(Hypertension. 2002;39:739.)
© 2002 American Heart Association, Inc.
Scientific Contributions |
From Department of Heart Disease, Haukeland University Hospital (E.G.), Bergen, Norway; Department of Medicine, Helsinki University Central Hospital (L.O.), Helsinki, Finland; Department of Medicine, Weill Medical College of Cornell University (V.P., R.B.D.), New York, NY; Department of Medicine, Vestfold Central Hospital (J.E.O.), Tönsberg, Norway, Department of Medicine, Copenhagen County University Hospital (K.W.), Glostrup, Denmark; Department of Medicine, Skellefteaa Hospital and Umeaa University (K.B.), Skellefteaa, Sweden; and Department of Medicine, Sahlgrenska University Hospital-Östra (B.D.), Gothenburg, Sweden.
Correspondence to Eva Gerdts MD, PhD, Department of Heart Disease, Haukeland University Hospital, N-5021 Bergen, Norway. E-mail evgerdts{at}online.no
| Abstract |
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Key Words: left atrial size hypertrophy age body mass index
| Introduction |
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Recent studies have shown that LA enlargement is a risk factor for atrial fibrillation and stroke, especially in men.7,8 LV hypertrophy has been suggested to mediate, at least partially, the relation between hypertension and LA enlargement. However, correlates of LA size in hypertensive patients with LV hypertrophy have so far not been assessed in a large-scale study. Thus, the aim of the present study was to describe factors associated with LA enlargement in hypertensive patients with electrocardiographic LV hypertrophy recruited into the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study.
| Methods |
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2440 mVxms). Baseline characteristics of the total LIFE study population and study design for the LIFE echocardiographic substudy have been previously published.9,10 Electrocardiographic LA enlargement was diagnosed by P-terminal forces in lead V1 criteria and considered present if terminal P-wave area was
-0.04 mVxsec.11 Sitting blood pressure and heart rate were measured at baseline clinical visits. Pulse pressure was calculated as the difference between systolic and diastolic blood pressure, and mean blood pressure as diastolic blood pressure plus one third of pulse pressure. All patients gave written informed consent to participate in the echocardiographic substudy.
Study Design
All examinations were performed with commercially available phased-array transducers, using frequencies between 2.5 and 3.5 MHz, and recorded on VHS videotapes. Recordings were made by a standardized previously published protocol.10,12 Blood pressure measured by mercury or regularly calibrated aneroid cuff manometer at the end of the echocardiographic examination was used for calculation of end-systolic stress, pulse pressure/stroke volume ratio, and total peripheral resistance. All video recordings were sent for blinded interpretation at the Echocardiographic Reading Center at The New York HospitalCornell Medical Center.
Echocardiographic Methods
Measurements at the Echocardiographic Reading Center were made using a computerized review station equipped with digitizing table and monitor screen overlay. LV internal diameters and wall thicknesses at end-diastole and end-systole were measured by M-mode echocardiography following the American Society of Echocardiography recommendations on up to 3 cardiac cycles.13,14
LA diameter was measured in the parasternal long-axis view from the trailing edge of the posterior aortic-anterior left atrial complex to avoid including the variable size of the connective tissue filled space between these structures erroneously in atrial diameter, as previously reported.15 The LA was considered enlarged when LA diameter exceeded 3.8 cm in women and 4.2 cm in men, the upper limit of the 95% confidence interval of LA size found in 413 apparently normal adults in another study from the Reading Center.15
LV mass was calculated by an anatomically validated formula (r=0.90 versus necropsy LV mass).16 LV mass showed excellent interstudy reliability (RHO=0.93) in a separate study of 183 patients from the Reading Center.17 LV hypertrophy was considered present when LV mass/body surface area exceeded 116 g/m2 in men and 104 g/m2 in women.18 Relative wall thickness (RWT) was calculated at end-diastole as posterior wall thickness/internal radius.19 Increased RWT was regarded present when the ratio was
