Nonobstructive coronary artery disease and risk of myocardial infarction.

IMPORTANCE Little is known about cardiac adverse events among patients with nonobstructive coronary artery disease (CAD). OBJECTIVE To compare myocardial infarction (MI) and mortality rates between patients with nonobstructive CAD, obstructive CAD, and no apparent CAD in a national cohort. DESIGN, SETTING, AND PARTICIPANTS Retrospective cohort study of all US veterans undergoing elective coronary angiography for CAD between October 2007 and September 2012 in the Veterans Affairs health care system. Patients with prior CAD events were excluded. EXPOSURES Angiographic CAD extent, defined by degree (no apparent CAD: no stenosis >20%; nonobstructive CAD: ≥1 stenosis ≥20% but no stenosis ≥70%; obstructive CAD: any stenosis ≥70% or left main [LM] stenosis ≥50%) and distribution (1, 2, or 3 vessel). MAIN OUTCOMES AND MEASURES The primary outcome was 1-year hospitalization for nonfatal MI after the index angiography. Secondary outcomes included 1-year all-cause mortality and combined 1-year MI and mortality. RESULTS Among 37,674 patients, 8384 patients (22.3%) had nonobstructive CAD and 20,899 patients (55.4%) had obstructive CAD. Within 1 year, 845 patients died and 385 were rehospitalized for MI. Among patients with no apparent CAD, the 1-year MI rate was 0.11% (n = 8, 95% CI, 0.10%-0.20%) and increased progressively by 1-vessel nonobstructive CAD, 0.24% (n = 10, 95% CI, 0.10%-0.40%); 2-vessel nonobstructive CAD, 0.56% (n = 13, 95% CI, 0.30%-1.00%); 3-vessel nonobstructive CAD, 0.59% (n = 6, 95% CI, 0.30%-1.30%); 1-vessel obstructive CAD, 1.18% (n = 101, 95% CI, 1.00%-1.40%); 2-vessel obstructive CAD, 2.18% (n = 110, 95% CI, 1.80%-2.60%); and 3-vessel or LM obstructive CAD, 2.47% (n = 137, 95% CI, 2.10%-2.90%). After adjustment, 1-year MI rates increased with increasing CAD extent. Relative to patients with no apparent CAD, patients with 1-vessel nonobstructive CAD had a hazard ratio (HR) for 1-year MI of 2.0 (95% CI, 0.8-5.1); 2-vessel nonobstructive HR, 4.6 (95% CI, 2.0-10.5); 3-vessel nonobstructive HR, 4.5 (95% CI, 1.6-12.5); 1-vessel obstructive HR, 9.0 (95% CI, 4.2-19.0); 2-vessel obstructive HR, 16.5 (95% CI, 8.1-33.7); and 3-vessel or LM obstructive HR, 19.5 (95% CI, 9.9-38.2). One-year mortality rates were associated with increasing CAD extent, ranging from 1.38% among patients without apparent CAD to 4.30% with 3-vessel or LM obstructive CAD. After risk adjustment, there was no significant association between 1- or 2-vessel nonobstructive CAD and mortality, but there were significant associations with mortality for 3-vessel nonobstructive CAD (HR, 1.6; 95% CI, 1.1-2.5), 1-vessel obstructive CAD (HR, 1.9; 95% CI, 1.4-2.6), 2-vessel obstructive CAD (HR, 2.8; 95% CI, 2.1-3.7), and 3-vessel or LM obstructive CAD (HR, 3.4; 95% CI, 2.6-4.4). Similar associations were noted with the combined outcome. CONCLUSIONS AND RELEVANCE In this cohort of patients undergoing elective coronary angiography, nonobstructive CAD, compared with no apparent CAD, was associated with a significantly greater 1-year risk of MI and all-cause mortality. These findings suggest clinical importance of nonobstructive CAD and warrant further investigation of interventions to improve outcomes among these patients.

[1]  J. Tardif,et al.  Prevalence of anginal symptoms and myocardial ischemia and their effect on clinical outcomes in outpatients with stable coronary artery disease: data from the International Observational CLARIFY Registry. , 2014, JAMA internal medicine.

[2]  Habib Samady,et al.  Prevalence and characteristics of TCFA and degree of coronary artery stenosis: an OCT, IVUS, and angiographic study. , 2014, Journal of the American College of Cardiology.

[3]  R. Califf,et al.  Outcomes among non-ST-segment elevation acute coronary syndromes patients with no angiographically obstructive coronary artery disease: observations from 37,101 patients , 2014, European heart journal. Acute cardiovascular care.

[4]  G. Grunwald,et al.  Normal coronary rates for elective angiography in the Veterans Affairs Healthcare System: insights from the VA CART program (veterans affairs clinical assessment reporting and tracking). , 2014, Journal of the American College of Cardiology.

[5]  D. Berman,et al.  Predicting outcome in the COURAGE trial (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation): coronary anatomy versus ischemia. , 2014, JACC. Cardiovascular interventions.

[6]  Jeroen J. Bax,et al.  2013 ESC guidelines on the management of stable coronary artery disease: the Task Force on the management of stable coronary artery disease of the European Society of Cardiology. , 2013, European heart journal.

[7]  James Brian Byrd,et al.  Data quality of an electronic health record tool to support VA cardiac catheterization laboratory quality improvement: the VA Clinical Assessment, Reporting, and Tracking System for Cath Labs (CART) program. , 2013, American heart journal.

[8]  Sankey V. Williams,et al.  2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Ass , 2012, Journal of the American College of Cardiology.

