This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Verdecchia, P. Articles by Porcellati, C. Search for Related Content PubMed PubMed Citation Articles by Verdecchia, P. Articles by Porcellati, C. Pubmed/NCBI databases Medline Plus Health Information High Blood Pressure

(Circulation. 1998;97:48-54.)
© 1998 American Heart Association, Inc.

Clinical Investigation and Reports

Prognostic Significance of Serial Changes in Left Ventricular Mass in Essential Hypertension

Paolo Verdecchia, MD; Giuseppe Schillaci, MD; Claudia Borgioni, MD; Antonella Ciucci, MD; Roberto Gattobigio, MD; Ivano Zampi, MD; Gianpaolo Reboldi, MD, PhD; ; Carlo Porcellati, MD

From Ospedale Generale Regionale Raffaello Silvestrini, Area Omogenea di Cardiologia e Medicina, Perugia (P.V., C.B., A.C., R.G., I.Z., C.P.); Ospedale Beato G. Villa, Città della Pieve (G.S.); and DIMISEM Università di Perugia (G.R.), Italy. Presented in part at the Twelfth Scientific Meeting of the American Society of Hypertension, San Francisco, Calif, May 27–31, 1996. Correspondence to Dr Paolo Verdecchia, Ospedale Generale Regionale R. Silvestrini, Area Omogenea di Cardiologia e Medicina, Località San Sisto, 06156 Perugia PG, Italy.

	Abstract

Top Abstract Introduction Methods Results Discussion References

 
Background—Increased left ventricular (LV) mass predicts an adverse outcome in patients with essential hypertension. The purpose of this study was to determine the relation between changes in LV mass during antihypertensive treatment and subsequent prognosis.

Methods and Results—Procedures including echocardiography and 24-hour ambulatory blood pressure (BP) monitoring were performed in 430 patients with essential hypertension before therapy and after 1217 patient-years. Months or years after the follow-up visit, 31 patients suffered a first cardiovascular morbid event. The patients with a decrease in LV mass from the baseline to follow-up visit were compared with those with an increase in LV mass. There were 15 events (1.78 per 100 person-years) in the group with a decrease in LV mass and 16 events (3.03 per 100 person-years) in the group with an increase in LV mass (P=.029). In a Cox model, the lesser cardiovascular risk in the group with a decrease in LV mass (hazard ratio [HR], 0.46; 95% CI, 0.22 to 0.99) remained significant (P=.04) after adjustment for age (HR, 1.06; 95% CI, 1.03 to 1.10; P=.0008) and baseline LVH at ECG (HR, 3.85; 95% CI, 1.52 to 9.78; P=.012). In that model, baseline LV mass bordered on statistical significance (HR, 1.01; 95% CI, 1.00 to 1.03; P=.06). In the subset with LV mass >125 g/m² at the baseline visit (26% of subjects), the event rate was lower among the subjects who achieved regression of LVH than in those who did not (1.58 versus 6.27 events per 100 person-years; P=.002). This difference held in the multivariate analysis (HR, 0.18; 95% CI, 0.05 to 0.68).

Conclusions—In essential hypertension, a reduction in LV mass during treatment is a favorable prognostic marker that predicts a lesser risk for subsequent cardiovascular morbid events. Such an association is independent of baseline LV mass, baseline clinic and ambulatory BP, and degree of BP reduction.

Key Words: hypertension • prognosis • hypertrophy • echocardiography • electrocardiography

	Introduction

Top Abstract Introduction Methods Results Discussion References

 
Left ventricular hypertrophy detected at echocardiography in a single session predicts an increased risk for cardiovascular disease in patients with essential hypertension.^{1 2 3 4 5 6} Although the mechanisms of this association are undefined, LV mass is generally considered a biological assay that reflects and integrates the long-term cumulative effect of several risk factors for cardiovascular disease.⁷ Antihypertensive therapy may lead to regression of LVH,^{8 9} but the prognostic significance of this finding is still undetermined. In the Framingham Heart Study, the subjects with an increase of a quartile in the sum of the R wave in the aVL lead plus the S wave in the V₃ lead were twice as likely to suffer a cardiovascular morbid event over the subsequent years than those with a decrease by a quartile in the voltage score.¹⁰ However, the ECG is less sensitive than echocardiography for detection of LVH.^{11 12} Some investigations found a link between regression of echocardiographic LVH and cardiovascular disease in essential hypertension,^{13 14 15} but none of these studies could provide conclusive evidence of an independent predictive effect of serial changes in LV mass, in subjects free of cardiovascular disease, on the subsequent cardiovascular event risk. In the setting of the PIUMA registry,^{6 16} the purpose of the present study was to determine the prognostic significance of serial changes in LV mass in subjects who attended the baseline and follow-up visits free of cardiovascular disease. Because ambulatory BP monitoring was carried out at both visits, we could adjust for the potential confounding effect of ambulatory BP. In fact, the changes in LV mass during treatment correlate more closely with the concomitant changes in ambulatory BP than with the changes in clinic BP,^{17 18} and data from our laboratory suggest that the prognostic value of ambulatory BP is superior to that of clinic BP.^{6 16}

	Methods

Top Abstract Introduction Methods Results Discussion References

 
Subjects
We studied 430 hypertensive subjects (54.0% men) 48.2±11 years old (mean±SD) who attended the baseline visit and a follow-up visit in the setting of the PIUMA study, a prospective registry of morbidity and mortality in subjects with essential hypertension whose off-therapy initial diagnostic workup included 24-hour noninvasive ambulatory BP monitoring according to a standardized protocol. Details of the PIUMA registry have been reported previously.^{6 16} At entry, all patients had 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 the following inclusion criteria: (1) no previous treatment for hypertension (n=293) or withdrawal from antihypertensive drugs at least 4 weeks before the study (n=137); (2) no clinic or laboratory evidence of heart failure, renal failure, coronary artery disease, valvular defects, or secondary causes of hypertension; and (3) at least one valid BP measurement per hour over the 24 hours.

BP Measurement
Clinic BP was measured with a standard mercury sphygmomanometer with the subject sitting for at least 10 minutes. Clinic heart rate was determined immediately thereafter. Caffeine ingestion and cigarette smoking were not permitted during the previous 2 hours. Ambulatory BP was recorded with SpaceLabs units 90202 and 90207 set to take a reading every 15 minutes throughout the 24 hours. Normal daily activities were allowed, and patients were told to keep their nondominant arm still and relaxed to the side during measurements. The spontaneous day-to-day variability of ambulatory BP was assessed in some of these patients.¹⁹

Echocardiography
The M-mode echocardiographic study of the LV was performed under cross-sectional control with commercially available machines according to standard laboratory procedures.^{6 16} Echocardiographic examinations were performed by two physicians, and tracings were read by two other investigators. The mean value from at least five measurements of the LV per observer was computed. At the time of the echocardiographic examination, all involved investigators were unaware of all patients' clinical data, including office BP, ambulatory BP, and cardiovascular complications. LV mass was determined according to the formula introduced by Devereux et al²⁰ : 0.80x{1.04x[(septal thickness+LV internal diameter+posterior wall thickness)³ -(LV internal diameter)³ ]}+0.6 g and was normalized by body surface area. In our laboratory, the intraobserver coefficients of variation are 4.50% for septal thickness, 1.65% for LV internal diameter, 4.81% for posterior wall thickness, and 6.33% for LV mass index. Interobserver coefficients of variation are 6.30% for septal thickness, 1.65% for LV internal diameter, 6.73% for posterior wall thickness, and 7.65% for LV mass index.

Electrocardiography
Standard 12-lead ECGs were recorded in all subjects at 25 mm/s and 1-mV/cm calibration. Tracings were coded and interpreted by two investigators without knowledge of other patient data. Interobserver differences occurred in <5% of readings and were resolved by consensus. Complete bundle-branch block and Wolff-Parkinson-White syndrome were exclusion criteria from ECG analysis for LVH. Previous myocardial infarction and atrial fibrillation were exclusion criteria from the study. None of the subjects were being treated with digitalis. LVH was diagnosed by a Romhilt-Estes²¹ score 5 points.

Follow-up
All subjects were followed up by their family doctors in cooperation with the outpatient clinic of the referring hospital and were treated with the aim of reducing clinic BP <140/90 mm Hg by standard lifestyle and pharmacological measures. By protocol, therapeutic strategies were based on clinic BP, although ambulatory BP reports remained accessible to patients and their doctors. Diuretics, ß-blockers, ACE inhibitors, calcium channel blockers, and ₁-blockers, alone or in various combinations, were the antihypertensive drugs most frequently used.

