Left ventricular structure in different types of chronic pressure overload
Institute of Medicine, University of Bergen and Department of Heart Diseases, Haukeland University Hospital, N-5021 Bergen, Norway
* Corresponding author. Tel: +47 55 97 21 70; fax: +47 55 97 58 90. E-mail address: gerdtsev{at}online.no
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Abstract |
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 Top Abstract IntroductionMethodsRelationship between left...Left ventricular structure in...SummaryConclusions and clinical...FundingAcknowledgementsReferences |
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Aims: Hypertension and aortic stenosis (AS) are different forms of chronic pressure overload that lead to changes in left ventricular (LV) geometry. This article explores the relationship between LV geometry and outcomes, as well as the distribution of LV geometric patterns in patients with hypertension and those with asymptomatic AS with or without concomitant hypertension.
Methods and results: Studies describing the distribution of LV geometry, or the relationship between LV geometry and outcome, in patients with hypertension and/or AS were reviewed. Abnormal LV geometry increases the risk of major cardiovascular events and mortality in patients with untreated hypertension, with concentric hypertrophy conferring the greatest risk, followed by eccentric hypertrophy and then concentric remodelling. Abnormal LV geometry during antihypertensive drug therapy also increases cardiovascular risk compared with normal geometry. In asymptomatic AS, the relationship between LV geometry and outcome remains to be clarified. A pooled analysis of data from two major clinical studies, Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) and Simvastatin and Ezetimibe in Aortic Stenosis (SEAS), showed that the prevalence of abnormal LV geometry increases with increasing chronic pressure overload—from 35% in normotensive patients with asymptomatic mild-to-moderate AS to 80% in patients with hypertension and electrocardiographic evidence of LV hypertrophy (LVH). In patients with asymptomatic AS, concentric LV geometry is most common, whereas eccentric hypertrophy is the most common LV geometric abnormality in patients with hypertension and LVH.
Conclusion: Abnormal LV geometry has been independently associated with adverse outcomes in hypertension. Patients with asymptomatic mild-to-moderate AS often have abnormal LV geometry irrespective of the presence of concomitant hypertension, and, accordingly, may be at higher cardiovascular risk than expected on the basis of their AS alone. In the future, ongoing clinical trials involving AS patients, such as the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study, may help to provide further information concerning relationships between abnormal LV geometry and clinical outcomes among individuals with asymptomatic AS.
Key Words: Left ventricular geometry • Left ventricular hypertrophy • Aortic stenosis • Hypertension
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Introduction |
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TopAbstractIntroductionMethodsRelationship between left...Left ventricular structure in...SummaryConclusions and clinical...FundingAcknowledgementsReferences |
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Hypertension and aortic stenosis (AS) represent two different types of chronic pressure overload, both of which lead to development of left ventricular hypertrophy (LVH). In this setting, four different patterns of LV geometry can be identified by echocardiography, each characterised by distinctive pathophysiological patterns and each associated with different cardiovascular risk. These LV geometric patterns are defined by increases in the LV mass/body surface area [LV mass index (LVMI)] or relative wall thickness (RWT) or both.1,2 To determine these parameters, LV internal diameters and wall thicknesses at end-diastole are measured by M-mode or two-dimensional echocardiography. This article explores the relationship between LV geometry and outcomes, as well as the distribution of LV geometric patterns in patients with different types of chronic pressure overload, including hypertension and AS with or without concomitant hypertension by reviewing key publications on this topic as well as providing some new insight into the Losartan Intervention for Endpoint reduction in hypertension (LIFE) Echo Substudy and Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study.5
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Methods |
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TopAbstractIntroductionMethodsRelationship between left...Left ventricular structure in...SummaryConclusions and clinical...FundingAcknowledgementsReferences |
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In large clinical trials, such as the LIFE and SEAS studies, clinicians and sonographers are trained to obtain electrocardiograms according to standardised procedures following international guidelines. Final readings and interpretation of the study echocardiograms are then performed at a central core echocardiography laboratory by an experienced echocardiographer who is blinded to the nature of the intervention. If more than one person is involved in final reading, the impacts of inter-observer variation in reading on performance are assessed.
