(Hypertension. 1996;28:284-289.)
© 1996 American Heart Association, Inc.
Articles |
Association Between Persistent Pressure Overload and Ventricular Arrhythmias in Essential Hypertension
the Ospedale "Beato G. Villa," Citta' della Pieve (G.S., N.S.), and the Ospedale Generale Regionale "R. Silvestrini," Area Omogenea di Cardiologia e Medicina, Perugia (P.V., C.B., A.C., I.Z., M.B., R.G., C.P.), Italy.
Correspondence to Dr Paolo Verdecchia, Ospedale Generale Regionale "R. Silvestrini," Area Omogenea di Cardiologia e Medicina, Localita San Sisto, 06156 Perugia PG, Italy.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Hypertension is a risk factor for sudden cardiac death, and some data indicate that frequent and complex ventricular arrhythmias may be additional risk markers in hypertensive individuals. We investigated the relation between ventricular arrhythmias and the persistence of increased blood pressure levels over 24 hours in subjects with essential hypertension. We studied 126 never-treated subjects with essential hypertension (83 men) who underwent 24-hour electrocardiographic monitoring, 24-hour ambulatory blood pressure monitoring, and echocardiography. Premature ventricular beats were detected in 71% of the subjects. Compared with subjects in Lown class 0-1, subjects with frequent or complex ventricular arrhythmias (Lown class
2) were older (54 versus 45 years) and had a longer duration of hypertension (5.4 versus 2.8 years), a greater left ventricular mass (147 versus 127 g·m-2), and a blunted nocturnal reduction in ambulatory blood pressure (7%/12% versus 12%/16%). The number of premature ventricular beats over 24 hours was associated with age (r=.25), left ventricular mass (r=.24), and pulse pressure (r=.18) and inversely associated with the percent reduction in blood pressure from day to night (r=-.29 for systolic and -.25 for diastolic pressures). In a multiple logistic regression analysis, frequent or complex ventricular arrhythmias (Lown class 2) were predicted by an age 60 years (odds ratio, 10.4; 95% confidence interval, 2.4-44.8), left ventricular hypertrophy at echocardiography (odds ratio, 4.2; 95% confidence interval, 1.5-11.6), and a <10% reduction in blood pressure from day to night ("nondipping" pattern: odds ratio, 2.9; 95% confidence interval, 1.2-7.0). We conclude that in addition to the strong effect of age and left ventricular hypertrophy at echocardiography, the persistence of high blood pressure levels over the 24 hours ("nondipping" pattern) is an independent predictor of the frequency and complexity of ventricular arrhythmias in never-treated subjects with essential hypertension.
Key Words: arrhythmia • blood pressure monitoring, ambulatory • circadian rhythm • echocardiography • hypertension, arterial • hypertrophy
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Hypertension is a risk factor for sudden cardiac death,1 and the risk of sudden death is increased in those hypertensive subjects who develop LV hypertrophy.2 However, the mechanisms underlying this association are not clear. According to many studies,3 4 5 6 7 8 9 10 but not all,11 12 ventricular arrhythmias are more frequent in hypertensive individuals with than in those without LV hypertrophy, and this finding suggests that ventricular arrhythmias might be involved in the mechanisms leading to sudden cardiac death in individuals with essential hypertension. However, some of these studies included subjects previously or currently treated,3 4 5 6 7 8 9 10 and this may introduce a bias because it has been shown that antihypertensive treatment may occasionally increase the risk of ventricular arrhythmias11 and sudden death13 in the long term. Only few data are available on the relation between LV hypertrophy and ventricular arrhythmias in untreated hypertensive subjects.11 12
The prognostic value of ventricular arrhythmias has been established in hypertrophic cardiomyopathy,14 ischemic heart disease,15 and a subset of subjects with LV hypertrophy from the Framingham cohort16 but not in subjects with essential hypertension. In the only prospective study conducted on hypertension, the prognostic value of ventricular arrhythmias did not remain significant after adjustment for potential confounding factors.4
