstressed" ventricle

Left ventricular hypertrophy in left ventricular pressure overload occurs in response to excessive work load imposed on the left ventricle by increased impedance to ejection. Right ventricular hypertrophy may occur in patients with these findings, but has been considered to be secondary to pulmonary hypertension. To determine the frequency of right ventricular hypertrophy and its relation to increased left ventricular wall thickness in patients with left ventricular pressure overload, right ventricular wall thickness was measured using M-mode echocardiography with two-dimensional echocardiographic guidance in 65 patients with left ventricular pressure overload; 49 patients had essential hypertension and 16 had aortic valve stenosis. These measurements were compared with data from 13 patients with "thin-walled" dilated cardiomyopathy and 20 normal subjects. Average right ventricular wall thickness in hypertensive patients (7 +/- 2 mm) and patients with aortic stenosis (6 +/- 2 mm) was significantly greater than that in normal subjects (4 +/- 1 mm) and patients with dilated cardiomyopathy (4 +/- 1 mm) who had normal left ventricular wall thickness, even though left ventricular mass was increased in all patient groups. Increased right ventricular wall thickness was present in 40 (80%) of 49 patients with hypertension and 10 (63%) of 16 patients with aortic stenosis. The magnitude of increase in right ventricular wall thickness was linearly correlated (r = 0.76, p less than 0.005) with left ventricular wall thickness, but was not associated with pulmonary hypertension. It is concluded that increased right ventricular wall thickness is common in patients with left ventricular pressure overload, is directly related to increases in left ventricular wall thickness, and is independent of right ventricular hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of left atrial volume parameters in detecting left ventricular diastolic dysfunction versus tissue Doppler recordings

Because of diastolic coupling between the left atrium and left ventricle, we hypothesized that left atrial (LA) function mirrors the diastolic function of left ventricle. The aims of this study were to assess whether LA volume parameters can be good indexes of left ventricular diastolic dysfunction. Six hundred fifty-nine patients underwent cardiac catheterization and measurements of left ventricular filling pressure (LVFP). Echocardiographic examinations including tissue Doppler and LA volumes were also assessed. Ratio of early diastolic mitral inflow velocity to early diastolic mitral annular velocity and LVFP tended to increase after progression of diastolic dysfunction. The inverse phenomenon existed in LA ejection and LA distensibility. LA distensibility was superior to LA ejection fraction and early diastolic mitral inflow velocity/early diastolic mitral annular velocity for identifying LVFP >15 mm Hg (areas under receiver operating characteristic curve 0.868, 0.834, and 0.759, respectively) and for differentiating pseudonormal from normal diastolic filling (areas under receiver operating characteristic curve 0.962, 0.907, and 0.741, respectively). Multivariate logistic regression showed that LA ejection fraction and LA distensibility were associated significantly with the presence of pseudonormal/restrictive ventricular filling. In conclusion, LA volume parameters can identify LVFP >15 mm Hg and differentiate among patterns of ventricular diastolic dysfunction. For assessing diastolic function LA parameters offer better performance than even tissue Doppler.     

Impaired control of vasopressin release in hypertensive subjects with cardiac hypertrophy

The effects of graded lower body negative pressure (-10 and -40 mm Hg) on vascular resistance and plasma vasopressin, norepinephrine, and renin activity were assessed in seven hypertensive subjects with left ventricular hypertrophy and seven sex-matched and age-matched normotensive subjects. In both groups increasing levels of lower body negative pressure induced a progressive decrease in right atrial pressure and an increase in vascular resistance. In normal subjects plasma vasopressin, norepinephrine, and renin activity were progressively raised, whereas only the higher level of stimulation increased plasma renin activity, norepinephrine, and vasopressin in hypertensive subjects. Propranolol induced a significant increase in plasma vasopressin in normal subjects (from 1.3 +/- 0.1 to 2.0 +/- 0.1 pg/ml; p less than 0.05) but not in hypertensive subjects. In this latter condition -10 mm Hg lower body negative pressure failed to increase plasma vasopressin, norepinephrine, and renin activity in normal subjects. Propranolol abolished the change in plasma renin activity in both groups, reduced the increase in vascular resistance induced by -40 mm Hg lower body negative pressure in normotensive subjects, but did not modify the rise in vasopressin elicited by this stimulus in normal subjects or the humoral and hemodynamic reflex responses evoked in hypertensive subjects. These results suggest that cardiopulmonary receptors are involved in the control of vasopressin release in normal subjects, whereas in hypertensive subjects with left ventricular hypertrophy, this control is altered because of an impaired function of cardiopulmonary receptors.     