0.43.20 LV geometry was assessed from LV mass/body surface area and RWT in combination.20 Midwall fractional shortening was calculated from parasternal short-axis using a formula previous validated formula.21 Circumferential end-systolic stress was estimated at midwall from M-mode tracings using a formula derived from the cylindric model by Gaasch et al.22,23 Stroke volume, calculated by an invasively validated Doppler echocardiographic method, was used to calculate cardiac output and total peripheral resistance.24
The leading edge of transmitral Doppler flow pattern was traced to derive the peak early (E) and atrial (A) LV filling phase and their ratio (E/A). Atrial filling fraction was calculated as the ratio of the A-wave time velocity integral to the total diastolic time velocity integral. E/A ratios of <0.6 and >1.5 measured at mitral anular level have previously been identified as the fifth and 95th percentiles of a reference range in 124 apparently normal adults in another study from the Reading Center.25 Using a previously published equation26 predicting E/A ratio at mitral leaflet tips from measurements at mitral anulus, E/A ratios of <0.7 and >1.5 were regarded as low or high for age, respectively, in the present study population. An isovolumic relaxation time (IVRT)
105 ms was regarded prolonged in all patients. Mitral regurgitation was assessed from color Doppler recordings using a previously described 4-point grading system based on the farthest distance reached from the mitral orifice adjusted for jet width when appropriate.27
Statistical Analyses
SPSS statistical computing program version 10.0 (SPSS Inc) was used for data management and analysis. Continuous variables are expressed as mean±SD; categorical data, as percentages. Differences in continuous and categorical variables between the groups of patients with normal and enlarged LA size were assessed by unpaired samples Students t tests and
2 analyses, respectively. Differences in LA size between groups of patients with different LV geometry and E/A ratios were assessed by one-way ANOVA followed by the Scheffé post hoc test. LA size in white and black participants was compared in a general linear model adjusting for age, height, weight, and gender. Bivariate correlations between LA size and LV geometric variables were assessed with Pearsons correlation coefficients. Binary logistic regression analysis was performed to identify covariates of LA enlargement. A 2-tailed P<0.05 was considered statistically significant.
| Results |
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Compared with patients with normal LA size, patients with LA enlargement had significantly larger LV internal chamber dimensions, stroke volume, and mass; a higher prevalence of echocardiographic LV hypertrophy; and a lower LV ejection fraction and relative wall thickness (Table 2). Similar results were found in alternative analyses that indexed LA diameter for body height. Doppler diastolic indices did not differ between the groups of patients with normal and enlarged LA, respectively. However, patients with high E/A ratio for age or prolonged IVRT and/or with low E/A ratio for age had significantly larger LA compared with patients with normal E/A ratio and IVRT for age (Table 3). Blood pressure, heart rate, gender distribution, and body mass index did not differ between these groups of patients.
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Both LA size and prevalence of LA enlargement differed significantly in relation to LV geometry, being larger in patients with eccentric LV hypertrophy (4.08±0.55 cm and 58%, respectively) than those with concentric LV hypertrophy (3.93±0.57 cm and 46%), normal LV geometry (3.73±0.47 cm and 28%), or concentric remodeling (3.70±0.52 cm and 32%), respectively (all, P<0.01).
Mitral regurgitation was present in 20% of patients with normal LA size and in 29% of patients with LA enlargement (P<0.01). The regurgitation was classified as grade 1 in the majority of patients (Table 2). Mitral regurgitation was more prevalent among women than men (30% versus 20%, P<0.001).
