Presence of concentric left ventricular (LV) geometry has important pathophysiologic and prognostic implications. However, little is known about its natural history in older adults. Of the 5,795 community-dwelling adults ≥65 years of age in the Cardiovascular Health Study, 1,871 without baseline heart failure had data on baseline and 7-year echocardiograms. Of these 343 (18%) had baseline concentric LV geometry (concentric remodeling 83%, concentric LV hypertrophy [LVH] 17%) and are the focus of the present study. LV geometry at year 7 was categorized into 4 groups based on LVH (LV mass indexed for height >51 g/m 2.7 ) and relative wall thickness (RWT): eccentric hypertrophy (RWT ≤0.42 with LVH), concentric hypertrophy (RWT >0.42 with LVH), concentric remodeling (RWT >0.42 without LVH), and normal (RWT ≤0.42 without LVH). At year 7, LV geometry normalized in 57%, remained unchanged in 35%, and transitioned to eccentric hypertrophy in 7% of participants. Incident eccentric hypertrophy occurred in 4% and 25% of those with baseline concentric remodeling and concentric hypertrophy, respectively, and was associated with increased LV end-diastolic volume and decreased LV ejection fraction at year 7. Previous myocardial infarction and baseline above-median LV mass (>39 g/m 2.7 ) and RWT (>0.46) had significant unadjusted associations with incident eccentric LVH; however, only LV mass >39 g/m 2.7 (odds ratio 17.52, 95% confidence interval 3.91 to 78.47, p <0.001) and previous myocardial infarction (odds ratio 4.73, 95% confidence interval 1.16 to 19.32, p = 0.031) had significant independent associations. In conclusion, in community-dwelling older adults with concentric LV geometry, transition to eccentric hypertrophy was uncommon but structurally maladaptive.
Concentric left ventricular (LV) geometry, defined by alterations in LV relative wall thickness (RWT) and LV mass, has important pathophysiologic and prognostic implications. Concentric remodeling commonly develops in response to persistent increased LV afterload caused by conditions such as arterial hypertension and aortic stenosis. Conversely, eccentric hypertrophy commonly develops in response to persistent increased LV preload caused by conditions such as persistent mitral regurgitation. Patients with heart failure (HF) may have concentric or eccentric hypertrophy, and it is unclear whether eccentric hypertrophy develops directly or progresses from concentric remodeling.
Findings from laboratory animals have suggested that persistent pressure overload may lead to concentric hypertrophy with compensated LV function that over time progresses to eccentric hypertrophy, LV dilation, and decreased LV systolic function. However, nearly 1/2 of all patients with HF may have diastolic HF with normal LV ejection fraction and LV volume. Most (≥90%) of these patients have antecedent hypertension and many (50% to 75%) have concentric geometry. These observations have led to the hypothesis that in humans LV progression from concentric to eccentric geometry may not be common. However, this hypothesis has not been previously examined in those with LV concentric geometry without a history of HF. Furthermore, little is known about the natural history of LV concentric geometry. Therefore, the purpose of this prospective study was to examine the natural history of concentric LV geometry with a focus on its progression to eccentric hypertrophy.
Methods
The Cardiovascular Health Study (CHS) is an ongoing epidemiologic study of cardiovascular disease in community-dwelling adults ≥65 years of age in the United States; details of the rationale, design, and implementation have been previously detailed. Of the 5,888 CHS participants, data on 5,795 participants were available in the de-identified public-use copies of the datasets (93 participants declined to be included in these datasets). Of the 5,795 CHS participants, 1,871 were free of HF at baseline and had echocardiographic data at baseline and at 7 years.
LV hypertrophy (LVH) was defined as a gender-neutral cut-off value for LV mass indexed for height >51 g/m 2.7 . RWT was computed by the ratio of the sum of interventricular septal and posterior wall thicknesses to LV end-diastolic dimension. LV structure at baseline and year 7 was categorized as normal (RWT ≤0.42 and no LVH), concentric remodeling (RWT >0.42 and no LVH), concentric hypertrophy (RWT >0.42 and LVH), and eccentric hypertrophy (RWT ≤0.42 and LVH). Of the 1,871 CHS participants without baseline HF, 343 (18%) had LV concentric geometry and are the focus of the present study; of these 284 (83%) had concentric remodeling and 59 (17%) had concentric hypertrophy.
A multivariable logistic regression model was developed to identify baseline characteristics that predicted incident eccentric hypertrophy. In the model, LV mass indexed for height and LV RWT were categorized based on median values >39g/m 2.7 and >0.46, respectively. The model was also adjusted for age, gender, race, baseline history of hypertension and previous acute myocardial infarction (AMI), and intercurrent (from baseline to year 7) AMI and HF. Because an intercurrent AMI may lead to eccentric hypertrophy by progressive remodeling with LV dilation and LV systolic dysfunction, reflecting pathophysiology of coronary heart disease rather than hypertensive heart disease, we repeated our analysis after excluding patients with intercurrent AMI.