The follow-up visit, including standard laboratory tests, 12-lead ECG, 24-hour ambulatory BP monitoring, and echocardiography, was undertaken after 1 to 10 years of follow-up (average, 2.8 years). The protocol for experimental procedures was the same as in the baseline studies. None of the patients had developed a cardiovascular morbid event at the time of the follow-up visit.

Contacts with family doctors of patients and telephone interviews were periodically undertaken to ascertain the incidence of major cardiovascular complications of hypertension. All interviews were conducted without knowledge of the results of echocardiographic studies or ambulatory BP monitoring. Many of the patients continued to be periodically referred to our institution for BP checks and other diagnostic procedures. A major effort was recently undertaken over 1 month to assess the vital status of all subjects.

End-Point Evaluation
Hospital record forms and other available original source documents were reviewed in conference by the authors of this study for the subjects who developed a cardiovascular morbid event. Cardiovascular events included new-onset coronary artery disease (myocardial infarction, or angina with concomitant ischemic ECG changes), stroke, transient cerebral ischemic attack, symptomatic aortoiliac occlusive disease verified at angiography, thrombotic occlusion of a retinal artery documented at fluoroangiography, progressive heart failure requiring hospitalization, and renal failure requiring dialysis. Transient ischemic attack was defined by the diagnosis, by a physician, of any sudden focal neurological deficit that cleared completely in <24 hours. Heart failure was defined by the simultaneous presence of at least two major criteria or one major plus two minor criteria as reported in the Framingham Heart Study.²² The international standard criteria used to diagnose cardiovascular events in the PIUMA study have been described elsewhere.^{6 16}

Data Analysis
Parametric data are reported as mean±SD. Standard descriptive and comparative statistical analyses were undertaken. Cardiovascular event rate is presented as the number of events per 100 patient-years based on the ratio of the observed number of events to the total number of patient-years of exposure. Survival curves were estimated by the Kaplan-Meier product-limit method²³ and compared by the Mantel (log-rank) test.²⁴ The effect of prognostic factors on survival was evaluated by the Cox semiparametric regression model.²⁵ In the Cox model, we tested the following covariates: age (years), sex (female, male), diabetes mellitus (no, yes), cardiac death in a parent at 55 years of age, baseline clinic systolic and diastolic BPs and their change from baseline to the follow-up visit, average 24-hour systolic and diastolic BPs and their change from baseline to the follow-up visit, smoking habits at the baseline visit (current smokers, previous smokers, never smokers) and failure of quitting smoking (those who continued smoking versus the others), serum cholesterol (mmol/L), body mass index (body weight in kilograms divided by the square of height in meters), ECG LVH defined by a Romhilt-Estes²¹ score 5 points (no, yes), and baseline LV mass index (grams divided by body surface area). Two groups were defined on the basis of changes in LV mass from baseline to follow-up: decrease in LV mass (group 1) or no change or increase in LV mass (group 2). Echocardiographic LVH was defined by an LV mass >125.0 g/m² because the prognostic value of such definition in uncomplicated subjects with essential hypertension is the most widely documented.^{4 5 6} We also tested the hypothesis of a different outcome between regressors and nonregressors in the subset with echocardiographic LVH at the baseline visit. The assumption of proportional hazard over time was verified before the analysis was performed and was met by all covariates. The assumption concerning risk linearity for continuous variables was verified by visual inspection. The other comparisons were made by Student's t test and ² test when appropriate. In two-tailed tests, values of P<.05 were considered statistically significant. BMDP package release 7 (BMDP Statistical Software) was used to perform the analyses.

	Results

Top Abstract Introduction Methods Results Discussion References

 
Table 1 shows the main characteristics of the whole population at baseline and follow-up visits. Basally, LV mass index was more closely correlated with average 24-hour ambulatory BP (r=.40 systolic and r=.37 diastolic, both P<.001) than with clinic BP (r=.22 systolic and r=.17 diastolic, both P<.001). There was a clinically consistent and statistically significant reduction in BP and LV mass over the follow-up period. There was also a small but significant increase in body weight and body mass index. The changes in LV mass index showed a closer association with the changes in 24-hour ambulatory systolic and diastolic BPs (r=.41 and r=.34, respectively, both P<.001) than with the changes in clinic BP (r=.34 and r=.34, respectively, all P<.001). Among routine laboratory tests, there was a small but statistically significant increase in total and HDL cholesterol and serum creatinine. Table 2 shows some demographic, BP, echocardiographic, and laboratory data in the two groups with reduction or no reduction in LV mass. Age at entry (48.3 versus 48.0 years) and sex distribution (44% versus 49% women) did not differ between the former and the latter groups (both P=NS).

View this table: [in this window] [in a new window]   Table 1. Main Clinical Characteristics in the Study Population at the Baseline and Follow-up Visits

View this table: [in this window] [in a new window]   Table 2. Demographic, Blood Pressure, Echocardiographic, and Biochemical Characteristics in the Study Groups Defined by Changes in LV Mass From Baseline to Follow-up

The proportions of subjects receiving lifestyle measures only, diuretics and/or ß-blockers alone or combined, ACE inhibitors and/or calcium channel blockers alone or combined, or various drug associations were 42.1%, 9.1%, 23.9%, and 24.9%, respectively, in the subset with reduction in LV mass and 49.7%, 13.1%, 15.2%, and 22.1% in the subset without any reduction in LV mass (P=.09).

Cardiovascular Morbidity
Months or years after the follow-up visit, there were 31 nonfatal cardiovascular morbid events. One additional patient died of intestinal cancer and another committed suicide, but there were no cardiovascular deaths. The 430 study subjects contributed 1367 person-years of observation over the entire study period up to the terminating event or censoring (mean, 3.2 years), and the overall event rate was 2.27 per 100 person-years. There were 10 subjects with stroke, 4 with myocardial infarction, 4 with transient ischemic attack, 9 with new-onset coronary artery disease, 1 with heart failure requiring hospitalization, 1 with new-onset aortoiliac occlusive disease, 1 with occlusion of the retinal artery, and 1 with renal failure requiring dialysis.

Distribution of antihypertensive treatments at the follow-up visit did not differ among the subjects with and those without future cardiovascular events (lifestyle measures only, diuretic and/or ß-blockers alone or combined, ACE inhibitors and/or calcium channel blockers alone or combined, or various drug associations in 16.1%, 9.7%, 38.7%, and 36.5% in the former versus 39.3%, 9.0%, 23.1%, and 28.6% in the latter, P=.06).

Only 5 of 162 subjects (3%) who were maintained on lifestyle interventions alone at the follow-up visit suffered morbid events in the future, versus 26 of the 268 subjects (9.7%) who received antihypertensive drugs (P=.017 between the groups [Yates' correction]). However, the former group had a lower cardiovascular risk profile at the baseline visit than the latter group. In fact, in this group the mean age (45 versus 50 years, P<.01), office BP (144/94 versus 160/100 mm Hg, both P<.01), average 24-hour BP (126/81 versus 142/91 mm Hg, both P<.01), and LV mass (97 versus 116 g/m², P<.01) were all lower than in the group that was subsequently treated with drugs.

ECG LVH and Cardiovascular Risk
At entry, the Romhilt-Estes²¹ score was 5 points in 23 subjects (prevalence, 5.3%). Consequently, the prognostic value of serial ECG changes could not be tested because of the small number of subjects with ECG LVH. However, the frequency of cardiovascular events was 26.1% among the subjects with baseline Romhilt-Estes score 5 points versus 5.8% among those with a lower score (P<.01), and the excess risk associated with ECG LVH held in the multivariate analysis (adjusted HR, 3.85; 95% CI, 1.52 to 9.78; P=.012). Therefore, despite its low prevalence, LVH diagnosed at ECG by the Romhilt-Estes score identified a subset at increased cardiovascular risk.

