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. Author manuscript; available in PMC: 2018 Jun 20.
Published in final edited form as: JACC Cardiovasc Imaging. 2017 Mar 15;10(9):1031–1038. doi: 10.1016/j.jcmg.2016.10.022

Non-obstructive CAD by coronary CTA improves risk stratification and allocation of statin therapy

Hamed Emami *, Richard AP Takx *, Thomas Mayrhofer *,†, Sumbal Janjua *, Jakob Park *, Amit Pursnani *, Ahmed Tawakol *, Michael Lu *, Maros Ferencik *,§, Udo Hoffmann *
PMCID: PMC6010207  NIHMSID: NIHMS966880  PMID: 28330658

Abstract

Background

Detection of non-obstructive coronary artery disease (CAD) by coronary CTA may improve risk stratification and permit individualized and more appropriate allocation of statin therapy.

Objectives

To determine prognostic value of non-obstructive CAD for ASCVD events and to determine whether incorporation of this information into the pooled cohort equation reclassifies recommendations for statin therapy as defined by the 2013 ACC/AHA guidelines for cholesterol management.

Methods

We determined the pooled hazard ratio (HR) non-obstructive CAD for ASCVD events from published studies and incorporated this information into the ACC/AHA Pooled Cohort equation. We calculated revised gender and ethnicity based 10 year ASCVD risk and determined boundaries corresponding to the original 7.5% risk for ASCVD events. We also assessed re-classification for statin eligibility by incorporating the results from meta-analysis to individual patients from a separate cohort.

Results

We included two studies (2295 subjects, 66% male, prevalence of non-obstructive CAD 47%, median follow-up 49 months, 67 ASCVD events). HR of non-obstructive CAD for ASCVD events was 3.2 [95% CI 1.5-6.7]. Incorporation of this information into the pooled cohort equation resulted in reclassification towards statin eligibility in individuals with non-obstructive CAD, with original ASCVD score of 3.0% and 5.9% or higher in African-American Women and Men, and 4.4% and 4.6% or higher in Caucasian Women and Men; respectively. The absence of non-obstructive CAD resulted in reclassification towards statin ineligibility if the original ASCVD score was as 10.0% and 17.9% or lower in African-American Women and Men, and 13.7% and 14.3% or lower in Caucasian Women and Men; respectively. Reclassification is observed in 14% of patients.

Conclusions

Detection of non-obstructive CAD by coronary CTA improves risk stratification and permits individualized and more appropriate allocation of statin therapy across gender and ethnicity groups.

Keywords: 2013 ACC/AHA Prevention Guidelines, Prognosis, Risk Factors, Coronary Artery Disease

INTRODUCTION

The 2013 ACC/AHA guidelines have introduced the 10-year event risk for atherosclerotic cardiovascular disease (ASCVD) as a benchmark for recommendations for statin therapy.1 These estimated event risks and thresholds are based on the pooled cohort risk calculator of ASCVD, which uses the demographic and clinical risk factors from observational cohorts to calculate the 10-year event risk.

Following the release of new ACC/AHA guidelines, it has been demonstrated that the new guidelines significantly improve the alignment of statin-eligibility (defined as >7.5% 10 year ASCVD risk) and presence of coronary artery disease (CAD); for example, Pursnani et al. showed that alignment of presence of coronary artery calcification (CAC) and statin eligibility in asymptomatic patients was improved from 23% to 63% as compared to the 2004 ATP III guidelines.2 Furthermore, studies suggest that assessment of CAD can reclassify statin eligibility in up to 50% of patients.3,4 For example, absence of CAC identifies a large group (33%) of statin eligible individuals that are at a similarly low risk as non-statin eligible individuals (1.0 vs. 1.1% 10 year ASCVD risk, respectively).2 Thus, although new guidelines improve detection of patients with CAD, cardiovascular imaging has demonstrated promising results to further improve the statin allocation.

Symptomatic patients undergo coronary CT Angiography (CTA) for the assessment of obstructive CAD but few (<15%) of these patients are diagnosed with obstructive CAD.5,6 However, the benefit of coronary CTA extends to the remaining 85% of patients because CAD can be either accurately excluded (30-40%) or non-obstructive CAD can be detected (around 50%)5,7, both of which provide tremendous prognostic information beyond traditional risk assessment in both asymptomatic and symptomatic patients.8 Nevertheless, neither current primary nor secondary prevention guidelines contain recommendations for medical therapy in patients with non-obstructive CAD beyond traditional cardiovascular (CV) risk factors. However, detailed knowledge of presence or absence of non-obstructive CAD may improve risk stratification and permit individualized and more appropriate allocation of statin therapy.

