Myocardial necrosis without significant coronary atherosclerosis was described in autopsy reports over 80 years ago.1,2 More recently, this phenomenon has been heavily researched as scientists and cardiologists have tried to explain the pathophysiology of myocardial necrosis without coronary obstruction and proposed diagnostic algorithms and treatment management protocols for this unique patient population.
The term myocardial infarction with nonobstructive coronary arteries (MINOCA) is the current term used to describe patients who have an acute myocardial infarction (MI) with normal coronary arteries or with atherosclerosis that is determined by angiography to not be severe enough to obstruct myocardial blood flow.3,4
However, many questions remain, beginning with the actual definition of MINOCA? The inclusion and exclusion criteria of studied MINOCA patient populations differ from study to study, making it very hard to draw conclusions and update clinical management. In this review article, we will update the most recent definition of MINOCA and discuss its epidemiology and etiology. We will also review the diagnostic workup, and discuss the current management options and the future of MINOCA.
DEFINITION OF MYOCARDIAL INFARCTION WITH NONOBSTRUCTIVE CORONARY ARTERIES
There is an effort to group patients diagnosed with an MI who on subsequent angiography have no evidence of significant coronary obstruction into a standardized group as this could increase clinical awareness and drive research to better understand and treat this pathological condition.5 Ischemia and no obstructive coronary arteries, myocardial infarction with normal coronary arteries, troponin positive nonobstructive coronary arteries, and acute coronary syndrome with normal or near-normal coronary arteries are a few of the terms that have been used for this patient presentation; but the constantly changing identifications and definitions underscore how difficult it has been for the medical community to come to any universal agreement.6–9
Recently, the European Society of Cardiology gave an updated international definition and criteria for MINOCA.4 The criteria are (a) MI as set in the “Fourth Universal Definition of Myocardial Infarction”;10 (b) no evidence of obstructive coronary disease as per angiography (defined as no lesions >50% obstruction in an epicardial vessel); and (c) no other clinically overt cause for this acute presentation.
The first part of the criteria for MINOCA is that an MI has to occur; an MI can be considered with high sensitivity cardiac troponins greater than the 99th percentile of the upper limit of normal with a rise or fall on serial troponin testing.11 An elevated cardiac troponin level indicates cardiac myocyte damage leading to membrane breakdown and the leakage of cardiac troponins into the systemic circulation. However, myocardial damage can occur from both ischemic and non-ischemic processes that can both lead to elevated cardiac troponin levels. This issue has caused the “Fourth Universal Definition of Myocardial Infarction” to delineate myocardial injury compared to MI as separate pathophysiological disease processes.10 Myocardial injury is a non-ischemic process leading to myocyte injury and troponin leakage, while MI is an ischemic process leading to myocyte injury and subsequent troponin leakage.
This terminology of myocardial injury versus infarction has made diagnosis difficult as both disease processes can present similar in the clinical setting.12 For example, myocarditis is a non-ischemic process and can present with an elevated troponin level and angiographic normal coronary arteries,13 but an MI has not occurred, therefore it cannot be diagnosed as MINOCA. This is still a controversial area in the field; many studies and reviews are still including myocarditis, Takotsubo cardiomyopathy, and other non-ischemic causes of myocardial injury within the scope of MINOCA, despite the absence of an MI.
The other difficult part of defining patients with MINOCA is to define what nonobstructive coronary arteries (NOCA) are. According to the American Heart Association/American College of Cardiology guidelines, NOCA is diagnosed in patients with <50% obstruction in the major epicardial vessels by angiography, without any significant lesions.14 However, angiographic assessments are subjective and have been shown in many studies to have wide variability between clinicians.15–17 Secondary invasive functional testing of an obstructive lesion is not usually done, so all future clinical decisions are made based on this initial subjective visual assessment by the interventional cardiologist during angiography. Because of the variability in obstruction measurements, recent MINOCA studies have separated patients into those with moderate obstructive disease-causing 30–50% obstruction and those with zero or minimal obstructive disease defined as <30% obstruction. Bainey et al.18 described this as a useful distinction as they found significantly lower mortality in the group with minimal obstruction.
