Icd 10 Code for Family History of Ischemic Heart Disease
Circulation. Writer manuscript; bachelor in PMC 2013 Apr 21.
Published in final edited grade as:
PMCID: PMC3631594
NIHMSID: NIHMS459143
Association Between Family History and Coronary Heart Affliction Decease Across Long-Term Follow-Up in Men
The Cooper Center Longitudinal Study
Justin G. Bachmann
Sectionalisation of Cardiology, Section of Internal Medicine University of Texas Southwestern Medical Center Dallas, TX
Benjamin 50. Willis
Cooper Institute University of Texas Southwestern Medical Center Dallas, TX
Colby R. Ayers
Reynolds Cardiovascular Clinical Inquiry Center Academy of Texas Southwestern Medical Centre Dallas, TX
Amit Khera
Division of Cardiology, Department of Internal Medicine University of Texas Southwestern Medical Middle Dallas, TX
Jarett D. Berry
Division of Cardiology, Department of Internal Medicine University of Texas Southwestern Medical Centre Dallas, TX
Abstract
Background
Family history of coronary heart disease (CHD) has been well studied equally an independent risk factor for CHD events in the brusque term (<x years). However, information are sparse on the association betwixt family unit history and risk for CHD beyond long-term follow-upward.
Methods and Results
We included 49 255 men from the Cooper Center Longitudinal Study. Premature family history of CHD was divers as the presence of angina, myocardial infarction, angioplasty, or bypass surgery in a relative <50 years of age. Cause-specific mortality was obtained from the National Death Alphabetize. The association between premature family history and cardiovascular disease (CVD) or CHD death was compared across three unique follow-upwardly periods (0–ten, >10–twenty, and >twenty years). Lifetime take chances was estimated past use of a modified survival analytic technique adjusted for competing hazard with non-CVD death as the competing effect. After 811 708 person-years of follow-up, in that location were 919 CHD deaths and 1456 CVD deaths. After adjustment for traditional risk factors, premature family unit history was associated with CHD bloodshed >10 to twenty years (1.59; 95% conviction interval, 1.14–two.22) and >20 years (1.43; 95% confidence interval, 1.05–1.95) with wider conviction intervals at 0 to x years (1.32; 95% confidence interval, 0.76–2.31). Similar findings were observed for CVD mortality. Compared with men without a family unit history of coronary artery disease, premature family history was associated with an ≈50% higher lifetime risk for both CHD and CVD mortality (13.7% versus viii.9% and 21% versus 14.1%, respectively).
Conclusion
Premature family history was associated with a persistent increase in both CHD and CVD bloodshed risk across long-term follow-upwards, resulting in significantly higher lifetime risk estimates.
Keywords: cardiovascular diseases, coronary disease, heredity, risk factors
Family history of coronary center disease (CHD) is a well-recognized take a chance factor, with multiple prospective studies demonstrating a consequent, independent clan with CHD.one–3 Although definitions vary, it is well established that the strength of the association betwixt family history and CHD is greatest with earlier age of presentation of CHD in the family member (ie, premature family history [pre-FHx]).four–6 Current prevention guidelines recommend that pre-FHx be incorporated into the risk interpretation process that guides treatment decisions,v and family history can be easily and systematically queried in the clinical setting.7 Yet, family history is included in some,8 but not all,9,10 brusk-term risk prediction equations because of its relatively pocket-size contribution to curt-term take chances.4,9,x
Clinical Perspective on p 3098
Although risk in the short term (ie, 10 years) represents a well-established approach to guide handling decisions, it may non completely reflect the brunt of CHD adventure beyond the lifespan.11–14 Specifically, a risk cistron that promotes a small but consequent increase in CHD gamble can interpret into substantial differences in risk across the lifespan despite a more modest increase in curt-term chance.15
To the all-time of our cognition, the association between a family unit history of CHD and long-term risk for CHD has not been studied. Therefore, we sought to determine the association betwixt the presence of a family history of CHD and both CHD and cardiovascular illness (CVD) bloodshed across short-term (0–10 years), intermediate-term (>10–twenty years), and long-term (>20 years) follow-up. We besides sought to determine the association between the presence of a family unit history of CHD and the lifetime risk for both CHD and CVD mortality.