Recently, the persistence of high BP values over 24 hours (nondipping pattern) has been associated with LV hypertrophy,17 18 19 vascular structural changes,19 and increased cardiovascular morbidity and mortality.20 21 In the present study, we investigated the prevalence and determinants of ventricular arrhythmias in never-treated subjects with essential hypertension. A primary aim of the study was the assessment of the relation between ventricular arrhythmias and the persistence of increased BP levels over 24 hours.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
We studied 126 subjects with essential hypertension (83 men and 43 women; mean age, 48 years [SD 11]), none of whom had been previously treated with antihypertensive drugs. All subjects were referred to our centers for baseline evaluation by a group of general practitioners operating in Umbria, Central Italy, in the setting of the Progetto Ipertensione Umbria Monitoraggio Ambulatoriale (PIUMA) study, a registry of morbidity and mortality in subjects with essential hypertension whose initial evaluation included 24-hour off-therapy ambulatory BP monitoring according to a standardized protocol.20 All of the subjects had a clinic systolic BP
140 mm Hg and/or diastolic BP 90 mm Hg on at least three visits at 1-week intervals and fulfilled all of the following inclusion criteria: no clinical or laboratory evidence of heart failure, coronary heart disease, previous stroke, valvular defects, or secondary causes of hypertension; high-quality echocardiographic tracings; and at least one valid BP measurement per hour over 24 hours. To exclude coronary heart disease, we performed exercise testing, thallium scintigraphy, or both when clinically indicated. Subjects engaged in regular physical training were excluded from the present study.
Clinic BP was measured by a physician with a mercury sphygmomanometer in the hospital clinic before ambulatory BP monitoring was begun, with the subject sitting for at least 10 minutes. The average of three measurements was considered for analysis. Ambulatory BP was recorded with the SpaceLabs 90207 monitor set to take a reading every 15 minutes throughout 24 hours. Overall, there were 92.1 valid BP readings per subject (SD 6; range, 74 to 112); the error percentage was 12% (SD 10). Normal daily activities were allowed and encouraged, and subjects were told to keep their nondominant arm still and relaxed at their side during measurements. To abide by the actual wakefulness-sleep rhythm reported in subjects' diaries, we defined daytime to be between 10 AM and 10 PM and nighttime between 1 and 6 AM. We excluded from the analysis the morning and evening transition hours, during which a varying number of subjects were awake and active; in fact, longer fixed nocturnal intervals, including transition hours, may lead to an overestimation of the true sleeping BP.22 Nighttime workers, as well as subjects going to bed later than 1 AM, were excluded from the present study; therefore, all study subjects were in bed during the entire nighttime period and were awake and active during the daytime interval. Subjects with a nocturnal reduction of systolic and/or diastolic BP 10% were defined as dippers (n=93, 74%) and the others as nondippers (n=33, 26%). There were 20 nondippers among men (24%) and 13 among women (30%, P=NS). Reading, editing, and analysis of data were done as previously described.20 The spontaneous day-to-day variabilities of 24-hour, daytime, and nighttime ambulatory BPs in our laboratory have previously been assessed.23
On the same day, all subjects underwent 24-hour ambulatory ECG recording. We used a two-channel bipolar recorder. The system was fully automatic and computerized; tracings were analyzed by two investigators who were unaware of the results of other investigations. Total PVBs were computed, and the arrhythmias were graded for complexity with the Lown-Wolf classification.24 A venous blood sample was obtained from all subjects for measurement of serum potassium concentration.