Clinical studies have identified the prevalence of MINOCA to be between 4% and 15% of total acute MI cases.19–21 A large meta-analysis of MINOCA prevalence in 2015 reported 6% of MIs occur without the presence of coronary artery disease (CAD).22
The MINOCA patient demographics tend to be younger, female and non-white compared to patients with other causes of MI.6,19 When compared to patients with MI and CAD, MINOCA patients were younger (58 years vs. 61 years), more likely women (50% vs. 25%), and more likely in non-white.23 The Variation in Recovery: Role of Gender on Outcomes of Young AMI Patients study reported MINOCA to be 5 times more likely in women than men.19
Common risk factors of MI-CAD, such as hypertension, diabetes mellitus, tobacco usage, and family history of MI were less frequent in patients diagnosed with MINOCA,19,23,24 but some studies have reported differently.22 A recent large population retrospective study in Japan found an increased prevalence of MINOCA in patients with medical comorbidities including pulmonary disease, peripheral vascular disease, cerebrovascular disease, liver disease, renal disease, and malignancy.25
MINOCA patients can present with ST-segment elevation MI (20–33%) or non-ST segment elevation MI (66–79%).6,26 Clinical outcomes of MINOCA vary across studies when compared to MI-CAD. Many previous studies have reported better outcomes for MINOCA patients compared to MI-CAD patients.22,27 However, in the recent literature, it has been reported that patients with MINOCA have similar or worse outcomes when compared to the MI-CAD population. The Variation in Recovery: Role of Gender on Outcomes of Young AMI Patients study reported no difference in mortality at 1 month and 1 year, and similar functional and psychomotor outcomes at 1 year.19 Other studies have also reported no difference or increased mortality rates in MINOCA patients compared to MI-CAD patients.25,28 Pelliccia et al.29 found that normal ejection fraction and normal coronary arteries by angiography were inversely related to long-term mortality risk, but ST depression on initial electrocardiogram and use of beta-blockers for follow-up management were directly related to increased mortality risk. The heterogeneity of MINOCA makes outcome reporting very difficult to interpret and analyze. There continues to be a strong need for better prognostic and outcome predictors for patients with MINOCA.
MINOCA is caused by a group of heterogeneous disease processes. In this section, we will briefly review the 6 established causes of a patient presenting with MINOCA.
One of the commonly reported causes of MINOCA is atherosclerotic disease which can lead to plaque disruption. Plaque disruption can be either plaque rupture or erosion; rupture is defined as a fibrous cap that ruptures leading to an open communication between the coronary lumen and the plaque cavity, while erosion occurs when the luminal surface of the plaque remains intact.30 Plaque rupture is caused by inflammation while plaque erosion is due to endothelial dysfunction.31 Plaque disruption can lead to thrombus formation which can cause MINOCA by transient thrombus obstruction with thrombolysis, distal embolization, or by leading to subsequent vasospasm.23 Plaque disruption can be a challenge to visualize on angiography and can only be defined with intracoronary imaging such as optical coherence tomography (OCT) or intravascular ultrasound (IVUS).6,32
Coronary vasospasm is defined as intense vasoconstriction leading to decreased myocardial blood flow;33 a prolonged vasospastic episode can lead to MINOCA. The pathophysiology of vasospasm is still being elucidated, but the prevailing current theory is that it occurs due to vascular smooth muscle hyperreactivity with an interplay of adventitia and endothelial cell layers.34 Coronary vasospasm is a more common cause of MINOCA in Asians compared to white people.22 Vasospasm can be diagnosed with coronary artery provocative testing. These tests were historically avoided due to deaths during the 1970s during testing, but recent new techniques have proven safe.35 The Coronary Vasomotion Disorders International Study Group proposed indications for when to perform provocative coronary artery spasm testing (Table 1).36
TABLE 1. -
Indications for Provocative Coronary Artery Spasm Testing
|Class I (strong indications)
||History suspicious of VSA without documented episode, especially if:
| -Nitrate-responsive rest angina, and/or
| -Marked diurnal variation in symptom onset/exercise tolerance, and/or
| -Rest angina without obstructive coronary artery disease
| -Unresponsive to empiric therapy
|Acute coronary syndrome presentation in the absence of a culprit lesion
|Unexplained resuscitated cardiac arrest
|Unexplained syncope with antecedent chest pain
|Recurrent rest angina following angiographically successful PCI
|Class IIa (good indications)
||Invasive testing for noninvasive diagnosed patients unresponsive to drug therapy
|Documented spontaneous episode of VSA to determine the “site and mode” of spasm
|Class IIb (controversial indications)
||Invasive testing for noninvasive diagnosed patients responsive to drug therapy
|Class III (contra-indications)
||Emergent acute coronary syndrome
|Severe fixed multi-vessel coronary artery disease including left main stenosis
|Severe myocardial dysfunction (class IIb if symptoms suggestive of vasospasm)
|Patients without any symptoms suggestive of VSA
With permission from Beltrame et al.36
PCI indicated percutaneous coronary intervention; VSA, vasospastic angina.