The SEAS study is an ongoing, randomised, double-blind, placebo-controlled multicentre trial that is evaluating the effects of lipid-lowering treatment with combined ezetimibe/simvastatin on progression of mild-to-moderate AS.5 Patients enrolled in the SEAS study had asymptomatic AS defined by aortic valve thickening on echocardiography and accompanied by a Doppler-measured aortic peak flow velocity of 2.5–4.0 m/s. Patients with other significant valvular disease, systolic heart failure, established vascular disease, diabetes, renal insufficiency, or other uncontrolled diseases and those already receiving lipid-lowering therapy were excluded. In the SEAS study, all patients were scheduled for study echocardiograms at baseline and thereafter annually. In addition, a preoperative echocardiogram was taken in all patients who underwent aortic valve replacement as a result of progression of AS. All echocardiographic measurements in the SEAS trial were performed in a blinded manner using an echocardiography core laboratory. By decreasing inter-observer variability through the use of standardised protocols, including consensus international echocardiographic guidelines, as well as consistent training, core laboratories can enhance the accuracy and reproducibility of findings. Clinical decisions, including patient inclusion and the timing of surgical procedures, were based on local assessments of AS.5
LVMI can be calculated from end-diastolic LV dimensions using an anatomically validated formula according to the American Society of Echocardiography (ASE) convention: 0.832 x [(LVID + IVS + PWT)3—(LVID)3]+0.6 g, where LVID is the LV internal diameter, IVS the interventricular septum diameter, and PWT the posterior wall thickness.6 LVH is considered present when LVMI exceeds 104 g/m2 in women and 116 g/m2 in men, or, alternatively, when the LV mass indexed for height in its allometric power is >46.7 g/m2.7 and 49.2 g/m2.7 in women and men, respectively.3,4 The non-gender-specific definition of LVH as LV mass/height2.7 
51 g/m2.7 grossly underestimates the diagnosis of LVH, particularly in women, and should not be preferred.7
In large trials, protocols specify which criteria will be used to define the presence of LVH. LV geometry is assessed from LVMI in combination with RWT. RWT can be calculated as the ratio of PWT to LV internal radius at end-diastole, and is considered to be increased when 0.43.2 These partition values for LVMI and RWT are used to identify the four different LV geometric patterns: (1) normal geometry, in which both LVMI and RWT are normal (i.e. below the partition value); (2) concentric remodelling, in which RWT is increased but LVMI is normal; (3) eccentric hypertrophy, in which LVMI is increased but RWT is normal; and (4) concentric hypertrophy, in which both LVMI and RWT are increased (Figure 1).2
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Echocardiography is also the method of choice in assessing the severity of AS, which can be estimated from transaortic velocity or gradient, or aortic valve area (AVA).8 In the ongoing SEAS study, patients were included based on diagnosis of AS severity from peak transaortic velocity measured by Doppler echocardiography made at the individual study sites.5 However, the echocardiograms following a standardised study protocol were recorded and submitted to the SEAS echocardiography core laboratory situated at Haukeland University Hospital in Bergen, Norway. Echocardiograms were preliminarily read by a first reader, then read again, and quality assured by a highly experienced echocardiologist. A total of 93% of baseline echocardiograms and 100% of annual follow-up echocardiograms were read by the same cardiologist (E.G.). All readers were blinded for study intervention and