Advances in the treatment of hypertension.
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Adult↗
Biomedical subjects
T G Pickering
Publications and source records attributed to T G Pickering.
Home blood pressure teletransmission for better diagnosis and treatment.
The rate of control of high blood pressure is disappointing, and noncompliance is one factor that contributes to this. The reasons for poor compliance are complex and include factors related to the patient, the healthcare provider, and the medical system. In general, the lack of regular communication between the patient and the physician, as occurs in the traditional model of clinic-based care, predicts a low rate of blood pressure control. In addition, clinic-based blood pressure rates are notoriously unreliable. A solution to this dilemma is teletransmission of self- measured blood pressure readings, which offers the dual advantages of more reliable measurements, and the establishment of regular telephone communication between the patient and the healthcare provider. Preliminary evidence with this type of system suggests that blood pressure control can be improved substantially.
Antihypertensive Agents↗
Prevention of recurrent pulmonary edema in patients with bilateral renovascular disease through renal artery stent placement.
Pulmonary edema and congestive heart failure (both referred to here as PE) have been reported to be complications of bilateral renal artery stenosis or unilateral stenosis in a solitary functioning kidney (both referred to as BRAS). The goals of this study were to determine whether a history of PE was more common in patients with BRAS than in those with unilateral stenosis and a normal contralateral kidney (URAS), and whether recurrent PE could be prevented by renal artery stent placement. We evaluated 90 consecutive patients with renovascular disease who were treated with percutaneous renal artery stent placement. History and clinical follow-up were obtained through chart review and phone contact with referring physicians. Mean follow-up was 18.4 months after stent placement. Twenty-three of 56 (41%) subjects with BRAS had a history of PE before revascularization, compared with four of 34 (12%) subjects with URAS (P = .05). Twenty-five of the 27 patients with history of PE had adequate clinical follow-up. Seventeen of the 22 (77%) subjects with BRAS and history of PE had no further PE after stent placement in one or both renal arteries. The five BRAS subjects with recurrent PE after stent placement had evidence of stent thrombosis or restenosis. In contrast, only one of three (33%) URAS subjects with a history of PE remained free of PE after stent placement. We conclude that PE is a common complication of BRAS, but not of URAS. In patients with BRAS, recurrent PE can be prevented by successful stent placement in one or both renal arteries.
Aged↗
Beta-adrenergic receptor blockade as a therapeutic approach for suppressing the renin-angiotensin-aldosterone system in normotensive and hypertensive subjects.
Although beta-adrenergic-blocking drugs suppress the renin system (RAAS), plasma angiotensin II (Ang II) responses during beta-blockade have not been defined. This study quantifies the effects of beta-blockade on the RAAS and examines its impact on prorenin processing by measuring changes in the ratio of plasma renin activity (PRA) to total renin. In normotensive (N = 14) and hypertensive (N = 16) subjects, blood pressure (BP), heart rate, PRA, plasma prorenin, plasma total renin (prorenin + PRA), ratio of PRA to total renin (%PRA), plasma Ang II, and urinary aldosterone were measured before and after 1 week of beta-blockade. Plasma renin activity, Ang II, and urinary aldosterone levels were similar for normotensive and hypertensive subjects. Plasma renin activity correlated with Ang II. Total renin, which is proportional to (pro)renin gene expression, was lower in hypertensive subjects and was inversely related to BP. Beta-blockade decreased BP and heart rate in both groups, with medium- and high-renin hypertensive subjects responding more frequently than those with low renin. Beta-blockade consistently suppressed PRA, Ang II, and aldosterone. Total renin was unchanged, thus, %PRA fell. These results indicate that beta-blockers suppress plasma angiotensin II levels, in parallel with the marked reductions in PRA and urinary aldosterone levels in normotensive and hypertensive subjects. The suppression of Ang II levels was comparable to that produced during angiotensin converting enzyme (ACE) inhibition. However, by reducing prorenin processing to renin, beta-blockers do not stimulate renin secretion, unlike ACE inhibitors and Ang II receptor antagonists. This unique action of beta-blockers has important implications for the treatment of cardiovascular disease.
Adrenergic beta-Antagonists↗
Differential effects of morning and evening dosing of nisoldipine ER on circadian blood pressure and heart rate.
