Postprandial blood pressure reduction in healthy elderly

Previous studies have identified postprandial systolic blood pressure reductions in old, frail institutionalized subjects, which do not occur in healthy, young subjects, after a morning meal. To evaluate the relative contributions of state of health and time of day to this potentially dangerous abnormality in cardiovascular homeostasis, we measured sitting systolic blood pressure and heart rate before and at intervals after a noon meal, and in identical fashion without a meal, in 21 healthy, community-dwelling elderly subjects (73 +/- 6 years of age) attending a nutrition program. Systolic blood pressure changed a maximum of -11 +/- 9 (SD) mmHg (P = .006, analysis of variance) by 60 minutes after the meal, in contrast to 1 +/- 7 mmHg (NS) by 60 minutes, when no meal was given (P less than .0001, meal versus control studies). There was a highly significant inverse correlation between postprandial and basal sitting systolic blood pressure changes (R = -0.60, P = .004). Healthy community-dwelling elderly demonstrate postprandial reductions in systolic blood pressure which correlate with basal sitting systolic blood pressure. This is consistent with age- and hypertension-related impairment in baroreflex compensation for the hypotensive stress of eating.     

Relationship of baroreflex sensitivity and blood pressure in an older population

OBJECTIVES: Ageing and hypertension are associated with reduced baroreflex sensitivity (BRS) in young and middle-aged populations. The effects of blood pressure level on BRS in the older population are unclear. We examined the association between blood pressure and BRS in older persons with blood pressure below 180 mmHg. METHODS: BRS, high (alphaHF 0.15-0.4 Hz) and low (alphaLF 0.04-0.15 Hz) frequency alpha-index, was determined in 75 normotensive subjects (aged 75 +/- 4 years, 41% female, 131 +/- 10/74 +/- 7 mmHg) and 64 untreated hypertensive subjects (aged 76 +/- 5 years, 48% female, 165 +/- 7/ 88 +/- 7 mmHg) by spectral analysis of 20 min continuous blood pressure and heart rate recordings using finger plethysmography. Subjects were recruited from 10 general practices and were taking no cardiovascular medications. RESULTS: High but not low frequency alpha-index was significantly blunted in hypertensive subjects (alphaHF 5.1 +/- 3.1 versus 8.4 +/- 7.4 ms/mmHg, P< 0.001 and alphaLF 4.7 +/- 3.0 versus 5.8 +/- 3.9 ms/mmHg, P= 0.07). Multivariate analysis of the relationship between age and blood pressure demonstrated systolic and to a lesser extent diastolic blood pressure were significant predictors of variance in BRS for alphaHF [systolic blood pressure (SBP) P< 0.0001, diastolic blood pressure (DBP) P< 0.05, r2 = 0.1] and alphaLF (SBP P=0.01, DBP P<0.05, r2 = 0.04). Age was not a significant predictor for either measure, in the 20 year range studied. CONCLUSIONS: In an older population blood pressure is associated with reduced BRS, particularly for the high frequency component. Such a change may place older subjects with hypertension at increased risk of orthostatic hypotension, vasovagal syncope and sudden cardiac death.     

EVAluation of the prognostic value of BARoreflex sensitivity in hypertensive patients: the EVABAR study

AIMS: The prognostic value of baroreflex sensitivity in hypertensive patients has not much been studied. METHOD: A cohort of 451 hypertensive patients without cardiovascular history was studied for an average of 6.2 +/- 2.8 years follow-up. Each patient had a baroreflex sensitivity measurement by the sequence method, which is represented by the slope of up-sequences (systolic blood pressure+/pulse interval+) and down-sequences (systolic blood pressure-/pulse interval-) of spontaneous fluctuations in systolic blood pressure and pulse interval. RESULTS: During the follow-up, there were 20 deaths from any cause and 30 patients presented a major adverse cardiovascular event. Deaths and major adverse cardiovascular events were associated with a reduction in baroreflex sensitivity (systolic blood pressure+/pulse interval+ and systolic blood pressure-/pulse interval-). In multivariate analysis, the reduction in baroreflex sensitivity systolic blood pressure+/pulse interval+ was associated with an increased risk of deaths from any cause (Odds ratio 1.23; 95% confidence interval 1.02-1.67, P = 0.04). A baroreflex sensitivity systolic blood pressure+/pulse interval+ under 4.5 ms/mmHg was associated with a 2.5-increased relative risk of major adverse cardiovascular event (95% confidence interval 1.11-5.93, P = 0.03). However, multivariate analysis showed that baroreflex sensitivity systolic blood pressure-/pulse interval- was not associated either with death or major adverse cardiovascular events. CONCLUSIONS: Reduction in baroreflex sensitivity marked by a reduction in vagal reflexes is an independent marker of the risk of mortality and major adverse cardiovascular events in hypertensive patients.     

