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J Am Coll Cardiol, 2000; 35:1628-1637 © 2000 by the American College of Cardiology Foundation |
* Division of Cardiology, Georgetown University Hospital, Washington, DC, USA
j St. Francis Hospital, Roslyn, New York, USA
Department of Biostatistics, Washington University, Seattle, Washington, USA
Division of Cardiology, University of Massachusetts Medical Center, Worcester, Massachusetts, USA
Department of Radiology, Tufts–New England Medical Center, Boston, Massachusetts, USA
|| Colchester Research Facility, University of Vermont, Colchester, Vermont, USA
¶ Wake Forest University, Winston-Salem, North Carolina, USA
# University of California at Irvine, Irvine, California, USA
** Division of Cardiovascular Medicine, University of California at Davis, Davis, California, USA
Division of Epidemiology and Clinical Applications, National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA
Manuscript received April 2, 1999; revised manuscript received December 7, 1999, accepted January 19, 2000.
Reprint requests and correspondence: Dr. John S. Gottdiener, Cardiology Research, St. Francis Hospital, 100 Port Washington Boulevard, Roslyn, New York 11576
gottdien{at}ziplink.net
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Abstract |
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We sought to characterize the predictors of incident congestive heart failure (CHF), as determined by central adjudication, in a community-based elderly population.
BACKGROUND
The elderly constitute a growing proportion of patients admitted to the hospital with CHF, and CHF is a leading source of morbidity and mortality in this group. Elderly patients differ from younger individuals diagnosed with CHF in terms of biologic characteristics.
METHODS
We analyzed data from the Cardiovascular Health Study, a prospective population-based study of 5,888 elderly people >65 years old (average 73 ± 5, range 65 to 100) at four locations. Multiple laboratory measures of cardiovascular structure and function, blood chemistries and functional assessments were obtained.
RESULTS
During an average follow-up of 5.5 years (median 6.3), 597 participants developed incident CHF (rate 19.3/1,000 person-years). The incidence of CHF increased progressively across age groups and was greater in men than in women. On multivariate analysis, other independent predictors included prevalent coronary heart disease, stroke or transient ischemic attack at baseline, diabetes, systolic blood pressure (BP), forced expiratory volume 1 s, creatinine >1.4 mg/dl, C-reactive protein, ankle-arm index <0.9, atrial fibrillation, electrocardiographic (ECG) left ventricular (LV) mass, ECG ST-T segment abnormality, internal carotid artery wall thickness and decreased LV systolic function. Population-attributable risk, determined from predictors of risk and prevalence, was relatively high for prevalent coronary heart disease (13.1%), systolic BP 
140 mm Hg (12.8%) and a high level of C-reactive protein (9.7%), but was low for subnormal LV function (4.1%) and atrial fibrillation (2.2%).
CONCLUSIONS
The incidence of CHF is high in the elderly and is related mainly to age, gender, clinical and subclinical coronary heart disease, systolic BP and inflammation. Despite the high relative risk of subnormal systolic LV function and atrial fibrillation, the actual population risk of these for CHF is small because of their relatively low prevalence in community-dwelling elderly people.
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The Cardiovascular Health Study (CHS) is a prospective, community-based, epidemiologic, observational study of 5,888 participants 65 years old from four different locations of the U.S. (11). The study was designed to investigate the risk factors for cardiovascular death and morbidity. This project contains an extensive array of physiologic and clinical functional measures, offering the opportunity to investigate the association of these measures with clinical events. The purpose of this report is describe the demographic, functional, anatomic and biochemical predictors of incident CHF in elderly subjects with and without prevalent coronary heart disease at enrollment.
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Methods |
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The design, rationale and examination details of the CHS, initiated and supported by the National Heart, Lung, and Blood Institute, have been published elsewhere (11). Briefly, interviews and questionnaires were used to obtain information on medications, functional status, quality of life, physical activity, nutrition and medical history. Participants reported to the CHS field center clinic after a 12-h overnight fast for assessment of blood chemistries, blood pressure (BP), heart rate and cognitive function, as well as anthropometric, electrocardiographic, echocardiographic, carotid artery ultrasound and other objective measurements (11).
