Left Ventricular Filling Profiles in Young White-Coat Hypertensive Patients Without Hypertrophy
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Abstract
Abstract This study was to assess left ventricular diastolic function in young white-coat hypertensive subjects <50 years of age without hypertrophy. Hypertensive patients (systolic or diastolic blood pressure ≥140 or ≥90 mm Hg on all three visits) were defined as white coat if their average 24-hour blood pressure was <127/81 mm Hg and at least 18/16 mm Hg lower than their average office values. We chose three groups balanced for sex, age, and body mass index: 50 sustained hypertensives, 25 white-coat hypertensives, and 25 normotensives. Office blood pressure was similar in white-coat and sustained hypertensives. Ambulatory blood pressure was comparable in white-coat hypertensives and normotensives. Compared with normotensives, white-coat hypertensives had more impaired diastolic function: increased ratio of late to early filling velocities, raised ratio of late to early time-velocity integral, prolonged deceleration time, and lengthened isovolumic relaxation time (P<.001, P<.001, P=.002, and P<.001, respectively). No difference was noticed between white-coat and sustained hypertensives. Compared with normotensives, white-coat hypertensives had higher values of plasma and urine norepinephrine (P<.001 and P<.001, respectively), plasma and urine aldosterone (P<.001 and P=.002, respectively), plasma renin activity (P=.04), total cholesterol (P=.001), and LDL cholesterol (P<.001). No difference was observed between white-coat and sustained hypertensives. Within white-coat hypertensives, 24-hour urinary aldosterone closely correlated with the ratio of late to early filling velocities (P=.008), and plasma and 24-hour urinary norepinephrine correlated well with total cholesterol (P=.037 and P=.006, respectively). No correlation was detected within the sustained hypertensives and normotensives. Heightened neurohumoral activity clearly supported the progression of diastolic dysfunction and metabolic abnormality in white-coat hypertensives.
- hypertension, white coat
- ventricular function
- echocardiography
- blood pressure monitoring
- angiotensin system
The term white-coat hypertension has been used to describe patients who have elevated BP in the doctor’s office but normal values during 24-hour ambulatory recording.1 2 3 Although white-coat hypertension has been recognized for a long time and is known to be common in clinical settings, its etiology is still unknown.3 4 5 In fact, even the prognosis in this condition has not been established; moreover, the contributing factors to its cause are not yet clear.3 4 5 Measurement of 24-hour BP values among clinically hypertensive patients have become the cornerstone for diagnosing white-coat hypertension.1 2 3 4 5 Until long-term follow-up results of white-coat hypertension based on this technique are available, the detection of target-organ changes is the most useful parameters in the clinical handling of these subjects.1 2 3 4 5 6 LVH, the major target-organ damage, has been widely recognized as a predictor of cardiovascular morbidity and mortality in hypertensive patients.7 8 Indeed, most of the previously published articles9 10 11 12 13 14 15 have discussed whether white-coat hypertensives showing LV muscle mass differ from sustained hypertensives and normotensives. Recently, LV diastolic dysfunction has begun to attract attention since it has been detected early in the course of hypertension and precedes the development of LVH.16 17 18 To the best of our knowledge, no study has been performed concerning the LV diastolic filling profile in young patients with white-coat hypertension but without LVH. Furthermore, there are few reports5 12 15 in the literature that describe neurohumoral and metabolic measurements, which have been considered to be related to the development of the white-coat phenomenon, and the resulting cardiac status in clinically hypertensive patients.
The aim of this study was to ascertain the LV diastolic filling profiles and neurohumoral and metabolic findings in young patients with white-coat hypertension who do not have LVH and to compare them with sustained hypertensives and normotensives.