Relationship of cardiac chamber volume to baroreflex activity in normal humans

The objectives of this study were to examine the effect of incremental lower body negative pressure (LBNP) on cardiac chamber volume and assess the relationship between cardiac chamber volume and baroreflex activation of the neurohormonal axis. Accordingly, echocardiographic determination of cardiac chamber volume and neurohormonal responses were studied in 14 normal subjects during incremental LBNP. LBNP -10 mm Hg decreased left atrial diameter and left ventricular systolic volume index, but did not alter heart rate, systolic or pulse pressure, or stroke volume. During LBNP -10 mm Hg, plasma norepinephrine levels increased, suggesting activation of the sympathetic nervous system. LBNP -40 mm Hg caused a significant decrease in left atrial diameter and left ventricular systolic, diastolic, and stroke volume indices. During LBNP -40 mm Hg, heart rate increased, and systolic and pulse pressure fell. With this more negative level of LBNP, norepinephrine, angiotensin II, aldosterone, and arginine vasopressin concentrations and PRA all increased. The findings that left atrial diameter decreased and plasma norepinephrine concentration increased during LBNP -10 mm Hg suggest that the sympathetic nervous system is sensitive to changes in atrial receptor activity. At higher levels of LBNP (-40 mm Hg), activation of the renin-angiotensin system and release of vasopressin were associated with a fall in left ventricular diastolic volume as well as a decrease in the pressure input to the arterial baroreceptors. Under this condition, the differential contribution of the cardiopulmonary and arterial baroreceptors to the regulation of the renin-angiotensin system and vasopressin release cannot be distinguished.     

Diminished nocturnal decline in blood pressure in elderly hypertensive patients with left ventricular hypertrophy.

To assess the circadian blood pressure (BP) changes in elderly hypertensive patients with left ventricular hypertrophy (LVH), the ambulatory BP was measured noninvasively every 30 minutes for 24 hours in those patients with LVH (n = 15) and without LVH (n = 23), and in normotensive elderly subjects (n = 11). Although the daytime systolic BP (SBP) was comparable in the two hypertensive groups, the nighttime SBP in patients with LVH tended to be higher than in patients without LVH (149.0 +/- 15.1 versus 138.4 +/- 20.1 mm Hg, p less than 0.10). The LV mass index correlated significantly with the nighttime SBP (r = 0.43, p less than 0.01), but not with the daytime SBP (r = 0.24, ns), with clinic SBP (r = 0.14, p = ns) or the SBP after handgrip exercise (r = 0.31, p = ns). The difference in the systolic BP between daytime and nighttime (D-N SBP) in patients with LVH (2.8 +/- 9.4 mm Hg) was significantly less than that in patients without LVH (12.8 +/- 16.0 mm Hg) (p less than 0.02). In addition, the D-N SBP correlated inversely with the left ventricular mass index (r = -0.33, p less than 0.05). It was concluded that hypertension in the elderly with LVH was associated with a diminished nocturnal decline in blood pressure.     

Left ventricular hypertrophy in patients with renal artery stenosis

Left ventricular hypertrophy (LVH) has been shown to be 3 times more prevalent in patients with renal artery stenosis (RAS) compared to essential hypertension, but factors that predict LVH in this population are not known. We identified 66 patients with unilateral renal artery stenosis and an interpretable electrocardiogram (ECG). LVH by either Cornell voltage-duration product or Sokolow-Lyon voltage criteria was present in 18 of the 66 patients (27%). The mean intra-aortic blood pressure was 100 +/- 14 mm Hg in patients with LVH, and 104 +/- 23 mm Hg in those without LVH (P = 0.37). The average stenosis by quantitative computerized angiography was 68 +/- 17% in patients with LVH, and 64 +/- 13% in those without LVH (P = 0.34). The mean translesional pressure gradient was 11 +/- 15 mm Hg in patients with LVH, and 13 +/- 20 mm Hg in those without LVH (P = 0.60). Using linear regression models, there was no correlation between intra-aortic blood pressure, percentage of stenosis, or translesional pressure gradient and either Cornell voltage-duration product or Sokolow-Lyon voltage criteria. In summary, LVH using ECG criteria was present in 27% of patients with unilateral RAS but was not associated with blood pressure at the time of the procedure or severity of renal artery stenosis.