Study group. To determine the relation between incident CHF and baseline demographic, clinical and laboratory variables, analyses were performed of the entire cohort without prevalent CHF (n = 5,625), as determined by adjudication of clinical records (see the following paragraph). Additional subgroup analyses were performed for participants with and without coronary heart disease at baseline (n = 973 and 4,652, respectively). Echocardiograms were obtained during the baseline examination for the original cohort (1989 to 1990) and again for surviving members of both cohorts in 1994 to 1995.
Adjudication of CHF. Methods used to assess cardiovascular events, including CHF, have been reported previously in detail (12,13). Potential clinical outcome events were identified at semi-annual visits. Self-report of a physician diagnosis of CHF was followed by confirmational review of the participant’s medical records. The presence of CHF was determined from both the diagnosis of CHF by a physician and treatment of CHF (i.e., a current prescription for a diuretic agent and either digitalis or a vasodilator). In addition, symptoms, signs and chest X-ray findings of CHF were reviewed by the CHS Events Committee, which classified all cardiovascular events. Congestive heart failure was termed "probable" rather than "definite" if the data were incomplete or unclear from the medical record or, more rarely, if the data were ambiguous. For cases of fatal CHF, the underlying cause of CHF (e.g., ischemic, valvular heart disease) was coded as the cause of death.
Electrocardiography. Twelve-lead electrocardiograms (ECGs) were obtained at baseline examination and yearly thereafter. Methods of analysis and classification by the ECG core laboratory (EPICARE Center, Winston-Salem, North Carolina), including estimation of left ventricular (LV) mass, have been published elsewhere (14–17). The prevalence and kinds of ECG abnormalities at baseline in this cohort have been previously reported (18).
LV function.
Global LV systolic function was qualitatively assessed from the baseline two-dimensional echocardiogram as showing normal, borderline or subnormal ejection fraction. Left ventricular function was scored in 99% of the original CHS cohort, with inter-reader agreement in 94% and intrareader agreement in 98% of paired studies (19). For comparison with the clinical evaluation of LV function, qualitatively assessed normal LV function on the echocardiogram approximately corresponds to an ejection fraction 55%. Analyses were performed on the entire cohort using baseline LV function as a covariate for the prediction of incident CHF.
Clinical assessments and measurements.
Prevalent coronary heart disease was determined by the participant’s report of physician diagnosis of angina pectoris, myocardial infarction, coronary artery bypass graft surgery or percutaneous transluminal coronary angioplasty before the initial evaluation. Diabetes mellitus was defined by self-report or by the current use of insulin or an oral hypoglycemic medication. Hypertension status was characterized as normal, borderline or definite. Borderline hypertension was defined by systolic BP 140 but <160 mm Hg or diastolic BP 90 but <95 mm Hg. Definite hypertension was defined by systolic BP 160 mm Hg or diastolic BP 95 mm Hg or a clinical history of hypertension requiring an antihypertensive medication. The ankle-arm index (i.e., the ratio of supine systolic ankle to brachial BP), a measure of lower extremity arterial occlusive disease, was obtained as described previously (8). Analyses of fasting serum chemistry values, fasting lipid values and plasma fibrinogen levels were performed by the core blood laboratory (University of Vermont, Colchester). Measures of pulmonary function included forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1). Common and internal carotid artery intimal-medial thickness, markers of atherosclerosis (20), were measured at baseline. Cognitive function was assessed using a Mini-Mental score obtained by observation of administered mental tasks (21).
Independent variables that were analyzed for their relation to incident CHF included demographic and clinical variables (age, gender, race, educational level, income, height, body weight, BP, ankle-arm index, smoking history, hypertension history, diabetes history, history of chronic obstructive pulmonary disease, stroke, transient ischemic attack [TIA], intermittent claudication), clinical chemistry values (fasting serum glucose levels, serum insulin, cholesterol, high and low density lipoproteins, serum creatinine), coagulation and inflammation variables (factor VII, fibrinogen, albumin, C-reactive protein), carotid ultrasound (common and internal carotid artery intimal-medial wall thickness), functional variables (Mini-Mental score, FEV1, FVC), ECG variables (presence of LV hypertrophy, estimated LV mass, atrial fibrillation, minor and major ST segment changes, Q wave myocardial infarction) and the echocardiographic categoric variable for LV systolic function at baseline.
