Women and Cardiovascular Health
When the Arteries Look Normal but the Symptoms Are Real: INOCA
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These articles provide education to enhance your healthcare partnership. All treatment decisions should involve your healthcare team. Use this knowledge to have informed discussions, not replace medical care.
In Brief
This article is for the woman who has had cardiac chest pain, undergone a coronary angiogram, been told the arteries look fine, and still has symptoms. For decades, women in that situation were routinely told their hearts were fine and the chest pain was something else. Two decades of research have established that the chest pain is often cardiac — caused by conditions the standard angiogram cannot see.
Ischemia with no obstructive coronary artery disease (INOCA) is a distinct clinical entity with two major mechanisms: coronary microvascular dysfunction (disease of the small downstream vessels) and epicardial vasospasm (transient squeezing of the larger arteries). (1) INOCA is more common in women than in men. In the Women’s Ischemia Syndrome Evaluation of 936 women referred for medically indicated angiography, only 39 percent had obstructive disease; approximately half of those without obstructions who underwent further intracoronary testing showed reduced coronary flow reserve consistent with microvascular dysfunction. (2,3) The 2018 CorMicA trial, the 2017 AHA INOCA scientific statement, and the 2021 ACC/AHA chest pain guideline establish that mechanism-specific diagnosis and treatment improves symptoms. (1,4,5) If a clinician dismisses your persistent chest pain after a clean angiogram as “not cardiac,” the contemporary guidelines do not support that position. This article walks through the diagnostic tools, treatments, and what to ask for.
Why the Standard Workup Misses INOCA
For decades, the clinical evaluation of cardiac chest pain proceeded along a familiar path: take the history, get the electrocardiogram, draw the blood tests for heart muscle damage, and if cardiac suspicion remained, perform coronary angiography. If the angiogram showed obstructive disease — typically defined as a narrowing of more than 50 percent in one or more major heart arteries — the diagnosis was made and treatment proceeded. If the angiogram was clean, the conclusion was that the symptoms were not cardiac.
That approach misses important cardiac pathology in many women, in two specific ways.
The absence of obstruction on the angiogram does not exclude cardiac ischemia. The angiogram visualizes the larger heart arteries on the surface of the heart — the epicardial arteries: the left main, the left anterior descending, the circumflex, the right coronary artery, and their major branches. These surface arteries are only the beginning of the heart’s blood supply. Downstream lies the coronary microvasculature — a vast network of small arteries, arterioles, and capillaries that actually distribute blood through the heart muscle. Disease in these small vessels can cause real ischemia but is below the resolution of standard angiography. (1)
The larger arteries can also go into transient spasm — a sudden squeezing called vasospasm — that produces episodes of obstruction without lasting structural disease. Spasm is, by its nature, transient. If the artery is not in spasm at the moment the angiogram is taken, the test looks normal. (1)
The Women’s Ischemia Syndrome Evaluation (WISE) study established the scale of the problem. WISE enrolled 936 women referred for medically indicated coronary angiography because of suspected ischemic heart disease.
| WISE findings — what the standard workup missed in women | Proportion |
| Obstructive coronary artery disease (≥50 percent stenosis) on angiography | 39 percent |
| Non-obstructive epicardial coronary disease (“clean” angiogram) | 61 percent |
| Among the subset with non-obstructive disease who underwent intracoronary testing: reduced coronary flow reserve indicating microvascular dysfunction | 47 percent |
Bairey Merz 2006 J Am Coll Cardiol; Reis 2001 Am Heart J.
The “clean angiogram, you’re fine” framework missed approximately half of the actual cardiac pathology in women with chest pain serious enough to warrant angiography. More than half of the women in WISE had chest pain serious enough to prompt angiography but did not have the obstructive disease the test was designed to find. Approximately half of those women had measurable small-vessel disease the test could not detect. (2,3)
INOCA: The Two Mechanisms
The 2017 American Heart Association scientific statement on INOCA established the framework that contemporary cardiovascular care now uses. (1) INOCA is not a single disease. It is an umbrella term covering two distinct mechanisms that can occur alone or together.
