Nocturnal Blood Pressure Drop Research Articles

Left ventricular hypertrophy and preclinical impaired glucose tolerance and diabetes mellitus contribute to abnormal left ventricular diastolic function in hypertensive patients

Impaired left ventricular diastolic function is not uncommon in patients with either diabetes mellitus or hypertension. This study was carried out to assess the contribution of left ventricular hypertrophy, high blood pressure, preclinical impaired glucose tolerance and diabetes mellitus to left ventricular diastolic function in patients attending a hypertension clinic. Echocardiography, 24-h ambulatory blood pressure monitoring and oral glucose tolerance tests were carried out in 152 consecutive hypertensive patients who had no evidence of ischaemic heart disease and were not known to be diabetic. From echocardiography, E/A (peak velocity of early/atrial filling waves of the transmitral flow) at rest and at peak standardized isometric exercise using handgrip, left ventricular mass index and deceleration time of the E wave were derived. Patients with impaired glucose tolerance and diabetes mellitus had lower E/A than the euglycaemic subjects both at rest (P=0.0073) and during isometric exercise (P<0.0001). E/A significantly reduced during isometric exercise in patients with impaired glucose tolerance and diabetes but not in euglycaemic patients. Deceleration time was shortened with a worsening degree of glucose intolerance in all the patients (P=0.0005), in those with left ventricular hypertrophy (P=0.0006) and in those without left ventricular hypertrophy (P=0.033). When adjusted for age, gender, race, body mass index, smoking history, ambulatory blood pressure findings, cholesterol and triglyceride levels and antihypertensive medications taken, E/A at isometric exercise was related to results of glucose tolerance tests and was inversely proportional to left ventricular mass index (P<0.0001). No significant differences were found whether patients were taking antihypertensive medications or not. In hypertensive patients, left ventricular diastolic function is determined by left ventricular mass index and the status of preclinical glucose intolerance, independent of age, gender, race, body mass index, blood pressure level, nocturnal drop in blood pressure or lipid level. These findings were not prejudiced by antihypertensive medications.

Abnormal vasoactive hormones and 24-hour blood pressure in obstructive sleep apnea

Background Patients with obstructive sleep apnea (OSA) are at increased risk for hypertension. The mechanisms responsible for the development of hypertension are controversial. We hypothesized that patients with OSA had an abnormal 24-h blood pressure (BP) and an abnormal activity in vasoactive hormones, and that both BP and hormones were normalized during treatment with long-term nasal continuous positive airway pressure (CPAP). Methods The 24-h BP and plasma levels of the vasoactive hormones (renin, angiotensin II, aldosterone, atrial natriuretic peptide, brain natriuretic peptide, vasopressin, and endothelin-1) were measured in 24 patients with OSA and in 18 control subjects. Thirteen patients with OSA were reexamined after 14 months of CPAP therapy. Results Patients with OSA had significantly increased BP and heart rate and a reduced nocturnal BP drop. Both angiotensin II (13.3 ± 1.6 v 7.8 ± 1.0 pmol/L) and aldosterone (94.0 ± 9.4 v 62.2 ± 4.5 pmol/L) were significantly higher in OSA than in control subjects. Positive correlations were found between angiotensin II and daytime BP (systolic: r = 0.49, P < .01; diastolic: r = 0.52, P < .01). The CPAP therapy resulted in a decrease in BP, and this CPAP-induced reduction in BP was correlated with a decrease in both plasma renin ( r = 0.76 to 0.92, all P < .01) and plasma angiotensin II concentration ( r = 0.58 to 0.81, all P < .05). Conclusions Plasma angiotensin II and aldosterone were elevated in OSA, and plasma angiotensin II was correlated with BP. Long-term CPAP reduced BP, and this decrease in BP was correlated with the reductions in plasma renin and angiotensin II levels. We suggest that OSA mediates hypertension, at least in part, via a stimulation of angiotensin II production.

Autonomic dysfunction associates with prolongation of QT intervals and blunted night BP in obese women with visceral obesity.