sequence of echocardiograms. From the submitted recordings, a standardised and accurate diagnosis of AS was made based on mean and peak velocities and time-velocity integral in the LV outflow tract measured by pulsed-wave Doppler and transaortic velocity measured by continuous-wave Doppler from different windows by imaging and non-imaging transducers.4 The highest transaortic velocity was used to trace the time-velocity integral. The aortic valve annulus was measured as the internal diameter at end-diastole in a zoomed two-dimensional parasternal long-axis view focusing on the aortic valve, and then the effective AVA was calculated using the continuity equation with time-velocity integral ratio.4 The severity is then determined on the basis of the peak transaortic velocity (mild: 2.5–3.0 m/s; moderate: 3.0–4.0 m/s; or severe: >4.0 m/s) or AVA (mild: >1.5 cm2; moderate: 1.0–1.5 cm2; or severe <1.0 cm2), as it is well known that the continuity equation tends to overestimate the severity of AS in milder cases. In the SEAS study, only asymptomatic patients with mild-to-moderate AS, characterised by a peak transaortic velocity of 2.5–4.0 m/s, and free of diabetes and a history of coronary heart disease were enrolled.5
In the SEAS study, LV systolic function was evaluated as LV ejection fraction (EF) by biplane Simpson's formula as well as fractional shortening both at the endocardial and the midwall level after adjusting for circumferential end-systolic stress (CESS), which was estimated at midwall using a cylindrical model.4 The ratio between the measured and predicted fractional shortening and midwall shortening was adjusted for the CESS in order to obtain the stress-corrected fractional shortening and the stress-corrected midwall shortening.
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Relationship between left ventricular geometry and outcome in hypertension |
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In patients with untreated mild-to-moderate hypertension, the prevalence of LVH by echocardiography is 30–50%, the most common patterns of abnormal LV geometry being concentric remodelling and eccentric LVH. For example, Ganau et al.2 found abnormal LV geometry in 48% of 165 patients with untreated hypertension, including 13% with concentric remodelling, 27% with eccentric LVH, and 8% with concentric LVH. In another series of 271 untreated hypertensive patients, Roman et al.9 found 35% abnormal LV geometry, including 20% with concentric remodelling, 9% with eccentric LVH, and 6% with concentric LVH.2
Koren et al.10 evaluated the prognostic significance of LV geometry in a prospective cohort of 280 hypertensive patients without pre-existing heart disease. After a mean follow-up of 10.2 years, patients with increased LVMI (125 g/m2) on their initial echocardiogram had higher rates of cardiovascular events (26 vs. 12%, P = 0.006), cardiovascular mortality (14 vs. 1%, P < 0.001), and all-cause mortality (16 vs. 2%, P = 0.001) than patients with lower LVMI values. In the multivariate analysis, only age and LVMI—and not gender, blood pressure (BP), or serum cholesterol—were independently associated with outcome. When LV geometry was considered, further risk stratification of adverse outcomes was seen in the following rank order: normal geometry (RWT <0.45 and LVMI <125 g/m2) < concentric remodelling < eccentric hypertrophy < concentric hypertrophy. For example, cardiovascular events occurred during follow-up in 11% of those with normal geometry compared with 15% in those with concentric remodelling, 23% in those with eccentric hypertrophy, and 31% in those with concentric hypertrophy (P = 0.03). Similarly, the rates of all-cause mortality in patients with these LV patterns were 1, 6, 10, and 24%, respectively (P < 0.001).