| The two major mechanisms of INOCA | |
| Coronary microvascular dysfunction | Epicardial vasospastic disease |
| Disease of the small downstream arteries and arterioles | Disease of the larger surface arteries (left main, left anterior descending, circumflex, right coronary) |
| Impaired ability of the small vessels to dilate when the heart needs more oxygen | Transient narrowing — the artery suddenly squeezes shut, then opens again |
| Cannot be seen on standard angiography (the vessels are below imaging resolution) | May not be present at the moment of imaging (spasm comes and goes) |
| Detected by: coronary flow reserve measurement with intracoronary adenosine | Detected by: provocative testing with intracoronary acetylcholine |
| Treatment includes anti-anginal medications (beta-blockers, calcium-channel blockers, ranolazine), ACE inhibitors, statins, and aggressive risk factor management | Treatment centers on calcium-channel blockers and long-acting nitrates; certain beta-blockers can paradoxically worsen spasm |
Both mechanisms can occur alone or together. Both produce genuine cardiac ischemia. Both have specific treatments.
Coronary microvascular dysfunction is the impaired ability of the heart’s small blood vessels to dilate in response to increased demand for oxygen or in response to medications that should normally dilate them. It is measured clinically using a ratio called coronary flow reserve — the ratio of maximum coronary blood flow (during stress or after a vasodilator drug) to resting coronary blood flow. A normal value is generally above 2.0 to 2.5; values below this range indicate microvascular dysfunction. (1) The mechanism is thought to involve a combination of dysfunction in the endothelium (the inner lining of blood vessels) and structural changes in the walls of the small vessels themselves.
Epicardial vasospastic disease is a tendency of the larger heart arteries to go into transient spasm — either spontaneously, in response to certain triggers, or in response to provocation during testing. Spasm produces temporary obstruction that can cause angina, abnormal stress test results, and in severe cases a heart attack. Vasospastic disease is diagnosed clinically by provocative testing during angiography, in which a drug (typically acetylcholine or ergonovine) is injected into the coronary arteries to attempt to provoke spasm. If spasm occurs and is reversed by nitroglycerin, the diagnosis is established. (1)
Both mechanisms produce genuine cardiac ischemia. Both can be detected with specific diagnostic tools. Both have specific treatments. Both can be present in the same person.
Why INOCA Is More Common in Women
INOCA is not a women-only condition. Men develop microvascular dysfunction and vasospastic disease too, and the diagnostic and treatment frameworks discussed in this article apply equally when these conditions occur in men. INOCA disproportionately affects women, and this section explains why.
Coronary microvascular dysfunction — the dominant INOCA mechanism — is more common in women. Vasospastic disease has a more complex gender distribution: classical variant angina was historically described as more common in men in certain populations, but the contemporary INOCA picture, in which vasospastic disease often accompanies or coexists with microvascular dysfunction, may be more common in women overall.
The reasons women are more likely than men to develop coronary microvascular dysfunction are not fully established, but several converging lines of evidence point to a coherent picture. The strongest evidence for why women develop more INOCA involves the convergence of three factors that operate together.
The first is coronary anatomy and biology. As discussed in Article 1 of this series, women’s epicardial coronary arteries are smaller than men’s even after adjusting for body size. The endothelium — the inner lining of blood vessels — is regulated differently in women, with substantial contributions from estrogen-related signaling. The decline in estrogen across the menopause transition produces measurable changes in how well the endothelium functions. Women in WISE and other cohorts have shown age-related and menopause-stage-related changes in the function of the heart’s small vessels. This is the strongest evidence for the sex difference in INOCA and is reflected in the major society guidance.
The second is how risk factors manifest differently. The standard cardiovascular risk factors — high blood pressure, abnormal cholesterol, diabetes, smoking — affect the small vessels of the heart as well as the larger arteries. In women, the cardiovascular consequences of these risk factors appear more often to manifest as small-vessel disease and INOCA. In men, obstructive disease of the larger arteries more often dominates the picture. The same underlying risk factor burden produces a different anatomic phenotype.
The third is inflammation. Women have higher prevalence of autoimmune and chronic inflammatory conditions (discussed in Article 9 of this series). The microvasculature is particularly susceptible to inflammatory injury, and decades of cumulative inflammatory exposure may contribute to the sex difference in microvascular disease. This contribution is plausible and supported by observational data but is less mechanistically established than the first two.