Reduced plasma renin activity in elderly subjects in response to vasovagal hypotension and head-up tilt

The sympathoadrenal and renin-angiotensin systems play an important role in the cardiovascular responses induced by head-up tilt. In young people, hypotension and postural changes induced by tilt produce significant increases in plasma renin activity. The response of plasma renin activity to prolonged tilt and subsequent vasovagal hypotension has not been assessed in the elderly. Seventeen elderly subjects (10 with carotid sinus syndrome and seven age-matched controls) were studied during 45 minutes of recumbency and 120 minutes of head-up tilt to 40 degrees. Intra-arterial systolic blood pressure and heart rate were monitored continuously and plasma renin activity was measured at frequent intervals. Ten subjects developed vasovagal syncope during tilt (at 32 +/- 18 min). Systolic blood pressure and heart rate fell by 70 +/- 20 mmHg and 20 +/- 7 beats . min-1 (P less than 0.001 and P less than 0.01, respectively). Plasma renin activity did not change in syncopal subjects and remained unchanged up to 60 min after syncope. In seven subjects who completed 120 min of tilt without symptoms, heart rate rose during tilt but plasma renin activity remained unchanged. Plasma renin activity is not influenced by marked hypotension or prolonged head-up tilt in the elderly.     

Baroreflex buffering in sedentary and endurance exercise-trained healthy men

Baroreflex buffering plays an important role in arterial blood pressure control. Previous reports suggest that baroreflex sensitivity may be altered in endurance exercise-trained compared with untrained subjects. It is unknown, however, if in vivo baroreflex buffering is altered in the endurance exercise-trained state in humans. Baroreflex buffering was determined in 36 healthy normotensive men (18 endurance exercise-trained, 41+/-5 [SEM] years; 18 untrained, 41+/-4 years) by measuring the potentiation of the systolic blood pressure responses to a phenylephrine bolus and to incremental phenylephrine infusion during compared with before ganglionic blockade with trimethaphan. The exercise-trained men had a lower resting heart rate and higher maximal oxygen consumption and heart rate variability than the sedentary control subjects (all P=0.01). Mean levels and variability of blood pressure, cardiovagal baroreflex sensitivity (change in heart rate/change in systolic blood pressure), and basal muscle sympathetic nerve activity were not different in the two groups. The systolic blood pressure responses to phenylephrine were not different in the endurance-trained and untrained men before or during ganglionic blockade (P>0.6). Measures of baroreflex buffering with the use of a phenylephrine bolus (3.9+/-0.8 versus 4.0+/-0.7, trained versus untrained, P=0.85) and incremental infusion (2.8+/-0.4 versus 2.5+/-0.6, P=0.67) were similar in the two groups. Baroreflex buffering does not differ in endurance exercise-trained compared with untrained healthy men. These results support the concept that habitual vigorous endurance exercise does not modulate in vivo baroreflex buffering in healthy humans.     

Nocturnal home hemodialysis improves baroreflex effectiveness index of end-stage renal disease patients

BACKGROUND: In patients with end-stage renal disease receiving conventional hemodialysis, both the frequency with which brief rises or falls in systolic blood pressure initiate concordant changes in pulse interval (arterial baroreflex effectiveness index), and the gain of reflex heart rate responses to these stimuli (arterial baroreflex sensitivity) are diminished. In chronic renal failure, low baroreflex effectiveness index and baroreflex sensitivity are associated with increased rates of all-cause mortality and sudden death, respectively. Conversion to home nocturnal hemodialysis augments baroreflex sensitivity but its effects on baroreflex effectiveness index have not been reported. METHODS: In 20 consecutive hypertensive conventional hemodialysis patients training to transition to nocturnal hemodialysis (age 41 +/- 2 years; mean +/- standard error), baroreflex effectiveness index, baroreflex sensitivity (sequence method) and total arterial compliance (stroke volume/pulse pressure) were determined during quiet rest before and 2 months after conversion. RESULTS: With nocturnal hemodialysis, dialysis frequency doubled, the dose per session increased by 70% and antihypertensive medications were withdrawn (from 2.5 +/- 0.3 to 0.2 +/- 0.1 drugs/patient, P < 0.01) because systolic blood pressure fell (from 139 +/- 5 to 119 +/- 4 mmHg, P < 0.05). Baroreflex effectiveness index increased from (0.33 +/- 0.03 to 0.42 +/- 0.03, P = 0.01). Baroreflex sensitivity increased from 5.60 +/- 0.88 to 8.48 +/- 1.60 ms/mmHg (P < 0.05). Changes in total arterial compliance correlated with changes in baroreflex sensitivity (r = 0.63, P = 0.004) but not baroreflex effectiveness index (r = 0.05, P = 0.95), suggesting independent mechanisms for their attenuation and recovery in end-stage renal disease. CONCLUSION: Nocturnal hemodialysis increases baroreflex effectiveness index in addition to baroreflex sensitivity. The hypothesis that such changes might reduce cardiovascular event rates in this high-risk population merits prospective evaluation. More frequent engagement of the arterial baroreflex after conversion to nocturnal hemodialysis may improve short-term cardiovascular regulation.     