The time of administration of once-daily antihypertensive agents may have a significant impact on blood pressure control during awake and sleep periods. Using 24-h ambulatory monitoring, we compared the effects of morning and evening dosing of the long-acting dihydropyridine calcium channel blocker, nisoldipine extended-release (ER), on circadian blood pressure (BP) and heart rate in patients with mild-to-moderate hypertension. After completing a 3-week placebo run-in period, 85 patients were randomized to morning versus evening nisoldipine ER treatment at a fixed 20-mg dose. Patients were treated for 4 weeks, followed by crossover to the alternate dosing regimen for 4 additional weeks. Twenty-four-hour ambulatory monitoring was performed at baseline and at 4 and 8 weeks after randomization. Awake and sleep times were determined by electronic activity recorders (Actigraphy). Similar least-squares (+/-SE) mean changes from baseline in 24-h BP (systolic BP/diastolic BP: -11.9/-7.4 +/- 0.6/0.5 v -11.6/-6.5 +/- 0.6/0.5 mm Hg) and heart rate (1.0/1.7 +/- 0.4/0.4 beats/min) occurred with morning and evening administration, respectively. A significantly greater effect on awake diastolic BP (systolic BP/diastolic BP: -12.6/-8.1 +/- 0.7/0.4 v -11.3/-6.4 +/- 0.7/0.4 mm Hg; P = .16/.01) was observed with morning dosing compared with evening dosing. In addition, small increases in sleep and early morning heart rate were seen with evening compared with morning administration of nisoldipine (sleep, 3.1 +/- 0.4 v 0.4 +/- 0.4 beats/min; P < .001; early morning, 3.5 +/- 0.7 v 0.5 +/- 0.7 beats/min; P = .002). These differential effects on awake BP and sleep heart rate were also observed in patients who had normal (dippers) and elevated (nondippers) BP values during sleep. Appropriate evaluation of the efficacy and safety of long-acting antihypertensive agents is essential when evening administration is being considered. In the present study, the timing of nisoldipine ER administration had no effect on mean changes in BP and heart rate over a 24-h period. However, nisoldipine ER had some differential effects during sleep and awake periods with morning relative to evening dosing.
Antihypertensive Agents↗
Comments on the study of Zakopoulos et al.
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Blood Pressure↗
Effect of body weight changes on changes in ambulatory and standardized non-physician blood pressures over three years.
PURPOSE: This study examines the relationship of changes in body mass index (BMI) to changes in measures of both casual and ambulatory blood pressures over three years. METHODS: In this prospective study of men aged 30-60 years, a cohort of 198 participants was followed for three years. Height, weight, demographic characteristics, and casual and ambulatory measures of blood pressure (BP) were obtained at baseline and 3-year follow-up. RESULTS: Change in BMI was significantly associated with change in all ambulatory (awake, work, home, and sleep) and casual systolic and diastolic blood pressures. After controlling for age and race/ethnicity, the association remained significant for nine of the twelve BP change measures. Further tests show that the effect of a change in BMI on BP change does not vary across the six systolic blood pressures or across the six diastolic measures. An average-height man gaining 5 kg (11 pounds) typically exhibited a 2.5 mm Hg increase in systolic and a 1.8 mm Hg increase in diastolic casual and ambulatory BPs. There is no evidence that changes in BP were associated with age, race/ethnicity (blacks vs. Hispanics vs. whites), or the average of the baseline and follow-up levels of BMI. In addition, the impact of weight gain is similar in magnitude, but in the opposite direction, to that of weight loss. CONCLUSIONS: Changes in BMI over three years predict changes in ambulatory and standardized non-physician BPs. These changes in BP are not related to average BMI level or age.
Adult↗
Impact of arterial elastance as a measure of vascular load on left ventricular geometry in hypertension.