Prolonged QT intervals and a reduced fall of nocturnal blood pressure (BP) both predict an increased risk of cardiovascular events in obese subjects. We evaluated circadian BP variations (24-h ambulatory BP monitoring), autonomic function (power spectral analysis of RR interval oscillations) and cardiac repolarization times (QTc-dispersion and QTc interval) in 70 obese women, aged 25-44 yr, grouped by WHR into group A (WHR > 0.85, no.=38) and group B (WHR < or = 0.85, no.=32). Compared with non-obese age-matched women (no.=25, BMI=23+/-1.8) and obese women of group B, obese women of group A had higher values of QTc-d (p<0.05) and QTc (p<0.05), an altered sympathovagal balance (ratio of low-frequency/high-frequency power, p<0.01), and a blunted nocturnal drop in BP (p<0.01). In group A, QTc-d and the QTc interval correlated with diastolic night BP (p<0.01) and sympathovagal balance (p<0.01). WHR and plasma insulin levels correlated with QT intervals, reduced nocturnal fall in diastolic BP and sympathovagal balance (p<0.01). Prolongation of cardiac repolarization times and the reduction of nocturnal fall in BP coexist in obese women with visceral obesity, and might contribute to their raised cardiovascular risk. Autonomic dysfunction may be the common mechanism for this association.

Blood pressure during siesta: effect on 24-h ambulatory blood pressure profiles analysis.

Blood pressure (BP) during siesta declines to levels similar to those of night time sleep. The objective of the study was to assess the effect of siesta on 24-h ambulatory BP (ABP) data. Two different approaches were employed for the definition of day and night periods: (1) actual patient reported day and night intervals (ACT) with siesta period analysed as a third time period; and (2) arbitrary day and night time intervals (ARB) with the presence of siesta being ignored. A total of 203 24-h ABP recordings were analysed, with a siesta during ABP monitoring reported in 154 of them. Mean siesta BP was very close to ACT night time BP. Among recordings with a siesta, ACT daytime BP was higher and night time BP lower than the corresponding ARB BPs (P < 0.001). The magnitude of night time BP drop was greater with ACT intervals, resulting in a lower percentage of non-dippers (P < 0.001). Among 49 recordings without a siesta, differences between ACT and ARB BPs were less pronounced for daytime but not for night time. Differences in the magnitude of nocturnal BP drop between ACT and ARB periods, although statistically significant, did not affect the prevalence of non-dippers. In conclusion, analysis of 24-h BP profiles by using ARB instead of ACT day and night intervals results in underestimation of the nocturnal BP drop and overestimation of the proportion of non-dippers. This bias is more pronounced in patients who take a siesta during ABP monitoring.

The diabetic patient with hypertension

Hypertension and diabetes co-exist more commonly than would be expected from their individual prevalences. Elevated blood pressure is most commonly due to coexisting essential hypertension, or diabetic renal disease. Early stages of diabetic renal disease can be identified by detecting microalbuminuria. Standard measures of blood pressure are not necessarily raised, but 24-hour ambulatory measures frequently identify a loss of nocturnal drop in blood pressure. Treating hypertension aggressively is important in slowing the inexorable decline in glomerular filtration rate. In diabetes there appears to be no 'J'-shaped relationship between blood pressure and cardiovascular events, thus removing any concern about attaining low blood pressures as long as the patient is asymptomatic. Morbidity and mortality in these patients is usually associated with cardiovascular events, and it is important to assess the effect of drugs on left ventricular hypertrophy and metabolic parameters. Many drugs are effective at lowering blood pressure, but angiotensin-converting enzyme inhibitors may have an additional renoprotective action. alpha-Adrenergic antagonists may improve lipid profiles and calcium antagonists are probably lipid neutral, making these drugs useful alternatives. Dihydropyridine calcium antagonists (eg, nifedipine) may augment protein-uria, and hence non-dihydropyridine calcium antagonists (eg, verapamil, diltiazem) would be preferred. beta-Blockers and thiazide diuretics have the disadvantage of causing a deterioration in glycaemic and lipid profiles, but can be useful on occasions.