Altered sympathetic and vagal modulations of the cardiovascular system in patients with pheochromocytoma: their relations to orthostatic hypotension.

To examine sympathetic and vagal cardiovascular regulatory mechanisms in the pathogenesis of orthostatic hypotension in pheochromocytoma, we continuously monitored blood pressure (Finapres) and RR interval (electrocardiogram) in supine and standing positions in 12 patients with pheochromocytoma, 43 patients with essential hypertension, and 30 normotensive subjects. Mayer wave power spectrum of systolic blood pressure variability (approximately 0.1 Hz) and respiratory power spectrum of the RR interval variability (approximately 0.25 Hz) were taken as measures of sympathetic vascular and cardiac vagal modulations, respectively. Systolic blood pressure decreased more upon standing in pheochromocytoma patients (-21 +/- 7 mm Hg) than in normotensive subjects (-5 +/- 2 mm Hg) or essential hypertensive patients (-3 +/- 2 mm Hg) (P < .005 for both), whereas heart rate tended to increase most in the pheochromocytoma group. Postural reduction in systolic blood pressure was highly correlated with postural increase in heart rate (reciprocal change in RR interval) in the pheochromocytoma group (r = 0.716, P < .01) suggesting that baroreflex is well functioning in those patients. The Mayer wave power spectrum in recumbency was extremely depressed in pheochromocytoma patients (1.1 +/- 0.2 mm Hg2) compared with normotensives (4.5 +/- 0.8 mm Hg2) or essential hypertensives (5.6 +/- 0.6 mm Hg2) (P < .001 for both). This parameter increased significantly with standing in all groups but remained lower in patients with pheochromocytoma (5.1 +/- 1.0 mm Hg2) than in normotensives (7.1 +/- 0.9 mm Hg2, P = NS), whereas essential hypertensive patients demonstrated far greater value (19.2 +/- 3.8, P < .01 for both). The respiratory power spectrum of the RR interval in recumbency of pheochromocytoma patients (189 +/- 54 msec2) was less than in normotensive subjects (714 +/- 100 msec2, P < .001) but did not differ from that in patients with essential hypertension (214 +/- 41 msec2). The respiratory power spectrum of the RR interval upon standing was markedly suppressed in pheochromocytoma patients (36.9 +/- 16.7 msec2) compared with normotensive subjects (129.5 +/- 23.6 msec2) or essential hypertensive patients (126.6 +/- 28.6 msec2) (P < .001 for both). Postural decrement in the respiratory power spectrum of the RR interval correlated positively with postural increase in heart rate (r = 0.577, P < .05) in patients with pheochromocytoma. After successful surgery (n = 9), the Mayer wave power spectrum of the systolic blood pressure and the blood pressure response to orthostasis were normalized. These data suggest that altered sympathetic vascular regulation is central to the pathogenesis of orthostatic hypotension in pheochromocytoma, whereas cardiac vagal regulation acts to compensate.     