Coronary thrombosis and/or embolism can result in MINOCA if partial or total thrombolysis results in a nonobstructive image on subsequent angiography. The most common cause of coronary thrombosis/embolism is a hypercoagulable state which includes inherited disorders such as Factor V Leiden and Protein C/S deficiency, antiphospholipid syndrome, thrombotic thrombocytopenic purpura, and malignancy. A systematic review of hypercoagulable workups in MINOCA patients found Factor V Leiden in 12% and Protein C/S deficiency in 3% of patients.22 However, a thrombophilia workup is not indicated on the index admission and should be completed based upon an individualized clinical plan with the hematologist.37
Microvascular coronary dysfunction can cause MINOCA, but is a difficult diagnosis to confirm as microvascular dysfunction can result as sequelae to MI or myocardial injury.38 The microcirculation of the coronary system (<0.5 mm diameter) is not visualized well on angiography and is responsible for 70% of total coronary resistance in the absence of obstructive disease.23 The coronary microvasculature cannot be visualized on coronary angiography so a patient with MINOCA secondary to coronary microvascular dysfunction will have a normal angiogram. Positron emission tomography has been used to quantify myocardial blood flow and coronary flow reserve in patients with coronary microvascular dysfunction.39 Coronary microvascular dysfunction can be diagnosed by a decreased coronary flow reserve or with chest discomfort during provocative testing with negative coronary vasospasm findings.
Spontaneous coronary artery dissection (SCAD) is an uncommon cause of MI, but increases in prevalence in women younger than 50 years of age, and has been associated with pregnancy.40 SCAD leading to MI is usually due to severe obstruction, but occasionally can also be a nonobstructive lesion leading to MINOCA.41 The origin layer of the dissection is unknown which has made diagnostics and treatment difficult.42 Invasive diagnostic and therapeutic approaches are not usually recommended at a risk of worsening or extending the dissection.
Supply-demand mismatch is often given as a diagnosis to patients with hypotension and tachycardia without suspicion of ischemia, but supply-demand mismatch can lead to a type 2 MI which falls under MINOCA.43 There is a wide spectrum of possible etiologies that can cause supply-demand mismatch, so diagnosis and treatment protocols are very difficult to develop.43 It is also extremely difficult to definitively diagnose supply-demand mismatch as the cause of MINOCA because it is challenging to determine if the mismatch is the actual cause of the infarction or a consequence of a preceding infarction.23
MINOCA is a heterogeneous disease process that has many different treatment and management options based on the underlying etiology causing the MINOCA presentation. Because of this, it has been recommended MINOCA should only be used as an initial, working diagnosis.6 Further diagnostic assessment is needed to rule out other causes of the presentation and to establish a more specific, underlying etiology that can be treated and managed appropriately (Fig 1).
A patient presenting with a rise and/or fall of cardiac troponins with 1 level greater than the 99th percentile, signs and symptoms of an ischemic event, and a subsequent angiographic evaluation that shows no obstructive processes should have MINOCA as a working diagnosis at that time. Further diagnostic tests must be done, but there is no standard algorithmic approach.
Following is a discussion of the different diagnostic options available and when they can be considered.
Cardiac magnetic resonance imaging (CMR) has become the most important test for suspected MINOCA patients. CMR can rule out myocarditis, Takotsubo Syndrome and other cardiomyopathies that mimic MINOCA clinically, and it can also confirm if an MI occurred.44 A recent cohort of 388 MINOCA patients underwent CMR imaging, showing that 25% had an MI, 25% had cardiomyopathy, 25% had myocarditis, and 25% had an undetermined pathology.44 CMR was able to show that half of the patients initially diagnosed did not have MINOCA; this allows for more directed treatment options and identification of unfavorable subsets of presentations and finer risk stratification. CMR is an effective diagnostic option for MINOCA patients presenting with both ST-elevation MI or non-ST elevation MI, as Hausvater et al found no difference in rates of identifying MI, myocarditis and cardiomyopathy in MINOCA patients with either presentation.26 Patients with an initial MINOCA diagnosis may also have a subsequent normal CMR with no evidence of myocardial necrosis, but this does not rule out that an MI has occurred, and so MINOCA cannot be excluded with a normal result.45 CMR imaging has been shown to be most effective and have greatest impact when done within 48 hours of initial presentation,44 but because this is a relatively specialized test and is not widely available, it is difficult to introduce CMR as a standard, necessary diagnostic step for any MINOCA diagnosis. However, new CMR techniques are being developed and currently researched that will hopefully allow for more accurate and quick diagnosis of MINOCA when CMR becomes widely available.