Thus, we used published data on the prognostic value of non-obstructive CAD to determine whether incorporation of this information into the pooled cohort equation reclassifies recommendations for statin therapy as defined by the 2013 ACC/AHA guidelines for cholesterol management. To do so, we performed a meta-analysis; used the results to modify the ASCVD risk calculator, and applied it to a separate population to assess the re-classification.

METHODS

Systematic literature review and data collection

A meta-analysis was conducted in adherence to the MOOSE Guidelines for Meta-Analyses and Systematic Reviews of Observational Studies.9 Two physician-scientists (H.E. and R.A.P.T) searched PubMed for eligible studies using pre-defined selection criteria (Figure 1) and pre-defined search syntax for selection of studies that had assessed the prognostic value of coronary CTA published up to May 2016 (please see the supplement). No search restrictions were employed and references of included studies were manually checked to identify eligible studies missed by the primary search strategy. We included the eligible articles based on the following criteria: study domain—patients with suspected CAD without a prior history of CAD; index test—coronary CTA (obstructive CAD, non-obstructive CAD). If there was an overlap in study populations, the study with the largest population was included. We excluded animal-studies, phantom studies, case-reports (N < 10), and studies that did not report hazard ratios for ASCVD events. Abstracts and unpublished studies were not included and no contact was made with authors.

Figure 1.

Figure 1

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Literature search and selection of eligible studies

The characteristics of study subjects at baseline and outcomes were collected in consensus by two physician-scientists (H.E. and R.A.P.T) for all selected studies. All the selected studies defined obstructive CAD as >50% luminal stenosis and non-obstructive CAD as any CAD <50% luminal narrowing in at least one coronary segment. Study quality was assessed in consensus (H.E. and R.A.P.T) using a modified (study confounding was omitted) version of the Quality In Prognosis Studies (QUIPS) tool.10 Our primary outcome of interest was ASCVD defined as cardiovascular death, non-fatal myocardial infarction, and stroke. Annualized ASCVD event risk in each study (if not reported) is calculated by using the median follow-up period. Average annual ASCVD risk of selected studies is calculated as mean of reported or calculated annualized event rates of the individual studies.

Meta-analysis - prognostic value of non-obstructive CAD

We identified studies that reported HR of non-obstructive CAD for ASCVD events. The types of events as well as observed overall event rates, annualized event rates, and HR with their corresponding 95% confidence intervals (CI) for ASCVD events were collected. We calculated log hazard ratios and their standard errors, as to perform a random effects generic inverse variance method for ascertaining pooled log-HR. Forest plots were generated for graphical display of the results. The I2 statistic was calculated to determine heterogeneity. For the meta-analysis, we used RevMan version 5.3 (The Nordic Cochrane Centre, The Cochrane Collaboration, Copenhagen).

Revision of ASCVD risk using information on the prognostic value of presence or absence of non-obstructive CAD

The 10-year risk for ASCVD was derived from the pooled cohort equation as described by Goff et al.11 We incorporated the study level pooled log-HR of non-obstructive CAD for ASCVD events into the original pooled cohort equation and calculated revised ASCVD score including the 95% confidence intervals for the revised risk thresholds by using the lower and upper bounds of the confidence intervals of the pooled HR. As the equation contains coefficients for gender and ethnicity, we calculated eight revised ASCVD scores for patients with and eight for patients without non-obstructive CAD. In patients without CAD, the calculation determined the highest original score that, in consideration of the prognostic value of absence of CAD, would correspond to a revised score of 7.5%. In patients with non-obstructive CAD, the calculation determined the lowest original score that, in consideration of the prognostic value of presence of non-obstructive CAD, would correspond to a revised score of 7.5%.

Reclassification of individuals for statin eligibility

In order to determine in how many patients undergoing coronary CTA the knowledge of presence or absence of non-obstructive CAD would reclassify statin recommendations, we applied the modified risk calculator in patients with acute chest pain in whom ACS was excluded.12 Please see the supplemental material for the details of selection of this patient population.

The 2013 ACC/AHA guidelines were used to determine statin eligibility as follows: (1) clinical ASCVD (not applicable to this patient population), (2) LDL≥190 mg/dl, (3) diabetes 40-75 years and LDL 70-189 mg/dl, or (4) without clinical ASCVD or diabetes, LDL 70-189 mg/dl, and estimated ASCVD risk ≥7.5%. Individual ASCVD risk was determined with and without knowledge of CAD status. Individuals with non-obstructive CAD could be reclassified to be newly statin eligible, only if their original ASCVD score was <7.5% and their new modified (after incorporating HR of non-obstructive CAD) ASCVD risk was ≥7.5%. Individuals without non-obstructive CAD could be reclassified to be not statin eligible, only if their original ASCVD score was >7.5% and their new modified (after incorporating HR of absence of non-obstructive CAD) ASCVD risk was <7.5%. McNemar’s test was used to determine whether a significant proportion of patients was reclassified. Stata software (Version 13.1, StataCorp, College Station, Texas) was used for all calculations regarding the modification and application of the ASCVD risk.