Baroreflex sensitivity changes with calcium antagonist therapy in elderly subjects with isolated systolic hypertension

In order to study the effects of calcium-blocking therapy on cardiovascular homeostasis in elderly subjects with isolated systolic hypertension, we performed a randomised double-blind placebo-controlled crossover study of 6 weeks therapy with modified-release nifedipine or placebo. Changes with calcium-blocker treatment in clinic and 24-h blood pressure (BP), heart rate, BP variability, baroreflex sensitivity (BRS) by three methods (Valsalva manoeuvre, phenylephrine and sodium nitroprusside injection), and in baroreflex- and non-baroreflex-mediated reflexes (tilt and cold face stimulus) were studied in 14 elderly subjects (mean age [+/- SEM] 70 +/- 1 years) with sustained isolated systolic hypertension (clinic BP 179 +/- 3/85 +/- 1 mm Hg). Clinic systolic BP, but not diastolic BP, was reduced with treatment (by 14 +/- 6 mm Hg, P = 0.03, diastolic BP 4 +/- 3 mm Hg, P = 0.16). Twenty-four hour BP was also reduced by nifedipine treatment (by 18 +/- 3/9 +/- 2 mm Hg, both P < 0.001). Clinic and 24-h heart rate, and daytime BP variability, were unchanged with treatment. BRS was significantly increased during nifedipine therapy by all three measurement methods (all P < 0.05). With 60 degrees tilt during active treatment, subjects exhibited a greater heart rate increase (P < 0.01), and a reduced fall in systolic (P < 0.05) and diastolic BP (P < 0.05). Thus despite the arteriosclerosis and reductions in large artery compliance described in elderly patients with isolated systolic hypertension, clinically important improvements in clinic and ambulatory BP and some aspects of cardiovascular homeostasis can be achieved with calcium-channel blocking therapy.     

Mechanism of lipid enhancement of alpha1-adrenoceptor pressor sensitivity in hypertension

OBJECTIVE AND DESIGN: Plasma lipids enhance alpha1-adrenoceptor pressor sensitivity, impair baroreflex function, and correlate with increased blood pressure. This clinical study was designed to determine whether the enhanced alpha1-pressor sensitivity induced by acute hyperlipidemia is primarily mediated by increased vascular alpha1 responsiveness, reduced baroreflex sensitivity (BRS) or both. METHOD: Regional alpha1-adrenoceptor vasoreactivity was measured using a graded brachial artery infusion of the alpha1 agonist, phenylephrine, in seven subjects with stage 1 hypertension. Forearm blood flow was estimated from venous occlusion plethysmography. The phenylephrine dose-forearm blood flow response curve was used to determine alpha1-vascular reactivity (slope of the dose-response curve) and sensitivity, EC50 (phenylephrine dose inducing 50% maximal response). BRS (ms/mmHg) was measured as the slope of the progressive rise in systolic blood pressure and the resultant lengthening in the subsequent R-R interval after systemic intravenous boluses of phenylephrine. Subsequently, plasma lipids were raised with a 1-h systemic co-infusion of intralipid and heparin, after which measurements of regional vasoreactivity and BRS were repeated. RESULTS: Mean arterial pressure was 109 +/- 4 versus 110 +/- 3 (P = NS), vasoreactivity was -0.71 +/- 0.10 versus -0.82 +/- 0.10 (P = NS) and log EC50 was 1.47 +/- 0.29 versus 1.52 +/- 0.34 nmol/l (P = NS) before and after raising non-esterified fatty acids, respectively. In contrast, mean BRS was acutely reduced from 8.2 +/- 2.1 to 6.2 +/- 1.8 ms/mmHg (P = 0.02) after the lipid infusion. CONCLUSIONS: These findings suggest that in hypertensive patients, the primary mechanism for short-term alpha1-pressor hypersensitivity in response to hyperlipidemia is via the acute impairment of BRS.     

Influence of gender and family history of hypertension on autonomic control of heart rate, diastolic function and brain natriuretic peptide

OBJECTIVE: To verify in a unitary view whether autonomic control of heart rate and cardiac structure and function are modified early in offspring of hypertensive families. METHODS AND RESULTS: We selected 87 age- and sex-matched young normotensive subjects with (n = 45) and without (n = 42) a family history of hypertension who underwent evaluations of arterial pressure, time-domain parameters of autonomic heart rate control (24-h ECG monitoring), spectral baroreflex sensitivity, left ventricular geometry and function (echo-Doppler) and plasma brain natriuretic peptide levels (BNP). The group with a family history of hypertension significantly differed from their counterparts for systolic pressure (119 +/- 11 versus 114 +/- 9 mmHg, P< 0.05), heart rate (RR interval, 766 +/- 64 versus 810 +/- 93 ms, P< 0.05), heart rate variability [the standard deviation of normal RR intervals (SDNN), 147 +/- 29 versus 171 +/- 33 ms, P < 0.051, diastolic function (isovolumetric relaxation time, 65 +/- 9 versus 60 +/- 8 ms, P< 0.05) and BNP (23 +/- 13 versus 37 +/- 10 pg/ml, P< 0.05). Baroreflex sensitivity values did not differ between the two groups. When gender was considered, all the above-mentioned measures, as well as baroreflex sensitivity, were significantly different between males with and without a family history of hypertension but not between females, except for BNP, which was lower in males and females with a history of hypertension (males, 24 +/- 11 versus 38 +/- 8 pg/ml, P< 0.01; females 21 +/- 14 versus 36 +/- 13 pg/ml, P < 0.05). CONCLUSIONS: Male, but not female, hypertensive offspring have modified diastolic function and autonomic control of heart rate; BNP is the only parameter able to characterize hypertensive offspring independently from the influence of gender. This provides the hypothesis that the impaired production of this hormone could play a primary role in the pre-hypertensive state.     