The cumulative effect is that the same underlying risk factor burden in women is more likely to produce INOCA than overt obstructive coronary disease, while in men the inverse is more often true.
Why INOCA Is Often Missed in Practice
The difficulty diagnosing INOCA is structural. The standard tests for cardiac ischemia were optimized to detect obstructive disease of the larger arteries — not the small-vessel or vasospastic conditions that can cause ischemia without obstruction.
Coronary angiography images the inside of the larger epicardial arteries. It does not visualize the small downstream vessels and, unless provocative testing is performed during the procedure, does not detect vasospasm. The angiographic image captures one moment in time; spasm that comes and goes may not be present at that moment.
Stress echocardiography and nuclear stress testing detect regional disturbances in heart wall motion or in blood supply that result from focal ischemia. These tests can pick up microvascular dysfunction in some cases, but they are less sensitive for the more diffuse pattern of microvascular disease than for the focal ischemia caused by obstructive epicardial disease.
Cardiac magnetic resonance imaging with stress perfusion is more sensitive for microvascular disease and is increasingly used in the workup of suspected INOCA, but it is not yet routinely available in many practice settings.
Coronary CT angiography evaluates the anatomy of the larger arteries non-invasively. It is a good alternative to invasive angiography for the question of obstruction. It does not directly assess the microvasculature.
Invasive coronary function testing is the gold standard for definitively diagnosing INOCA. It is performed during a coronary angiography procedure using small amounts of medication injected directly into the coronary arteries — adenosine to measure how well the small vessels can dilate (giving the coronary flow reserve value), and acetylcholine to test whether the arteries are prone to spasm. The procedure adds approximately 20 to 30 minutes to a standard angiogram and adds modest additional risk. In patients with chest pain and non-obstructive coronary disease, the diagnostic yield is substantial. (4)
The 2021 ACC/AHA Chest Pain Guideline explicitly addresses the diagnostic pathway for patients with persistent chest pain and non-obstructive epicardial disease, recommending that the workup not end with the angiogram. Invasive coronary function testing received a Class 2a recommendation (a reasonable choice supported by moderate evidence) for patients with persistent symptoms and non-obstructive coronary disease. (5)
The CorMicA Trial
The strongest randomized evidence on the management of INOCA comes from the 2018 CorMicA trial, conducted across the Golden Jubilee National Hospital and Hairmyres Hospital in Scotland and published in the Journal of the American College of Cardiology. (4)
CorMicA enrolled 151 patients who had chest pain and signs of ischemia, underwent coronary angiography, and were found to have no significant obstruction in their larger heart arteries. Patients were randomized to one of two arms (75 to intervention, 76 to control). In the intervention group, an additional invasive coronary function test was performed during the angiogram, using intracoronary adenosine and acetylcholine to determine which mechanism was responsible for the chest pain — microvascular dysfunction, vasospasm, both, or neither. The diagnosis was then shared with the patient and clinician, and treatment was tailored to the underlying mechanism. In the control group, the angiogram was performed without coronary function testing, and standard care proceeded based on the angiogram alone. (4)
The primary outcome was change in the Seattle Angina Questionnaire summary score at six months — a validated patient-reported measure of how much angina symptoms affect daily life. The intervention produced a significant 11.7-point improvement in the Seattle Angina Questionnaire summary score compared with usual care (95% CI 5.0–18.4; p=0.001). Quality-of-life measures also improved. The benefit persisted at one-year follow-up. (4)
CorMicA was a single-trial study of modest size and was not designed to detect differences in major cardiac events. It established a principle, not a final answer: when chest pain persists after a clean angiogram, mechanism-specific diagnosis and treatment improves symptoms and quality of life. Whether it also reduces major cardiac events — heart attack, stroke, death — has not yet been tested in a randomized trial of the necessary size and duration. The testing itself is not therapeutic. It enables the right treatment to be chosen.
Long-Term Outcomes
The clinical conclusion that “the angiogram is clean, so this is not cardiac” carried the implicit assumption that the prognosis was favorable. Long-term follow-up has refuted this assumption.
The WISE study’s ten-year mortality analysis found that women with chest pain and non-obstructive coronary disease had cumulative cardiovascular event rates substantially higher than women without symptoms, though lower than women with obstructive disease. (6) Adverse outcomes included heart attack, heart failure, stroke, and cardiovascular death.