Methods
Study Sample and Definitions
The Cooper Center Longitudinal Study (CCLS) is an ongoing, prospective study at the Cooper Clinic in Dallas, TX, that began over 40 years ago.16–eighteen The Cooper Center is a preventive medical practice that focuses on periodic health examinations. Patients come from all fifty states and are referred past their employer or personal doc or are self-referred. Fewer than five% of patients are nonwhite. For the present study, nosotros included all men between 20 and ninety years of age who underwent a complete clinical test and completed a family history questionnaire at the Cooper Center between 1970 and 2006 (n=49 956). Afterwards excluding 701 men with a prior myocardial infarction, nosotros had a terminal study sample of 49 255. Women were excluded from the present study because of the small number of CHD end points in each decade of follow-upwards (6 CHD deaths at 0–10 years, 27 CHD deaths at >10–xx years, and 32 CHD deaths at >20 years), particularly when stratifying past family history status.
The CCLS undergoes annual review past the Institutional Review Board of the Cooper Institute. The present study was approved past the Institutional Review Board of University of Texas Southwestern Medical Center at Dallas.
Measurements
All participants underwent a comprehensive clinical examination that included self-reported personal medical history and smoking habits, a physical exam, and measurement of claret pressure level, fasting blood glucose, and cholesterol. Details of anthropometric and laboratory measurements and other variable definitions have been given previously.17 Diabetes mellitus was defined by self-written report or a fasting claret glucose >125 mg/dL. Smoking habits (current smoker or not) were obtained from a standardized questionnaire. Systolic and diastolic blood pressures were measured in standard style with a sphygmomanometer.
Definition of Family History
Participants completed a standardized questionnaire on their family unit history status. A positive family history was defined as the presence of angina, myocardial infarction, angioplasty, or coronary artery bypass surgery in a sibling, aunt or uncle, parent, or grandparent (excluding cousins, relatives by union, and one-half-relatives). If a patient had a family unit fellow member with a history of CHD, the patient was asked to betoken whether the event occurred before 50 years of age (pre-FHx) or thereafter (tardily-FHx); if not, the patient was defined equally having no family history (no-FHx). The 3 categories of family history (no-FHx, pre-FHx, and late-FHx) were mutually exclusive. No specific data was recorded in the questionnaire on the type of CHD event or family member.
Outcome
Participants were followed upwardly from the engagement of initial test until death or the end of follow-up on Dec 31, 2006 (range of follow-up period, 0.01–36 years), through the use of information from the National Death Alphabetize. CHD mortality was defined as the primary cause of death indicated by International Classification of Diseases, 9th revision (ICD-nine), codes 410 to 414 or equivalent codes from ICD-8 or ICD-10. CVD bloodshed was defined equally ICD-9 codes 390.0 to 458.9 or their equivalents from ICD-8 or ICD-10.
Statistical Analysis
The follow-upwards period was partitioned into iii unique, mutually sectional time periods: 0 to 10 inclusive, >ten to twenty inclusive, and >20 years. For instance, a participant surviving for 25 years provided 10 years of follow-up for the first follow-upwards interval (0–10 years), 10 years of follow-up for the 2nd interval (>10–xx years), and v years of follow-up for the third interval (>20 years). Family history was characterized every bit a single categorical variable with three levels (no-FHx, pre-FHx, and tardily-FHx), and a Cox proportional hazards model was synthetic for each follow-up flow with no-FHx every bit the referent group. The model was multivariable and included historic period, systolic blood pressure, serum total cholesterol, body mass index, smoking, and diabetes mellitus. Secondary analyses with further adjustment for fitness were too performed.
Finally, to estimate lifetime hazard for CHD mortality, we applied a modified survival analytic technique that has been described previously.12,19 In this type of analysis, participants contributed information on CHD expiry and decease costless of CHD for each age attained during follow-up. Because the Kaplan-Meier cumulative incidence does not reflect the competing take chances for death from other causes before the development of CHD, adjustment was made for this competing gamble to yield a true remaining lifetime take a chance for CHD. Lifetime take a chance estimates were calculated separately for each family history category (no-FHx, pre-FHx, and belatedly-FHx) beginning at 45 and 55 years of age. Like analyses were performed to judge the lifetime chance for CVD mortality. All statistical analyses were performed with SAS for Windows (release 9.2; SAS Institute, Inc, Cary, NC).
Results
Baseline Characteristics
Among 49 255 men in the report sample, 7832 (16%) had a tardily-FHx and 3203 (vi.5%) had a pre-FHx. Baseline characteristics of the written report sample are shown in Table 1, demonstrating similar overall levels of traditional risk factors with and without a family history of CHD. Afterward a median follow-upwards of 16 years, in that location were 919 CHD deaths and 1456 CVD deaths beyond 811 708 person-years of follow-up, with a big number of person-years and events beyond all periods of follow-up (Table 2).