OBJECTIVE: Effective arterial elastance (Ea), integrating the pulsatile component of left ventricular (LV) afterload, is an estimate of aortic input impedance. We evaluated relationships of Ea with left ventricular anatomy and function in essential hypertension. DESIGN: A cross-sectional analysis in 81 normotensive and 174 untreated hypertensive individuals enrolled in a referral hypertension centre. METHODS: Using echocardiography we determined left ventricular mass index (LVMI), relative wall thickness (RWT), stroke volume (SV), endocardial (FSe) and midwall (FSm) fractional shortening and total peripheral resistance (TPR). Carotid pressure waveforms were obtained by arterial tonometry, and end-systolic pressure (Pes) was measured at the dicrotic notch. Ea index (EaI) was calculated as Pes/(SV index); LV elastance (Ees) was estimated as Pes/LV end-systolic volume, and ventriculo-arterial coupling was evaluated by the Ea/Ees ratio. RESULTS: EaI was higher in hypertensives than in normotensives (3.02 +/- 0.63 versus 2.40 +/- 0.52 mmHg/l per m2; P< 0.0001). Using the 95% upper confidence limit in normotensives, hypertensives were divided in two groups with normal or elevated EaI. The 38 hypertensives with elevated EaI had higher RWT (0.41 +/- 0.06 versus 0.37 +/- 0.05), lower LVMI (87.5 +/- 18.5 versus 96.8 +/- 19.3 g/m2), higher TPR (2247 +/- 408 versus 1658 +/- 371 dynes/cm s(-5)) and lower FSe and FSm (35 +/- 5 versus 39 +/- 5 and 16 +/- 2 versus 18 +/- 2%; all P< 0.05) than patients with normal EaI. Ea/Ees ratio was increased and cardiac output was reduced in hypertensives with elevated EaI. CONCLUSIONS: High values of EaI identify a minority of hypertensive patients characterized by elevated TPR, left ventricular concentric remodelling, depressed left ventricular systolic function and impaired ventriculo-arterial coupling.
Adult↗
Blood Pressure Monitoring. Task force V: White-coat hypertension.
TERMINOLOGY: Two terms are in current use to describe patients whose blood pressures are high only in a medical setting (white-coat hypertension and isolated office or clinic hypertension). The term white-coat effect is also commonly used to describe the pressor response to the clinic setting. DEFINITIONS: White-coat hypertension is generally defined as a persistently elevated clinic blood pressure in combination with a normal ambulatory blood pressure (ABP). There is disagreement regarding the optimal cutoff point for ABP. The white-coat effect is operationally defined as the difference between the clinic blood pressure and daytime ABP. PREVALENCE OF WHITE-COAT HYPERTENSION: This varies according to the definition of white-coat hypertension and the population studied, but is approximately 20% among mild hypertensives, and increases with age. METABOLIC AND BIOCHEMICAL ASPECTS: Authors of some studies have suggested that white-coat hypertension is associated with metabolic abnormalities such as hyperlipidemia that lead to an increase in cardiovascular risk, but most have not found this. TARGET-ORGAN DAMAGE: Several measures of target-organ damage have been compared among normotensives, white-coat hypertensives, and sustained hypertensives; these include left ventricular mass, microalbuminuria, and carotid atherosclerosis. In general, target-organ damage in white-coat hypertension is less than that in sustained hypertension, but in some studies it has been found to be more prevalent than in normotensives. MORBIDITY AND MORTALITY: Authors of a relatively small number of prospective studies have concluded that white-coat hypertensives have a lower risk of morbidity than do sustained hypertensives, but a larger number have drawn the more general conclusion that, when there is a discrepancy between the clinic blood pressure and ABP, the prognosis is more closely related to the ABP. MANAGEMENT: When white-coat hypertensives are prescribed antihypertensive medication there is usually a decrease in clinic blood pressure, but little or no change in ABP. Thus drug treatment is not necessarily indicated. Another issue is the follow-up of white-coat hypertensives; there is general agreement that blood pressure outside the office should be monitored indefinitely. Some patient may have been wrongly classified as white-coat hypertensives, and others may progress to develop sustained hypertension.
Antihypertensive Agents↗
The effect of job strain on ambulatory blood pressure in men: does it vary by socioeconomic status?
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Adult↗
Assessment of arterial compliance by carotid midwall strain-stress relation in normotensive adults.
Examining left ventricular midwall as opposed to endocardial mechanics enhances understanding of left ventricular function in individuals with abnormal cardiac geometry. Accordingly, we used carotid ultrasound and applanation tonometry of arterial pressure to derive carotid midwall strain and its relation to carotid peak-systolic and end-diastolic stresses in 82 apparently normal, employed subjects (56 men, 26 women; median age, 47 years; 70% white; 21% overweight) with no evidence of coronary or valvular heart disease. Regression equations relating carotid luminal and midwall strain to the increment in carotid stress during systole (Deltacarotid stress) were used to predict strain for the observed Deltastress. Observed/predicted carotid luminal or midwall strain was calculated as a measure of carotid luminal or midwall strain for imposed stress, termed stress-corrected strain. Midwall carotid strain was similar in women and men but was negatively related to older age (r=-0.35, P=0.001) and higher body mass index (r=-0.31, P=0.005) and brachial and carotid blood pressure (r=-0.30 to -0.45, all P<0.01). The pulsatile change in arterial load, measured by Deltacarotid stress, was positively related to midwall strain (r=0. 44, P<0.001) more closely than was carotid luminal strain. Regression analyses revealed that carotid midwall strain was positively related to Deltastress, with additional negative relations to age and carotid diastolic diameter (all P<0.001). Stress-corrected carotid midwall strain was strongly and negatively correlated with midwall elastic modulus and Young's modulus (both r=-0.77, P<0.001), followed by elastic modulus (r=-0.74, P<0.001), midwall Young's modulus (r=-0.73, P<0.001), midwall stiffness index (r=-0.70, P<0.001), and stiffness index (r=-0.66, P<0.001). Thus, in normal adults, carotid midwall strain is unrelated to gender, is positively related to pulsatile carotid load as measured by Deltacarotid stress, and is negatively related to age, overweight, and standard measures of arterial stiffness.