The M-mode echocardiographic study of the left ventricle was performed under two-dimensional control. Measurements were taken according to the American Society of Echocardiography recommendations.25 Only frames with optimal visualization of interfaces and showing simultaneously septum, LV internal diameter, and posterior wall were used for reading. Tracings were read by two observers, and the mean value from at least five measurements per observer was computed. LV mass was calculated according to Devereux et al26 and normalized both by body surface area and by height2.727 to correct for the effect of overweight. LV hypertrophy was defined as LV mass 51 g·m-2 in both sexes, as suggested by De Simone et al.28 The intraobserver and intratracing variabilities in our laboratory have been reported elsewhere.29
All subjects underwent standard 12-lead ECG; LV hypertrophy was defined by the sex-specific Cornell voltage criterion30 and a recently developed criterion incorporating modified Cornell voltage, Romhilt-Estes score, and LV strain.31 The latter criterion has shown a higher sensitivity than Cornell voltage, without compromising specificity.31
Data were stored with a DBASE IV package (Borland Inc), and statistical analyses were done with the SPSS/PC+ software, version 3.0 (SPSS Inc). We performed Student's t and 
2 tests and Pearson's correlation analysis when appropriate. Stepwise multiple linear regression tested the independent relation of several variables to the number of PVBs per 24 hours. Since the PVB showed a nongaussian distribution with a significant positive skewness (coefficient of skewness, 3.38; P<.0001), data are presented before and after logarithmic transformation. We performed multiple logistic regression analysis to test the determinants of complex ventricular arrhythmias (Lown-Wolf class 2 versus 0-1). This categorization of Lown-Wolf classification was chosen because it has been associated with increased mortality in a general population sample.16 Values of P<.05 were considered statistically significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
During 24-hour ECG monitoring, PVBs were detected in 71% of the subjects (n=89); the other 29% (n=37) were in Lown class 0. Thirty-three percent (n=42) of the subjects were scored as Lown 1, 2% (n=2) as Lown 2, 17% (n=22) as Lown 3, 13% (n=17) as Lown 4a, and 5% (n=6) as Lown 4b. On average, there were 250 (SD 664) PVBs over the 24 hours. Thirty-one percent (n=39) had polymorphic PVBs, 15% (n=19) ventricular pairs, and 5% (n=6) unsustained ventricular tachycardia runs. There was no R-on-T phenomenon.
The demographic and clinical characteristics of the study subjects are shown in Table 1
. The subjects with frequent or complex ventricular arrhythmias (Lown class 2) were older than those in Lown class 0-1 and had a longer duration of hypertension. Sex, smoking habits, body mass index, serum potassium level, and clinic and daytime ambulatory BPs did not differ between the two groups. Only four subjects (3%) had mild hypokalemia (serum potassium <3.5 mmol/L; range, 3.2 to 3.4), and none of them had complex ventricular arrhythmias. Subjects in Lown class 2 had significantly higher nocturnal and 24-hour systolic BPs (P<.002 and <.05) and a blunted day-night BP reduction for both systolic and diastolic BPs (P<.002/.004). The degree of nocturnal BP reduction progressively dampened with increasing complexity of ventricular arrhythmias (Fig 1). Subjects with unsustained ventricular tachycardia (Lown class 4b, n=6) had a nearly flat circadian BP profile, with an average nocturnal systolic/diastolic BP reduction of 0.8%/6.1%. Compared with dippers, hypertensive nondippers had more PVBs (584 versus 131, P<.0006; see Fig 2) and a significantly higher prevalence of frequent or complex ventricular arrhythmias (Lown class 2) (20/33, 61%, versus 27/93, 29%; P<.002). Compared with dippers, nondippers also showed a reduced nocturnal heart rate fall (13.3% versus 19.0%, P<.0006), despite similar clinic (74 versus 74 beats per minute, P=.97) and 24-hour (76 versus 74 beats per minute, P=.30) heart rate values.
|
|
|
The echocardiographic data are reported in Table 2. Seventy-four subjects (59%) had LV hypertrophy at echocardiography. Compared with the subjects in Lown class 0-1, subjects in Lown class 2 showed a greater LV mass (147 versus 127 g·m-2, P<.004, or 67 versus 56 g·m-2.7, P<.0004) and a higher prevalence of LV hypertrophy (74% [35/47] versus 49% [39/79], P<.01). As shown in Fig 2
, the total number of PVBs over the 24 hours was greater in subjects with LV hypertrophy than in those without LV hypertrophy (339 versus 66, P<.02). A lower percentage of subjects had LV hypertrophy at ECG (16% using Cornell voltage, 32% using the multifactorial criterion30 ). Nevertheless, the group with ECG LV hypertrophy identified by the multifactorial criterion had likewise a higher prevalence of Lown class 2 arrhythmias (54% versus 31%, P<.02) compared with the group without ECG LV hypertrophy. The difference was not significant with the use of the less-sensitive Cornell voltage criterion (55% versus 36%, P=.10).