Echocardiographic LVH and Cardiovascular Risk
Total Population
The prevalence of LVH at echocardiography (LV mass >125.0 g/m²) was 26%, and the event rate in this group was higher (3.9 events per 100 person-years) than among subjects with normal LV mass (1.6 events per 100 person-years). Fig 1 shows event-free survival curves in the two groups. There were 15 events (1.78 per 100 person-years) among the 285 subjects with a decrease in LV mass from baseline to follow-up visit and 16 events (3.03 per 100 person-years) in the group with no change or an increase in LV mass (P=.029, log-rank test). The different event rates in the two groups are depicted in Fig 2. In a Cox model, the lesser cardiovascular risk in the group with a decrease in LV mass (adjusted HR, 0.46; 95% CI, 0.22 to 0.99) remained significant (P=.04) after adjustment for age (adjusted HR, 1.06; 95% CI, 1.03 to 1.10; P=.0008) and baseline LVH at ECG (adjusted HR, 3.85; 95% CI, 1.52 to 9.78; P=.012). Baseline LV mass bordered on statistical significance (adjusted HR, 1.01; 95% CI, 1.00 to 1.03; P=.06). None of the other covariates (see Data Analysis), including clinic and ambulatory BPs and their changes from baseline to follow-up visit, attained statistical significance to enter the model. Because highly correlated risk variables, particularly clinic and ambulatory BPs, did not enter the model, collinearity between significant predictors was not a problem in the present study.

View larger version (22K): [in this window] [in a new window]   Figure 1. Event-free survival in the two groups with (thick line) and without (thin line) echocardiographic LVH at the baseline visit. BSA indicates body surface area.

View larger version (16K): [in this window] [in a new window]   Figure 2. Event rate in the two groups with LV mass reduction (open column) or increase (solid column) from baseline to follow-up visit.

Subset With Increased LV Mass
Among the subjects with LV mass >125 g/m² at the baseline visit, the event rate was considerably lower in the subset (n=52; 47%) with regression of LVH (LV mass <125 g/m² at the follow-up visit) than in that with LV mass persistently >125 g/m² (1.58 versus 6.27 events per 100 person-years; P=.002, log-rank test). Fig 3 shows survival curves in the two groups. In a Cox model, the lesser event risk in regressors compared with nonregressors (adjusted HR, 0.18; 95% CI, 0.05 to 0.68; P=.004) held after adjustment for age (adjusted HR, 1.08; 95% CI, 1.02 to 1.14; P=.0001), whereas none of the other covariates attained statistical significance to enter the model. A representative tracing of a patient with regression of echocardiographic LVH is reported in Fig 4.

View larger version (26K): [in this window] [in a new window]   Figure 3. Event rate in subset with echocardiographic LVH at baseline visit. Survival curves differed between those with regression (thin line) or persistence (thick line) of LVH at follow-up visit. BSA indicates body surface area.

View larger version (60K): [in this window] [in a new window]   Figure 4. Representative tracings of a patient with regression of LVH.

	Discussion

Top Abstract Introduction Methods Results Discussion References

 
The most important result of this study is that a serial reduction in LV mass in uncomplicated subjects with essential hypertension has a favorable prognostic value by predicting a lesser risk for subsequent cardiovascular disease. This association was independent of baseline LV mass, baseline clinic and ambulatory BPs, and BP changes from baseline to follow-up visit. These results were obtained in a 100% white population and may not be applicable to other racial groups.

Previous Studies
In contrast to previous echocardiographic studies that assessed the prognostic value of baseline LVH,^{1 2 3 4 5 6 26} we evaluated the implications of serial changes in LV mass on the subsequent cardiovascular risk. To the best of our knowledge, only three studies^{13 14 15} examined the relation between changes in LV mass and cardiovascular disease risk in patients with essential hypertension. In one study, available in abstract form,¹³ 166 hypertensive patients had echocardiographic examinations before and after an average of 5 years of treatment. Over the subsequent years, there were 18 cardiovascular morbid events, which occurred more frequently in the subjects with an increase (16%) than in those with a decrease (6%) in LV mass.¹³ In another study,¹⁴ 304 hypertensive men with echocardiographic LVH were followed for 4 years with an echocardiographic check every year, and during this period, LV mass decreased by 30 g in the subjects without new cardiovascular events, versus an increase of 0.3 g in those with new events. However, LV mass was measured by the Teichholz formula, which underestimates anatomic LV mass,²⁰ and data analysis did not take into account the potential confounding effect of several associated risk factors. In another study,¹⁵ 151 white subjects underwent echocardiography before therapy and after 7 to 13 years of follow-up. The frequency of cardiovascular morbid events was higher in the subjects who failed to achieve regression of LVH at follow-up than in those with persistently normal LV mass, whereas the event rate in the group with regression of LVH did not differ from that with persistently normal LV mass.¹⁵ However, a limitation of that study was that some of the events occurred before the follow-up echocardiographic study,¹⁵ and therefore, apart from a link between changes in LV mass and cardiovascular morbidity, that study could not determine the predictive effect on the subsequent outcome of serial changes in LV mass in subjects still free of cardiovascular disease. In contrast, the present study was carried out in subjects still free of cardiovascular morbid events when they attended the follow-up examination.

Our results are in agreement with a recent report from Framingham based on serial ECG examinations in a general population sample.¹⁰ In the present study, we targeted uncomplicated hypertensive subjects to specifically examine LV structural changes secondary to essential hypertension.

ECG LV Hypertrophy
The prevalence of LVH was 5.3% by the Romhilt-Estes ECG score and 26% by echocardiographic LV mass. The low prevalence of LVH at the baseline ECG study precluded the prognostic assessment of its regression over time. However, the frequency of cardiovascular events was considerably higher (P<.01) in the subset with (26.1%) than in that without (5.8%) LVH at the baseline ECG. Hence, despite its low prevalence, ECG LVH allowed identification of a subset at increased cardiovascular risk.

Echocardiographic LVH
An important finding in this study was that the favorable prognostic impact of LV mass reduction remained significant in a multivariate analysis that considered baseline LV mass and ECG LVH. In contrast, neither clinic nor ambulatory BP nor the other covariates yielded statistical significance to enter the model. Because the changes in LV mass over time showed a significant association with the changes in ambulatory BP and a weaker association with those in clinic BP, the degree of 24-hour BP control over time may have been important in influencing the degree of LVH regression. However, clinic BP on a single follow-up visit and even ambulatory BP on a single follow-up day might not be adequate to express the degree of BP control over years, and this may explain why the changes in LV mass, as "time-integrated markers of exposure to hypertension,"²⁶ were more potent than the recorded changes in clinic or ambulatory BP for prediction of cardiovascular risk. Moreover, progression of coronary artery lesions²⁶ and other risk factors for LVH and cardiovascular disease⁷ may have continued to be active in the high-risk subjects who failed to achieve reduction of LV mass or regression of LVH despite a reduction in BP.

An unexpected finding was the lower frequency of subsequent cardiovascular events in the subset maintained on lifestyle intervention alone than in that treated with antihypertensive drugs. Because the former group did show a lower cardiovascular risk profile at the baseline visit, treatment decisions may have selectively turned from nonpharmacological to pharmacological therapy in those patients who were identified on the basis of clinical judgment as being at highest risk of morbid events.

Limitations of the Study
A limitation of this study is the lack of fatal cardiovascular end points, which might be accounted for by the relatively young age of the subjects (48.2 years), the low prevalence of diabetes (3.0%), the absence of previous cardiovascular morbid events, and the relatively short duration of follow-up (average, 3.2 years). Consequently, the results of this study need further assessment in large, ongoing observational studies, including the CARDIA Study,²⁷ the Cardiovascular Health Study,²⁸ the Strong Heart Study,²⁹ and the Framingham Heart Study. Furthermore, several outcome trials comparing different antihypertensive regimens include echocardiography among experimental procedures.^{30 31 32 33} These trials have been specifically designed to see whether a particular antihypertensive therapeutic strategy is more advantageous over another in inducing regression of LVH, with subsequent prognostic implications. Compared with the present observational study, these intervention megatrials are also structured to permit a greater control of the time course of BP levels over several visits and long-term adherence to antihypertensive therapy.

Clinical Implications
In hypertensive patients, a "limited echocardiographic study" is clinically valuable and cost-effective,^{34 35} and in this setting, M-mode echocardiography may be cheaper than ECG per case of LVH detected.³⁶ Although limited by the relatively small sample size and by the lack of fatal end points, the present study suggests the clinical usefulness of periodic measurements of LV mass in patients with essential hypertension to improve cardiovascular risk stratification. The patients who fail to achieve reduction in LV mass or regression of LVH should be considered at increased risk for subsequent cardiovascular disease, and a more aggressive therapeutic approach is justified in these subjects.

	Selected Abbreviations and Acronyms

 

BP = blood pressure HR = hazard ratio LV = left ventricular, left ventricle LVH = left ventricular hypertrophy PIUMA = Progetto Ipertensione Umbria Monitoraggio Ambulatoriale

	Acknowledgments

 
This study was supported in part by grants from the Associazione Umbria Cuore e Ipertensione, Perugia, Italy. Appreciation is expressed to the Medical Department of Novartis Farma S.p.A., Italy, for technical assistance.