Tabular array 1
Participant Characteristics in the Cooper Center Longitudinal Study
| Feature | No Family unit History (northward=38 220) | Late-Onset Family History (n=7832) | Premature Family History (due north=3203) |
|---|---|---|---|
| Baseline age, y | 45.1 (9.eight) | 43.two (9.6) | twoscore.5 (8.7) |
| SBP, mm Hg | 122.eight (13.7) | 120.4 (13.5) | 121.0 (13.ii) |
| DBP, mm Hg | 82.1 (nine.7) | 80.iii (9.5) | fourscore.7 (nine.4) |
| Total cholesterol, mg/dL | 206.6 (40.ii) | 212.5 (40.1) | 214.3 (40.4) |
| Triglycerides, mg/dL | 139.2 (120.3) | 139.two (112.9) | 145.1 (107.2) |
| BMI, kg/chiliadtwo | 27.0 (iv) | 26.1 (iii.v) | 26.1 (iii.6) |
| Diabetes mellitus, n (%) | 1740 (4.6) | 320 (four.1) | 161 (5) |
| Smoking, n (%) | 6361 (16.6) | 1623 (xx.7) | 702 (21.nine) |
| CHD deaths, n | 582 | 230 | 107 |
| Age-adjusted rate per 1000 person-y | 1.0 | one.3 | 1.9 |
| CVD deaths, n | 905 | 387 | 387 |
| Age-adjusted rate per 1000 person-y | 1.6 | 2.two | two.ix |
| All-cause deaths, n | 2657 | 1057 | 407 |
| Age-adjusted rate per m person-y | iv.6 | vi.0 | 7.0 |
Table 2
Mortality Rates by Cause of Death for 0 to 10, >10 to twenty, and >twenty Years of Follow-Up Amidst 49 255 Men in the Cooper Eye Longitudinal Written report
| Follow-Upwardly of 0–10 y (n=49 255) | Follow-Up of >10–20 y (n=32 789) | Follow-Upwards of >20 y (due north=20 282) | |
|---|---|---|---|
| Person-y | 411 648 | 270 036 | 130 024 |
| CHD deaths, n | 203 | 356 | 360 |
| Rate (per g person-y) | 0.49 | ane.32 | 2.77 |
| CVD deaths, due north | 281 | 540 | 635 |
| Rate (per k person-y) | 0.68 | 2.00 | iv.88 |
| All-cause deaths, n | 810 | 1499 | 1812 |
| Rate (per 1000 person-y) | 1.97 | v.55 | 13.94 |
Family unit History of CHD and Run a risk at 0 to 10, >10 to twenty, and >xx Years of Follow-Up
The associations between tardily-FHx and CHD, CVD, and all-cause death across short-term, intermediate-term, and long-term follow-upwards are shown in Table iii. The association betwixt tardily-FHx and CHD mortality was strongest in the curt term (0–10 years) with no apparent association across intermediate- and long-term follow-up. Findings were similar in both age-adapted and multivariable-adapted models and for both CHD and all-cause mortality.