Methods
Study Population
We surveyed 235 successive clinically hypertensive patients from our hypertensive outpatient clinic and 76 healthy normotensive volunteers. All individuals fulfilled all of the inclusion criteria for this study and underwent 2-D, pulsed Doppler, and color Doppler echocardiographic examinations and 24-hour ambulatory BP monitoring. Of the 235 clinically hypertensive patients, 151 patients had never been treated previously, and 84 patients had discontinued their previous antihypertensive drug therapy at least 6 months prior to this study. The following criteria were used to define subject eligibility for inclusion in this study: (1) age <50 years old (mean, 39.1±8.5 years; age range, 28 to 49 years); (2) a diagnosis of clinical hypertension based on the average of three office readings at 5-minute intervals, taken at each of three different occasions during a 3- to 4-week period, excluding his/her first visit. All subjects were asked not to smoke or ingest caffeine within 2 hours of each visit. All subjects were ordered not to take herb drugs within 2 months prior to enrollment. Clinical hypertension was defined when all three visits showed an average systolic BP ≥140 mm Hg or diastolic BP ≥90 mm Hg, as recommended by the Fifth Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure.19 Healthy normotensive subject had average office systolic and diastolic BPs <140 and 90 mm Hg, respectively, at all three visits; (3) no evidence of cardiovascular (coronary artery disease, valvular heart disease, congestive heart failure, or rhythm abnormality) or cerebrovascular disease detected by means of history taking, physical examinations, resting electrocardiogram, treadmill exercise test, chest x-ray, and echocardiographic examination; (4) no evidence of any kind of secondary hypertension; (5) no evidence of renal and liver function abnormality or any metabolic disease; (6) normal 2-D echo: normal systolic function expressed as FS, no LVH expressed as normal LVMI and normal RWT, normal LVDd and LVDs, normal LAD (the normal limits for these measurements were established from 60 age- and sex-matched healthy volunteers. Data were considered abnormal if they were 2 SDs greater than the mean in the normal subjects), and no regional wall motion abnormality; (7) no more than a mild degree of mitral or aortic regurgitation as determined by color Doppler study; (8) no obesity, expressed by normal BMI; (9) well hydrated; and (10) subjects with adequate echocardiographic acoustic windows and well-documented 24-hour BP recordings. Among 235 clinically hypertensive patients, 183 were defined as having sustained hypertension, and 52 were classified as having white-coat hypertension (see below for definition of white-coat hypertension). The prevalence of white-coat hypertension was 22% in our study population. From all of these participants, we chose three groups balanced for sex, age, and BMI: 50 sustained hypertensives, 25 white-coat hypertensives, and 25 normotensives. These subjects were selected for a further comparative study. Subjects who could not be matched appropriately were not used for comparisons between groups, although they were used for the within-group correlation study. The study was in accordance with the Second Declaration of Helsinki. All procedures were approved by the Committee on Human Studies of our College Hospital, and informed consent was completed by all subjects.
Clinical and 24-Hour Blood Pressure Recording
Clinical BP recordings were performed on the nondominant arm, with the patient in the supine position after 10 minutes of rest. Twenty-four-hour BP recording was achieved by a portable noninvasive recorder (SpaceLabs 90207), with cuffing on the nondominant arm. Recording was done during an ordinary daily activity within 2 weeks of the last office interview. BP readings and pulse rates were recorded every 20 minutes from 6 am to 11 pm and every 30 minutes from 11 pm to 6 am. The data were edited to a 24 consecutive 1-hour average. Systolic readings of >260 or <70 mm Hg, diastolic readings of >150 or <40 mm Hg, and pulse pressure readings of >150 or <20 mm Hg were automatically deleted. The correctness of the recorder was confirmed by carrying out three simultaneous readings with a standard mercury manometer through a Y-tube at the beginning and end of the monitoring time. We measured several parameters including average 24-hour, daytime, and nighttime systolic and diastolic BPs and pulse rates. Average daytime and nighttime BPs were recalculated according to each individual’s awake and sleep periods, which were recorded in a diary. Twenty-four-hour BP recordings that had more than four measurement deficits were reexamined. All recordings were analyzed by an investigator (Z.-Y.L.) who was unaware of other data of any patient.