A separate WISE analysis examined the prognostic value of coronary flow reserve specifically. Among 189 women undergoing invasive coronary function testing, lower coronary flow reserve was associated with significantly increased risk of major adverse cardiovascular events — defined as death, nonfatal myocardial infarction, nonfatal stroke, or hospital stay for heart failure — at a mean follow-up of 5.4 years. An exploratory analysis identified a coronary flow reserve threshold below 2.32 as best discriminating outcomes (event rate 26.7 percent below the threshold, versus 12.2 percent above it). Per unit decrease in coronary flow reserve, the hazard ratio for the overall cohort was 1.16 (95% CI 1.04–1.30); in the 152 women without obstructive coronary artery disease specifically, the hazard ratio was 1.20 (95% CI 1.05–1.38). (7) The signal was as strong in the women without obstructive disease as in the overall cohort.
The mechanisms linking INOCA to long-term adverse outcomes are biologically plausible. Microvascular dysfunction is associated with progressive structural changes in the heart, including stiffening of the heart muscle and a specific form of heart failure called heart failure with preserved ejection fraction (HFpEF) — where the pumping function of the heart looks normal on standard echocardiography, but the heart cannot relax and fill properly. Vasospastic disease can produce heart attacks in arteries that appear normal on follow-up angiography. The shared underlying biology — endothelial dysfunction, inflammation, and small-vessel and large-vessel disease — connects INOCA to the broader cardiovascular trajectory.
The clinical implication is direct. A diagnosis of INOCA should trigger the same intensity of cardiovascular risk factor management as a diagnosis of obstructive coronary disease. Cholesterol-lowering medications, blood pressure control, blood sugar management, weight management, physical activity, dietary patterns, and smoking cessation matter just as much in INOCA as in obstructive disease — possibly more.
Treatment
The treatment of INOCA depends on what the diagnostic workup uncovers. The 2017 American Heart Association scientific statement and the 2021 ACC/AHA chest pain guideline both structure this approach. (1,5)
For coronary microvascular dysfunction, the approach combines aggressive risk factor management with anti-anginal medications targeted at the small vessels. Lifestyle interventions — physical activity, dietary patterns, weight management, smoking cessation — are foundational. Statins are recommended both for risk factor modification and for their potential beneficial effects on blood vessel function. Anti-anginal medications used include beta-blockers, calcium-channel blockers, ranolazine (a medication that reduces angina without affecting heart rate or blood pressure), or combinations of these. Angiotensin-converting enzyme inhibitors (ACE inhibitors), commonly used for blood pressure control, have shown specific benefit in some studies of microvascular dysfunction. (1)
For epicardial vasospastic disease, the cornerstone of treatment is calcium-channel blockers, which directly counter the tendency to spasm. Long-acting nitrates can be added. Beta-blockers — particularly non-selective types like propranolol — can paradoxically worsen vasospastic disease because they block the vessel-relaxing receptors while leaving the constricting receptors unopposed. Beta-blocker choice in vasospastic disease therefore requires careful selection. Smoking cessation is particularly important, as tobacco is a known trigger of coronary spasm. (1)
For combined microvascular and vasospastic disease, treatment is layered — addressing both mechanisms simultaneously.
For acute angina episodes in either mechanism, sublingual nitroglycerin is a reasonable first-line treatment. It dilates both the small vessels and the larger epicardial arteries and can relieve angina from either microvascular dysfunction or vasospasm. A patient with diagnosed INOCA who has not been prescribed sublingual nitroglycerin should ask about it — having it available for acute symptom episodes is part of standard INOCA management.
For all patients with INOCA, conventional cardiovascular risk factor management is essential regardless of which mechanism is dominant. The biology that causes INOCA shares much with the biology that causes obstructive coronary disease, and the same long-term risk modification matters.
What Your Care Should Cover
If you have had cardiac chest pain that was not explained by a standard angiogram, several specific things should be part of your ongoing care.
Ask whether coronary function testing was performed during the angiogram. This refers specifically to intracoronary adenosine (to measure coronary flow reserve and assess the small vessels) and intracoronary acetylcholine (to test for vasospasm). If neither was done, the angiogram has only ruled out obstructive disease in the larger arteries. It has not ruled out INOCA.