|
As reported in Table 3, the number of PVBs over the 24 hours showed a positive association with age (r=.25, P<.01), LV mass (r=.24, P<.01), and pulse pressure (r=.18 for clinic and r=.19 for 24-hour values, both P<.05) and an inverse relation with the day-night BP reduction (r=-.29 for systolic BP and r=-.25 for diastolic BP, both P<.01). The number of PVBs showed no significant relation with systolic and diastolic BPs, both clinic (r=.13/-.06) and 24-hour (r=.08/-.04), and with serum potassium concentration (r=.08).
|
With multiple linear regression analysis, we tested the independent relation of several variables to the number of PVBs over the 24 hours, after logarithmic correction. Older age (P<.0001), increased LV mass (P<.002), the amount of daily cigarette smoking (P<.01), and a blunted day-night systolic BP reduction (P<.04) predicted a higher number of PVBs. The resulting equation was log(PVBs Over the 24 Hours+1)=-1.683+(0.037xAge)+(0.018xLV Mass/Height2.7)+(0.212xCigarettes per Day)-(0.022xDay-Night Systolic BP Reduction). Overall, 35% of the observed variation in the number of PVBs was explained by the model (multiple r=.59). Sex, serum potassium, clinic BP (systolic and diastolic), 24-hour BP (systolic and diastolic), and 24-hour heart rate did not enter the equation.
In a multiple logistic regression analysis, we tested the determinants of frequent or complex ventricular arrhythmias (Lown 2 versus Lown 0-1). In this analysis, Lown class 2 was independently predicted by older age (>60 years: odds ratio, 10.40; 95% confidence interval, 2.4-44.8), LV hypertrophy at echocardiography (odds ratio, 4.19; 95% confidence interval, 1.5-11.6), and a day-night BP reduction <10% (nondipping pattern: odds ratio, 2.86; 95% confidence interval, 1.2-7.0). The analysis of deviance revealed a good fit of the model to the perfectly fitting model containing all main effects and all interactions (overall log-likelihood=-68.2, Lemeshow-Hosmer goodness-of-fit 2=7.8 with 6 df, P=NS). When the determinants were analyzed as continuous variables, age (P<.0002), LV mass/height2.7 (P<.003), and day-night systolic BP reduction (P<.04) entered the model. Sex, serum potassium, clinic BP (systolic and diastolic), 24-hour BP (systolic and diastolic), and 24-hour heart rate did not enter the equation.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The present study provides new insight into the prevalence and determinants of ventricular arrhythmias in subjects with essential hypertension. In our cohort of never-treated subjects, advancing age and echocardiographic LV hypertrophy were significant predictors of ventricular arrhythmias. However, the most important finding of this study was the inverse relation between nocturnal BP decline and the prevalence and complexity of ventricular arrhythmias. In a multivariate analysis, this association remained significant after correction for potential confounding factors.