White-Coat Hypertension
Clinically hypertensive patients were classified as white coat if their average 24-hour BP was <127/81 mm Hg and at least 18/16 mm Hg less than their average office values. The remaining hypertensive subjects were placed into the category of sustained hypertension. Because geographic factors may contribute to the normal limits of the 24-hour BP values, we did not use the previously reported cutoff point.3 5 20 21 Instead, we chose the upper limit as 2 SDs above the average 24-hour systolic and diastolic BP values taken from 50 healthy clinically normotensives in our geographic area (Shin-E area, Taipei, Taiwan). These 50 subjects included 25 men and 25 women (age, 39.1±7.2 years; age range, 30 to 50 years). The resulting upper limit for the average 24-hour BP values was 127/81 mm Hg. Hence, the major criterion of white-coat hypertension was based on a clinically hypertensive patient who showed an average 24-hour systolic BP <127 and diastolic BP <81 mm Hg. The later criterion was taken from examination of our normotensives in whom the mean±SD of their average office and 24-hour systolic and diastolic differences were 10±8 and 9±7 mm Hg, respectively. The values of 18 and 16 mm Hg were measured as the mean+SD. Intraindividual reproducibilities of white-coat and sustained hypertension were determined from three successive 24-hour BP monitorings in a randomly selected subsample of 20 sustained and 20 white-coat hypertensive subjects. We arranged 5 to 18 days (mean, 12±8 days) as the interval between recordings.
Echocardiography
Echocardiographic studies were performed on an ATL (Advanced Technology Laboratories) Ultramark 7, phased-array, ultrasound system with a 2.5-MHz transducer. 2-D echo, pulsed Doppler, and color Doppler ultrasound images were recorded within 2 weeks of the 24-hour BP recording in all subjects. Mitral inflow velocity was recorded from the apical four-chamber view by the pulsed Doppler technique with patients in passive end-expiration. The sample volume was placed at the level of the mitral leaflet tips. All parameters were calculated by the averaging of at least five successive cardiac cycles. The LVMI (g/m2) was calculated as (Vepi−Vendo)×1.05/BSA, where BSA is the body surface area. The LV epicardial enclosed volume (Vepi) and endocardial enclosed volume (Vendo) were measured at end-diastole (the R-wave peak of the simultaneously recorded electrocardiogram). Volume measurements were calculated from apical four-chamber (A1) and two-chamber (A2) views by use of the biplane area-length formula (V=8A1A2/3πL), where L is the lesser of the lengths of the long axes of these two views. The RWT was calculated as 2×(PWT/LVDd). LV PWT and LVDd were measured at end-diastole from the parasternal long-axis view of the 2-D echo image. FS was calculated as (LVDd−LVDs/LVDd)×100. LVDs was measured as the shortest systolic dimension taken from the parasternal long-axis view of the 2-D echo image. LAD was measured as the largest systolic dimension taken from the parasternal long-axis view of the 2-D echo image. LV diastolic filling indexes22 included the following measurements: peak late diastolic filling velocity (A) (cm/s), peak early diastolic filling velocity (E) (cm/s), A:E ratio, atrial time-velocity integral (Ai) (cm), early time-velocity integral (Ei) (cm), Ai:Ei ratio, early filling time (EFT, ms), and deceleration time of early filling (DT, ms). In addition, isovolumic relaxation time (IVRT, ms) was also measured as the time interval from the Doppler sampling information of aortic valve closure artifacts to the onset of mitral valve flow. Echocardiography was carried out and analyzed by the same operator (N.-C.C.) throughout the study, who was blinded with regard to all other data of all subjects. Intraobserver variations in calculating all echocardiographic parameters were estimated by a randomly selected subsample of 100 sustained hypertensives, 30 white-coat hypertensives, and 40 normotensives on two occasions by one physician (N.-C.C.) with an interval of 2 months between measurements. Variability in measurement was outlined as the difference between the first and second readings divided by the first reading. Percentage variabilities for the readings of two identical echocardiograms were obtained.