The prognostic significance of concentric remodelling was further evaluated by Verdecchia et al.11 in 694 hypertensive patients with LVMI < 125 g/m2. Concentric remodelling using a partition value for RWT 0.45 was identified in 39% of the study cohort. Patients with concentric remodelling were older (mean age, 52 vs. 49 years), had a longer duration of hypertension (5.1 vs. 3.8 years), and were more likely to have been treated for hypertension (36 vs. 23%) (all P < 0.01). After a mean follow-up of 2.7 years, patients with concentric remodelling had a higher rate of cardiovascular events than those with normal geometry (2.39 vs. 1.12 events per 100 patient-years). In multivariate analysis, concentric remodelling was found to increase the risk of cardiovascular events compared with normal LV geometry [relative risk (RR) = 2.56, 95% confidence interval (CI): 1.20–5.45, P < 0.01] independent of age, gender, diabetes, LVMI, or BP.11
Taken together, these studies illustrate that LV geometry stratifies risk of adverse outcomes in patients with hypertension independent of BP and other conventional risk factors. Recently, LV geometry was also demonstrated as a predictor of cardiovascular risk during antihypertensive drug therapy in the LIFE Echocardiography (Echo) Substudy. LIFE was a randomised, double-blind, multicentre trial that compared the effect of losartan-based vs. atenolol-based therapy on combined cardiovascular death, non-fatal or fatal myocardial infarction, and fatal or non-fatal stroke over 4.8 years in 9194 patients with essential hypertension.12 Patients enrolled in LIFE were aged 55–80 years, had clinic systolic BP (SBP) of 160–200 mmHg and/or diastolic BP (DBP) of 95–115 mmHg while receiving placebo for one to two weeks, and had electrocardiography (ECG)-documented LVH at inclusion.
The LIFE Echo Substudy was prospectively planned to include 10% of the entire LIFE study population, and a cohort of 960 patients were recruited.13 LVMI was measured by echocardiography at baseline and then annually. The study demonstrated at baseline that, also among hypertensive patients with ECG signs of LVH, the most common LV geometry was eccentric LVH (46%), followed by concentric LVH (24%).13 However, LV geometry changed significantly during follow-up as a result of systematic, aggressive antihypertensive treatment, and baseline LV geometry did not predict outcome in the LIFE study. Of the 660 patients with either eccentric or concentric LVH at baseline, 52% had normal LV geometry in the final study echocardiogram. Moreover, 80 of 98 patients (82%) with concentric remodelling at baseline had normal LV geometry at the end of the study.13
The LIFE Echo Substudy was the first to demonstrate a strong, independent association between on-treatment LVMI and cardiovascular events during antihypertensive treatment.14 After adjusting for baseline LVMI, randomised study treatment, and degree of BP-lowering, the risk of the composite primary endpoint in the LIFE Echo Substudy was reduced by 22% for each 1 SD decrease in LVMI (i.e. per 25.3 g/m2) while on treatment (P = 0.009). Similarly, the risk of important secondary study endpoints were reduced with lower on-treatment LVMI: cardiovascular mortality by 38% (P = 0.001), stroke by 24% (P = 0.02), and all-cause mortality by 28% (P = 0.002).
In the LIFE Echo Substudy, the presence and absence of LVH defined by sex-specific LVMI partition values (i.e. >104 g/m2 in women and >116 g/m2 in men) were substituted for the LVMI values as a continuous time-varying covariate.14 The absence of LVH was associated with lower risk of the composite endpoint compared with the presence of LVH [hazard ratio (HR) = 0.58, 95% CI: 0.38–0.86, P = 0.008] (Figure 2).14 The absence of LVH was also associated with a 66% lower risk of cardiovascular mortality (P = 0.004) and 64% lower risk of all-cause mortality (P < 0.001), documenting the usefulness of these LVH partition values in a clinical setting. Notably, the absence vs. presence of LVH was a stronger predictor of cardiovascular risk than the actual LVMI value.
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LV geometry was also assessed as a continuous time-varying covariate in the LIFE Echo Substudy cohort.14 The distribution of LV geometry using the sex-specific partition values for LVMI and an RWT partition value
0.43 changed from baseline to the end of the follow-up period. At baseline, 19% of the cohort had normal geometry, 11% had concentric remodelling, 46% had eccentric hypertrophy, and 24% had concentric hypertrophy, whereas by the end of the follow-up period, the proportions with each of these LV geometries were 63, 3, 30, and 4%, respectively (P < 0.001). In multivariate Cox regression analysis, each abnormal LV pattern independently predicted risk of the composite endpoint compared with normal LV geometry (Figure 3).13 After adjusting for study treatment, Framingham risk score, race, and time-varying SBP, the hazard ratios (95% CI) for the composite endpoint were 2.99 (1.16–7.71) for concentric remodelling, 1.79 (1.17–2.73) for eccentric hypertrophy, and 2.71 (1.13–6.45) for concentric hypertrophy (all P < 0.05). When the individual components of the composite endpoint were considered separately in similar multivariate models, concentric remodelling was associated with increased risk of cardiovascular death and stroke, eccentric hypertrophy with increased risk of cardiovascular death and MI, and concentric hypertrophy with increased risk of MI. This analysis demonstrates that on-treatment evaluation of LV geometry adds prognostic information to clinical evaluation and assessment of LVH alone, in cardiovascular risk assessment in patients with hypertension.