When questions remain about the diagnosis after CMR, further imaging modalities should be considered to further visualize the coronary vasculature to uncover the underlying etiology of the patient presentation. OCT and IVUS have been used to visualize and diagnose plaque disruption, coronary emboli or thrombus, or SCAD.32,46 A prospective study on OCT use in 38 MINOCA patients found 24% to have plaque disruption and 18% to have a coronary thrombus.47 Reynolds et al.48 showed similar findings using IVUS; they reported 38% of female patients with MINOCA had plaque disruption. OCT is preferred over IVUS because IVUS can only identify plaque rupture while OCT can identify both plaque rupture and plaque erosion.49 Tamis-Holland et al.23 hypothesize that as coronary imaging using OCT becomes more common, the prevalence of plaque disruption will increase. As invasive coronary imaging becomes more common and widely available, undetermined causes of MINOCA will decrease.
When coronary vasospasm is the suspected underlying cause, provocative testing should be considered. The current gold standard test is an intracoronary acetylcholine bolus with invasive contrast angiography to visualize the epicardial vessels.35 Montone et al.50 showed 46% of MINOCA patients had a positive vasospasm test during their index admission. As further safety guidelines and regulations are enacted for provocative testing and cardiologists become more comfortable with this procedure, provocative testing will become an important part of the diagnostic workup for MINOCA patients.
The diagnostic work-up can become very complicated when a patient is suspected to have MINOCA. It is important to treat MINOCA as a working diagnosis and further investigate the specific cause using these different diagnostic tests based on clinical suspicion and availability within the hospital (Fig. 1). Clinicians should also always exclude a missed obstruction by carefully re-reviewing angiographic findings before ordering these more invasive and costly tests, as well as consider alternate diagnosis that may present with a similar clinical situation, such as pulmonary embolism, sepsis, and other non-cardiac causes of a cardiac troponin elevation with NOCA.
CONCLUSION AND FUTURE RESEARCH
MINOCA has become a difficult clinical presentation for management and treatment. The different specific causes of MINOCA each have different treatment protocols—there is no singular treatment plan for any MINOCA patient. The diagnostic process has become essential to uncover the cause of the MI, but there is no standard consensus on how to approach diagnosis. CMR has shown a lot of promise in recent research, but is unfortunately not widely available in the community setting. There are ongoing clinical trials to further explore the use of CMR as well as other imaging modalities including OCT, IVUS, and computed tomography coronary angiography.26,44
But there is still a lot of uncertainty and skepticism about MINOCA within the cardiology community. There is still disagreement about myocardial injury (ie, myocarditis) not being a cause of MINOCA as many studies still include confirmed myocarditis patients within their MINOCA cohort. There is disagreement on how much obstruction is allowable to still be considered NOCA, and disagreement on what specific CMR findings indicate ischemic or non-ischemic processes.51,52 Most of the studies reviewed in this article have separated obstructive lesions to <50% obstruction and <30% obstruction, but the Stockholm Myocardial Infarction with Normal Coronaries study uses inclusion criteria of <20% obstruction.53 The lack of standardization around a MINOCA definition and inclusion criteria makes this an even more difficult disease process to treat and study. Our understanding of MINOCA can progress once a standardized definition is agreed upon; this will lead to improved research and a better understanding of the pathophysiology, and hopefully to improved prevention and treatment.