Received August 17, 1997; revision received September 17, 1997; accepted September 25, 1997.

	References

Top Abstract Introduction Methods Results Discussion References

 
1. Casale PN, Devereux RB, Milner M, Zullo G, Harshfield GA, Pickering TG, Laragh JH. Value of echocardiographic measurement of left ventricular mass in predicting cardiovascular morbid events in hypertensive men. Ann Intern Med. 1986;105:173–178.

2. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Left ventricular mass and incidence of coronary heart disease in an elderly cohort. Ann Intern Med. 1989;110:101–107.

3. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham heart study. N Engl J Med. 1990;322:1561–1566.[Abstract]

4. Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med. 1991;114:345–352.

5. Mensah GA, Koren MJ, Ulin R, Pappas TW, Nicholson J, Laragh JH, Devereux RB. Comparison of classification of the severity of hypertension by blood pressure level and by World Health Organization criteria in the prediction of concurrent cardiac abnormalities and subsequent complications in essential hypertension. J Hypertens. 1993;11:1429–1440.[Medline] [Order article via Infotrieve]

6. 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.[Abstract/Free Full Text]

7. Devereux RB, Roman MJ. Hypertensive cardiac hypertrophy: pathophysiologic and clinical characteristics. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis and Management. 2nd ed. New York, NY: Raven Press, Ltd; 1995:409–424.

8. Dahlof B, Pennert K, Hannson L. Reversal of left ventricular hypertrophy in hypertensive patients: a meta-analysis of 109 treatment studies. Am J Hypertens. 1992;5:95–110.[Medline] [Order article via Infotrieve]

9. Schmieder RE, Martus P, Klingbeil A. Reversal of left ventricular hypertrophy in essential hypertension: a meta-analysis of randomized double-blind studies. JAMA. 1996;275:1507–1513.[Abstract/Free Full Text]

10. Levy D, Salomon M, D'Agostino RB, Belanger AJ, Kannel WB. Prognostic implications of baseline electrocardiographic features and their serial changes in subjects with left ventricular hypertrophy. Circulation. 1994;90:1786–1793.[Abstract/Free Full Text]

11. 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.[Abstract/Free Full Text]

12. Woythaler JN, Singer SL, Kwan OL, Meltzer RS, Reubner B, Bommer W, DeMaria A. Accuracy of echocardiography versus electrocardiography in detecting left ventricular hypertrophy: comparison with postmortem mass measurements. J Am Coll Cardiol. 1983;2:305–311.[Abstract]

13. Koren MJ, Ulin RJ, Laragh JH, Devereux RB. Reduction of left ventricular mass during treatment of essential hypertension is associated with improved prognosis. Am J Hypertens. 1991;4:IA. Abstract.

14. Yurenev AP, Dyakonova HG, Novikov ID, Vitols A, Pahl L, Haynemann G. Management of essential hypertension in patients with different degrees of left ventricular hypertrophy: multicenter trial. Am J Hypertens. 1992;5(pt 2):182S–189S.

15. Muiesan ML, Salvetti M, Rizzoni D, Castellano M, Donato F, Agabiti-Rosei E. Association of change in left ventricular mass with prognosis during long-term antihypertensive treatment. J Hypertens. 1995;13:1091–1095.[Medline] [Order article via Infotrieve]

16. Verdecchia P, Schillaci G, Gatteschi C, Zampi I, Battistelli M, Bartoccini C, Porcellati C. Blunted nocturnal fall in blood pressure in hypertensive women with future cardiovascular morbid events. Circulation. 1993;88:986–992.[Abstract/Free Full Text]

17. Porcellati C, Verdecchia P, Schillaci G, Boldrini F, Motolese M. Long-term effects of benazepril on ambulatory blood pressure, left ventricular mass, diastolic filling and aortic flow in essential hypertension. Int J Clin Pharmacol Ther Toxicol. 1991;29:187–197.[Medline] [Order article via Infotrieve]

18. Mancia G, Zanchetti A, Agabiti Rosei E, Benemio G, De Cesaris R, Fogari R, Pessina A, Porcellati C, Salvetti A, Trimarco B, for the SAMPLE Study Group. Ambulatory blood pressure is superior to clinic blood pressure in predicting treatment-induced regression of left ventricular hypertrophy. Circulation. 1997;95:1464–1470.[Abstract/Free Full Text]

19. 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.

20. 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]

21. Romhilt DW, Estes EH. A point-score system for the ECG diagnosis of left ventricular hypertrophy. Am Heart J. 1968;75:752–759.[Medline] [Order article via Infotrieve]

22. McKee PA, Castelli WP, McNamara PM, Kannel WB. The natural history of congestive heart failure. N Engl J Med. 1971;285:1441–1446.

23. Kaplan ER, Meier P. Nonparametric estimation from incomplete observations. J Am Stat Assoc. 1958;53:457–481.

24. Mantel N. Evaluation of survival data and two new rank order statistics arising in its consideration. Cancer Chemother Rep. 1966;50:163–170.[Medline] [Order article via Infotrieve]

25. Cox DR. Regression models and life-tables. J R Stat Soc (B). 1972;34:187–220.

26. Liao Y, Cooper RS, McGee DL, Mensah G, Ghali JK. The relative effects of left ventricular hypertrophy, coronary artery disease, and ventricular dysfunction on survival among black adults. JAMA. 1995;273:1592–1597.[Abstract/Free Full Text]

27. Maron BJ, Gardin JM, Flack JM, Gidding SS, Kurosaki TT, Bild DE. Prevalence of hypertrophic cardiomyopathy in a general population of young adults: echocardiographic analysis of 4111 subjects in the CARDIA Study: Coronary Artery Risk Development in (Young) Adults. Circulation. 1995;92:785–789.[Abstract/Free Full Text]

28. Gardin J, Siscovick D, Anton-Culver H, Lynch JC, Smith VE, Klopfenstein HS, Bommer WJ, Fried L, O'Leary D, Manolio TA. Sex, age, and disease affect echocardiographic left ventricular mass and systolic function in the free-living elderly: the Cardiovascular Health Study. Circulation. 1995;91:1739–1748.[Abstract/Free Full Text]

29. Devereux RB, Roman MJ, Paranicas M, O'Grady MJ, Wood EA, Howard BV, Welty TK, Lee ET, Fabsitz RR. Relations of Doppler stroke volume and its components to left ventricular stroke volume in normotensive and hypertensive American Indians: the Strong Heart Study. Am J Hypertens. 1997;10:619–628.[Medline] [Order article via Infotrieve]

30. Devereux RB, Dahlof B, Levy D, Pfeffer MA. Comparison of enalapril vs nifedipine to decrease left ventricular hypertrophy in systemic hypertension (the PRESERVE trial). Am J Cardiol. 1996;78:61–65.[Medline] [Order article via Infotrieve]

31. Dahlof B, Devereux RB, de Faire U, Fyrquist F, Hedner T, Ibsen H, Julius S, Kjeldsen S, Kristianson K, Lederballe-Pedersen O, Lindholm L, Nieminen M, Omvik P, Oparil S, Wedel H. Losartan Intervention for Endpoint Reduction in Hypertension (the LIFE study). J Hypertens. 1996;14(suppl 1):S219. Abstract.

32. Bond G, Dal Palù C, Hansson L, Magnani B, Mancia G, Neiss A, Rahn KH, Reid JL, Rodicio JL, Safar M, Zanchetti A, on behalf of the ELSA Investigators. The ELSA trial: protocol of a randomized trial to explore the differential effect of antihypertensive drugs on atherosclerosis in hypertension. J Cardiovasc Pharmacol. 1994;23(suppl 5):S85–S87.

33. Liebson PR, Grandits GA, Dianzumba S, Prineas RJ, Grimm RH Jr, Neaton JD, Stamler J, for The Treatment of Hypertension Study Research Group. Comparison of five antihypertensive monotherapies and placebo for change in left ventricular mass in patients receiving nutritional-hygienic therapy in the Treatment of Mild Hypertension Study (TOMHS). Circulation. 1995;91:698–706.[Abstract/Free Full Text]

34. Black HR, Weltin G, Jaffe CC. The limited echocardiogram: a modification of standard echocardiography for use in routine evaluation of patients with systemic hypertension. Am J Cardiol. 1991;67:1027–1030.[Medline] [Order article via Infotrieve]

35. 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]

36. Devereux RB, Casale PN, Wallerson DC, Kligfield P, Hammond IW, Liebson PR, Campo E, Alonso DR, Laragh JH. Cost-effectiveness of echocardiography and electrocardiography for detection of left ventricular hypertrophy in patients with systemic hypertension. Hypertension. 1987;9(suppl II):II-69-II-76.