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Left ventricular structure in aortic stenosis |
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Concentric hypertrophy has been reported as the most common LV geometric pattern in patients with severe symptomatic AS irrespective of the presence of concomitant hypertension.15 Antonini-Canterin et al.15 evaluated LV geometry in 193 consecutive patients with symptomatic AS, of whom 32% also had hypertension. Concentric hypertrophy—using partition values of LVMI > 125 g/m2 and RWT > 0.44—was identified in 50% of patients with coexisting AS and hypertension and in 50% of those having AS without hypertension. Eccentric hypertrophy was found in 29% of patients with AS and hypertension and in 31% of patients with AS and without hypertension, and concentric remodelling was found in 15% of patients in both subsets. However, few studies have assessed determinants of LV geometry in patients with asymptomatic AS.
Chambers et al.17 reported LV structure in a cohort of 91 consecutive patients with thickening of the aortic valve cusps and peak transaortic velocity >2 m/s. LVMI was significantly related to the effective AVA (r = 0.22) and peak transvalvular pressure gradient (r = 0.36) in the univariate analysis, but on multivariate analysis, the determinants of LVMI varied according to the severity of AS. DBP was predictive in mild AS (P = 0.028); peak transvalvular pressure gradient was predictive in moderate AS (P = 0.03), and both peak transvalvular pressure gradient (P < 0.0001) and gender (P = 0.02) were predictive in severe AS. Moreover, the prevalence of LVH in this cohort increased with AS severity: 63% in mild AS, 78% in moderate AS, and 80% in severe AS. This study illustrated that LVH is common in AS, even when the condition is at a mild stage.17
We recently reported determinant and covariates of LVH in a large series of asymptomatic patients with AS recruited into the SEAS study.4 In the analysis by Cramariuc et al., gender differences in LV structure and systolic function were reported. In this report, women (n = 674) were older than men (n = 1046), had a smaller AVA index than men, and included more obese and hypertensive patients (all P < 0.05). Women also tended to have significantly higher stress-corrected fractional shortening and stress-corrected midwall shortening compared with men. Despite these differences, LVH was more prevalent among men, and increased in prevalence with increasing AS severity. On multivariate analysis, the degree of AS, presence of hypertension, and lower stress-corrected midwall shortening were independent predictors of LVH in both men and women (all P < 0.01). The presence of aortic regurgitation was also predictive of LVH in men (P < 0.05). This study was cross-sectional, and differences in various parameters according to baseline AS severity by tertiles of peak transaortic velocity may not be consistent with long-term data. The ongoing prospective SEAS trial may assist researchers in evaluating the impact of gender on longitudinal LV responses to AS progression.4
Rieck et al.16 evaluated the impact of concomitant hypertension on baseline LV geometry in the SEAS study. LV geometry could be assessed in 1762 of the 1873 included patients at baseline, of whom 872 patients were normotensive and 890 patients were hypertensive. Normotensive and hypertensive patient groups had similar degrees of AS based on the AVA/body surface area ratio (0.66 vs. 0.68 cm2/m2). However, the hypertensive group was significantly older and had higher body mass index (BMI), systolic BP, and diastolic BP than the normotensive group. The hypertensive group also had higher LVMI (106 vs. 101 g/m2, P < 0.001) and RWT (0.36 vs. 0.35, P < 0.05), as well as a higher prevalence of LVH (39 vs. 30%, P < 0.05) and increased RWT (20 vs. 16%, P < 0.05) compared with the normotensive group.