A polymorphism in the endothelin-A receptor gene is linked to baroreflex sensitivity

BACKGROUND: The baroreflex plays an essential role in regulating the cardiovascular system. However, very few studies have focused on the links between genetic polymorphisms and baroreflex sensitivity (BRS). METHODS: A total of 146 hypertensive individuals who had never been treated, and 105 healthy individuals (controls) were included in the study. The genotypes of 17 polymorphisms of 11 genes involved in the regulation of the cardiovascular system were studied. BRS was measured using a sequence method: BRS was evaluated as the slope of spontaneous increases [systolic blood pressure (SBP)+/reflex response (RR)+] or decreases (SBP-/RR-) in SBP and pulse interval by recording blood pressure (BP) continuously for 20 min. RESULTS: Following univariate analysis, the genetic polymorphism of endothelin receptor A EDNRA/C+1222T was found to be significantly correlated with the BRS (SBP-/RR-) level in both populations. In normotensive subjects, mean BRS values (SBP-/RR-) were 11.93 +/- 3.69 ms/mmHg in EDNRA CC homozygotes, 9.94 +/- 2.97 ms/mmHg in CT heterozygotes and 9.51 +/- 3.16 ms/mmHg in TT homozygotes (P = 0.01). In hypertensive subjects, mean BRS values (SBP-/RR-) were 9.26 +/- 3.59 ms/mmHg in EDNRA CC homozygotes, 9.03 +/- 4.14 ms/mmHg in CT heterozygotes and 6.60 +/- 2.42 ms/mmHg in TT homozygotes (P = 0.01). After adjustment for age, sex, SBP and diastolic blood pressure and body mass index, the EDNRA/C+1222T polymorphism remained significantly correlated with BRS in both normotensive (P = 0.01) and hypertensive (P = 0.01) subjects. CONCLUSIONS: These results suggest that the endothelin system may be involved in the regulation of BRS in humans. In particular, the T allele of the EDNRA/C+1222T polymorphism is associated with a reduction in BRS in both healthy and hypertensive subjects.     

The effect of age and sodium depletion on cardiovascular response to orthostasis

To test the hypothesis that normal age-related limitations in cardiovascular homeostasis may become clinically significant under stress, the cardiovascular response to postural change was assessed in six young and six old healthy subjects before and after modest diuretic-induced sodium depletion. Before diuresis, systolic blood pressure was maintained (from 110 +/- 4 to 113 +/- 6 mm Hg) while heart rate increased 22% (from 67 +/- 2 to 82 +/- 5 beats/min) at 3 minutes after 60-degree upright tilt in young subjects. After a significant diuretic-induced weight reduction and natriuresis, the young again maintained systolic blood pressure (from 110 +/- 4 to 110 +/- 6 mm Hg) and increased heart rate 49% (from 68 +/- 2 to 101 +/- 5 beats/min; p less than 0.05, compared with prediuresis values) in response to the same postural stimulus. During the prediuresis tilt, the older subjects showed no change in systolic blood pressure (from 132 +/- 4 to 134 +/- 6 mm Hg) and a 9% increase in heart rate (from 68 +/- 3 to 74 +/- 2 beats/min). After a similar significant weight reduction and sodium loss, the older subjects showed a significant reduction in systolic blood pressure (from 132 +/- 6 to 108 +/- 6 mm Hg; p less than 0.05) and a 17% increase in heart rate (from 69 +/- 4 to 81 +/- 3 beats/min; p less than 0.05) during tilt compared with values in young subjects. Three of six elderly subjects noted postural symptoms. These results suggest that, although the healthy old may appear well compensated under optimal conditions, decreased cardiovascular reserve renders them susceptible to postural change following mild sodium depletion.     