If invasive testing is not appropriate or not available, ask about cardiac MRI with stress perfusion. This is a non-invasive imaging study that can detect microvascular dysfunction and is increasingly available at academic medical centers.
Bring symptoms back if they persist or recur. Microvascular angina and vasospastic angina respond to specific medications. Persistent chest pain after a clean angiogram is not the end of the workup. It is often the point at which the workup begins in earnest.
Manage conventional cardiovascular risk factors with the same intensity as if you had been diagnosed with obstructive coronary disease. The biology of INOCA — endothelial dysfunction, inflammation, and small-vessel disease — overlaps substantially with the biology of obstructive coronary disease. Cholesterol management, blood pressure control, glucose management, weight, physical activity, dietary pattern, and tobacco status all matter just as much, and possibly more.
Recognize what the contemporary guidance actually says. The 2017 AHA scientific statement on INOCA and the 2021 ACC/AHA Chest Pain Guideline both formally establish INOCA as a recognized clinical entity with defined diagnostic tools and defined treatments. If a clinician dismisses your symptoms as non-cardiac because the angiogram looked clean, the current guidelines do not support that position. You are entitled to a workup that does not stop at the standard angiogram. The 2021 chest pain guideline says so explicitly.
Consider a second opinion at a specialized center if the workup feels incomplete. Many community cardiologists do not yet routinely offer invasive coronary function testing or stress cardiac MRI as part of their standard workup. Larger academic medical centers and specialized women’s cardiovascular programs have more experience with these tools and with the mechanism-specific treatment approach. A second opinion at such a center is a reasonable step.
Article 8 of this series covers three additional syndromes that disproportionately affect women — spontaneous coronary artery dissection, MINOCA, and Takotsubo cardiomyopathy — that the standard heart attack framework has historically missed or mischaracterized.
The Bottom Line
A woman with cardiac chest pain whose coronary angiography shows no obstructive disease has a question that has not yet been answered, not a diagnosis of “no heart disease.” The reflexive response to a clean angiogram — reassurance and discharge — has been shown to miss a substantial fraction of treatable cardiac pathology. INOCA is a distinct clinical entity with two major mechanisms (microvascular dysfunction and epicardial vasospasm), defined diagnostic tools (invasive coronary function testing remains the gold standard, with stress cardiac MRI as a non-invasive alternative), defined treatments (chosen based on which mechanism is responsible), and a prognosis that is meaningfully worse than the historical “clean angiogram, you’re fine” framing suggested.
The contemporary standard of care reflects this. The 2017 AHA scientific statement on INOCA, the 2018 CorMicA randomized trial, and the 2021 ACC/AHA Chest Pain Guideline all establish that mechanism-specific diagnosis and treatment improves outcomes in patients with chest pain and non-obstructive coronary disease.
What remains is closing the gap between what the contemporary guidelines say and what routine practice does. A meaningful share of that work depends on women themselves — knowing that the angiogram alone does not rule out cardiac ischemia, knowing that coronary function testing and stress cardiac MRI exist, asking whether they were performed, asking for them if they were not, and not accepting “your heart looks fine” as the final answer if symptoms persist. A clean angiogram redirects the cardiac workup. It does not end it.
Next: Article 8 covers spontaneous coronary artery dissection (SCAD), myocardial infarction with non-obstructed coronary arteries (MINOCA), and Takotsubo cardiomyopathy — three syndromes that disproportionately affect women and that the standard cardiovascular framework has historically missed or mischaracterized.
Key Terms
Acetylcholine: A medication that, when injected into a coronary artery during angiography, can provoke spasm in arteries that are prone to it. Used in provocative testing for vasospastic disease.
Adenosine: A medication that, when injected into a coronary artery during angiography, causes the small vessels of the heart to dilate. Used to measure coronary flow reserve.
Angiography (coronary): The standard test for examining the larger arteries of the heart, in which dye is injected into the arteries and X-ray images are taken. Excellent at detecting obstructions in the larger arteries; cannot directly see the small vessels or detect transient spasm.