LA size as a continuous variable was positively related to age (r=0.13), weight (r=0.38), height (r=0.24), body mass index (r=0.26), systolic blood pressure (r=0.15), pulse pressure (r=0.11), LV mass (r=0.48), LV internal end-systolic (r=0.38) and end-diastolic diameter (r=0.43), interventricular septal and posterior wall thickness (r=0.24 and 0.23, respectively), stroke volume (r=0.18), end-systolic stress (r=0.22), E/A ratio (r=0.10), and IVRT (r=0.07) (all, P<0.01). Furthermore, LA size was negatively related to LV ejection fraction (r=-0.22), endocardial and midwall shortening (r=-0.21 and -0.14, respectively), relative wall thickness (r=-0.10), total peripheral resistance, and atrial filling fraction (both r=-0.07) (all, P<0.05).
A binary logistic regression model was created, using an indicator variable for LA enlargement as dependent variable, with age, body mass index, and indicator variables for LV geometry and hypertrophy, as well as for gender, and presence of atrial fibrillation and mitral regurgitation, respectively, as independent variables. LA enlargement was related to presence of LV hypertrophy, eccentric LV geometry, higher body mass index, systolic blood pressure and age, female gender, and presence of mitral regurgitation and atrial fibrillation (Nagelkerke R2=0.24, P<0.001) (Table 4). In another model replacing LV hypertrophy with LV mass, a similar result was found. Diastolic Doppler indices and indicator variables for previous myocardial infarction and stroke did not enter when included in additional models.
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ECG LA enlargement was present in 38% of patients in the study population. By echocardiography, patients with ECG LA enlargement had higher peak A velocity (0.83 versus 0.80 m/s, P<0.05), whereas left atrial diameter and LV mass/body surface area did not differ significantly (3.95±0.59 versus 3.90±0.52 cm, and 125±28 versus 122±24 g/m2, respectively, both P=0.06).
| Discussion |
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The first finding, that LA size was significantly related to LV mass, is in accordance with previous findings in older patients with isolated systolic hypertension.1 However, the present study adds to their findings by demonstrating a relation of LA size with LV geometry, as well as with LV mass and the prevalence of echocardiographic LV hypertrophy in a large group of patients, including both combined systolic-diastolic and isolated systolic hypertension. In particular, LA enlargement was associated with eccentric LV hypertrophy in these middle-aged and older hypertensive patients.
Obesity has previously been suggested to mediate the relation between LA size and LV mass in veteran studies.5,6 The present study modifies this conclusion by finding independent associations of both obesity and LV hypertrophy with LA enlargement. The different findings may be explained by major differences in patient characteristics including the presence of women, less obesity, and a higher prevalence of LV hypertrophy in the present study. Still, the impact of obesity on LA size in hypertensive patients is demonstrated both by the significantly larger body mass index found in patients with LA enlargement and by the independent relation between body mass index and absolute LA size. The mechanism by which overweight leads to LA enlargement is unclear, but a relation to hemodynamic changes seen in obese patients, including increased intravascular volume and larger stroke volume and cardiac output, has been suggested.28,29 This view is supported by our findings, as stroke volume, cardiac output, and body mass index were higher in patients with LA enlargement in the present study.
Systolic blood pressure is a well-established determinant of LV mass in hypertensives.30,31 A relation between systolic blood pressure and LA size has previously been reported in the Framingham Heart Study.32 Their report demonstrated LA enlargement to be associated both with the duration of elevated blood pressure and with the level of systolic pressure in a general population, and suggested LV hypertrophy to mediate the effect of systolic blood pressure on LA size.32 The present study adds to previous findings by showing that systolic pressure influences LA size in middle-aged and older hypertensive patients independent of LV hypertrophy.