This article has been cited by other articles:

				A. S.P. Sharp, R. J. Tapp, S. A. M. Thom, D. P. Francis, A. D. Hughes, A. V. Stanton, A. Zambanini, E. O'Brien, N. Chaturvedi, S. Lyons, et al. Tissue Doppler E/E' ratio is a powerful predictor of primary cardiac events in a hypertensive population: an ASCOT substudy Eur. Heart J., November 26, 2009; (2009) ehp498v1. [Abstract] [Full Text] [PDF]

				N. Reichek, R. B. Devereux, R. A. Rocha, R. Hilkert, D. Hall, D. Purkayastha, and B. Pitt Magnetic Resonance Imaging Left Ventricular Mass Reduction With Fixed-Dose Angiotensin-Converting Enzyme Inhibitor-Based Regimens in Patients With High-Risk Hypertension Hypertension, October 1, 2009; 54(4): 731 - 737. [Abstract] [Full Text] [PDF]

				S.-A Chang, Y.-J. Kim, H.-W. Lee, D.-H. Kim, H.-K. Kim, H.-J. Chang, D.-W. Sohn, B.-H. Oh, and Y.-B. Park Effect of Rosuvastatin on Cardiac Remodeling, Function, and Progression to Heart Failure in Hypertensive Heart With Established Left Ventricular Hypertrophy Hypertension, September 1, 2009; 54(3): 591 - 597. [Abstract] [Full Text] [PDF]

				M. S. Willis, M. Rojas, L. Li, C. H. Selzman, R.-H. Tang, W. E. Stansfield, J. E. Rodriguez, D. J. Glass, and C. Patterson Muscle ring finger 1 mediates cardiac atrophy in vivo Am J Physiol Heart Circ Physiol, April 1, 2009; 296(4): H997 - H1006. [Abstract] [Full Text] [PDF]

				M. J. Raher, H. B. Thibault, E. S. Buys, D. Kuruppu, N. Shimizu, A.-L. Brownell, S. L. Blake, J. Rieusset, M. Kaneki, G. Derumeaux, et al. A short duration of high-fat diet induces insulin resistance and predisposes to adverse left ventricular remodeling after pressure overload Am J Physiol Heart Circ Physiol, December 1, 2008; 295(6): H2495 - H2502. [Abstract] [Full Text] [PDF]

				G. E. Peterson, T. de Backer, A. Gabriel, V. Ilic, T. Vagaonescu, L. J. Appel, G. Contreras, C. Kendrick, S. Rostand, R. A. Phillips, et al. Prevalence and Correlates of Left Ventricular Hypertrophy in the African American Study of Kidney Disease Cohort Study Hypertension, December 1, 2007; 50(6): 1033 - 1039. [Abstract] [Full Text] [PDF]

				M. Burnier, O. Phan, and Q. Wang High salt intake: a cause of blood pressure-independent left ventricular hypertrophy? Nephrol. Dial. Transplant., September 1, 2007; 22(9): 2426 - 2429. [Full Text] [PDF]

				A. Struthers and C. Lang The potential to improve primary prevention in the future by using BNP/N-BNP as an indicator of silent 'pancardiac' target organ damage: BNP/N-BNP could become for the heart what microalbuminuria is for the kidney Eur. Heart J., July 2, 2007; 28(14): 1678 - 1682. [Abstract] [Full Text] [PDF]

				E. S. Buys, M. J. Raher, S. L. Blake, T. G. Neilan, A. R. Graveline, J. J. Passeri, M. Llano, T. M. Perez-Sanz, F. Ichinose, S. Janssens, et al. Cardiomyocyte-restricted restoration of nitric oxide synthase 3 attenuates left ventricular remodeling after chronic pressure overload Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H620 - H627. [Abstract] [Full Text] [PDF]

				C. J. Barrick, M. Rojas, R. Schoonhoven, S. S. Smyth, and D. W. Threadgill Cardiac response to pressure overload in 129S1/SvImJ and C57BL/6J mice: temporal- and background-dependent development of concentric left ventricular hypertrophy Am J Physiol Heart Circ Physiol, May 1, 2007; 292(5): H2119 - H2130. [Abstract] [Full Text] [PDF]

				J. Burns, M. U. Sivananthan, S. G. Ball, A. F. Mackintosh, D. A.S.G. Mary, and J. P. Greenwood Relationship Between Central Sympathetic Drive and Magnetic Resonance Imaging-Determined Left Ventricular Mass in Essential Hypertension Circulation, April 17, 2007; 115(15): 1999 - 2005. [Abstract] [Full Text] [PDF]

				M J. S Zaman, J. Sanders, A. M Crook, G. Feder, M. Shipley, A. Timmis, and H. Hemingway Cardiothoracic ratio within the "normal" range independently predicts mortality in patients undergoing coronary angiography Heart, April 1, 2007; 93(4): 491 - 494. [Abstract] [Full Text] [PDF]

				V. Barrios, C. Escobar, A. Calderon, J. Pablo Tomas, S. Ruiz, J. L. Moya, A. Megias, O. Vegazo, and R. Fernandez Regression of left ventricular hypertrophy by a candesartan-based regimen in clinical practice The VIPE study Journal of Renin-Angiotensin-Aldosterone System, December 1, 2006; 7(4): 236 - 242. [Abstract] [PDF]

				N. B. Mascarenhas, R. Muthupillai, B. Cheong, M. Pereyra, and S. D. Flamm Fast 3D cine steady-state free precession imaging with sensitivity encoding for assessment of left ventricular function in a single breath-hold. Am. J. Roentgenol., November 1, 2006; 187(5): 1235 - 1239. [Abstract] [Full Text] [PDF]

				R. S. Vasan Biomarkers of Cardiovascular Disease: Molecular Basis and Practical Considerations Circulation, May 16, 2006; 113(19): 2335 - 2362. [Full Text] [PDF]

				Abstracts Heart, May 1, 2006; 92(suppl_2): A4 - A121. [Full Text] [PDF]

				G. Schillaci, M. Pirro, G. Pucci, M. R. Mannarino, F. Gemelli, D. Siepi, G. Vaudo, and E. Mannarino Different Impact of the Metabolic Syndrome on Left Ventricular Structure and Function in Hypertensive Men and Women Hypertension, May 1, 2006; 47(5): 881 - 886. [Abstract] [Full Text] [PDF]

				A. Morganti Randomized Clinical Trials on Surrogate End Points: Are They Useful for Evaluating Cardiovascular and Renal Disease Protection in Hypertension? The Case for Yes J. Am. Soc. Nephrol., April 1, 2006; 17(4_suppl_2): S141 - S144. [Abstract] [Full Text] [PDF]

				S. Ichihara, A. Noda, K. Nagata, K. Obata, J. Xu, G. Ichihara, S. Oikawa, S. Kawanishi, Y. Yamada, and M. Yokota Pravastatin increases survival and suppresses an increase in myocardial matrix metalloproteinase activity in a rat model of heart failure Cardiovasc Res, February 15, 2006; 69(3): 726 - 735. [Abstract] [Full Text] [PDF]

				W. H T Smith, R U. Nair, D. Adamson, M. T Kearney, S. G Ball, and A. J Balmforth Somatostatin receptor subtype expression in the human heart: differential expression by myocytes and fibroblasts J. Endocrinol., December 1, 2005; 187(3): 379 - 386. [Abstract] [Full Text] [PDF]

				K Y K Wong, S McSwiggan, N S J Kennedy, S Y S Wong, A Gavin, R S MacWalter, and A D Struthers Spectrum of cardiac abnormalities associated with long QT in stroke survivors Heart, October 1, 2005; 91(10): 1306 - 1310. [Abstract] [Full Text] [PDF]

				A. Sciacqua, A. Scozzafava, A. Pujia, R. Maio, F. Borrello, F. Andreozzi, M. Vatrano, S. Cassano, M. Perticone, G. Sesti, et al. Interaction between vascular dysfunction and cardiac mass increases the risk of cardiovascular outcomes in essential hypertension Eur. Heart J., May 1, 2005; 26(9): 921 - 927. [Abstract] [Full Text] [PDF]

				G. Mancia and G. Grassi Joint National Committee VII and European Society of Hypertension/European Society of Cardiology Guidelines for Evaluating and Treating Hypertension: A Two-Way Road? J. Am. Soc. Nephrol., March 1, 2005; 16(3_suppl_1): S74 - S77. [Abstract] [Full Text] [PDF]