Sustained effect of continuous positive airway pressure on baroreflex sensitivity in congestive heart failure patients with obstructive sleep apnea

BACKGROUND: Patients with either heart failure or obstructive sleep apnea have a reduced baroreflex sensitivity for heart rate, a sign of poor prognosis. We previously demonstrated that nocturnal application of continuous positive airway pressure to heart failure patients with obstructive sleep apnea increased baroreflex sensitivity acutely, but it is not known whether these effects persist into wakefulness. OBJECTIVE: To determine whether treating obstructive sleep apnea in heart failure patients with continuous positive airway pressure improves baroreflex sensitivity during wakefulness. METHODS: Spontaneous baroreflex sensitivity was assessed during wakefulness in 33 heart failure patients (left ventricular ejection fraction < or = 45%) with obstructive sleep apnea (apnea-hypopnea index > or = 20). Subsequently, baroreflex sensitivity was reassessed 1 month after patients were randomly allocated to nocturnal continuous positive airway pressure treatment or no treatment (control). RESULTS: Compared with the 14 control patients, the 19 continuous positive airway pressure-treated patients experienced a greater increase in baroreflex sensitivity [median, (25%, 75%)] [from 5.4 (2.2, 8.3) to 7.9 (4.4, 9.4) ms/mmHg; P = 0.01] and left ventricular ejection fraction (P < 0.001). In addition, daytime systolic blood pressure and heart rate decreased more in the continuous positive airway pressure group (from 122 +/- 15 to 113 +/- 12 mmHg; P = 0.02, and from 66 +/- 8 to 62 +/- 8 bpm; P < 0.001, respectively) than in the control group. CONCLUSION: Treatment of coexisting obstructive sleep apnea by continuous positive airway pressure in heart failure patients improves baroreflex sensitivity during wakefulness in addition to improving left ventricular ejection fraction and lowering blood pressure and heart rate. These data indicate that the improved autonomic regulation of heart rate in heart failure patients treated for obstructive sleep apnea during sleep persists into wakefulness.     

Decreased exercise capacity in mild essential hypertension: non-invasive indicators of limiting factors.

Available data suggest that exercise capacity is limited in hypertension. The mechanism of this reduced maximal exercise capacity has not been fully elucidated. In this study 22 patients with mild essential hypertension (162 +/- 22 mmHg systolic and 95 +/- 8 mmHg diastolic) and 36 normotensive control subjects (128 +/- 13 mmHg systolic and 80 +/- 7 mmHg diastolic) (P less than 0.01) performed an ergometer test till exhaustion. Body mass index in the two groups did not differ. The maximal oxygen consumption VO2 was lower in the hypertensive group (18 +/- 7 versus 23 +/- 8 ml/kg/min; P less than 0.02) as was the maximal workload (141 +/- 52 vs. 185 +/- 70 Watt; P less than 0.01). Rate pressure product rose only 2.7 fold in hypertensive patients versus 3.5 fold in the control group (P less than 0.001). In hypertensive patients maximal workload decreased with increasing resting systolic blood pressure (P less than 0.05) while in the normotensive subjects maximal workload rose with increasing resting systolic blood pressure (P less than 0.05). In conclusion both high and low blood pressure was associated with a decreased maximal voluntary exercise capacity. Even mild hypertension was accompanied by lower maximal exercise capacity. Hypertensive patients also had a lower maximal VO2 and lower maximal rate pressure product than did normotensive subjects.     

Slow breathing improves arterial baroreflex sensitivity and decreases blood pressure in essential hypertension

Sympathetic hyperactivity and parasympathetic withdrawal may cause and sustain hypertension. This autonomic imbalance is in turn related to a reduced or reset arterial baroreflex sensitivity and chemoreflex-induced hyperventilation. Slow breathing at 6 breaths/min increases baroreflex sensitivity and reduces sympathetic activity and chemoreflex activation, suggesting a potentially beneficial effect in hypertension. We tested whether slow breathing was capable of modifying blood pressure in hypertensive and control subjects and improving baroreflex sensitivity. Continuous noninvasive blood pressure, RR interval, respiration, and end-tidal CO2 (CO2-et) were monitored in 20 subjects with essential hypertension (56.4+/-1.9 years) and in 26 controls (52.3+/-1.4 years) in sitting position during spontaneous breathing and controlled breathing at slower (6/min) and faster (15/min) breathing rate. Baroreflex sensitivity was measured by autoregressive spectral analysis and "alpha angle" method. Slow breathing decreased systolic and diastolic pressures in hypertensive subjects (from 149.7+/-3.7 to 141.1+/-4 mm Hg, P<0.05; and from 82.7+/-3 to 77.8+/-3.7 mm Hg, P<0.01, respectively). Controlled breathing (15/min) decreased systolic (to 142.8+/-3.9 mm Hg; P<0.05) but not diastolic blood pressure and decreased RR interval (P<0.05) without altering the baroreflex. Similar findings were seen in controls for RR interval. Slow breathing increased baroreflex sensitivity in hypertensives (from 5.8+/-0.7 to 10.3+/-2.0 ms/mm Hg; P<0.01) and controls (from 10.9+/-1.0 to 16.0+/-1.5 ms/mm Hg; P<0.001) without inducing hyperventilation. During spontaneous breathing, hypertensive subjects showed lower CO2 and faster breathing rate, suggesting hyperventilation and reduced baroreflex sensitivity (P<0.001 versus controls). Slow breathing reduces blood pressure and enhances baroreflex sensitivity in hypertensive patients. These effects appear potentially beneficial in the management of hypertension.     