Table 3
Multivariable- and Age-Adjusted Run a risk Ratios (95% Confidence Intervals) for Premature Family History, Late-Onset Family History, and Coronary Heart Disease Mortality, Cardiovascular Illness Bloodshed, and All-Crusade Mortality Among Men in the Cooper Center Longitudinal Study*
| Variable | Follow-Upward of 0–x y | Follow-Up of >10–20 y | Follow-Up of >20 y |
|---|---|---|---|
| CHD mortality | |||
| Historic period-adjusted | |||
| No-FHx | 1 | 1 | 1 |
| Late-FHx | 1.25 (0.89–ane.76) | 1.10 (0.87–1.39) | 0.99 (0.76–1.27) |
| P, late-FHx vs no-FHx | 0.196 | 0.436 | 0.910 |
| pre-FHx | ane.41 (0.81–2.45) | 1.59 (one.14–2.22) | 1.46 (1.07–1.99) |
| P, pre-FHx vs no-FHx | 0.226 | 0.006 | 0.017 |
| Multivariable | |||
| No-FHx | 1 | one | 1 |
| Belatedly-FHx | 1.25 (0.88–1.76) | one.fifteen (0.91–ane.46) | 1.00 (0.78–1.29) |
| P, tardily-FHx vs no-FHx | 0.210 | 0.250 | 0.984 |
| pre-FHx | 1.32 (0.76–2.31) | 1.59 (1.14–two.22) | 1.43 (1.05–1.95) |
| P, pre-FHx vs no-FHx | 0.324 | 0.006 | 0.025 |
| Log-rank P | 0.644 | 0.001 | <0.0001 |
| CVD mortality | |||
| Age-adjusted | |||
| No-FHx | one | 1 | 1 |
| Tardily-FHx | 1.42 (1.07–1.88) | i.fifteen (0.95–1.39) | 1.ten (0.91–i.32) |
| P, late-FHx vs no-FHx | 0.016 | 0.155 | 0.345 |
| pre-FHx | i.60 (1.02–2.53) | 1.44 (1.09–1.92) | 1.47 (ane.16–1.86) |
| P, pre-FHx vs no-FHx | 0.042 | 0.011 | 0.002 |
| Multivariable | |||
| No-FHx | 1 | ane | one |
| Late-FHx | 1.forty (1.06–1.86) | 1.twenty (0.99–one.45) | ane.xi (0.92–1.33) |
| P, tardily-FHx vs no-FHx | 0.019 | 0.065 | 0.299 |
| pre-FHx | one.51 (0.96–ii.39) | 1.46 (one.ten–1.94) | 1.43 (ane.thirteen–i.82) |
| P, pre-FHx vs no-FHx | 0.078 | 0.009 | 0.003 |
| Log-rank P | 0.347 | <0.0001 | <0.0001 |
| All-cause bloodshed | |||
| Age-adjusted | |||
| No-FHx | one | 1 | ane |
| Belatedly-FHx | 1.32 (i.eleven–1.56) | ane.09 (0.97–one.22) | ane.01 (0.90–i.13) |
| P, late-FHx vs no-FHx | 0.001 | 0.132 | 0.858 |
| pre-FHx | 1.26 (0.95–i.67) | 1.21 (1.02–1.44) | one.xiv (0.98–1.32) |
| P, pre-FHx vs no-FHx | 0.115 | 0.033 | 0.098 |
| Multivariable | |||
| No-FHx | 1 | 1 | i |
| Late-FHx | 1.30 (1.ten–1.54) | 1.ten (0.98–1.24) | 0.99 (0.89–1.11) |
| P, belatedly-FHx vs no-FHx | 0.002 | 0.094 | 0.887 |
| pre-FHx | i.19 (0.90–i.58) | one.xx (1.01–1.43) | 1.09 (0.94–i.27) |
| P, pre-FHx vs no-FHx | 0.228 | 0.040 | 0.248 |
| Log-rank P | 0.091 | <0.0001 | <0.0001 |
The associations betwixt pre-FHx and CHD, CVD, and all-cause expiry across the short-term, intermediate-term, and long-term follow-up are also shown in Table 3. pre-FHx was associated with both CVD and CHD mortality across intermediate-term (>10–20 years) and long-term (>20 years) follow-upwards in both age-adapted and multivariable-adjusted models, with a similar pattern of results in curt-term follow-upwards merely with wider conviction intervals. Secondary analyses with boosted adjustment for cardiorespiratory fitness levels demonstrated similar results (data non shown). In add-on, we stratified our analyses by high (x-yr chance ≥ten%) and depression (10-year gamble <10%) Framingham Risk Score groups. The magnitude of the clan between pre-FHx and CHD mortality at >20-yr follow-up was similar in the groups with high (hazard ratio, 1.45; 95% confidence interval, 0.89–two.34) and low (hazard ratio, ane.37; 95% confidence interval, 0.91–2.06) Framingham Risk Score but with wider conviction intervals as expected.
Family History and Lifetime Risk of CVD Mortality
For men 55 years of age, the presence of a pre-FHx was associated with a 6.9% higher lifetime risk for CVD mortality (Figure one). For men 45 years of age, pre-FHx was associated with a 4.7% higher lifetime risk for CVD mortality (Figure 2). Like findings were observed for men at both ages for lifetime hazard for CHD mortality (at 55 years of age, xiii.7% with pre-FHx versus 8.9% with no family unit history; at 45 years of age, 8.1% versus 5.5%). In contrast, in that location was no apparent departure in the lifetime hazard for either CHD or CVD mortality between the no-FHx and late-FHx groups (data non shown).