Atrial fibrillation was present in only 1.6% of the study population. The prevalence is lower than expected from the age of this hypertensive population, probably because of exclusion from LIFE of patients that needed ß-blocker treatment for rate control of atrial fibrillation.9,33 Still, atrial fibrillation was independently associated with LA enlargement in the present study population, and was also associated with concomitant diabetes mellitus. These findings are in accordance with previous publications identifying hypertension and diabetes as major predictors of incident atrial fibrillation in general and hypertensive populations.33,34
The present study is to our knowledge the first to report mitral regurgitation as a predictor of LA enlargement, independent of other covariates, including LV hypertrophy and atrial fibrillation, in middle-aged and older hypertensives. Mitral regurgitation assessed by color Doppler echocardiography was present in 24% of the present study population. The prevalence is, as expected, somewhat higher than the about 20% prevalence reported from surveys of slightly younger population based samples.27,35
The present study also shows that LA enlargement was particularly common in women. Our finding that mitral regurgitation was more prevalent in women is in accordance with previous reports.27,35 However, female gender was associated with LA enlargement independent of mitral regurgitation and other known covariates of LA size in the present study. Previous reports in general population and population-based case control studies have found LA size in women to be associated with mitral regurgitation, but not with risk of stroke.8,27,35 The prognostic value of LA enlargement in men and women with respect to stroke will be addressed in a follow-up study of the present study population.
Theoretically, LA enlargement in hypertensive patients with LV hypertrophy can be secondary both to changes in systolic and diastolic LV function. In particular, electrocardiographic signs of LA enlargement has been regarded as an early clinical sign of reduced diastolic LV function in patients with normal systolic LV function.4 This clinical view is supported by several findings in the present study: patients with normal E/A ratio for age had smaller mean LA size; LA size was weakly but significantly associated with longer IVRT, higher E/A ratio, and lower atrial filling fraction, suggesting that both impaired relaxation and increased passive stiffness influence LA size. However, as most patients included in the present study had impaired diastolic function (in particular abnormal relaxation) as evaluated by diastolic Doppler indices, the relations between LA enlargement and diastolic Doppler indices were less striking, and none of the diastolic Doppler variables were identified as independent correlates of LA size in multivariate analyses.
In conclusion, echocardiographic LA enlargement is commonly found in hypertensive patients with electrocardiographic LV hypertrophy. In such patients, LA enlargement is particularly prevalent in older and more obese patients, as well as in women and patients with eccentric LV geometry, independent of the degree of LV hypertrophy or the presence of additional atrial fibrillation and mitral valve regurgitation.
| Acknowledgments |
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Received June 5, 2001; first decision September 13, 2001; accepted January 11, 2002.
| References |
|---|
|
|
|---|
2. Dunn FG, Chandraratna P, Decarvalho JGR, Basta LL, Frohlich ED. Pathophysiologic assessment of hypertensive heart disease with echocardiography. Am J Cardiol. 1977; 39: 789795.[CrossRef][Medline] [Order article via Infotrieve]
3.
Tarazi RC, Miller A, Frohlich ED, Dustan HP. Electrocardiographic changes reflecting left atrial abnormality in hypertension. Circulation. 1966; 34: 818822.
4.
Frohlich ED, Tarazi RC, Dustan HP. Clinical-physiological correlations in the development of hypertensive heart disease. Circulation. 1971; 44: 446455.
5. Gottdiener JS, Reda DJ, Williams DW, Materson BJ. Left atrial size of hypertensive men: influence of obesity, race and age. J Am Coll Cardiol. 1997; 29: 651658.[Abstract]
6.
Gottdiener JS, Domenic J, Reda MS, Williams DW, Materson BJ, Cushman W, Anderson RJ. Effect of single-drug therapy on reduction of left atrial size in mild to moderate hypertension. Circulation. 1998; 98: 140148.
7.
Benjamin EJ, DAgostino RB, Belanger AJ, Wolf PA, Levy D. Left atrial size and the risk of stroke and death: the Framingham Heart Study. Circulation. 1995; 92: 835841.
8.
Di Tullio MR, Sacco RL, Sciacca RR, Homma S. Left atrial size and the risk of ischemic stroke in an ethnically mixed population. Stroke. 1999; 30: 20192024.
9.