Previous Studies
The finding of increased ventricular arrhythmias in individuals with LV hypertrophy is in agreement with most,3 4 5 6 7 8 9 10 but not all,11 12 previous studies. This association has been questioned12 because most published studies included subjects previously or currently treated.3 4 5 6 7 8 9 10 This may introduce a bias since long-term antihypertensive treatment might affect the association between BP, LV hypertrophy, and ventricular arrhythmias because it may induce changes in LV mass and occasionally increase the risk of ventricular arrhythmias11 and sudden cardiac death.13 So far, only two studies11 12 have investigated the relation between LV hypertrophy and ventricular arrhythmias in never-treated hypertensive individuals, and both failed to demonstrate an increased prevalence of arrhythmias in the subset with LV hypertrophy compared with that without it. However, the smaller sample size in those studies compared with the present study (38 subjects with and 16 without hypertrophy in one study,11 21 subjects with and 29 without hypertrophy in the other12 ) might have precluded the detection of a difference between the groups. Moreover, at variance with James and Jones,12 who used ECG, the present study used echocardiography, a more-sensitive technique for determination of LV hypertrophy.31 32 In the present study, we found an increased complexity of arrhythmias (Lown class 2) in subjects with ECG LV hypertrophy only when hypertrophy was defined with the more-sensitive multifactorial criterion.31
The present study provides the first evidence of an association between LV hypertrophy and ventricular arrhythmias in never-treated subjects with essential hypertension. However, the mechanisms underlying this association remain unclear. LV hypertrophy could be a marker of silent coronary disease; furthermore, cardiac hypertrophy may predispose to ventricular arrhythmias even in the absence of coronary artery disease.5 Hypertrophied hearts show prolongation and greater dispersion of the action potential duration33 34 35 and altered conduction velocity due to myocardial fibrosis,36 37 38 which may be a potential source of reentry.
Persistence of High BP Values
Two previous articles reported simultaneous 24-hour ambulatory BP and ECG recordings in hypertensive subjects,3 39 but in those studies, the relation between diurnal BP variations and ventricular arrhythmias was not analyzed. In hypertensive individuals, the persistence of high BP values over 24 hours (nondipping pattern) has been associated with increased LV mass,17 18 19 more advanced vascular structural changes,19 higher target-organ damage score,40 and increased silent cerebrovascular damage.41 Recently, increased cardiovascular morbidity and mortality have been found in hypertensive individuals with a blunted nocturnal reduction in BP.20 21
In the present study, we observed a significant independent association between a blunted reduction in systolic BP from day to night and the number and complexity of ventricular arrhythmias. It is tempting to speculate that a constant, long-standing hemodynamic burden might predispose the ventricular myocardium to initiate an arrhythmic event in response to trigger factors, such as a sudden rise in BP.42 Average BP levels did not show any significant relationship with ventricular arrhythmias. Only pulse pressure, both clinic and 24-hour, showed significant univariate correlations with the number and complexity of ventricular arrhythmias (Table 3), but these associations were not significant in a multivariate model. These results are in keeping with those obtained by Melina et al,39 who did not find any association between ambulatory BP levels and ventricular arrhythmias in 78 subjects with borderline hypertension. The finding of a lower reduction in heart rate from day to night in nondippers than in dippers suggests the possibility that nondippers may fail to downregulate sympathetic tone during sleep or that they may not increase their daytime activity as much as dippers.
The present study identified some important determinants of ventricular arrhythmias in hypertension. However, the best-fitting regression equation, including age, LV hypertrophy, cigarette smoking, and day-night BP changes, accounted for only 35% of the observed variance in the number of PVBs over the 24 hours. This suggests that other factors make an appreciable contribution to the development of arrhythmias in hypertensive subjects.
Study Limitations
We carried out a 24-hour session of ambulatory ECG recording, whose reproducibility is inferior to that achievable with more prolonged recording periods.43 Moreover, we studied untreated and normokalemic hypertensive subjects, and our conclusions perhaps cannot be extrapolated to treated hypertensive subjects.
Conclusions
In addition to age and LV hypertrophy at echocardiography, a persistent pressure overload (nondipping pattern) detected with ambulatory BP monitoring is an independent predictor of the frequency and complexity of ventricular arrhythmias in never-treated subjects with essential hypertension. These findings suggest a hypothetical relation between persistent pressure overload and sudden cardiac death in individuals with essential hypertension, particularly when LV hypertrophy and old age coexist. Large prospective studies are needed to address this important issue.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
This work was supported in part by grants provided by the Associazione Umbra Cuore e Ipertensione, Perugia, Italy.
Received January 29, 1996; first decision February 21, 1996; accepted April 18, 1996.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Kannel WB, McGee DL. Epidemiology of sudden death: insights from the Framingham study. In: Josephson MS, ed. Sudden Cardiac Death. Philadelphia, Pa: FA Davis Co; 1985:93-105.