Cumulative incidence of cardiovascular affliction (CVD) death adjusted for competing gamble (lifetime chance) for men co-ordinate to family history status at 55 years of historic period. Family unit history of premature coronary centre disease (CHD) denotes a CHD event in a outset-caste family fellow member before l years of historic period. north=26 447 for patients with attained age ≥55 years.
Cumulative incidence of cardiovascular disease (CVD) death adjusted for competing chance (lifetime risk) for men according to family unit history status at 45 years of age. Family history of premature coronary heart disease (CHD) denotes a CHD consequence in a first-degree family fellow member earlier 50 years of historic period. due north=37 036 for patients with attained age ≥45 years.
Give-and-take
In the present study, we observed several important findings. First, the association between pre-FHx and both CHD and CVD mortality relative to overall bloodshed was consequent across short-term (0–10 years), intermediate-term (>x–20 years), and long-term (>20 years) follow-upward. In contrast, the presence of late-FHx was associated with an increased risk in the short term with no credible clan across subsequently follow-up periods. In add-on, the presence of pre-FHx was associated with an ≈v% absolute and l% relative deviation in the lifetime run a risk for CVD and CHD mortality. These findings suggest that the presence of a pre-FHx of CHD represents a clinically meaning increase in CHD and CVD gamble across the lifespan.
Current prevention guidelines recommend the use of short-term risk estimation (ie, ten years) to guide handling decisions (ie, statin therapy).5,twenty–25 Although these hazard prediction algorithms accept some limitations, the ability to improve their performance through the improver of novel hazard markers has had merely express success.26 In particular, the addition of pre-FHx to a traditional risk factor model was not associated with a pregnant improvement in risk classification.4
In contrast, lifetime gamble estimation has been proposed as a novel strategy to provide clinically meaningful improvements in risk prediction.12,xiv,27 Near Usa adults ≤fifty years of age are at low curt-term take a chance for CHD (ie, <x%); still, more ane one-half accept a high lifetime risk.12,28 This discordance reflects the dominant furnishings of historic period in curt-term gamble equations and the sustained contribution of modest risk gene levels on CHD risk across the remaining lifespan.13,29,xxx Therefore, extending the fourth dimension horizon for run a risk estimation beyond the ten-year window to include the remaining lifespan represents a novel approach to risk estimation that could have important clinical implications.
In the present study, nosotros extend our prior work in long-term risk interpretation to include family history, demonstrating that pre-FHx is associated with a five% absolute and 50% relative difference in the lifetime adventure for CVD mortality. Earlier literature from the CCLS11 and from other information sets13,14 suggests that this increment represents a clinically pregnant difference in lifetime take a chance and is similar to the effect of a major take chances gene. For instance, nosotros recently observed that the presence of a major take chances factor was associated with a lifetime risk for CVD bloodshed of 23% compared with a lifetime risk of just 17% among participants without a major risk factor.xi Similarly, compared with participants without a family unit history, the presence of a pre-FHx was associated with an increased lifetime take a chance of CVD expiry (viii.four% versus 13.1% at 45 years of age). Thus, when making handling decisions, clinicians could consider the contribution of a pre-FHx to the lifetime risk of CVD every bit similar to a major hazard cistron.
The discordance between the clinical touch on short-term and long-term risk is not unexpected. For example, nonsense mutations in PCSK9 resulting in a 15% reduction in depression-density lipoprotein cholesterol were associated with a 47% reduction in the gamble of CHD.15 Thus, the more than typical 1:1 relationship between cholesterol and CHD risk in clinical trials was increased 3-fold, consistent with the cumulative effects of lower depression-density lipoprotein cholesterol beyond the lifespan. Similarly, sustained exposure to the genetic factors involved in a pre-FHx could be expected to consequence in a significant, cumulative CHD run a risk over the lifespan.
Although the association between family history and CHD risk in the short term (ie, ≤10 years) has been well studied,1,6,31–twoscore relatively limited information are available on the clan between family history and long-term hazard. In 1 study from the Swedish Twin Registry, the heritability of CHD death was assessed across different follow-upward periods.41 An additional 10 years of follow-upwardly was associated with a small but statistically insignificant decrease in the heritability of CHD death (0.66 versus 0.57 in men; 0.44 versus 0.38 in women). These data are consistent with our observations that a pre-FHx was associated with CHD and CVD death across longer-term follow-up.