Age Factors↗
Assessment of arterial compliance by carotid midwall strain-stress relation in hypertension.
To elucidate the relations between arterial hypertrophy and compliance in hypertension, we studied 205 unmedicated hypertensive patients (129 men and 76 women) and 82 normotensive adults (56 men and 26 women) from an employed population by carotid ultrasound, noninvasive applanation tonometry, and echocardiography. Carotid midwall strain and circumferential stress were calculated at end diastole and peak systole. The relations of luminal and midwall strain to the increment in circumferential stress from end diastole to peak systole (Deltacarotid stress in normal subjects) were used to calculate ratios of observed/predicted carotid luminal and midwall strain. Mean stress-corrected luminal strain (82+/-26%) and midwall strain (78+/-23%) were lower (both P<0.001) in hypertensive patients than in normal adults. Stress-corrected luminal strain identified 14% of hypertensive patients with low arterial compliance, while stress-corrected midwall strain was low in 18% of patients. Patients with subnormal carotid midwall strain were older (61+/-12 versus 54+/-12 years, P<0.01) and had larger carotid diameters (6. 6+/-0.8 versus 5.7+/-0.8 mm, P=0.002) and higher brachial pulse pressures (71+/-25 versus 63+/-17 mm Hg, P<0.05) than other patients. Patients with arterial hypertrophy had lower stress-corrected midwall strain than those without hypertrophy (70+/-24% versus 79+/-23%, P=0.05), whereas no difference was observed in stress-corrected luminal strain (P=0.40). Stress-corrected midwall strain tended to be lower in patients with discrete atherosclerotic plaques than in those without (74+/-20% versus 79+/-24%, P=0.15). Compared with patients with normal left ventricular geometry, those with concentric hypertrophy had larger carotid diameters (6.6+/-0.7 versus 5.8+/-0.9 mm, P<0.05) and lower stress-corrected luminal strain (62+/-11% versus 85+/-25%, P<0.05) and midwall strain (59+/-10% versus 81+/-22%, P<0.05). Therefore, stress-corrected midwall strain identifies patients with reduced arterial compliance, increased arterial wall thickness, and abnormal left ventricular geometry better than conventional measures based on arterial lumen diameters.
Blood Pressure↗
Ambulatory physical activity as a determinant of diurnal blood pressure variation.
There are reports that indicate that diurnal blood pressure (BP) variation, in addition to high BP per se, is related to target organ damage and the incidence of cardiovascular events. However, the determinants of diurnal BP variation are not adequately understood. We used actigraphy and ambulatory BP monitoring to study the diurnal variation of BP and physical activity in 160 adults. Within individuals, activity was more strongly related to pulse rate than to BP. The correlation between BP and activity was stronger during sleep than when awake, but the correlation between activity and pulse rate was higher during the awake period than during sleep. Between individuals, the sleep/awake ratio of systolic BP (SBP) was correlated with mean sleep activity (r=.17, P<0.05), mean awake activity (r=-0.16, P<0.05), and, especially, the ratio of sleep/awake activity (r=.24, P<0.01). Awake BP variability (SD of awake SBP) was positively correlated with awake activity (r=.16, P<0. 05). In regard to the effect of position, the standing-supine SBP difference was negatively correlated with the sleep/awake SBP ratio (r=-0.39, P<0.01) and positively correlated with awake SBP variability (r=.33, P<0.01). When we divided the subjects into 3 groups, 19 extreme dippers (with a sleep SBP decrease of >/=20% of awake SBP), 102 dippers (with decreases of >/=10% to <20%), and 39 nondippers (with decreases of <10%), no significant differences existed in awake activity among the groups. However, the nondippers exhibited greater sleep activity than extreme dippers (P<0.05) and an increased sleep/awake activity ratio compared with extreme dippers and dippers (P<0.01). Extreme dipping may also be associated with increased BP variability (P=0.08). Individual SBP responses to activity (the within-person slope of awake SBP regressed on activity) did not differ significantly among the 3 subgroups. In conclusion, physical activity is one of the determinants of ambulatory BP and its diurnal variation. We hypothesize that the association of sleep activity to sleep BP and dipping reflects differences in sleep quality.