2. Kannel WB, Schatzkin A. Sudden death: lessons from subsets in population studies. J Am Coll Cardiol. 1985;5:141B-149B.
3. Messerli FH, Ventura HO, Elizardi DJ, Dunn FG, Frohlich ED. Hypertension and sudden death: increased ventricular ectopic activity in left ventricular hypertrophy. Am J Med. 1984;77:18-22.[Medline] [Order article via Infotrieve]
4.
Zehender M, Meinertz T, Hohnloser S, Geibel A, Gerisch U, Olschewski M, Just H. Prevalence of circadian variations and spontaneous variability of cardiac disorders and ECG changes suggestive of myocardial ischemia in systemic arterial hypertension. Circulation. 1992;85:1808-1815.
5. Ghali JK, Kadakia S, Cooper RS, Liao Y. Impact of left ventricular hypertrophy on ventricular arrhythmias in the absence of coronary artery disease. J Am Coll Cardiol. 1991;17:1277-1282.[Abstract]
6. Levy D, Anderson KM, Savage DD, Balkus SA, Kannel WB, Castelli WP. Risk of ventricular arrhythmias in left ventricular hypertrophy: the Framingham Heart Study. Am J Cardiol. 1987;60:560-565.[Medline] [Order article via Infotrieve]
7. McLenachan JM, Henderson E, Morris KI, Dargie HJ. Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy. N Engl J Med. 1987;317:787-792.[Abstract]
8. Siegel D, Cheitlin MD, Black DM, Seeley D, Hearst N, Hulley SB. Risk of ventricular arrhythmias in hypertensive men with left ventricular hypertrophy. Am J Cardiol. 1990;65:742-747.[Medline] [Order article via Infotrieve]
9. Kostis JB, Lacy CR, Shindler DM, Borhani NO, Dallas Hall W, Wilson AC, Krieger S, Chelton S. Frequency of ventricular ectopic activity in isolated systolic systemic hypertension. Am J Cardiol. 1992;69:557-559.[Medline] [Order article via Infotrieve]
10. Schmieder RE, Messerli FH. Determinants of ventricular ectopy in hypertensive cardiac hypertrophy. Am Heart J. 1992;123:89-95.[Medline] [Order article via Infotrieve]
11. Mayet J, Shahi M, Poulter NR, Sever PS, Thom SAM, Foale RA. Ventricular arrhythmias in hypertension: in which patients do they occur? J Hypertens. 1995;13:269-276.[Medline] [Order article via Infotrieve]
12. James MA, Jones JV. Ventricular arrhythmias in untreated newly presenting hypertensive patients compared with a matched normal population. J Hypertens. 1989;7:409-415.[Medline] [Order article via Infotrieve]
13.
Hoes AW, Grobbee DE, Lubsen J, Man in't Veld AJ, van der Does E, Hofman A. Diuretics, ß-blockers, and the risk for sudden cardiac death in hypertensive patients. Ann Intern Med. 1995;123:481-487.
14. Maron BJ, Savage DD, Wolfson JK, Epstein SE. Prognostic significance of 24-hour ambulatory electrocardiographic monitoring in patients with hypertrophic cardiomyopathy: a prospective study. Am J Cardiol. 1981;48:252-257.[Medline] [Order article via Infotrieve]
15. Ruberman W, Weinblatt E, Goldberg JD, Frank CW, Shapiro S. Ventricular premature beats and mortality after myocardial infarction. N Engl J Med. 1977;297:750-757.[Abstract]
16. Bikkina M, Larson MG, Levy D. Asymptomatic ventricular arrhythmias and mortality risk in subjects with left ventricular hypertrophy. J Am Coll Cardiol. 1993;22:1111-1116.[Abstract]
17.
Verdecchia P, Schillaci G, Guerrieri M, Gatteschi C, Benemio G, Boldrini F, Porcellati C. Circadian blood pressure changes and left ventricular hypertrophy in essential hypertension. Circulation. 1990;81:528-536.
18. Kuwajima I, Suzuki Y, Shimosawa T, Kanemaru A, Hoshino S, Kuramoto K. Diminished nocturnal decline in blood pressure in elderly hypertensive patients with left ventricular hypertrophy. Am Heart J. 1992;67:1307-1311.