Coronary flow reserve (CFR): The ratio of maximum coronary blood flow (under stress or pharmacologic stimulation) to resting coronary blood flow. A normal value is generally above 2.0 to 2.5. Values below indicate microvascular dysfunction. A WISE analysis found that a CFR below 2.32 was the threshold best discriminating major adverse cardiovascular events in women with non-obstructive coronary disease. (7)
Coronary microvascular dysfunction (CMD): Impaired function of the small blood vessels of the heart — those downstream of the larger arteries visible on a standard angiogram. A major mechanism of INOCA.
Endothelial dysfunction: Impaired ability of the inner lining of blood vessels (the endothelium) to perform its normal functions, including maintaining vessel tone and limiting inflammation. A common underlying mechanism in both microvascular and large-vessel disease.
Epicardial arteries: The larger heart arteries on the surface of the heart that are visible on a standard angiogram — including the left main, left anterior descending, circumflex, and right coronary arteries.
Epicardial vasospastic disease: A tendency of the larger heart arteries to undergo transient spasm. Diagnosed by provocative testing during coronary angiography.
Heart failure with preserved ejection fraction (HFpEF): A form of heart failure in which the heart’s pumping function on standard echocardiography looks normal but the heart cannot properly relax and fill. Linked to microvascular dysfunction.
INOCA: Ischemia with no obstructive coronary arteries. An umbrella term covering patients with documented evidence of cardiac ischemia whose epicardial coronary arteries on standard angiography show less than 50 percent narrowing.
Invasive coronary function testing: A procedure performed during coronary angiography using intracoronary medications (adenosine and acetylcholine) and pressure-wire measurements to characterize the function of the small vessels and to test for vasospasm. The gold standard for definitively diagnosing INOCA.
Major adverse cardiovascular events (MACE): A composite outcome used in cardiovascular research. In the Pepine 2010 WISE analysis cited here, MACE was defined as death, nonfatal myocardial infarction, nonfatal stroke, or hospital stay for heart failure.
Microvascular angina: Angina caused by coronary microvascular dysfunction. One of the two major INOCA mechanisms.
Seattle Angina Questionnaire (SAQ): A validated patient-completed questionnaire that measures how much angina symptoms affect daily life and physical activity. Used as a standard outcome measure in trials of anti-anginal treatments.
Vasospastic angina: Angina caused by epicardial vasospasm. Also called variant angina or Prinzmetal’s angina in older terminology. One of the two major INOCA mechanisms.
WISE study: The Women’s Ischemia Syndrome Evaluation. A prospective cohort study of 936 women sponsored by the National Heart, Lung, and Blood Institute that established much of the modern evidence base for INOCA.
References
- Bairey Merz CN, Pepine CJ, Walsh MN, Fleg JL, et al. Ischemia and no obstructive coronary artery disease (INOCA): developing evidence-based therapies and research agenda for the next decade. Circulation.2017;135(11):1075–1092.
- Bairey Merz CN, Shaw LJ, Reis SE, et al. Insights from the NHLBI-Sponsored Women’s Ischemia Syndrome Evaluation (WISE) Study: Part II: gender differences in presentation, diagnosis, and outcome with regard to gender-based pathophysiology of atherosclerosis and macrovascular and microvascular coronary disease. J Am Coll Cardiol. 2006;47(3 Suppl):S21–S29.
- Reis SE, Holubkov R, Conrad Smith AJ, et al. Coronary microvascular dysfunction is highly prevalent in women with chest pain in the absence of coronary artery disease: results from the NHLBI WISE study. Am Heart J.2001;141(5):735–741.
- Ford TJ, Stanley B, Good R, et al. Stratified medical therapy using invasive coronary function testing in angina: the CorMicA trial. J Am Coll Cardiol. 2018;72(23 Pt A):2841–2855.
- Gulati M, Levy PD, Mukherjee D, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR guideline for the evaluation and diagnosis of chest pain: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2021;78(22):e187–e285.
- Kenkre TS, Malhotra P, Johnson BD, et al. Ten-year mortality in the WISE study (Women’s Ischemia Syndrome Evaluation). Circ Cardiovasc Qual Outcomes. 2017;10(12):e003863.
- Pepine CJ, Anderson RD, Sharaf BL, et al. Coronary microvascular reactivity to adenosine predicts adverse outcome in women evaluated for suspected ischemia: results from the National Heart, Lung and Blood Institute WISE (Women’s Ischemia Syndrome Evaluation) Study. J Am Coll Cardiol. 2010;55(25):2825–2832.
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