Neurohumoral and Metabolic Measurements
The possible different impact of neurohumoral profiles, ie, renin-angiotensin-aldosterone profile (plasma renin activity, plasma aldosterone, and urinary aldosterone) and the sympathetic nervous system profile (plasma and urinary epinephrine and norepinephrine) on the cardiac and metabolic changes between the white-coat hypertensive group and the other two groups were evaluated. All subjects were ordered to maintain a normal diet without sodium restriction. We directed all subjects to take nothing at home after midnight before obtaining a blood sample and to sit quietly for 30 minutes in the early morning after arriving at our laboratory. Fasting blood samples were drawn for the measuring of lipid profiles, glucose, insulin level, plasma renin activity, aldosterone, norepinephrine, and epinephrine concentrations. Twenty-four-hour urine samples were also collected on the same day during which ordinary daily activities were performed for examination of urinary aldosterone, norepinephrine, and epinephrine excretion. Correlations were estimated for the relationships between plasma renin activity, plasma aldosterone, plasma norepinephrine, plasma epinephrine, 24-hour urinary aldosterone excretion, 24-hour urinary norepinephrine excretion, and 24-hour urinary epinephrine excretion, with the values of total cholesterol, triglyceride, LDL cholesterol, and left ventricular diastolic filling profiles in all subjects.
Statistics
Values were expressed as mean±1SD. All analyses were executed with the SPSS/PC+ package. For multiple comparisons, the means of continuous variables were compared with one-way ANOVA followed by Scheffé’s test. Frequencies were analyzed by Fisher’s exact test and continuity-adjusted χ2 test where suitable. Study of correlations was performed by linear-regression analysis. A value of P<.05 was considered statistically significant.
Results
Clinical Data and Blood Pressure Values
The demographic data for 50 sustained hypertensive patients, 25 white-coat hypertensive subjects, and 25 normotensive volunteers are summarized in Table 1⇓. Age, sex distribution, and BMI did not differ among the three groups (ANOVA; P=.798, P=.707, P=.905, respectively). In addition, the mean duration of hypertension was virtually identical in both hypertension groups. Table 2⇓ shows the clinical and ambulatory BP values in these three groups. The clinical systolic and diastolic BP values were not different between white-coat and sustained hypertensives. The average 24-hour, daytime, and nighttime systolic and diastolic BPs were similar in the white-coat hypertensives and normotensives. Intraindividual reproducibility among white-coat hypertensives and sustained hypertensives between the first and second and between the second and third 24-hour BP recordings were both 100% (sample size, 40).
Demographic Data of Study Populations
Clinical and 24-Hour BP Values of Study Populations
Echocardiographic Findings
The LVMI, RWT, FS, LVDs, LVDd, LAD, and HR in 60 age- and sex-matched healthy volunteers (age, 38.6±6.9 years; range, 31 to 49 years) on 2-D echo were 76±8 g/m2, 33±.03, 37±6%, 29±3 mm, 47±3 mm, 31±3 mm, and 73±6 beats/min, respectively. These data served to establish the normal reference values for 2-D echo measurements. Transmitral peak A, E, A:E ratio, Ai, Ei, Ai:Ei ratio, EFT, DT, and IVRT in healthy volunteers were 47±5 cm/s, 65±9 cm/s, .75±.09, 6±2 cm, 14±3 cm, .44±.05, 271±39 ms, 183±28 ms, and 78±10 ms, respectively. Table 3⇓ indicates the percentage variabilities for LVMI, RWT, FS, LVDs, LVDd, LAD, and Doppler indexes of two identical echocardiograms in 170 subjects. Table 4⇓ demonstrates echocardiographic data in these three groups. In our study, no remarkable changes in LVMI, RWT, FS, LVDs, LVDd, and LAD were identified among these three groups (ANOVAs are displayed in Table 4⇓), and the differences between any two of these three groups were within the range of intraobserver variability. However, compared with the normotensive group, the white-coat hypertensive group had significantly more impaired left ventricular diastolic filling profiles; it showed increased A (P=.023), decreased E (P=.004), elevated A:E ratio (P<.001), raised Ai (P=.029), reduced Ei (P<.001), heightened Ai:Ei ratio (P<.001), prolonged DT (P=.0016), and lengthened IVRT (P<.001). The diastolic filling profiles were similar in both white-coat and sustained hypertensive groups.