In dissimilarity to the results for pre-FHx, the association between tardily-FHx and CHD mortality attenuated over time. This is consequent with prior studiesiv,6 and probable reflects the heterogeneous nature of self-reported family unit history, which influences CHD take chances through both genetic and environmental mechanisms.33,37,42 Although premature CHD events likely take a greater genetic component, belatedly CHD events may reverberate a greater contribution of ecology factors and behaviors that are less heritable. Thus, the run a risk associated with the likely stronger genetic component of pre-FHx appeared to persist with time, in contrast to the attenuation in risk observed with tardily-FHx.
Several limitations of our written report should exist best-selling. Commencement, the definition of family history of CHD in our study was broad (including grandparents, aunts, and uncles) and was acquired within the context of a clinical study. Yet, these effects would tend to benumb the observed association between family history and CHD adventure, and a more rigorous definition of family unit history would exist expected to have an even larger outcome size. In improver, family history of CHD was obtained through patient report and was non validated. Nevertheless, in the National Middle, Lung, and Blood Institute Family Heart Study and other cohorts, self-report of a family history of premature CHD has a sensitivity of >fourscore% and a specificity approaching 90%.43–45 In the Newcastle Family unit History Study, the net bias in call up of family unit history of CHD was toward the zip.46 Therefore, at a minimum, nosotros believe that our data stand for conservative estimates on the association between family history and long-term take chances.
Second, the prevalence of pre-FHx and tardily-FHx is lower than in comparative studiesfour and likely reflects multiple factors, including the age restrictions in our definition of family history. Data on family size and the specific age at which a family unit member's CHD or CVD event occurred were not available in the CCLS database, preventing us from exploring more traditional age cut points. As a result, we were not able to use sexual practice-specific age restrictions with college age thresholds in women. Although our definition of family history may have resulted in some misclassification, the large sample size and long-term follow-upwardly provided adequate statistical power to assess the association between family history and long-term CHD gamble.
Tertiary, the CCLS is a unique cohort of predominantly white participants with a lower risk factor burden and college socioeconomic status than the full general population. Although the prevalence of prior CHD and traditional risk factors is lower,47 the effect of these risk factors is quite like. For instance, we accept recently shown that the presence of a major chance factor in middle age in the CCLS is associated with a comparable lifetime risk for CVD in other cohorts within the Lifetime Risk Pooling Project, a pooled assay of eighteen cohorts.eleven,14 Moreover, we believe that the overall healthy nature of the cohort represents an important strength, illustrating the contribution of family history to an otherwise depression-risk population. Finally, our analyses were restricted to men considering of the overall low prevalence of family history and the pocket-sized number of events in women across the different follow-upward periods.
Conclusions
We observed a persistent association betwixt pre-FHx and both CHD and CVD bloodshed across intermediate-term (>ten–20 years) and long-term (>twenty years) follow-up. We also observed that pre-FHx was associated with a clinically significant increase in the lifetime risk for both CVD and CHD mortality. We believe these findings could exist useful to clinicians, providing a broader context with which to consider the effects of a pre-FHx on the lifetime take chances of CVD.
Acknowledgments
We give thanks Dr Kenneth H. Cooper for establishing the Cooper Center Longitudinal Written report, the Cooper Center staff for collecting clinical data, and the Cooper Plant for maintaining the database.
Sources of Funding Dr Berry receives funding from the Dedman Family unit Scholar in Clinical Care endowment at University of Texas–Southwestern Medical Centre; grant K23 HL092229 from the National Heart, Lung, and Blood Institute; and grant 10BG1A4280091 from the American Heart Association. Dr Berry had full access to all the data in the study and had the terminal responsibleness for the decision to submit for publication. All authors have read and concord to the manuscript equally written.
Footnotes
Disclosures Dr Drupe is a member of the Speaker's Bureau for Merck & Co. The other authors report no conflicts.
Contributor Information
Justin M. Bachmann, Division of Cardiology, Section of Internal Medicine University of Texas Southwestern Medical Center Dallas, TX.
Benjamin L. Willis, Cooper Establish University of Texas Southwestern Medical Middle Dallas, TX.
Colby R. Ayers, Reynolds Cardiovascular Clinical Inquiry Center University of Texas Southwestern Medical Middle Dallas, TX.
Amit Khera, Partitioning of Cardiology, Department of Internal Medicine University of Texas Southwestern Medical Centre Dallas, TX.
Jarett D. Berry, Division of Cardiology, Department of Internal Medicine University of Texas Southwestern Medical Eye Dallas, TX.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3631594/
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