Statistical methods. Incidence rates for CHF were calculated in units of person-years due to differences in follow-up times between the original and new cohorts. Statistical significance of observed differences in rates across levels of categoric variables was determined by unadjusted Cox survival models. Bivariate differences in mean values by CHF status for continuously measured risk factors were assessed by t tests.
Cox proportional hazards models were used to identify risk factors for incident CHF in multivariate models for all participants free of CHF at entry, and then stratified by coronary heart disease status at baseline. The models were generated in stages, with demographic, history, laboratory and clinic examination measures taken first, followed by measures of subclinical disease, including ankle arm index, carotid artery wall thicknesses, ECG abnormalities and LV systolic function. Once significant predictors were identified, time-dependent variables (i.e., new or recurrent angina or myocardial infarction) were added to each model to evaluate the risk of new episodes of coronary disease on CHF. In the group without coronary heart disease at baseline, incident coronary heart disease was added, and in the group with coronary heart disease at baseline, the occurrence of a new MI was added. At each stage, stepwise selection was used with a p value of 0.05. Interactions between significant variables and gender, race and prevalent coronary artery disease were examined. When significant linear relations were identified for continuously measured risk factors, quintiles of the risk factor based on the CHF cases were examined to explore the relation of the risk factor to CHF. If all of the risk appeared to be confined to an upper quintile, the upper quintile cut point was used to calculate an indicator variable. Because covariates that have a high relative risk may have little population impact if the prevalence of the covariate in the population is low, the population-attributable risk was computed (22). This calculation combines the prevalence of a risk factor with its relative risk to estimate that risk factor’s contribution to the incidence of a clinical end point in the population as a whole. To calculate the prevalence of risk factors measured on a continuous scale, these risk factors were dichotomized, with a clinically relevant cut point chosen when known. The cut point for the internal carotid artery thickness is the 80th percentile point, and for low FEV1 it is the lower limit of normal from published reference equations that provide predicted FEV1 as a function of age and height for gender and race subgroups (23,24).
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Results |
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80 years old. There were no racial differences in incident CHF (18.8/1,000 person-years for African-Americans vs. 19.4/1,000 person-years for non–African-Americans). The incidence rates of CHF for selected risk factors are presented separately by gender (Table 2). Diabetes status, stroke or TIA, hypertension status (normal, borderline, definite), intermittent claudication, ankle-arm index, atrial fibrillation, minor and major ST-T segment changes, LV function, chronic obstructive lung disease, income, educational status and self-perceived general health were all associated with the incidence rate of CHF in both men and women. Smoking was associated with the incidence rate of CHF only in men. Baseline biomedical variables. The values for biomedical variables of interest measured at baseline in men and women, with and without subsequent CHF, are shown in Table 3. In comparison with men and women who did not develop CHF during follow-up, men and women with incident CHF were older, less educated and slightly shorter and had a higher systolic BP (but no difference in diastolic BP), greater LV mass, greater common and internal carotid artery intimal-medial wall thickness, lower ankle-arm index, lower FVC and FEV1, higher serum fibrinogen, higher C-reactive protein, higher fasting plasma glucose and higher serum insulin. Pack-years of cigarette smoking was greater in men with incident CHF and displayed a similar trend in women. Mental acuity was lower at baseline in men with incident CHF and showed a similar trend in women. Total cholesterol at baseline was lower in women, and high density lipoprotein fraction of cholesterol was lower in men and women with incident CHF than in those without CHF. On bivariate analyses, self-report of estrogen use was negatively associated with CHF incidence (incidence 16.9/1,000 patient-years for those who never used it vs. 10.9 for past users and 12.0 for current users) (p = 0.007). However, after adjustment for age, estrogen use became nonsignificant (p = 0.17).
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Table 4 shows the results of a multivariate analysis that added measures of subclinical atherosclerotic disease (ankle-arm index, intimal-medial carotid artery wall thickness), ECG measures (LV mass, repolarization abnormality, atrial fibrillation) and echocardiographic estimation of LV systolic function to the previous demographic, BP and blood chemistry variables. For the model including all participants, the initial demographic and other variables retained significance. Moreover, subclinical atherosclerosis, atrial fibrillation, ST-T segment abnormalities and diminished systolic function were also independently predictive of incident CHF.