Adult↗
Ambulatory blood pressure and metabolic abnormalities in hypertensive subjects with inappropriately high left ventricular mass.
Appropriateness of left ventricular (LV) mass to cardiac workload can be evaluated by the ratio of observed LV mass to the value predicted for an individual's gender, height(2.7), and stroke work at rest (%PLVM). It is unclear which pathophysiological factors are associated with inappropriately high LV mass in hypertensive subjects. Adequate LV mass was defined by the 90% confidence interval (73% to 128%) of the distribution of %PLVM in 393 normal-weight normotensive subjects. In 185 hypertensive subjects (aged 56+/-11 years; 60% male, 29% black), according to %PLVM, 164 (88%) had adequate LV mass, 16 (9%) had inappropriately high LV mass (%PLVM >128%), and 5 (3%) had %PLVM <73% (low LV mass). Age, gender, smoking habit, proportion of never-treated subjects, total cholesterol, triglycerides, and creatinine levels did not differ significantly between subjects with adequate and inappropriately high LV mass. Body mass index, fasting glucose, and proportion of black subjects were higher (all P<0.05), while HDL cholesterol was lower (P<0.05) in subjects with inappropriately high LV mass. Blood pressure at the echocardiogram was comparable between subjects with adequate and inappropriately high LV mass, but the latter group had higher ambulatory blood pressure (P<0.01). Subjects with inappropriately high LV mass also had higher aortic root dimension and LV relative wall thickness and relatively lower LV systolic performance than those with adequate LV mass (all P<0.001). Larger aortic root diameter and lower systolic function were also found in hypertensive subjects with inappropriate LV hypertrophy compared with those with adequate LV hypertrophy. In an exploratory case-control study that compared subjects with low %PLVM with age-matched counterparts with adequate LV mass, low %PLVM was associated with lower body mass index, more favorable metabolic profile, and higher LV myocardial contractility. Higher body mass index, larger aortic root, and black race were independent correlates of increased %PLVM. Thus, in arterial hypertension, levels of LV mass inappropriately high for gender, cardiac workload, and height(2.7) are associated with higher body mass index, higher ambulatory blood pressure, larger aortic root diameters, and relatively low myocardial contractility.
Adult↗
Is nocturnal blood pressure dipping reproducible?
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Adult↗
Blood Pressure Monitoring. Task force I: Methodological aspects.
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Activities of Daily Living↗
What is the 'normal' 24 h, awake, and asleep blood pressure?
The clinical use of ambulatory blood pressure monitoring requires that a 'normal' limit be identified. However, because the relationship between blood pressure and risk is continuous, any such limit is arbitrary. Various different methods have been used to define a normal limit, and can be divided into those that rely solely on blood pressure measurement, and those that relate blood pressure to target-organ damage or risk. First, several population studies of 'normotensive' people have identified the 95th centile of ambulatory blood pressure, with generally consistent findings, but with the methodological flaw that 'hypertensive' individuals must first be excluded. Second, the ambulatory blood pressure that corresponds to a threshold value of clinic blood pressure (e.g. 140/90 mmHg) can be identified from the regression equation linking the two measures of blood pressure. Third, the percentage of readings greater than a threshold value (the 'blood pressure load') can be specified; this method is arbitrary, and makes the unwarranted assumption that there is a threshold value above which blood pressure causes harm. Fourth, the ambulatory blood pressure above which the prevalence of target-organ damage begins to increase significantly can be identified. Fifth, the relationship between ambulatory blood pressure and cardiovascular risk can be examined in prospective studies. Despite these very different approaches, with a few notable exceptions there is reasonable agreement between the methods, the consensus being that, for daytime ambulatory blood pressure, the normal value is about 135/85 mmHg.
Blood Pressure↗
White coat hypertension: time for action.
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Blood Pressure Determination↗