[9]  Daniel S. Berman,et al.  What have we learned from CONFIRM? Prognostic implications from a prospective multicenter international observational cohort study of consecutive patients undergoing coronary computed tomographic angiography , 2012, Journal of Nuclear Cardiology.

[10]  Erik Jørgensen,et al.  Stable angina pectoris with no obstructive coronary artery disease is associated with increased risks of major adverse cardiovascular events. , 2012, European heart journal.

[11]  H. Hod,et al.  Non-obstructive coronary artery disease upon multi-detector computed tomography in patients presenting with acute chest pain--results of an intermediate term follow-up. , 2012, European heart journal cardiovascular Imaging.

[12]  G. Levine,et al.  2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. , 2011, Journal of the American College of Cardiology.

[13]  Mouaz Al-Mallah,et al.  Age- and sex-related differences in all-cause mortality risk based on coronary computed tomography angiography findings results from the International Multicenter CONFIRM (Coronary CT Angiography Evaluation for Clinical Outcomes: An International Multicenter Registry) of 23,854 patients without know , 2011, Journal of the American College of Cardiology.

[14]  Daniel S. Berman,et al.  Mortality risk in symptomatic patients with nonobstructive coronary artery disease: a prospective 2-center study of 2,583 patients undergoing 64-detector row coronary computed tomographic angiography. , 2011, Journal of the American College of Cardiology.

[15]  M. Budoff,et al.  Mortality incidence of patients with non-obstructive coronary artery disease diagnosed by computed tomography angiography. , 2011, The American journal of cardiology.

[16]  J. Rumsfeld,et al.  Utilization of Secondary Prevention Therapies in Patients With Nonobstructive Coronary Artery Disease Identified During Cardiac Catheterization: Insights From the National Cardiovascular Data Registry Cath-PCI Registry , 2010, Circulation. Cardiovascular quality and outcomes.

[17]  Dudley J Pennell,et al.  Low diagnostic yield of elective coronary angiography. , 2010, The New England journal of medicine.

[18]  Stephan D. Fihn,et al.  Strategies from a Nationwide Health Information Technology Implementation: The VA CART STORY , 2010, Journal of General Internal Medicine.

[19]  D. Berman,et al.  SCCT guidelines for the interpretation and reporting of coronary computed tomographic angiography. , 2009, Journal of cardiovascular computed tomography.

[20]  J. Redfern,et al.  Low utilisation of cardiovascular risk reducing therapy in patients with acute coronary syndromes and non-obstructive coronary artery disease. , 2008, International journal of cardiology.

[21]  C. Bauters,et al.  [Pathophysiology of coronary artery disease]. , 2008, La Revue du praticien.

[22]  P. Shah.  Molecular mechanisms of plaque instability , 2007, Current opinion in lipidology.

[23]  Manesh R. Patel,et al.  Prevalence, predictors, and outcomes of patients with non-ST-segment elevation myocardial infarction and insignificant coronary artery disease: results from the Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA Guidelines (CR , 2006, American heart journal.

[24]  R. Bugiardini,et al.  Unanswered questions for management of acute coronary syndrome: risk stratification of patients with minimal disease or normal findings on coronary angiography. , 2006, Archives of internal medicine.

[25]  P. Box.  Long-term adherence to evidence-based secondary prevention therapies in coronary artery disease , 2006 .

[26]  P. Libby,et al.  Pathophysiology of Coronary Artery Disease , 2005, Circulation.

[27]  C Noel Bairey Merz,et al.  Angina with "normal" coronary arteries. , 2005 .

[28]  Jeroen J. Bax,et al.  Prognostic and clinical correlates of angiographically diffuse non-obstructive coronary lesions , 2003, Heart.

[29]  W. Cherng,et al.  Comparison of white blood cell counts in acute myocardial infarction patients with significant versus insignificant coronary artery disease. , 2003, The American journal of cardiology.

[30]  Chao-Hung Wang,et al.  Coronary vasospasm as a possible cause of elevated cardiac troponin I in patients with acute coronary syndrome and insignificant coronary artery disease. , 2002, American heart journal.

[31]  H V Anderson,et al.  The American College of Cardiology-National Cardiovascular Data Registry™ (ACC-NCDR™): building a national clinical data repository , 2001 .

[32]  Deepak L. Bhatt,et al.  Clinical and therapeutic profile of patients presenting with acute coronary syndromes who do not have significant coronary artery disease.The Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) Trial Investigators. , 2000, Circulation.

[33]  V. Fuster,et al.  Coronary plaque disruption. , 1995, Circulation.

[34]  V. Fuster,et al.  Lewis A. Conner Memorial Lecture. Mechanisms leading to myocardial infarction: insights from studies of vascular biology. , 1994, Circulation.

[35]  B Meier,et al.  Relation of the site of acute myocardial infarction to the most severe coronary arterial stenosis at prior angiography. , 1992, The American journal of cardiology.

[36]  T. Marwick,et al.  A new method of scoring coronary angiograms to reflect extent of coronary atherosclerosis and improve correlation with major risk factors. , 1990, American heart journal.

[37]  L. J. Wei,et al.  The Robust Inference for the Cox Proportional Hazards Model , 1989 .

[38]  W. Santamore,et al.  Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease? , 1988, Circulation.

[39]  V. Fuster,et al.  Angiographic progression of coronary artery disease and the development of myocardial infarction. , 1988, Journal of the American College of Cardiology.

[40]  R. Wilson,et al.  Prediction of the physiologic significance of coronary arterial lesions by quantitative lesion geometry in patients with limited coronary artery disease. , 1987, Circulation.