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New occurrence of coronary heart disease and incident CHF. Of the 397 incident CHF cases in the subgroup with no coronary heart disease at baseline, 174 (43.8%) had a new occurrence of clinically evident coronary heart disease (i.e., angina pectoris, myocardial infarction, coronary artery bypass graft surgery or coronary angioplasty) before or concurrent with their episode of CHF. The analysis showed a very large relative risk (13.8; confidence interval [CI] 10.9 to 17.4) of incident coronary heart disease in the prediction of CHF. A similar risk was found for the occurrence of a new myocardial infarction as predictive of CHF in the subgroup with coronary heart disease at baseline. In participants with baseline coronary heart disease, of 200 patients with incident CHF, 53 (26.5%) had a new myocardial infarction before or concurrent with their first episode of CHF. Hence, multivariate analyses were performed to adjust for incident coronary heart disease in those without prevalent coronary heart disease and for new or recurrent myocardial infarctions in those with prevalent coronary heart disease. In participants without prevalent coronary heart disease, adjustment for incident coronary heart disease occurring before incident CHF led to a loss of significance of stroke or TIA at baseline and a history of diabetes as predictors of incident CHF. In participants with prevalent coronary heart disease, myocardial infarction at baseline was predictive of incident CHF, and because it is also predictive of recurrent myocardial infarction, its relative risk decreased after adjustment for a new myocardial infarction. The inclusion of a new myocardial infarction resulted in a loss of predictive significance for male gender.
LV systolic function and CHF.
LV function before the onset of CHF
Of the 597 cases of incident CHF, LV systolic function on the echocardiogram was determined in 553 at baseline examination, 504 (91%) of whom had intact systolic function before incident CHF and 49 (9%) of whom had depressed LV function. Of 240 women with evaluable echocardiograms who developed CHF, 228 (95%) had intact systolic LV function at baseline. In contrast, of 313 men with incident CHF and evaluable baseline echocardiograms, 276 (88%) had intact systolic LV function (p = 0.006, men vs. women).
Predictive value of baseline LV function for incident CHF
The relative risk of CHF in participants with abnormal baseline LV function in the absence of prevalent CHF was 2.84 (CI 1.63 to 4.93); in those with prevalent coronary disease it was 2.11 (CI 1.34 to 3.32). The association of abnormal LV function with subsequent CHF was present both in participants with and those without prevalent coronary heart disease. The relation persisted after adjustment for LV mass and other ECG covariates, after adjustment for incident coronary heart disease in participants free of it at baseline and after adjustment for a new myocardial infarction in participants with baseline coronary heart disease.
Population-attributable risk. The population-attributable risk for selected risk factors is shown in Table 5. Prevalent coronary heart disease was associated with the greatest population-attributable risk for incident CHF (13.1%), followed by uncontrolled systolic BP (12.8%), elevated C-reactive protein (9.7%) and low ankle-arm index (9.2%). In contrast, the risks attributable to subnormal LV systolic function (4.1%) and atrial fibrillation (2.2%) were low, secondary to their low population prevalence.
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Discussion |
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Bivariate relations were found between incident CHF and anthropometric, demographic and functional variables that have not been widely appreciated. For example, incident CHF was inversely related to body height, mental function, educational level and pulmonary function, as well as directly to measures of subclinical atherosclerosis, inflammation and coagulation. Short stature has been associated with adverse cardiovascular outcome (28–30). Diminished mental function may reflect atherosclerotic or hypertensive brain disease, and hence an increased likelihood of comorbid cardiac disease. Low educational level and other markers of decreased socioeconomic status have been linked to cardiovascular outcomes (31,32), possibly in relation to health-damaging behavior (33). Mental function, short stature and socioeconomic measures did not retain significance in multivariate models. This may be a reflection of their association with biologic predictors, such as coronary heart disease and hypertension, that are more directly linked to CHF.
When the relative risk of predictors was interpreted within the context of the population prevalence of those predictors (population-attributable risk), prevalent coronary heart disease, poorly controlled systolic BP and elevated C-reactive protein were the three leading predictors of incident CHF in the elderly.
