Clinical Characteristics, Sex Differences, and Outcomes in Patients With Normal or Near‐Normal Coronary Arteries, Non‐Obstructive or Obstructive Coronary Artery Disease

Figures

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  Figure 1. Prevalence of referral indications for invasive coronary angiography. The number of patients in each subgroup is shown below the bars. NSTEMI indicates non‐ST‐elevation myocardial infarction.

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  Figure 2. Prevalence of normal or near‐normal coronary arteries (NNCAs; ≤20% stenosis), no‐obstructive CAD (21–49% stenosis), and obstructive CAD (≥50% stenosis) in all patients and subdivided into male vs female sex for each invasive coronary angiography referral indication. For each indication, the combined prevalence of NNCA and nonobstructive CAD is significantly higher in female patients compared with male patients. CAD indicates coronary artery disease; F, female; M, male; NSTEMI, non‐ST‐elevation myocardial infarction.

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  Figure 3. Severity of coronary artery stenosis in the 217 patients who underwent imaging before ICA and had an interpretable stress ECG subdivided according to absence or presence of ischemia by stress ECG and stress imaging criteria. Prevalence of obstructive CAD (≥50% stenosis) was highest in patients exhibiting ischemia on both the stress ECG and imaging (P<0.001) and lowest with both negative (P=0.015). CAD indicates coronary artery disease; ICA, invasive coronary angiography.

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  Figure 4. Severity of coronary artery stenosis subdivided by findings on stress single‐photon emission computed tomography myocardial perfusion imaging. Although the rate of NNCAs or nonobstructive CAD was higher in those without ≥10% of the LV ischemic (P=0.029), it remained substantial even in this subgroup with severe ischemia (25.0%). CAD indicates coronary artery disease; LV, left ventricle; NNCAs, near‐normal coronary arteries. *P<0.05.

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  Figure 5. Severity of coronary stenosis subdivided by presence of borderline elevated, low, intermediate, and high troponin levels. There is a progressive increase in prevalence of obstructive CAD with increasing levels of troponin I (P<0.001). CAD indicates coronary artery disease.

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  Figure 6. Severity of coronary stenosis in the 186 patients with stable or unstable angina referred for invasive coronary angiography. The group is subdivided by 10‐year ASCVD risk of ≥7.5% (n=140) and <7.5% (n=46). Although the prevalence of obstructive CAD was greater in the subgroup with elevated pretest 10‐year ASCVD risk (P=0.032), more than 50% had either normal/near‐normal coronary arteries (≤20% stenosis) or nonobstructive CAD (21–49% stenosis). ASCVD, atherosclerotic cardiovascular disease; CAD, coronary artery disease. *P<0.05.

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  Figure 7. Kaplan–Meier survival curves of freedom from cardiac death and nonfatal myocardial infarction (MI) (A) and freedom from cardiac events (cardiac death, nonfatal MI, and late revascularization) (B) in those referred for abnormal stress, NSTEMI, or CP syndrome with NNCAs, nonobstructive CAD, and obstructive CAD stratified by sex. C, Freedom from cardiac events in high‐risk patients with ischemia on stress testing or a troponin level ≥1 ng/mL. There was a consistently higher risk of events for those with obstructive CAD across all groups. CAD indicates coronary artery disease; CP, chest pain; NNCAs, near‐normal coronary arteries; NSTEMI, non‐ST‐elevation myocardial infarction.