19. Rizzoni D, Muiesan ML, Montani G, Zulli R, Calebich S, Agabiti-Rosei E. Relationship between initial cardiovascular structural changes and daytime and nighttime blood pressure monitoring. Am J Hypertens. 1992;5:180-186.[Medline] [Order article via Infotrieve]
20.
Verdecchia P, Porcellati C, Schillaci G, Borgioni C, Ciucci A, Battistelli M, Guerrieri M, Gatteschi C, Zampi I, Santucci A, Santucci C, Reboldi G. Ambulatory blood pressure: an independent predictor of prognosis in essential hypertension. Hypertension. 1994;24:793-801.
21. Kuwajima I, Araki A, Suzuki Y, Watanabe S, Shibata S, Ozawa T, Kuramoto K. Prognostic value of 24-hour ambulatory blood pressure: a prospective study in the elderly. J Hypertens. 1994;12(suppl 3):S13. Abstract.
22. van Ittersum FJ, Ijzerman RG, Stehouwer CDA, Donker AJM. Analysis of twenty-four-hour blood pressure monitoring: what time period to assess blood pressure during waking and sleeping. J Hypertens. 1995;13:1053-1058.[Medline] [Order article via Infotrieve]
23. Verdecchia P, Schillaci G, Boldrini F, Guerrieri M, Zampi I, Porcellati C. Quantitative assessment of day-to-day spontaneous variability in non-invasive ambulatory blood pressure measurements in essential hypertension. J Hypertens. 1991;9(suppl 6):S322-S323.
24.
Lown B, Wolf M. Approaches to sudden death from coronary heart disease. Circulation. 1971;44:130-142.
25.
Sahn DJ, DeMaria A, Kisslo J, Weyman A, the Committee on M-Mode Standardization of the American Society of Echocardiography. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation. 1978;58:1072-1083.
26. Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, Reichek N. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol. 1986;57:450-458.[Medline] [Order article via Infotrieve]
27. De Simone G, Daniels SR, Devereux RB, Meyer RA, Roman MJ, De Divitiis O, Alderman MH. Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and the impact of overweight. J Am Coll Cardiol. 1992;20:1251-1260.[Abstract]
28. De Simone G, Devereux RB, Daniels SR, Koren MJ, Meyer RA, Laragh JH. Effect of growth on variability of left ventricular mass: assessment of allometric signals in adults and children and their capacity to predict cardiovascular risk. J Am Coll Cardiol. 1995;25:1056-1062.[Abstract]
29. De Simone G, Ganau A, Verdecchia P, Devereux RB. Echocardiography in arterial hypertension: when, why and how? J Hypertens. 1994;12:1129-1136.[Medline] [Order article via Infotrieve]
30. Casale PN, Devereux RB, Kligfield P, Eisenberg RR, Miller DH, Chaudhary BS, Phillips MC. Electrocardiographic detection of left ventricular hypertrophy: development and prospective validation of improved criteria. J Am Coll Cardiol. 1985;6:572-580.[Abstract]
31. Schillaci G, Verdecchia P, Borgioni C, Ciucci A, Guerrieri M, Zampi I, Battistelli M, Bartoccini C, Porcellati C. Improved electrocardiographic diagnosis of left ventricular hypertrophy. Am J Cardiol. 1994;74:714-719.[Medline] [Order article via Infotrieve]
32.
Levy D, Labib SB, Anderson KM, Christiansen JC, Kannel WB, Castelli WP. Determinants of sensitivity and specificity of electrocardiographic criteria for left ventricular hypertrophy. Circulation. 1990;81:815-820.
33. Cameron JS, Myerburg RJ, Wong SS, Gaide MS, Epstein K, Alvarez TR, Gelband H, Guse PA, Bassett AL. Electrophysiological consequences of chronic experimentally induced left ventricular pressure overload. J Am Coll Cardiol. 1983;2:481-487.[Abstract]
34.