Diastolic versus systolic CHF: role of LV mass. A principal finding of the study was the presence of intact LV systolic function commonly preceding the onset of incident CHF, particularly among women. This finding is consistent with the findings of others in noting that CHF in the elderly is commonly "diastolic" (10,25,34,35). Other analyses of the CHS cohort (36) demonstrated a relation between diastolic filling and subsequent CHF. Moreover, the independent association of LV mass with incident CHF has been reported by others (26) and is consistent with data from our group (36,37) showing the predictive value of both diastolic filling velocity and LV mass for subsequent CHF.
Age, gender and race. The present study of an older population with a greater incidence of CHF supports the findings of the Framingham investigators (38) and others (3,39,40) in finding that incident CHF is associated with male gender and age. Although the predictive value of age persisted even after adjustment for age-related covariates, the greater incidence in men, in part explained by greater prevalent and incident atherosclerosis, is consistent with the results of the Eastern Finland Surveillance Study (39).
We failed to find greater incidence rates of CHF in African-American participants. However, the smaller number of African-American participants relative to white participants reduces the power of the study to make meaningful comparisons of the effects of race on the incidence of CHF.
Diabetes and impaired glucose tolerance. Insulin resistance facilitates atherogenesis (41) as well as LV hypertrophy (42), both of which may lead to CHF, and diabetes has been previously associated with CHF (38,43). In our cohort of elderly individuals, the incidence of CHF was also substantially higher (approximately twofold) in diabetic men and women than in nondiabetics. Serum insulin had an independent predictive value for CHF only in men.
Inflammation. Increased C-reactive protein retained independent predictive value for CHF in multivariate models. Because of its high prevalence in the study group, elevated C-reactive protein was associated with substantial population-attributable risk for CHF. Although studies show that inflammation may be mechanistically associated with atherogenesis (44,45), the association of C-reactive protein with incident CHF persisted in models that adjusted for clinically prevalent as well as subclinical atherosclerotic disease. The increase in C-reactive protein may reflect a general increase in proinflammatory cytokines, which are elevated in CHF (46,47) and which have been implicated in its pathophysiology (48,49).
Pulmonary function and incident CHF. The inverse relation between FEV1 and incident CHF in this study may reflect a misclassification of dyspnea due to lung disease as CHF, as well as the concordance of age-related decreases in pulmonary function with increases in incident CHF. However, the relation persisted after adjustment for age and chronic obstructive lung disease, supporting the previous findings in the Framingham study (50). In addition, decreased FVC may exacerbate the clinical presentation of CHF. Pulmonary function in the elderly is independently associated with elevated LV mass, hypertension and ischemic cardiac disease (51,52). Multiorgan effects of aging, possibly encoded at birth (53), may account for pulmonary as well cardiac dysfunction.
Study limitations. The clinical diagnosis of CHF presumes that there is pulmonary and/or systemic congestion consequent to sufficient elevation of left and/or right heart filling pressure to produce transudation of fluid into the pulmonary interstitium and alveoli or into the systemic tissue interstitium. This may occur in the presence or absence of systolic LV dysfunction. Because it is impractical in clinical practice or in clinical studies (in particular, population-based studies) to measure intracardiac filling pressures, the diagnosis of CHF is based on clinical criteria. Those used in CHF are similar to those used in the Framingham study and in other studies. Nonetheless, it is possible that dyspnea from other causes, such as pulmonary disease, could be misclassified as CHF. Because participants with depressed baseline LV systolic function may have greater mortality associated with CHF, as well as a lower mean time to death, than those with intact baseline LV function, survivor effects may have resulted in overestimation of the proportion of participants with intact systolic function preceding CHF.
Clinical implications. Prevention of CHF in the elderly is an increasingly important clinical and public health goal for physicians. The present study underscores the contribution of poorly controlled systolic BP and of clinically evident coronary heart disease for incident CHF in community-based elderly people, many of whom have preserved LV systolic function. A reduction of systolic BP (54), possibly in relation to a reduction of LV mass (55,56) or left atrial size (57), or both, with the use of diuretic agents, beta-blockers (58–60) or other therapy, may be helpful in averting CHF.
Clinical trials of CHF have generally evaluated patients whose biologic characteristics differ substantially from those of elderly patients with CHF. Most major clinical trials have required severe LV dysfunction as a criterion for recruitment and have restricted recruitment to patients substantially younger than those in the present study. Hence, the optimal therapy for the treatment of CHF remains to be determined in appropriately designed clinical trials specifically addressing the particular characteristics of elderly patients with CHF (61).
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