The findings, published in the recent edition of Clinical Chemistry, are part of the ongoing Atherosclerosis Risk in Communities (ARIC) study designed to investigate the causes of atherosclerosis and its clinical outcomes.
The clinically used models for predicting heart failure rely on a combination of lifestyle, demographic and cardiovascular risk factor information. While the biomarkers improved the clinical models, the investigators were surprised to find that a simpler design, which included age, race and the blood concentrations of two biomarkers, troponin T and N-terminal-pro-B-type natriuretic peptide (NT-proBNP), was found to be statistically no different than the more complex model.
Major public health issue
“Heart failure already is and will continue to be a major cardiovascular public health issue in the coming decades. Identifying simpler and better ways to predict heart failure can help clinicians and researchers improve and better target their preventive strategies,” said Dr. Vijay Nambi, assistant professor of medicine – section of cardiovascular research at BCM, staff cardiologist at the Michael E. DeBakey Veterans Affairs Hospital, Ben Taub Hospital and the Houston Methodist Center for Cardiovascular Disease Prevention.
Troponin T is commonly used by doctors to diagnose a heart attack. It is an indication of damaged heart muscle, but by using improved assays (testing methods) researchers have been able to detect the protein in low levels even in individuals with no symptoms. In fact, in the middle-older aged ARIC study participants, approximately 2 out of every 3 individuals had measurable levels. NT-proBNP is an inactive peptide fragment left over from the production of brain natiuretic peptide (BNP), a small neuropeptide hormone that has been shown to have value in diagnosing congestive heart failure.
Predicting highest risks
The researchers used both these markers in the prediction of future heart failure (over 10 years), thereby understanding which individuals among a general population are at the highest risk of heart failure.
Applying the model to patient data from the ongoing ARIC study, the researchers found their simple heart failure risk model was comparable to more complex models that take into account age, race, systolic blood pressure, antihypertensive medication use, smoking or former smoking, diabetes, body-mass index, prevalent coronary heart disease and heart rate.
“We are now able to predict who will develop heart failure better then we can predict who will have a heart attack, so the critical issues that we must now address is what lifestyle and drug therapies can prevent the development of heart failures for individuals who are at high risk,” said Dr. Christie Ballantyne, professor of medicine and section chief of cardiology and cardiovascular research at BCM and of the Houston Methodist Center for Cardiovascular Disease Prevention.
Others who took part in the study include Salim S. Virani, Ron C. Hoogeveen, David Aguilar and Anita Deswal, with BCM; Xiaoxi Liu, Lloyd E. Chambless, Gerardo Heiss, with the University of North Carolina; James A. de Lemos, with the University of Texas Southwestern Medical Center; Eric Boerwinkle, with the University of Texas Health Science Center School of Public Health; Brad C. Astor, with the University of Wisconsin; Pothur R. Srinivas, with the National Heart, Lung and Blood Institute; Thomas H. Mosley, with the University of Mississippi Medical Center; Josef Coresh and Sunil Agarwal, with Johns Hopkins Bloomberg School of Public Health; and Aaron R. Folsom, with University of Minnesota School of Public Health.
Virani and Deswal are also with the Michael E. DeBakey Veterans Affairs Medical Center.
Ballantyne is also the director of the Maria and Alando J. Ballantyne Atherosclerosis Clinical Research Laboratory at BCM and director of the Center for Cardiovascular Disease Prevention at the Methodist DeBakey Heart Center and co-director of the Lipid Metabolism and Atherosclerosis Clinic at Houston Methodist.
The Atherosclerosis Risk in Communities 374 Study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts (HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C).
Astor and Coresh are supported by the National Institute of Diabetes and Digestive and Kidney Diseases (1 R01 DK076770-01). Nambi is supported by a National Heart, Lung, and Blood Institute grant (5K23HL096893-02). Virani is supported by a Department of Veterans Affairs Health Services Research and Development Services (HSR&D) Career Development Award (CDA 09-028) Reagents were supported by a grant from Roche.
Graciela Gutierrez 713-798-4710