Results
Participants (n = 343) had a mean ± SD age of 73 ± 5 years and a mean ± SD LV mass of 155 ± 51 g, 63% were women, 8% were African-Americans, and 59% had a history of hypertension ( Table 1 ). At year 7, LV geometry normalized in 57% of participants, remained unchanged in 35%, and progressed to eccentric hypertrophy in 7%. Of those with LV concentric remodeling at baseline, LV geometry normalized in 63%, remained unchanged in 31%, and progressed to concentric hypertrophy in 3% and eccentric hypertrophy in 4% of patients at year 7 ( Table 2 ). Of those with LV concentric hypertrophy at baseline, LV geometry normalized in 29%, regressed to concentric remodeling in 24%, remained unchanged in 22%, and progressed to eccentric hypertrophy in 25% of patients at year 7 ( Table 2 ).
| Age (years) | 73 ± 5 |
| Women | 217 (63%) |
| African-American | 26 (8%) |
| Smoking (pack-years) | 16 ± 25 |
| Height (cm) | 164 ± 9 |
| Weight (pounds) | 155 ± 28 |
| Body surface area (m 2 ) | 1.74 ± 0.19 |
| Body mass index (kg/m 2 ) | 26.1 ± 3.9 |
| Systolic blood pressure (mm Hg) | 137 ± 23 |
| Diastolic blood pressure (mm Hg) | 72 ± 12 |
| Echocardiography | |
| Left ventricular systolic dysfunction ⁎ | 9 (3%) |
| Left ventricular fractional shortening (%) | 45 ± 8 |
| Left ventricular end-diastolic dimension (cm) | 4.3 ± 0.5 |
| Left ventricular end-diastolic interventricular septal thickness (cm) | 1.1 ± 0.2 |
| Left ventricular end-diastolic posterior wall thickness (cm) | 1.0 ± 0.1 |
| Left ventricular mass (g) | 155.2 ± 50.7 |
| Relative wall thickness | 0.48 ± 0.07 |
| Co-morbidities | |
| Coronary heart disease | 50 (15%) |
| Previous myocardial infarction | 16 (5%) |
| Hypertension | 201 (59%) |
| Diabetes mellitus | 48 (14%) |
| Left ventricular hypertrophy (electrocardiogram) | 16 (5%) |
| Medications | |
| Angiotensin-converting enzyme inhibitors | 19 (6%) |
| β Blockers | 51 (15%) |
| Laboratory data | |
| Serum creatinine (mg/dl) | 0.91 ± 0.28 |
| Serum cholesterol (mg/dl) | 2,156 ± 39 |
| Serum C-reactive protein (mg/dl) | 3.8 ± 4.8 |
⁎ Based on qualitative 2-dimensional echocardiogram with estimated left ventricular ejection fraction <55%.
| Normal | Concentric Remodeling | Concentric Hypertrophy | Eccentric Hypertrophy | |||||
|---|---|---|---|---|---|---|---|---|
| Year 0 | Year 7 | Year 0 | Year 7 | Year 0 | Year 7 | Year 0 | Year 7 | |
| Baseline concentric remodeling (n = 284) | ||||||||
| Participants | 178 (63%) | 87 (31%) | 8 (3%) | 11 (4%) | ||||
| Left ventricular end-diastolic dimension (cm) | 4.2 ± 0.4 | 4.7 ± 0.5 | 4.1 ± 0.4 | 4.1 ± 0.4 | 4.3 ± 0.5 | 5.0 ± 0.5 | 4.5 ± 0.3 | 5.5 ± 0.5 |
| Left ventricular mass (g) | 141 ± 32 | 132 ± 33 | 133 ± 35 | 137 ± 35 | 151 ± 53 | 236 ± 67 | 157 ± 26 | 205 ± 27 |
| Left ventricular fractional shortening (%) | 44.8 ± 7.7 | 42.9 ± 7.7 | 46.8 ± 6.6 | 43.4 ± 8.4 | 40.6 ± 12.4 | 43.7 ± 10.0 | 41.7 ± 6.5 | 33.4 ± 16.0 |
| Left ventricular systolic dysfunction † | 3 (1%) | 6 (4%) | 3 (1%) | 4 (5%) | 1 (1%) | 2 (25%) | 2 (1%) | 4 (36%) |
| Baseline concentric hypertrophy (n = 59) | ||||||||
| Participants | 17 (29%) | 14 (24%) | 13 (22%) | 15 (25%) | ||||
| Left ventricular end-diastolic dimension (cm) | 5.0 ± 0.3 | 5.1 ± 0.4 | 4.6 ± 0.5 | 4.1 ± 0.4 | 5.1 ± 0.6 | 4.8 ± 0.3 | 4.8 ± 0.4 | 5.5 ± 0.6 |
| Left ventricular mass (g) | 222 ± 41 | 164 ± 35 | 218 ± 44 | 167 ± 32 | 251 ± 60 | 238 ± 45 | 233 ± 59 | 229 ± 60 |
| Left ventricular fractional shortening (%) | 41.7 ± 7.2 | 36.6 ± 8.6 | 42.7 ± 8.5 | 39.7 ± 7.0 | 41.6 ± 6.2 | 48.6 ± 10.5 | 41.0 ± 10.2 | 37.1 ± 11.7 |
| Left ventricular systolic dysfunction † | 1 (1%) | 4 (24%) | 1 (1%) | 1 (2%) | 1 (1%) | 0 (0%) | 3 (1%) | 6 (43%) |
⁎ Left ventricular structure at year 7 was categorized as normal (relative wall thickness ≤0.42 and no left ventricular hypertrophy), concentric remodeling (relative wall thickness >0.42 and no left ventricular hypertrophy), concentric hypertrophy (relative wall thickness >0.42 and left ventricular hypertrophy), and eccentric hypertrophy (relative wall thickness ≤0.42 and left ventricular hypertrophy).
† Defined as left ventricular ejection fraction <55% as qualitatively assessed on baseline echocardiogram.
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