Relation between diurnal variation of blood pressure and left ventricular mass in a Chinese population

In western populations, patients with hypertension who have a nocturnal decrease in blood pressure (BP) may have less left ventricular (LV) hypertrophy and cardiovascular morbidity than those without a diurnal variation in BP. To further examine this association between nocturnal BP reduction and LV mass index, we studied 720 normotensives (<140/90 mm Hg), 380 borderline hypertensives (140 to159/90 to 94 mm Hg), and 582 hypertensives (≥160/95 mm Hg) from Taiwan and Quemoy island by using 24-hour ambulatory BP monitoring and 2-dimensional echocardiography to obtain LV mass index during a community-based cardiovascular 3 survey. After controlling for age, sex, height, weight, daytime BP, and daytime heart rate, the nocturnal reduction of systolic BP was found to associate weakly with LV mass index, for the whole population (partial correlation coefficient = −0.06, p < 0.05), as well as for the patients with hypertension (partial correlation coefficient = −0.09, p < 0.05), but these associations were eliminated when 24-hour BP and heart rate were accounted for. The average and percent nocturnal decrease of systolic BP (mean ± SD; mm Hg, [%]) of 3.2 ± 5.9 (2.7 ± 4.8%); 3.3 ± 7.3 (2.4 ± 5.4%); and 4.6 ± 9.0 (3.0 ± 6.1%) in normotensives, borderline hypertensives, and hypertensives, respectively, was smaller than that found in previous studies. Hence, in this large Chinese population, a small nocturnal BP drop was found and it was only weakly associated with LV mass index. These results emphasize the general need for ambulatory BP reference values based on internal controls.

Diurnal variation in blood pressure in patients with biventricular assist devices and retained, nonpumping native hearts.

Studies indicate that centrally mediated rhythms in sympathetic tone play a prominent role in diurnal cardiovascular variability. Recent evidence from heart transplant recipients, in whom blood pressure does not decline during sleep despite normal variability in plasma norepinephrine, however, suggests that afferent cardiac nervous traffic is necessary for the generation of diurnal variability. This implies that in the presence of an innervated heart excluded from the systemic circulation, blood pressure would still decrease during sleep. To assess this hypothesis, we studied 24-hour blood pressure, heart rate, and neuroendocrine variability in patients with biventricular assist devices in whom the retained native hearts had ceased to pump. Eight patients were free of medication and were studied every 3 hours. Pump rates and output were kept constant throughout the study. Blood pressure showed a significant decline during sleep, as did norepinephrine and epinephrine (all P < .05). Atrial natriuretic factor showed a significant increase around midnight (P < .01). Significantly elevated levels were found for all hormones studied except for aldosterone and endothelin. Our results suggest that diurnal variations in cardiac function or in catecholamine levels (indicative of sympathetic activity) as found in cardiac transplant recipients alone are not responsible or sufficient for producing a nocturnal drop in blood pressure. The presence of an innervated heart appears crucial in this respect. This could be of importance for the understanding of circadian cardiovascular pathophysiology.

Nocturnal sleep and blood pressure in essential hypertension.

Blood pressure and sleep-wakefulness patterns were monitored in the sleep laboratory over four consecutive nights in six patients with mild hypertension and six age- and sex-matched controls. In both hypertensives and normals, blood pressure levels decreased during sleep compared with presleep levels by 16.6 and 8.4%, respectively; levels for hypertensives, however, remained significantly above those for the normals. The nocturnal drop in blood pressure for both groups appeared to be related primarily to the general state of sleep rather than to any specific sleep stage. Nocturnal patterns of sleep stages and sleep cycling were almost identical for the two groups. Nocturnal blood pressure fluctuation was correlated positively with the distribution of nocturnal wakefulness in hypertensives but not in normotensives. This suggests that with hypertension there is some diminution of the dampening effect of sleep itself upon blood pressure which normally carries over into periods of nocturnal wakefulness. This alteration in patients with mild hypertension may reflect a decrease in the sensitivity of the baroreceptor reflex or some other pathophysiological process.