Dahlöf B, Beevers G, Devereux RB, de Faire U, Fyhrquist F, Ibsen H, Julius S, Kjeldsen SE, Lederballe-Pedersen O, Lindholm LH, Nieminen M, Omvik P, Oparil S, Wedel H, for the LIFE Study Group. The Losartan Intervention For Endpoint (LIFE) reduction in hypertension study: baseline characteristics of 9194 patients with left ventricular hypertrophy. Hypertension. 1998; 32: 989997.
10. Devereux RB, Roman MJ, Palmieri V, Okin PM, Boman K, Gerdts E, Nieminen MS, Papademetriou V, Wachtell K, Dahlöf B. Left ventricular wall stresses and wall stress-mass-heart rate products in hypertensive patients with electrocardiographic left ventricular hypertrophy: the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. J Hypertens. 2000; 18: 11291138.[CrossRef][Medline] [Order article via Infotrieve]
11.
Morris JJ Jr, Estes HE, Whalen RE, Thompson HK, McIntosh HD. P wave analysis in valvular heart disease. Circulation. 1964; 29: 242252.
12.
Wachtell K, Bella JN, Liebson PR, Gerdts E, Dahlöf B, Aalto T, Roman MJ, Papademetriou V, Ibsen H, Rokkedal J, Devereux RB. Impact of different partition values on prevalence of left ventricular hypertrophy and concentric geometry in a large hypertensive population: the LIFE study. Hypertension. 2000; 35: 612.
13.
Sahn DJ, De Maria A, Kisslo J, Weyman A. Recommendations regarding quantitation in M-mode echocardiography: results from a survey of echocardiographic measurements. Circulation. 1978; 58: 10721083.
14. Schiller NB, Shah PM, Crawford M, De Maria A, Devereux R, Feigenbaum H, Gutgesell H, Reichek N, Sahn D, Schnittger I, Silvermax NH, Tajik AJ. Recommendations for quantification of the left ventricle by two-dimensional echocardiography: American Society of Echocardiography Committee on Standards: Subcommittee on Quantification of Two-Dimensional Echocardiograms. J Amer Soc Echocardiogr. 1989; 2: 358367.[Medline] [Order article via Infotrieve]
15. Ilercil A, OGrady MJ, Roman MJ, Paranicas M, Lee ET, Welty TK, Fabsitz RR, Howard BV, Devereux RB. Reference values for echocardiographic left ventricular measurements in urban and rural populations of differing ethnicity: the Strong Heart Study. J Am Soc Echocardiogr. 2001; 14: 606611.
16. 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: 450458.[CrossRef][Medline] [Order article via Infotrieve]
17.
Palmieri V, Dahlöf B, DeQuattro V, Sharpe N, Bella JN, de Simone G, Paranicas M, Fishman D, Devereux RB. Reliability of echocardiographic assessment of left ventricular structure and function: the PRESERVE study. J Am Coll Cardiol. 1999; 34: 16251632.
18. Devereux RB, Dahlöf B, Levy D, Pfeffer MA. Comparison of enalapril versus nifedipine to decrease left ventricular hypertrophy in systemic hypertension (the PRESERVE trial). Am J Cardiol. 1996; 78: 6165.[Medline] [Order article via Infotrieve]
19. Reichek N, Devereux RB. Reliable estimation of peak left ventricular systolic pressure by M-mode echocardiographic-determined end-diastolic relative wall thickness: identification of severe valvular aortic stenosis in adult patients. Am Heart J. 1982; 103: 202209.[CrossRef][Medline] [Order article via Infotrieve]
20. Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB. Relation of arterial structure and function to left ventricular geometric patterns in hypertensive adults. J Am Coll Cardiol. 1996; 28: 751756.[Abstract]
21. de Simone G, Devereux RB, Roman MJ, Ganau A, Saba PS, Alderman MH, Laragh JH. Assessment of left ventricular function by midwall fractional shortening/end-systolic stress relation in human hypertension. J Am Coll Cardiol. 1994; 23: 14441451.[Abstract]
22.