Diurnal variation of hemodynamic indices in non-dipper hypertensive patients.

The purpose of this study was to elucidate the underlying mechanisms of blunted nocturnal blood pressure reduction in non-dipper hypertensive patients. We studied the diurnal variations in systemic hemodynamic indices and baroreflex sensitivity. In 45 subjects with essential hypertension (24 men; mean age, 49+/-1 years), intra-arterial pressure was monitored telemetrically. Non-dippers were defined as those with a nocturnal reduction of systolic blood pressure of less than 10% of daytime systolic blood pressure. Stroke volume was determined using Wesseling's pulse contour method, calibrated with indocyanine green dilution. Baroreflex sensitivity was calculated as deltapulse interval/deltasystolic blood pressure on spontaneous variations. The mean values of the hemodynamic parameters were calculated every 30 min. Twenty-six subjects were classified as non-dippers. Daytime blood pressure was not significantly different between dippers (149+/-4/87+/-3 mmHg) and non-dippers (147+/-3/82+/-2 mmHg), while the nighttime blood pressure was significantly reduced in dippers (131+/-3/77+/-2 mmHg) but not in non-dippers (145+/-3/80+/-2 mmHg). Nocturnal decreases in both cardiac index and stroke index were smaller in non-dippers (-12.0+/-1.2% and 1.5+/-1.0%) than in dippers (-17.5+/-1.4% and -2.2+/-1.1%). Baroreflex sensitivity significantly increased at nighttime both in dippers (6.5+/-0.6 to 8.0+/-0.7 ms/mmHg) and in non-dippers (5.1+/-0.3 to 6.4+/-0.4 ms/mmHg). Neither daytime nor nighttime baroreflex sensitivity was significantly different between the groups. We conclude that the hemodynamics of non-dipper essential hypertension are characterized by an inadequate nocturnal decrease in cardiac index and stroke index, suggestive of relative volume expansion or malsuppressed sympathetic activity.     

Sleep disturbance during ambulatory blood pressure monitoring of hypertensive patients

BACKGROUND: Hypertensive patients who fail to exhibit a normal fall in blood pressure at night may have a greater risk of target-organ damage. Sleep, with associated cessation of physical activity, is the principal determinant of nocturnal blood pressure 'dip'. OBJECTIVE: To ascertain whether hypertensive patients, who experience the discomfort of higher cuff-inflation pressures during ambulatory blood pressure monitoring, experience more interference with sleep, manifested by greater nocturnal physical activity. DESIGN: A retrospective case- control study. METHODS: Subjects were selected from a database of 475 patients who had undergone simultaneous 24 h ambulatory blood pressure monitoring and monitoring of physical activity with a wrist-mounted piezoelectric accelerometer. Sixty-one hypertensives (average daytime systolic blood pressure >/= 150 mmHg) were age matched to 61 subjects with average daytime systolic blood pressures 相似文献   