In contrast to previous findings reported by Chambers et al.,17 in the SEAS study cohort most patients had normal LV geometry, including 65% of those in the normotensive subset and 59% in the hypertensive subset (Figure 4).18 Eccentric hypertrophy was the most common abnormal LV geometry, being identified in 19% and 21% of normotensive and hypertensive patients, respectively. Concentric remodelling and concentric hypertrophy were identified less often, although the latter was more likely to be found in hypertensive patients than in normotensive patients (11 vs. 6%, P < 0.01).
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A pooled analysis of baseline clinical and echocardiographic data from subgroups of patients in the LIFE and SEAS trials was conducted to compare the influence of different types of chronic pressure overload on LV structure.18 Because the LIFE and SEAS studies did not have identical inclusion and exclusion criteria, a harmonisation strategy was used to select patients for comparison. Patients who were <45 or >80 years of age and those with diabetes, known cardiovascular disease, or greater than grade 1 aortic valve regurgitation were excluded from the analysis.
In this analysis, hypertension was defined by a history of hypertension or a clinical measurement of systolic BP >140 mmHg or diastolic BP >90 mmHg. As a result, three cohorts were identified: 649 patients with hypertension and ECG evidence of LVH from the LIFE study (hypertension group), 265 normotensive patients with asymptomatic AS from the SEAS study (AS group), and 761 patients with hypertension and asymptomatic AS from SEAS (AS + hypertension group).
The three groups differed significantly with respect to certain demographic and clinical characteristics. Blood pressure was higher in the group with hypertension (mean, 173/99 mmHg) than in the AS + hypertension group (151/84 mmHg) or AS group (126/76 mmHg) (P < 0.01 across groups). Patients in the hypertension group were younger (65 vs. 68–70 years) and had higher heart rates (72 vs. 65–67 b.p.m.), and lower LVEF (62 vs. 66–67%) than those in the AS + hypertension and AS groups (all P < 0.01). The hypertension group also had a higher LV mass/height2.7 ratio than those in the AS + hypertension and AS groups (55.1 vs. 47.2 vs. 41.3 g/m2.7), as well as a higher prevalence of LVH (72 vs. 41 vs. 25%) (P < 0.01 across groups). The degree of AS did not differ between the AS and AS + hypertension groups.
The distribution of LV geometry also differed significantly across the three groups, with the prevalence of normal LV geometry decreasing with increasing chronic pressure overload severity (AS > AS + hypertension > hypertension alone). The hypertension group had a higher prevalence of eccentric and concentric hypertrophy and a lower prevalence of concentric remodelling than the groups with mild-to-moderate AS (Figure 5).18 In logistic regression analyses of data from this pooled cohort, the presence of hypertension increased the odds of LVH [odds ratio (OR) = 1.70, 95% CI: 1.21–2.38, P = 0.002), whereas the presence of AS reduced the odds of LVH (OR = 0.24, 95% CI: 0.18–0.32, P < 0.001). Other independent covariates of LVH were age, BMI, and LVEF (all P 
0.001).
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In the entire pooled cohort, the prevalence of concentric LV geometry (i.e. either concentric remodelling or concentric hypertrophy) was more common in the hypertension group (34%) than in the AS + hypertension group (22%) or AS group (18%) (P < 0.01 between groups). However, when only patients with abnormal LV geometry were considered, the prevalence of concentric LV geometry tended to be higher in the AS group (42 vs. 44 vs. 53%, P = 0.161).
In logistic regression analysis, concentric LV geometry was associated with AS (OR = 7.60, 95% CI: 4.78–12.10, P < 0.001) as well as older age (P = 0.002), lower body weight (P < 0.001), and lower peak systolic wall stress and midwall shortening (both P < 0.001). Conversely, eccentric LV geometry was associated with hypertension (OR = 1.92, 95% CI: 1.12–3.29).