Gaasch WH, Zile MR, Hoshino PK, Apstein CS, Blaustein AS. Stress-shortening relations and myocardial blood flow in compensated and failing canine hearts with pressure-overload hypertrophy. Circulation. 1989; 79: 872883.
23. Gaasch WH, Battle WE, Oboler AA, Banas-JS J, Levine HJ. Left ventricular stress and compliance in man: with special reference to normalized function curves. Circulation. 1972; 42: 746762.
24. Dubin J, Wallerson DC, Cody RJ, Devereux RB. Comparative accuracy of Doppler echocardiographic methods for clinical stroke volume determination. Am Heart J. 1990; 120: 11623.[CrossRef][Medline] [Order article via Infotrieve]
25. Bella JN, Palmieri V, Roman MJ, Liu JE, Welty TK, Fabsitz RR, Howard BV, Devereux RB. Prognostic significance of abnormal peak early to late diastolic filling ratio in middle-aged to elderly American Indians: the Strong Heart Study. J Am Coll Cardiol. 2000; 35: 293A. Abstract.
26. Palmieri V, Bella JN, DeQuattro V, Roman MJ, Hahn RT, Dahlöf B, Sharpe N, Lau CP, Chen WC, Paran E, de Simone G, Devereux RB. Relations of diastolic left ventricular filling to systemic chamber contractility in hypertensive patients with left ventricular hypertrophy: the PRESERVE study. Am J Cardiol. 1999; 84: 558562.[CrossRef][Medline] [Order article via Infotrieve]
27. Jones EC, Devereux RB, Roman MJ, Liu JE, Fishman D, Lee ET, Welty TK, Fabsitz RR, Howard BV. Prevalence and correlates of mitral regurgitation in a population-based sample: the Strong Heart Study. Am J Cardiol. 2001; 87: 298304.[CrossRef][Medline] [Order article via Infotrieve]
28.
Messerli FH, Ventura HO, Reisin E, Dreslinski GR, Dunn FG, MacPhee AA, Frohlich ED. Borderline hypertension and obesity: two prehypertensive states with elevated cardiac output. Circulation. 1982; 66: 5560.
29.
de Simone G, Devereux RB, Daniels SR, Mureddu GF, Roman MJ, Kimball TR, Greco R, Witt S, Contaldo F. Stroke volume and cardiac output in normotensive children and adults: assessment of relations with body size and impact of overweight. Circulation. 1997; 95: 18371843.
30. Gerdts E, Lund-Johansen P, Omvik P. Factors influencing left ventricular mass in salt sensitive and salt resistant essential hypertensive patients. Blood Press. 1998; 7: 223230.[Medline] [Order article via Infotrieve]
31. Hammond IW, Devereux RB, Alderman MH, Laragh JH. Relation of blood pressure and body build to left ventricular mass in normotensive and hypertensive employed adults. J Am Coll Cardiol. 1988; 12: 9961004.[Abstract]
32.
Vaziri SM, Larson MG, Lauer MS, Benjamin EJ, Levy D. Influence of blood pressure on left atrial size: the Framingham Heart Study. Hypertension. 1995; 25: 11551160.
33. Kannel B, Wolf PA, Benjamin EJ, Levy D, Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates. Am J Cardiol. 1998; 82 (8A): 2N9N.[CrossRef][Medline] [Order article via Infotrieve]
34. Ciaroni S, Cuenoud L, Bloch A. Clinical study to investigate the predictive parameters for the onset of atrial fibrillation in patients with essential hypertension. Am Heart J. 2000; 139: 814819.[Medline] [Order article via Infotrieve]
35. Singh J, Evans JC, Levy D, Larson MG, Freed LA, Fuller DL, Lehman B, Benjamin EJ. Prevalence and clinical determinants of mitral, tricuspid, and aortic regurgitation: the Framingham Heart Study. Am J Cardiol. 1999; 83: 897902.[CrossRef][Medline] [Order article via Infotrieve]
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