Intraobserver Percentage Variability of All Measurements of Identical Echocardiograms on Two Occasions in a Randomly Selected Subsample of 170 Subjects
Echocardiographic Data of Study Populations
Laboratory Findings
Table 5⇓ is a record of the laboratory data. Compared with the normotensive group, the white-coat hypertensive group showed significantly higher values for total cholesterol (P=.001), LDL cholesterol (P<.001), plasma renin activity (P=.04), plasma and 24-hour urinary norepinephrine (P<.001 and P<.001, respectively), and plasma and 24-hour urinary aldosterone (P<.001 and P=.0017, respectively). No difference was observed between white-coat and sustained hypertensive groups. The values for triglyceride, glucose, insulin, and plasma and 24-hour urinary epinephrine excretion were approximately similar between any two of these three groups. Table 6⇓ demonstrates that 24-hour urinary aldosterone excretion correlated significantly with transmitral A:E ratio within the white-coat hypertensive group (γ=.353, P=.008) but not within either of the other two groups. Furthermore, plasma and 24-hour urinary norepinephrine correlated closely with total cholesterol value within the white-coat hypertensive group (γ=.327, P=.037 and γ=.388, P=.006, respectively), although not within either of the other two groups. There were no significant correlations between plasma renin activity, plasma aldosterone concentration, plasma epinephrine concentration, or 24-hour urinary epinephrine and any of the other metabolic measurements or LV diastolic filling indexes within any of these three groups.
Laboratory Data of Study Populations
Correlation Coefficient Within the Study Populations
When the chosen sustained and white-coat hypertensive subjects in our study were reclassified according to the reference limits suggested by the consensus document on noninvasive ambulatory BP monitoring, ie, 135/85 mm Hg,23 two subjects with sustained hypertension were reclassified as white-coat hypertensives. If the critical point was set at 146/91 mm Hg, as derived from a meta-analysis of 23 studies21 using both invasive and noninvasive ambulatory recordings in clinically normotensive subjects or in general populations, four subjects with sustained hypertension were reclassified as white-coat hypertensives. However, this redistribution did not affect the results in our present study.
Discussion
There are apparently perplexing results in the literature that deal with cardiac involvement in white-coat hypertension. Some investigators9 10 11 12 have reported that white-coat hypertension does not result in any cardiac damage, whereas others13 14 15 have shown that white-coat hypertension results in a greater LV muscle mass and should not be considered as completely harmless. In view of the fact that the ambulatory BP determines LV mass,9 24 25 26 this discrepancy might be due to the divergence of ambulatory BP levels between white-coat hypertensive and normotensive groups observed in these studies. To date, no article has reported on the status of LV diastolic filling profile in white-coat hypertension without increased LV muscle mass. Again, the causal relationships between neurohumoral status in this subset of hypertensive patients and their cardiac changes and metabolic profiles have never been examined.
There are complex interactions involved in the measurement of the transmitral velocity profiles as Doppler indexes of diastolic function. Many cardiac factors, such as ischemic and valvular heart disease, LV size and mass, LV systolic function, left atrial size, and heart rate, and some extracardiac factors such as age, sex, and obesity, complicate the interpretation.27 28 We selected a study population <50 years old with a normal LV muscle mass; normal systolic function; normal LVDs, LVDd, and LAD; normal BMI; and regular sinus rhythm to exclude these disconcerting influences. We also took care to minimize the likelihood of ischemic and valvular heart disease by clinical means. Left atrial pressure, another confounding factor, was not an enigmatic problem in our study because in the situation of an A:E ≥1, the LV hemodynamic abnormality would be diastolic dysfunction, normal systolic function, and normal left atrial pressure. An elevated left atrial pressure would present an E-dominant or pseudonormalization pattern, despite the coexistence of diastolic dysfunction.29 We selected all subjects in our study who showed no evidence of congestive heart failure and were well hydrated to eliminate the possibility of alteration in left atrial pressure.