Light-headedness and defective cardiovascular reflexes after neck radiotherapy

METHODS: We investigated the possibility of carotid baroreflex dysfunction as the cause of cerebral insufficiency in head and neck cancer patients treated with neck radiotherapy. Three patients cured with radiation therapy were evaluated for light-headedness and syncope. Orthostatic blood pressure, heart rate responses to esmolol and atropine, and baroreceptor sensitivity to amyl nitrite and phenylephrine were measured. The results were compared with measurements in six normal control subjects. RESULTS: All three patients had intact sympathetic and parasympathetic cardiac innervation. Nevertheless, their heart rate responses to amyl-nitrite-induced hypotension and phenylephrine hypertension were only one-third normal (P = 0.013), indicating poor baroreceptor function. Upon standing, diastolic pressure of control participants increased but that of the three patients decreased by 3 mmHg. After inhalation of amyl nitrite their systolic and diastolic blood pressures decreased by 70+/-9 and 28+/-2 mmHg, much more than the control participants' decrease of 33+/-5 and 17+/-3 mmHg (P = 0.006, P = 0.02). CONCLUSION: The baroreflex is the most important mechanism for short-term blood pressure homeostasis. Patients with transient light-headedness or syncope after radiotherapy to the neck may have baroreceptor damage. This defect is unlikely to be apparent on routine cardiovascular testing. However, testing with a rapidly acting hypotensive stimulus can reveal gross deficits in the regulation of heart rate and blood pressure.     

Comparison between office and ambulatory blood pressure in young and elderly subjects with isolated systolic hypertension

BACKGROUND: It has been claimed that isolated systolic hypertension (ISH) in the elderly is not a sustained condition but a short-lasting increase in office systolic blood pressure magnified by arterial stiffness. DESIGN: Office and ambulatory blood pressures werecompared at baseline and after 3 months of observation of young and elderly subjects with ISH. METHODS: The study was carried out in 39 young (mean age 27.1+/-9.8 years) and 37 elderly patients (mean age 72.5+/-5.7 years). Office blood pressure was defined as the mean of six readings. All subjects underwent two non-invasive 24 h blood pressure monitorings performed 3 months apart and echocardiography (n = 50). RESULTS: The difference between office and mean 24 h systolic/diastolic blood pressure was 27.9/8.2 mmHg in the young and 18.9/6.9 mmHg in the elderly patients (P < 0.01 for systolic blood pressure). Twenty-four-hour (P < 0.001), daytime (P = 0.001) and night-time (P < 0.001) systolic blood pressures were higher in the elderly and the difference between daytime and night-time systolic blood pressure was greater in the young (P < 0.05). Office and ambulatory heart rates were significantly higher in the young subjects. The elderly patients showed a greater left ventricular wall thickness ( P = 0.005 for posterior wall; P < 0.005 for septum), relative wall thickness (P = 0.01) and left ventricular mass index (P = 0.001) and impaired left ventricular filling rate ( P = 0.05), whereas systolic performance and stroke volume were no different in the two groups. Due to the higher heart rate, cardiac output was greater in the young (P = 0.03). CONCLUSION: These data show that larger differences between office and ambulatory systolic blood pressure are not unique to elderly patients with ISH. Increased ambulatory blood pressure levels and a decreased nocturnal blood pressure fall were associated with left ventricular structural and functional abnormalities in the elderly subjects.     

Effect of systolic blood pressure and carotid stiffness on baroreflex gain in elderly subjects

BACKGROUND: Aging is associated with diminished baroreflex sensitivity (gain), which predisposes elderly people to orthostatic hypotension, syncope, and cardiovascular morbidity. Aging is also associated with systolic blood pressure (SBP) elevation and carotid artery stiffness, which may both affect baroreflex gain. METHODS: We examined the relation between SBP, carotid artery stiffness, and baroreflex gain in 34 healthy elderly (71 +/- 4 years) and 10 healthy young (31 +/- 3 years) subjects. SBP (Finapres) and carotid artery stiffness (ultrasound measures of relative carotid artery diameter changes during each blood pressure pulse) were measured. The gain of the transfer function relating the R-R interval to SBP fluctuations at a frequency of 0.05-0.15 Hz was used to assess cardiovagal baroreflex gain. RESULTS: Elderly subjects had higher carotid artery stiffness (14.2 +/- 5.1 vs 6.6 +/- 1.8, p <.05), higher SBP (146 +/- 24 vs 125 +/- 8 mmHg, p =.012), and lower baroreflex gain (8.2 +/- 6.4 vs 16.3 +/- 7.4, p <.05) than young subjects. Among all subjects, SBP and carotid artery stiffness both correlated with baroreflex gain (r = -.39, p =.02 for both). Although SBP was related to stiffness across all subjects, this relation was not present among the elderly subjects. Within the elderly group, only SBP was independently related to baroreflex gain (R(2) =.51, p =.009). CONCLUSIONS: SBP elevation in elderly people may affect the neural or cardiac response to blood pressure fluctuations, independent of the mechanical properties of barosensory regions in the carotid artery. Future studies should examine the effect of pharmacologic treatment of hypertension on baroreflex gain in elderly people.