RESULTS

Prognostic Value of non-obstructive CAD

We identified two studies reporting on ASCVD event HR for non-obstructive CAD, which included symptomatic individual patients without known CAD who had non-cardiac chest pain or were asymptomatic individuals with a high lifetime risk of CVD profile.13 They included 2,295 subjects (66% male, 55% with hypertension, 51% with dyslipidemia, 8% with diabetes, prevalence of non-obstructive CAD 46% (n=1075/2295), median follow-up period of 50 months and 67 ASCVD events. The average annual ASCVD event rate was 0.5% (Table 1). The presence of non-obstructive CAD by coronary CTA was associated with a significantly increased risk of future ASCVD events (pooled unadjusted HR = 3.20 [1.53, 6.70], Figure 2). The I2 statistic was 0%.

Table 1.

Selected Studies

First Author, Year Study design Characteristics of Study Population Events
Age
[mean±SD]		 Male
gender
[n (%)]		 HTN
[n (%)]		 DLP
[n (%)]		 DM
[n (%)]		 Smoking [n (%)] Asymptomatic Symptomatic Unknown
Status		 Non-
obstructive
CAD
[n (%)]		 No CAD [n (%)] Median
Follow-up
[months]		 Total
Number
of
Events		 Event
rate
[%]		 Annualized
event rate
[%]		 ASCVD
Events
Acute Stable
Hadamitzky, 201320 Prospective Cohort (n=1584) 58±11 1091 (69) 934 (59) 846 (53) 122 (8) 551 (35) * * * 794 (50) 464 (29) 67 61 3.9 0.7 61
Plank, 201421 Prospective cohort (n=711) 62 422 (59) 332 (47) 327 (46) 62 (9) 197 (28) * 281 (40) 201 (28) 32 6 0.8 0.3 6
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*

Star represents status of included subjects in regards to their symptoms in the studies.

Figure 2.

Figure 2

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Risk estimates of ASCVD events for presence of non-obstructive CAD

Revision of ASCVD risk using information on the prognostic value of presence or absence of non-obstructive CAD

In patients without CAD, the highest original ASCVD score that, in consideration of the prognostic value of absence of CAD would correspond to a revised score of 7.5%, ranged from 3.0% to 5.9% in African-America Women and Men, and 4.4% to 4.6% in Caucasian Women and Men; respectively.

In patients with non-obstructive CAD, the lowest original ASCVD score that, in consideration of the prognostic value of presence of non-obstructive CAD would correspond to a revised score of 7.5%, ranged from 10.0% to 17.9% in African-America Women and Men, and 13.7% to 14.3% in Caucasian Women and Men; respectively (Figure 3). The degree of revision was more prominent in African Americans than in Caucasians and more prominent in men as compared to women.

Figure 3.

Figure 3

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Reclassification thresholds (including 95% confidence intervals) of original ASCVD risk calculator to determine statin eligibility based on coronary CTA findings

Reclassification of individuals for statin eligibility

In order to determine the number of patients with coronary CTA in whom the knowledge of presence or absence of non-obstructive CAD would reclassify statin recommendations, the modified risk scores were calculated in 169 patients with acute chest pain without ACS (age 53 ± 9 years, 56% male).12 The mean original 10-year ASCVD risk in this population was 7.2% ± 7.7%, 101 (60%) were without CAD, and 68 (40%) had non-obstructive CAD. After including the pooled log-HR for non-obstructive CAD, statin eligibility was revised in 14% of the population (n=24/169). Specifically, 12/101 patients (12%) who had an original ASCVD score of >7.5% and who had no CAD were reclassified as non-statin eligible while 12/68 patients (18%) who had non-obstructive CAD but an original ASCVD score <7.5% were reclassified as statin eligible (Supplemental Figure 1).

For example, based on the original ASCVD risk calculation, a 49-year-old non-smoker Caucasian male with total cholesterol of 212, HDL-C of 40, Systolic blood pressure of 136, has a 5.5% 10-year event risk and is not statin eligible. However, this patient had non-obstructive CAD on coronary CTA. Incorporation of this information into the pooled cohort equation resulted in a revised 10-year ASCVD risk of 9%, making him eligible for statin therapy. Other examples of individual patients from our cohort with both up- and down- classification are shown in Figure 4.