				P. Verdecchia, F. Angeli, R. Gattobigio, M. Sardone, and C. Porcellati Asymptomatic Left Ventricular Systolic Dysfunction in Essential Hypertension: Prevalence, Determinants, and Prognostic Value Hypertension, March 1, 2005; 45(3): 412 - 418. [Abstract] [Full Text] [PDF]

				E. Nunez, D. K. Arnett, E. J. Benjamin, P. R. Liebson, T. N. Skelton, H. Taylor, and M. Andrew Optimal Threshold Value for Left Ventricular Hypertrophy in Blacks: The Atherosclerosis Risk in Communities Study Hypertension, January 1, 2005; 45(1): 58 - 63. [Abstract] [Full Text] [PDF]

				V. Kedar, H. McDonough, R. Arya, H.-H. Li, H. A. Rockman, and C. Patterson Muscle-specific RING finger 1 is a bona fide ubiquitin ligase that degrades cardiac troponin I PNAS, December 28, 2004; 101(52): 18135 - 18140. [Abstract] [Full Text] [PDF]

				P. M. Okin, R. B. Devereux, S. Jern, S. E. Kjeldsen, S. Julius, M. S. Nieminen, S. Snapinn, K. E. Harris, P. Aurup, J. M. Edelman, et al. Regression of Electrocardiographic Left Ventricular Hypertrophy During Antihypertensive Treatment and the Prediction of Major Cardiovascular Events JAMA, November 17, 2004; 292(19): 2343 - 2349. [Abstract] [Full Text] [PDF]

				R. B. Devereux, K. Wachtell, E. Gerdts, K. Boman, M. S. Nieminen, V. Papademetriou, J. Rokkedal, K. Harris, P. Aurup, and B. Dahlof Prognostic Significance of Left Ventricular Mass Change During Treatment of Hypertension JAMA, November 17, 2004; 292(19): 2350 - 2356. [Abstract] [Full Text] [PDF]

				R. H. Fagard, J. A. Staessen, L. Thijs, H. Celis, W. H. Birkenhager, C. J. Bulpitt, P. W. de Leeuw, G. Leonetti, C. Sarti, J. Tuomilehto, et al. Prognostic Significance of Electrocardiographic Voltages and Their Serial Changes in Elderly With Systolic Hypertension Hypertension, October 1, 2004; 44(4): 459 - 464. [Abstract] [Full Text] [PDF]

				R. B. Devereux, B. Dahlof, E. Gerdts, K. Boman, M. S. Nieminen, V. Papademetriou, J. Rokkedal, K. E. Harris, J. M. Edelman, and K. Wachtell Regression of Hypertensive Left Ventricular Hypertrophy by Losartan Compared With Atenolol: The Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) Trial Circulation, September 14, 2004; 110(11): 1456 - 1462. [Abstract] [Full Text] [PDF]

				G. Selvetella, E. Hirsch, A. Notte, G. Tarone, and G. Lembo Adaptive and maladaptive hypertrophic pathways: points of convergence and divergence Cardiovasc Res, August 15, 2004; 63(3): 373 - 380. [Abstract] [Full Text] [PDF]

				P. Verdecchia, G. Reboldi, F. Angeli, C. Borgioni, R. Gattobigio, L. Filippucci, S. Norgiolini, C. Bracco, and C. Porcellati Adverse Prognostic Significance of New Diabetes in Treated Hypertensive Subjects Hypertension, May 1, 2004; 43(5): 963 - 969. [Abstract] [Full Text] [PDF]

				P. M. Okin, M. J. Roman, E. T. Lee, J. M. Galloway, B. V. Howard, and R. B. Devereux Combined Echocardiographic Left Ventricular Hypertrophy and Electrocardiographic ST Depression Improve Prediction of Mortality in American Indians: The Strong Heart Study Hypertension, April 1, 2004; 43(4): 769 - 774. [Abstract] [Full Text] [PDF]

				F. Ichinose, K. D. Bloch, J. C. Wu, R. Hataishi, H. T. Aretz, M. H. Picard, and M. Scherrer-Crosbie Pressure overload-induced LV hypertrophy and dysfunction in mice are exacerbated by congenital NOS3 deficiency Am J Physiol Heart Circ Physiol, March 1, 2004; 286(3): H1070 - H1075. [Abstract] [Full Text] [PDF]

				M.D. Witham, J.I. Davies, A. Dawson, P.G. Davey, and A.D. Struthers Hypothetical economic analysis of screening for left ventricular hypertrophy in high-risk normotensive populations QJM, February 1, 2004; 97(2): 87 - 93. [Abstract] [Full Text] [PDF]

				M. Kyuma, T. Nakata, A. Hashimoto, K. Nagao, H. Sasao, T. Takahashi, K. Tsuchihashi, and K. Shimamoto Incremental Prognostic Implications of Brain Natriuretic Peptide, Cardiac Sympathetic Nerve Innervation, and Noncardiac Disorders in Patients with Heart Failure J. Nucl. Med., February 1, 2004; 45(2): 155 - 163. [Abstract] [Full Text] [PDF]

				R. Pontremoli, G. Leoncini, F. Viazzi, D. Parodi, E. Ratto, S. Vettoretti, M. Ravera, C. Tomolillo, and G. Deferrari Cardiovascular and Renal Risk Assessment as a Guide for Treatment in Primary Hypertension J. Am. Soc. Nephrol., January 1, 2004; 15(90010): S34 - 36. [Abstract] [Full Text]

				T. F. Griffith, D. N. Reddan, P. S. Klassen, and W. F. Owen Left ventricular hypertrophy: a surrogate end point or correlate of cardiovascular events in kidney disease? Nephrol. Dial. Transplant., December 1, 2003; 18(12): 2479 - 2482. [Full Text] [PDF]

				M. R. Di Tullio, D. R. Zwas, R. L. Sacco, R. R. Sciacca, and S. Homma Left Ventricular Mass and Geometry and the Risk of Ischemic Stroke Stroke, October 1, 2003; 34(10): 2380 - 2384. [Abstract] [Full Text] [PDF]

				R. B. Devereux, B. Dahlof, S. E. Kjeldsen, S. Julius, P. Aurup, G. Beevers, J. M. Edelman, U. de Faire, F. Fyhrquist, Sigrid Helle Berg, et al. Effects of Losartan or Atenolol in Hypertensive Patients without Clinically Evident Vascular Disease: A Substudy of the LIFE Randomized Trial Ann Intern Med, August 5, 2003; 139(3): 169 - 177. [Abstract] [Full Text] [PDF]

				T. V. Cloward, J. M. Walker, R. J. Farney, and J. L. Anderson Left Ventricular Hypertrophy Is a Common Echocardiographic Abnormality in Severe Obstructive Sleep Apnea and Reverses With Nasal Continuous Positive Airway Pressure Chest, August 1, 2003; 124(2): 594 - 601. [Abstract] [Full Text] [PDF]

				G. Selvetella, A. Notte, A. Maffei, V. Calistri, V. Scamardella, G. Frati, B. Trimarco, C. Colonnese, and G. Lembo Left Ventricular Hypertrophy Is Associated With Asymptomatic Cerebral Damage in Hypertensive Patients Stroke, July 1, 2003; 34(7): 1766 - 1770. [Abstract] [Full Text] [PDF]

				A.D. Struthers and J. Davies Should we add screening for and treating left ventricular hypertrophy to the management of all patients needing secondary prevention of cardiovascular disease? QJM, June 1, 2003; 96(6): 449 - 452. [Full Text] [PDF]

				G. de Simone, R. B. Devereux, S. G. Myerson, and D. J. Pennell What Is Bright Is Not Always Gold * Response: What Is Old Is Not Always Best Hypertension, June 1, 2003; e10(6): . [Full Text] [PDF]

				K Y K Wong, R S M. Walter, D Douglas, H W Fraser, S A Ogston, and A D Struthers Long QTc predicts future cardiac death in stroke survivors Heart, April 1, 2003; 89(4): 377 - 381. [Abstract] [Full Text] [PDF]

				C. Morisco, J. Sadoshima, B. Trimarco, R. Arora, D. E. Vatner, and S. F. Vatner Is treating cardiac hypertrophy salutary or detrimental: the two faces of Janus Am J Physiol Heart Circ Physiol, April 1, 2003; 284 (4): H1043 - H1047. [Full Text] [PDF]