The criteria used for defining white-coat hypertension might influence the study outcome. Weber and colleagues15 used a more demanding diastolic BP criterion for defining white-coat hypertension. The diagnosis of white-coat hypertension in their study was based on an office diastolic BP ≥90 mm Hg, an average 24-hour diastolic BP <85 mm Hg, and a difference between average 24-hour diastolic and office diastolic values of at least 15 mm Hg. The latter standard was the result of the observance of the mean±SD between office and 24-hour average diastolic difference in normal volunteers of 9±6 mm Hg. The reason for this was due to the fact that the 24-hour average, which included a low nighttime value, was probably 10 mm Hg below the office reading; therefore, some truly mild hypertensive patients would be misclassified as white-coat hypertensive subjects. In our present study, the differences between the average 24-hour and office systolic and diastolic values in the white-coat hypertensive group were 40 and 30 mm Hg, respectively, which were much greater than the mean+SD of the differences in our normal subjects of 18 and 16 mm Hg, respectively. Likewise, we determined the normalcy of the ambulatory BPs by considering geographic factors rather than using discretionary cutoff points and took an upper limit of mean+2 SD in our normal control subjects to diminish the possibility of some patient misnomers. Also, we conformed both average 24-hour systolic and diastolic BP values, as well as standards named from clinically normotensive subjects, rather than the general population. Thus, the selection bias was minimal in our study.
It was observed by us that impaired LV diastolic filling profiles were similar in both hypertensive groups. These findings support the concept of pathophysiologic similarities between patients with white-coat and sustained hypertension. According to the article of Stoddard and colleagues,30 the influence of impaired LV relaxation and increased chamber stiffness on Doppler filling profiles are different. Impairment of relaxation impedes early filling with a compensatory increase in late filling, whereas increased chamber stiffness impairs atrial filling and may enhance early filling. The increased A:E ratio observed in both hypertension groups in our study indicates an abnormal LV relaxation. This early change in LV is due to a loading condition that might have been exerted by clinical hypertension.30 31
The causality between neurohumoral profiles and the cardiac and metabolic changes in white-coat hypertensive patients has not been clarified but might be related to increased activities in the sympathetic and renin-angiotensin-aldosterone systems. Julius et al1 5 and Weber et al15 previously have noted a connection between sympathetic thrust and increased lipid level in borderline and white-coat hypertensives, respectively. However, there were disparities among several authors5 12 15 dealing with the lipid profiles in white-coat hypertension. These discriminations may be contingent on different populations studied, eating and smoking habits, and sample size. Furthermore, overweight might modify cardiovascular performance as well as some metabolic features. Thus, we have balanced the groups for this potential determinant. Our data about lipids, however, are partly in agreement with earlier observations.1 5 15 In addition, Weber et al15 reported that plasma norepinephrine correlated significantly with plasma cholesterol and triglyceride levels within the white-coat hypertensive patients but not in either the normal control subjects or established hypertensive patients. Our data are consistent with the recent report by Weber et al15 indicating that plasma and 24-hour urinary norepinephrine values correlated significantly with total cholesterol level within the white-coat hypertensive group only. These findings suggest that sympathetic activity plays a key role in defining the features of white-coat hypertension. Further, Weber et al15 have verified that white-coat hypertensive patients may be distinguished by a plasma aldosterone level similar to that in sustained hypertensive patients and reported a correlation between plasma aldosterone level and LV muscle mass within the white-coat hypertensive group but not in either the sustained hypertensive or normotensive group. Our data, however, are partially in accord with those reported by Weber et al.15 We have observed equivalent increased plasma and 24-hour urinary aldosterone and plasma renin activity in white-coat and sustained hypertensive groups and noticed a crucial correlation between 24-hour urinary aldosterone level and LV diastolic filling profile, specifically the transmitral A:E ratio, within the white-coat hypertensive group only. This is supported by the work by Weber and Brilla,32 who suggested that aldosterone directly stimulates LV remodeling in hypertensive patients. Moreover, several previous investigators33 34 35 have suggested that myocardial angiotensin II may lead to a change in the ratio of collagen phenotypes and increase in collagen content, which result in deterioration in the diastolic function in experimental rats with LVH. Extrapolating from the results from laboratory animals, we suggest that the alterations in the quantity and quality of the myocardial collagen matrix occur in white-coat hypertension mediated at least partly by increased activity in the renin-angiotensin-aldosterone system, before the development of a clinically detectable LVH, are related to LV diastolic dysfunction.