Figure 4.

Figure 4

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Application of original and modified ASCVD risk calculators in primary prevention patient population

DISCUSSION

We demonstrate that non-obstructive CAD carries a 3 times higher risk for incident ASCVD events as compared to no CAD. More importantly, by incorporating this information into the AHA/ACC pooled cohort equation; we demonstrate that patients with non-obstructive CAD with an original score as low as 3.0% would be reclassified as statin eligible while patients without CAD with an original ASCVD score as high as 17.9% would be reclassified as not statin eligible. In a separate cohort of patients with acute chest pain but without ACS, this would result in reclassification of statin eligibility in 14% of patients.

The new 2013 ACC/AHA guidelines for cholesterol management are estimated to identify almost 12 million more individuals as statin eligible.14 However, they accurately identify patients as statin eligible that are at a relatively higher risk as compared to those not statin eligible in regard to: 1) ASCVD events: HR 6.8 (95%CI: 3.8-11.9) vs. 3.1 (95%CI: 1.9-5.0),2 2) CAC score >300: 85% vs. 34%,2 and 3) obstructive CAD: 90% vs. 60% as compared to the ATP III guidelines.15 In addition, absence of CAC identifies a large group of patients that are at very low risk for ASCVD events despite being statin eligible by pooled cohort equation (33%2 in the Framingham Heart Study and 40%4 in the MESA study) (1.0% vs. 1.1% 10 year ASCVD risk, respectively). Although, the caveat with absence of CAC is that it does not necessarily exclude presence of other ASCVDs such as stroke.

Our study goes one step further and directly determines how prognostic information on non-obstructive CAD can revise ASCVD risk and subsequent statin recommendations in symptomatic patients undergoing coronary CTA in whom no obstructive CAD is present. It is indeed a challenge to determine whether patients with chest pain who have non-obstructive CAD should be treated by primary or secondary prevention guidelines. One could argue that they represent an intermediate group, as they are not asymptomatic but do have coronary disease associated with an increased risk for future cardiovascular events. As a result of the lack of guidelines and the uncertainty of benefits of modifications in preventive medical therapy beyond traditional risk factors about half of the patients with non-obstructive CAD are currently not on statin treatment.2,16-18 It is worth mentioning that in this study, we did not include the patients with obstructive CAD; because in the current clinical practice, these patients would be treated with statins as part of optimal medical management.

Our data suggest that about 14% of these patients would benefit from incorporation of non-obstructive CAD into the pooled cohort equation. The effect reaches across gender and ethnicity but was more prominent in men as compared to women and more prominent in African Americans as compared to Caucasians. Reclassification of statin eligibility based on the absence of CAD constitutes a relatively new concept but is supported by many studies demonstrating the excellent negative predictive value. This option may be especially important for patients who are at higher risk for adverse effects of medical therapy such as pre-diabetes patients. Nevertheless, the final decision for initiation of statin therapy is made after a clinician-patient discussion having all the risk factors considered.

Limitations

The main limitation of our study is the small number of eligible studies as the selection process resulted in two studies. Additionally, our results are limited by the small number of events as well as short follow-up period (4.2 years). The results of this study such as the prognostic value of non-obstructive CAD and the modification of the ASCVD score are derived from study level data since authors did not have access to individual level data. However, the 95% confidence intervals for the revision of the original ASCVD risk did not overlap with 7.5% threshold in both directions, thus indicating robustness of our estimates. In addition, we acknowledge that according to AHA/ACC guidelines, even patients with 5-7.5% ASCVD risk are considered for statin therapy by a level II evidence and that statin eligibility concept based on ASCVD risk is a recommendation rather than an absolute measure for therapy owning to personal preferences and variable risk profile of patients. Additionally, the risk thresholds are used for risk quantification and patients with lower ASCVD risk might also benefit from statin therapy they are deemed high-risk based on a discussion with their clinician.

Conclusion

Detection of non-obstructive CAD by coronary CTA improves risk stratification and permits individualized and more appropriate allocation of statin therapy across gender and ethnicity groups.

Supplementary Material

Supplement

Acknowledgments

No funding from any source was provided for this study.

Abbreviations

ASCVD

atherosclerotic cardiovascular disease

CAD

coronary artery disease

CTA

CT Angiography

Footnotes

Disclosures:

Authors have nothing to disclose relevant to this study.

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Associated Data

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Supplementary Materials

Supplement
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