				Y. Sakata, K. Yamamoto, T. Mano, N. Nishikawa, J. Yoshida, T. Miwa, M. Hori, and T. Masuyama Temocapril prevents transition to diastolic heart failure in rats even if initiated after appearance of LV hypertrophy and diastolic dysfunction Cardiovasc Res, March 1, 2003; 57(3): 757 - 765. [Abstract] [Full Text] [PDF]

				F. Angeli, P. Verdecchia, C. Pellegrino, R. G. Pellegrino, G. Pellegrino, L. Prosciutti, C. Giannoni, S. Cianetti, and M. Bentivoglio Association Between Periodontal Disease and Left Ventricle Mass in Essential Hypertension Hypertension, March 1, 2003; 41(3): 488 - 492. [Abstract] [Full Text] [PDF]

				P. Verdecchia, G. Reboldi, R. Gattobigio, M. Bentivoglio, C. Borgioni, F. Angeli, E. Carluccio, M. G. Sardone, and C. Porcellati Atrial Fibrillation in Hypertension: Predictors and Outcome Hypertension, February 1, 2003; 41(2): 218 - 223. [Abstract] [Full Text] [PDF]

				N. D. Desai and G. T. Christakis Stented Mechanical/Bioprosthetic Aortic Valve Replacement Card. Surg. Adult, January 1, 2003; 2(2003): 825 - 856. [Full Text]

				S. G. Myerson, H. E. Montgomery, M. J. World, and D. J. Pennell Left Ventricular Mass: Reliability of M-Mode and 2-Dimensional Echocardiographic Formulas Hypertension, November 1, 2002; 40(5): 673 - 678. [Abstract] [Full Text] [PDF]

				C. Indolfi, E. Di Lorenzo, C. Perrino, A. M. Stingone, A. Curcio, D. Torella, A. Cittadini, L. Cardone, C. Coppola, L. Cavuto, et al. Hydroxymethylglutaryl Coenzyme A Reductase Inhibitor Simvastatin Prevents Cardiac Hypertrophy Induced by Pressure Overload and Inhibits p21ras Activation Circulation, October 15, 2002; 106(16): 2118 - 2124. [Abstract] [Full Text] [PDF]

				A. D'Aloia, C. Fiorina, E. Vizzardi, P. Faggiano, and L. D. Cas Hypertensive crisis and acute, reversible, left ventricular systolic dysfunction: a case report Eur J Heart Fail, October 1, 2002; 4(5): 655 - 660. [Full Text] [PDF]

				A. Sharp and J. Mayet Regression of left ventricular hypertrophy: hoping for a longer life Journal of Renin-Angiotensin-Aldosterone System, September 1, 2002; 3(3): 141 - 144. [Abstract] [PDF]

				J. M. Gardin, D. Brunner, P. J. Schreiner, X. Xie, C. L. Reid, K. Ruth, D. E. Bild, and S. S. Gidding Demographics and correlates of five-year change in echocardiographic left ventricular mass in young black and white adult men and women: the Coronary Artery Risk Development in Young Adults (CARDIA) Study J. Am. Coll. Cardiol., August 7, 2002; 40(3): 529 - 535. [Abstract] [Full Text] [PDF]

				R. Schrier, K. McFann, A. Johnson, A. Chapman, C. Edelstein, G. Brosnahan, T. Ecder, and L. Tison Cardiac and Renal Effects of Standard Versus Rigorous Blood Pressure Control in Autosomal-Dominant Polycystic Kidney Disease: Results of a Seven-Year Prospective Randomized Study J. Am. Soc. Nephrol., July 1, 2002; 13(7): 1733 - 1739. [Abstract] [Full Text] [PDF]

				G. Schillaci, L. Pasqualini, P. Verdecchia, G. Vaudo, S. Marchesi, C. Porcellati, G. de Simone, and E. Mannarino Prognostic significance of left ventricular diastolic dysfunction in essential hypertension J. Am. Coll. Cardiol., June 19, 2002; 39(12): 2005 - 2011. [Abstract] [Full Text] [PDF]

				P. Verdecchia, G. Schillaci, C. Borgioni, R. Gattobigio, G. Ambrosio, and C. Porcellati Prevalent influence of systolic over pulse pressure on left ventricular mass in essential hypertension Eur. Heart J., April 2, 2002; 23(8): 658 - 665. [Abstract] [Full Text] [PDF]

				J. J. G. De Lima, M. L. C. Vieira, L. F. Viviani, C. J. Medeiros, L. E. Ianhez, L. Kopel, J. L. de Andrade, E. M. Krieger, and S. G. Lage Long-term impact of renal transplantation on carotid artery properties and on ventricular hypertrophy in end-stage renal failure patients Nephrol. Dial. Transplant., April 1, 2002; 17(4): 645 - 651. [Abstract] [Full Text] [PDF]

				S. G. Myerson, N. G. Bellenger, and D. J. Pennell Assessment of Left Ventricular Mass by Cardiovascular Magnetic Resonance Hypertension, March 1, 2002; 39(3): 750 - 755. [Abstract] [Full Text] [PDF]

				A D Struthers Introducing a new role for BNP: as a general indicator of cardiac structural disease rather than a specific indicator of systolic dysfunction only Heart, February 1, 2002; 87(2): 97 - 98. [Full Text] [PDF]

				J. C. Spratt, D. J Webb, A. Shiels, and B. Williams Effects of candesartan on cardiac and arterial structure and function in hypertensive subjects Journal of Renin-Angiotensin-Aldosterone System, December 1, 2001; 2(4): 227 - 232. [Abstract] [PDF]

				P. Verdecchia, G. Carini, A. Circo, E. Dovellini, E. Giovannini, M. Lombardo, P. Solinas, M. Gorini, A. P. Maggioni, and the MAVI Study Group Left ventricular mass and cardiovascular morbidity in essential hypertension: the MAVI study J. Am. Coll. Cardiol., December 1, 2001; 38(7): 1829 - 1835. [Abstract] [Full Text] [PDF]

				G. M. London, B. Pannier, A. P. Guerin, J. Blacher, S. J. Marchais, B. Darne, F. Metivier, H. Adda, and M. E. Safar Alterations of Left Ventricular Hypertrophy in and Survival of Patients Receiving Hemodialysis: Follow-up of an Interventional Study J. Am. Soc. Nephrol., December 1, 2001; 12(12): 2759 - 2767. [Abstract] [Full Text] [PDF]

				V. Palmieri, A. Celentano, M. J. Roman, G. de Simone, M. R. Lewis, L. Best, E. T. Lee, D. C. Robbins, B. V. Howard, and R. B. Devereux Fibrinogen and Preclinical Echocardiographic Target Organ Damage: The Strong Heart Study Hypertension, November 1, 2001; 38(5): 1068 - 1074. [Abstract] [Full Text] [PDF]

				P. Verdecchia, C. Porcellati, G. Reboldi, R. Gattobigio, C. Borgioni, T. A. Pearson, and G. Ambrosio Left Ventricular Hypertrophy as an Independent Predictor of Acute Cerebrovascular Events in Essential Hypertension Circulation, October 23, 2001; 104(17): 2039 - 2044. [Abstract] [Full Text] [PDF]

				U. E. Heidland and B. E. Strauer Left Ventricular Muscle Mass and Elevated Heart Rate Are Associated With Coronary Plaque Disruption Circulation, September 25, 2001; 104(13): 1477 - 1482. [Abstract] [Full Text] [PDF]

				R. B. Devereux, V. Palmieri, N. Sharpe, V. De Quattro, J. N. Bella, G. de Simone, J. F. Walker, R. T. Hahn, and B. Dahlof Effects of Once-Daily Angiotensin-Converting Enzyme Inhibition and Calcium Channel Blockade-Based Antihypertensive Treatment Regimens on Left Ventricular Hypertrophy and Diastolic Filling in Hypertension: The Prospective Randomized Enalapril Study Evaluating Regression of Ventricular Enlargement (PRESERVE) Trial Circulation, September 11, 2001; 104(11): 1248 - 1254. [Abstract] [Full Text] [PDF]

				F. Perticone, R. Ceravolo, A. Pujia, G. Ventura, S. Iacopino, A. Scozzafava, A. Ferraro, M. Chello, P. Mastroroberto, P. Verdecchia, et al. Prognostic Significance of Endothelial Dysfunction in Hypertensive Patients Circulation, July 10, 2001; 104(2): 191 - 196. [Abstract] [Full Text] [PDF]