White and colleagues36 indicated that LV filling rate is more dependent on age and 24-hour ambulatory BP. In our present study, the ages of the subjects in these three groups were identical; thus, the influence of aging on LV diastolic function was considered to be similar. Furthermore, the 24-hour ambulatory BP values were similar in white-coat hypertensive and normotensive groups. Therefore, the abnormal filling profiles in the white-coat hypertensives are not dependent on ambulatory BP values. Our results indicate that office systolic and diastolic BPs in white-coat hypertensives are similar to those in sustained hypertensives and significantly higher than those in normotensives. Thus, the temporary increase in BP due to enhanced BP responsiveness to visiting a doctor may play a role in the development of cardiac functional change in white-coat hypertension. Neurohumoral determination in the white-coat hypertensive group might support a part in mediating these findings. It should be stressed that neurohumoral indexes are more important than the level of BP itself in characterizing white-coat hypertension, since the urinary level of aldosterone and norepinephrine represents an integrated value over the 24-hour ambulatory monitoring, whereas elevated BP are only temporary and sporadic.
There are potential limitations of this study. To determine conclusively whether white-coat hypertension differs from either sustained hypertension or normotension, precisely matched pairs of patients with identical office systolic and diastolic BP values should be enrolled for comparison between white-coat and sustained hypertensive groups. Likewise, matched pairs of subjects with the same average 24-hour, daytime, and nighttime BP values should be selected for comparison between white-coat hypertensive and normotensive groups. A larger sample size would be necessary to achieve such stringent matching criteria. An important issue should be addressed: ie, that diastolic dysfunction may be a consequence of myocardial tissue injury and only partly related to the neurohumoral profiles. Multiple scattered foci of myocardial damage may be present, although they are not detectable by the limited resolution of the procedure employed here. In addition, angiotensin II measurement may be essential for a more apparent appraisal of the causality between the renin-angiotensin-aldosterone axis and diastolic function in white-coat hypertension.
In summary, the present study clearly demonstrates for the first time some data about the young white-coat hypertensive population without LVH, showing that in these subjects the impaired LV diastolic function is similar to that in sustained hypertensive subjects. Our present studies also indicate that white-coat hypertensive patients present with intensified neurohumoral activities similar to an early form or a variant form of sustained hypertension. Therefore, we conclude that white-coat hypertension may not represent a group at low risk for organ damage. A longitudinal study is necessary to reveal more clearly the long-term prognostic value of impaired diastolic function in white-coat hypertension.
Selected Abbreviations and Acronyms
2-D | = | two-dimensional |
BMI | = | body mass index |
BP | = | blood pressure |
FS | = | fractional shortening |
HR | = | heart rate |
LAD | = | left atrial dimension |
LV | = | left ventricular |
LVDd, LVDs | = | LV end-diastolic, end-systolic dimension |
LVH | = | LV hypertrophy |
LVMI | = | LV mass index |
PWT | = | posterior wall thickness |
RWT | = | relative wall thickness |
- Received March 15, 1997.
- Revision received April 15, 1997.
- Accepted April 30, 1997.
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- Left Ventricular Filling Profiles in Young White-Coat Hypertensive Patients Without HypertrophyNen-Chung Chang, Zhi-Yang Lai, Paul Chan and Tze-Che WangHypertension. 1997;30:746-752, originally published September 1, 1997https://doi.org/10.1161/01.HYP.30.3.746
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