Scamps F, Mayoux E, Charlemagne D, Vassort G. Calcium current in single cells isolated from normal and hypertrophied rat heart. Circ Res. 1990;67:199-208.
35.
Keung CE, Aronson RS. Non-uniform electrophysiological properties and electrotonic interaction in hypertrophied rat myocardium. Circ Res. 1981;49:150-158.
36. Caspari PG, Newcomb M, Gibson K, Harris P. Collagen in the normal and hypertrophied human ventricle. Cardiovasc Res. 1977;11:554-558.[Medline] [Order article via Infotrieve]
37. Toyoshima H, Park Y-D, Ishikawa Y, Nagata S, Hirata Y, Sakakibara H, Shimomura K, Nakayama R. Effects of ventricular hypertrophy on conduction velocity of activation front in the ventricular myocardium. Am J Cardiol. 1982;49:1938-1945.[Medline] [Order article via Infotrieve]
38. McLenachan JM, Dargie HJ. Ventricular arrhythmias in hypertensive left ventricular hypertrophy: relationship to coronary artery disease, left ventricular dysfunction, and myocardial fibrosis. Am J Hypertens. 1990;3:735-740.[Medline] [Order article via Infotrieve]
39. Melina D, Colivicchi F, Guerrera G, Melina G, Frustaci A, Caldarulo M, Guerrera C. Prevalence of left ventricular hypertrophy and cardiac arrhythmias in essential hypertension. Am J Hypertens. 1992;5:570-573.[Medline] [Order article via Infotrieve]
40.
Palatini P, Penzo M, Racioppa A, Zugno E, Guzzardi G, Anaclerio M, Pessina AC. Clinical relevance of nighttime blood pressure and of daytime blood pressure variability. Arch Intern Med. 1992;152:1855-1860.
41. Shimada K, Kawamoto A, Matsubayashi K, Nishinaga M, Kimura S, Ozawa T. Diurnal blood pressure variations and silent cerebrovascular damage in elderly patients with hypertension. J Hypertens. 1992;10:875-878.[Medline] [Order article via Infotrieve]
42.
Sideris A, Kontoyannis DA, Michalis L, Adractas A, Moulopoulos SD. Acute changes in blood pressure as a cause of cardiac arrhythmias. Eur Heart J. 1987;8:45-52.
43.
Morganroth J, Michelson EL, Horowitz LN, Josephson ME, Pearlman AS, Dunkman WB. Limitations of routine long-term electrocardiographic monitoring to assess ventricular ectopic frequency. Circulation. 1978;58:408-414.
This article has been cited by other articles:
 |
|
 |
|
  K. Wachtell, P. M. Okin, M. H. Olsen, B. Dahlof, R. B. Devereux, H. Ibsen, S. E. Kjeldsen, L. H. Lindholm, M. S. Nieminen, and K. Thygesen Regression of Electrocardiographic Left Ventricular Hypertrophy During Antihypertensive Therapy and Reduction in Sudden Cardiac Death: The LIFE Study Circulation, August 14, 2007; 116(7): 700 - 705. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A Yildirir, M. K Batur, and A Oto Hypertension and arrhythmia: blood pressure control and beyond Europace, January 1, 2002; 4(2): 175 - 182. [Abstract] [PDF]
|
|
|
|
 |
|
 A. Caplea, D. Seachrist, G. Dunphy, and D. Ely SHR Y chromosome enhances the nocturnal blood pressure in socially interacting rats Am J Physiol Heart Circ Physiol, July 1, 2000; 279(1): H58 - H66. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Wolk Arrhythmogenic mechanisms in left ventricular hypertrophy Europace, January 1, 2000; 2(3): 216 - 223. [Abstract] [PDF]
|
|
|
|
 |
|
 V. Palmieri, G. de Simone, M. J. Roman, J. E. Schwartz, T. G. Pickering, and R. B. Devereux Ambulatory Blood Pressure and M;etabolic Abnormalities in Hypertensive Subjects With Inappropriately High Left Ventricular Mass Hypertension, November 1, 1999; 34(5): 1032 - 1040. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||