				G. Schillaci, G. Reboldi, and P. Verdecchia High-Normal Serum Creatinine Concentration Is a Predictor of Cardiovascular Risk in Essential Hypertension Arch Intern Med, March 26, 2001; 161(6): 886 - 891. [Abstract] [Full Text] [PDF]

				S. Perlini, M. L. Muiesan, C. Cuspidi, L. Sampieri, B. Trimarco, G. P. Aurigemma, E. Agabiti-Rosei, and G. Mancia Midwall Mechanics Are Improved After Regression of Hypertensive Left Ventricular Hypertrophy and Normalization of Chamber Geometry Circulation, February 6, 2001; 103(5): 678 - 683. [Abstract] [Full Text] [PDF]

				V. Palmieri, J. N. Bella, D. K. Arnett, J. E. Liu, A. Oberman, M.-Y. Schuck, D. W. Kitzman, P. N. Hopkins, D. Morgan, D. C. Rao, et al. Effect of Type 2 Diabetes Mellitus on Left Ventricular Geometry and Systolic Function in Hypertensive Subjects : Hypertension Genetic Epidemiology Network (HyperGEN) Study Circulation, January 2, 2001; 103(1): 102 - 107. [Abstract] [Full Text] [PDF]

				J. H. O'Keefe, M. Wetzel, R. R. Moe, K. Brosnahan, and C. J. Lavie Should an angiotensin-converting enzyme inhibitor be standard therapy for patients with atherosclerotic disease? J. Am. Coll. Cardiol., January 1, 2001; 37(1): 1 - 8. [Abstract] [Full Text] [PDF]

				P. Verdecchia, G. Schillaci, G. Reboldi, F. Santeusanio, C. Porcellati, and P. Brunetti Relation Between Serum Uric Acid and Risk of Cardiovascular Disease in Essential Hypertension : The PIUMA Study Hypertension, December 1, 2000; 36(6): 1072 - 1078. [Abstract] [Full Text] [PDF]

				P.O. Lim and T.M. MacDonald Step test in hypertension QJM, November 1, 2000; 93(11): 703 - 705. [Full Text] [PDF]

				J. Mayet, B. Ariff, B. Wasan, N. Chapman, M. Shahi, N. R. Poulter, P. S. Sever, R. A. Foale, and S. A. McG. Thom Improvement in Midwall Myocardial Shortening With Regression of Left Ventricular Hypertrophy Hypertension, November 1, 2000; 36(5): 755 - 759. [Abstract] [Full Text] [PDF]

				K. Rajappan, N. G. Bellenger, L. Anderson, and D. J. Pennell The role of cardiovascular magnetic resonance in heart failure Eur J Heart Fail, September 1, 2000; 2(3): 241 - 252. [Abstract] [Full Text] [PDF]

				T. Tamura, S. Said, J. Harris, W. Lu, and A. M. Gerdes Reverse Remodeling of Cardiac Myocyte Hypertrophy in Hypertension and Failure by Targeting of the Renin-Angiotensin System Circulation, July 11, 2000; 102(2): 253 - 259. [Abstract] [Full Text] [PDF]

				J. S. Gottdiener, A. M. Arnold, G. P. Aurigemma, J. F. Polak, R. P. Tracy, D. W. Kitzman, J. M. Gardin, J. E. Rutledge, and R. C. Boineau Predictors of congestive heart failure in the elderly: the cardiovascular health study J. Am. Coll. Cardiol., May 1, 2000; 35(6): 1628 - 1637. [Abstract] [Full Text] [PDF]

				R. N. FOLEY, P. S. PARFREY, G. M. KENT, J. D. HARNETT, D. C. MURRAY, and P. E. BARRE Serial Change in Echocardiographic Parameters and Cardiac Failure in End-Stage Renal Disease J. Am. Soc. Nephrol., May 1, 2000; 11(5): 912 - 916. [Abstract] [Full Text]

				P. Verdecchia Prognostic Value of Ambulatory Blood Pressure : Current Evidence and Clinical Implications Hypertension, March 1, 2000; 35(3): 844 - 851. [Abstract] [Full Text] [PDF]

				G. Schillaci, P. Verdecchia, C. Porcellati, O. Cuccurullo, C. Cosco, and F. Perticone Continuous Relation Between Left Ventricular Mass and Cardiovascular Risk in Essential Hypertension Hypertension, February 1, 2000; 35(2): 580 - 586. [Abstract] [Full Text] [PDF]

				G. Parati, L. Ulian, L. Sampieri, P. Palatini, A. Villani, A. Vanasia, and G. Mancia Attenuation of the "White-Coat Effect" by Antihypertensive Treatment and Regression of Target Organ Damage Hypertension, February 1, 2000; 35(2): 614 - 620. [Abstract] [Full Text] [PDF]

				R. D. Feldman, N. Campbell, P. Larochelle, P. Bolli, E. D. Burgess, S. G. Carruthers, J. S. Floras, R. B. Haynes, G. Honos, F. H.H. Leenen, et al. 1999 Canadian recommendations for the management of hypertension Can. Med. Assoc. J., December 14, 1999; 161(90120): S1 - 17. [Abstract] [Full Text] [PDF]

				V. Palmieri, B. Dahlof, V. DeQuattro, N. Sharpe, J. N. Bella, G. de Simone, M. Paranicas, D. Fishman, and R. B. Devereux Reliability of echocardiographic assessment of left ventricular structure and function: The PRESERVE study J. Am. Coll. Cardiol., November 1, 1999; 34(5): 1625 - 1632. [Abstract] [Full Text] [PDF]

				M. G. Modena, N. Muia Jr, P. Aveta, R. Molinari, and R. Rossi Effects of Transdermal 17{beta}-Estradiol on Left Ventricular Anatomy and Performance in Hypertensive Women Hypertension, November 1, 1999; 34(5): 1041 - 1046. [Abstract] [Full Text] [PDF]

				P. Verdecchia, G. Reboldi, G. Schillaci, C. Borgioni, A. Ciucci, M. P. Telera, F. Santeusanio, C. Porcellati, and P. Brunetti Circulating Insulin and Insulin Growth Factor-1 Are Independent Determinants of Left Ventricular Mass and Geometry in Essential Hypertension Circulation, October 26, 1999; 100(17): 1802 - 1807. [Abstract] [Full Text] [PDF]

				A. Mosterd, R. B. D'Agostino, H. Silbershatz, P. A. Sytkowski, W. B. Kannel, D. E. Grobbee, and D. Levy Trends in the Prevalence of Hypertension, Antihypertensive Therapy, and Left Ventricular Hypertrophy from 1950 to 1989 N. Engl. J. Med., April 22, 1999; 340(16): 1221 - 1227. [Abstract] [Full Text] [PDF]

				F. Perticone, R. Maio, R. Ceravolo, C. Cosco, C. Cloro, and P. L. Mattioli Relationship Between Left Ventricular Mass and Endothelium-Dependent Vasodilation in Never-Treated Hypertensive Patients Circulation, April 20, 1999; 99(15): 1991 - 1996. [Abstract] [Full Text] [PDF]

				H. Schirmer, P. Lunde, and K. Rasmussen Prevalence of left ventricular hypertrophy in a general population; The Tromso Study Eur. Heart J., March 2, 1999; 20(6): 429 - 438. [Abstract] [PDF]

				R. A. Phillips, L. R. Krakoff, A. Dunaif, D. T. Finegood, R. Gorlin, and S. Shimabukuro Relation among Left Ventricular Mass, Insulin Resistance, and Blood Pressure in Nonobese Subjects J. Clin. Endocrinol. Metab., December 1, 1998; 83(12): 4284 - 4288. [Abstract] [Full Text]

				P. Verdecchia, G. Schillaci, C. Borgioni, A. Ciucci, S. Pede, and C. Porcellati Ambulatory Pulse Pressure : A Potent Predictor of Total Cardiovascular Risk in Hypertension Hypertension, December 1, 1998; 32(6): 983 - 988. [Abstract] [Full Text] [PDF]

				A. W. Haider, M. G. Larson, E. J. Benjamin, and D. Levy Increased left ventricular mass and hypertrophy are associated with increased risk for sudden death J. Am. Coll. Cardiol., November 1, 1998; 32(5): 1454 - 1459. [Abstract] [Full Text] [PDF]

				Left Ventricular Hypertrophy and Hypertension Journal Watch Cardiology, February 17, 1998; 1998(217): 10 - 10. [Full Text]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Verdecchia, P. Articles by Porcellati, C. Search for Related Content PubMed PubMed Citation Articles by Verdecchia, P. Articles by Porcellati, C. Pubmed/NCBI databases Medline Plus Health Information High Blood Pressure