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Summary |
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TopAbstractIntroductionMethodsRelationship between left...Left ventricular structure in...SummaryConclusions and clinical...FundingAcknowledgementsReferences |
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The studies reviewed in this paper show that LV geometry influences outcomes of patients with hypertension independently of BP and other conventional risk factors, and that the distribution of LV geometry differs according to the type and extent of chronic pressure overload. Eccentric hypertrophy is the most common abnormal LV geometry in patients with hypertension. As shown in the LIFE Echo Substudy, abnormal LV geometry during antihypertensive drug therapy is also associated with increased cardiovascular risk, with concentric hypertrophy conferring the greatest risk followed by eccentric hypertrophy, and then concentric remodelling. Information on how abnormal LV geometry influences outcome in mild-to-moderate AS is not yet available. However, data from the SEAS study showed that 35% of normotensive patients with asymptomatic mild-to-moderate AS had abnormal LV geometry, most commonly a concentric pattern. Moreover, in the pooled analysis of the LIFE and SEAS studies, hypertension was independently associated with eccentric LV geometry, whereas AS was associated with concentric LV geometry.
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Conclusions and clinical implications |
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TopAbstractIntroductionMethodsRelationship between left...Left ventricular structure in...SummaryConclusions and clinical...FundingAcknowledgementsReferences |
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LV geometry differs according to the type and extent of chronic pressure overload, as illustrated by data from a pooled analysis of the LIFE and SEAS trials. Approximately two-thirds of asymptomatic normotensive patients with mild-to-moderate AS had normal LV geometry. However, when an abnormal LV geometry was present in this population, a concentric pattern was the most common geometry. In patients with hypertension and mild-to-moderate AS without clear symptoms, nearly half had normal LV geometry. However, in individuals with abnormal patterns, eccentric hypertrophy was the most common geometry. Finally, in patients with hypertension and ECG evidence of LVH, only about 20% had normal LV geometry, and once again, eccentric hypertrophy was the most common abnormal pattern.
In patients with hypertension, each abnormal LV geometric pattern is associated with an increased risk of major cardiovascular events and mortality: concentric hypertrophy is associated with the greatest risk, followed by eccentric hypertrophy and then concentric remodelling. The prognostic significance of these abnormal LV patterns has been observed in hypertension, both in untreated patients and in those receiving antihypertensive drug therapy using baseline and on-treatment assessments. The influence of abnormal LV patterns on outcomes of AS patients remains to be determined. Ongoing studies may provide further information concerning relationships between abnormal LV geometry and clinical outcomes in patients with asymptomatic mild-to-moderate AS.
Clinical implications of these findings include the fact that abnormal LV geometry as determined by echocardiography may impart meaningful information to cardiologists in risk-stratifying and targeting treatment to their patients with hypertension beyond what is readily attainable from clinical assessments alone. Relationships between abnormal LV geometry and clinical outcomes in patients with mild-to-moderate AS in the absence of clear symptoms of AS are as yet unclear. However, preliminary data from the SEAS study suggest that concomitant hypertension and asymptomatic AS significantly influence LV geometry and the prevalence of LVH. Whether patients with both hypertension and asymptomatic AS are also at higher cardiovascular risk than expected based on AS alone will be assessed in follow-up analyses of the SEAS population.
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Funding |
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The Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) Echocardiography Substudy was supported by grant COZ 368 from Merck Sharpe and Dohme. The Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) echocardiography core laboratory is supported by Merck/Schering-Plough.
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Acknowledgements |
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Assistance in manuscript preparation was provided by Rete Biomedical Communications Corp. (Ridgewood, NJ, USA).
Conflict of interest: E.G. is a member of the steering committee in the SEAS study. The SEAS echocardiography core laboratory is sponsored by Merck Schering Plough Joint Venture.
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References |
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