1. Miller RD, Burchell HB, Edwards JE. Myocardial infarction with and without acute coronary occlusion; a pathologic study. AMA Arch Intern Med. 1951; 88:597–604
2. Bean WB. Infarction of the Heart. III. Clinical course and morphological findings. Anna Intern Med. 1938; 12:71–94
3. Beltrame JF. Assessing patients with myocardial infarction and nonobstructed coronary arteries (MINOCA). J Intern Med. 2013; 273:182–185
4. Agewall S, Beltrame JF, Reynolds HR, et al.; WG on Cardiovascular Pharmacotherapy. ESC working group position paper on myocardial infarction with non-obstructive coronary arteries. Eur Heart J. 2017; 38:143–153
5. Bairey Merz CN, Pepine CJ, Walsh MN, et al. Ischemia and no obstructive coronary artery disease
(INOCA): developing evidence-based therapies and research agenda for the next decade. Circulation. 2017; 135:1075–1092
6. Pustjens TFS, Appelman Y, Damman P, et al. Correction to: guidelines for the management of myocardial infarction/injury with non-obstructive coronary arteries (MINOCA): a position paper from the Dutch ACS working group. Neth Heart J. 2020; 28:59
7. Terefe YG, Niraj A, Pradhan J, et al. Myocardial infarction with angiographically normal coronary arteries in the contemporary era. Coron Artery Dis. 2007; 18:621–626
8. Kardasz I, De Caterina R. Myocardial infarction with normal coronary arteries: a conundrum with multiple aetiologies and variable prognosis: an update. J Intern Med. 2007; 261:330–348
9. Pacheco Claudio C, Quesada O, Pepine CJ, et al. Why names matter for women: MINOCA/INOCA (myocardial infarction/ischemia and no obstructive coronary artery disease
). Clin Cardiol. 2018; 41:185–193
10. Thygesen K, Alpert JS, Jaffe AS, et al.; Executive Group on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction. Fourth universal definition of myocardial infarction (2018). Circulation. 2018; 138:e618–e651
11. Kozinski M, Krintus M, Kubica J, et al. High-sensitivity cardiac troponin assays: from improved analytical performance to enhanced risk stratification. Crit Rev Clin Lab Sci. 2017; 54:143–172
12. Morrow DA. The fourth universal definition of myocardial infarction and the emerging importance of myocardial injury. Circulation. 2020; 141:172–175
13. Gannon MP, Schaub E, Grines CL, et al. State of the art: evaluation and prognostication of myocarditis using cardiac MRI. J Magn Reson Imaging. 2019; 49:e122–e131
14. Scanlon PJ, Faxon DP, Audet AM, et al. ACC/AHA guidelines for coronary angiography. A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee on Coronary Angiography). Developed in collaboration with the Society for Cardiac Angiography and Interventions. J Am Coll Cardiol. 1999; 33:1756–1824
15. Sen T, Kilit C, Astarcioglu MA, et al. Comparison of quantitative and qualitative coronary angiography: computer versus the eye. Cardiovasc J Afr. 2018; 29:278–282
16. Nallamothu BK, Spertus JA, Lansky AJ, et al. Comparison of clinical interpretation with visual assessment and quantitative coronary angiography in patients undergoing percutaneous coronary intervention in contemporary practice: the assessing angiography (A2) project. Circulation. 2013; 127:1793–1800
17. Zhang H, Mu L, Hu S, et al.; China PEACE Collaborative Group. Comparison of physician visual assessment with quantitative coronary angiography in assessment of stenosis severity in China. JAMA Intern Med. 2018; 178:239–247
18. Bainey KR, Alemayehu W, Gupta AK, et al. Ethnic and sex differences in ambulance activation among hospitalized patients with acute coronary syndromes: Insights from the Alberta contemporary acute coronary syndrome patients invasive treatment strategies (COAPT) study. Int J Cardiol. 2018; 272:33–39
19. Safdar B, Spatz ES, Dreyer RP, et al. Presentation, clinical profile, and prognosis of young patients with myocardial infarction with nonobstructive coronary arteries (MINOCA): results from the VIRGO study. J Am Heart Assoc. 2018; 7:e009174
20. Ballesteros-Ortega D, Martínez-González O, Gómez-Casero RB, et al. Characteristics of patients with myocardial infarction with nonobstructive coronary arteries (MINOCA) from the ARIAM-SEMICYUC registry: development of a score for predicting MINOCA. Vasc Health Risk Manag. 2019; 15:57–67
21. Gulati R, Behfar A, Narula J, et al. Acute myocardial infarction in young individuals. Mayo Clin Proc. 2020; 95:136–156
22. Pasupathy S, Air T, Dreyer RP, et al. Systematic review of patients presenting with suspected myocardial infarction and nonobstructive coronary arteries. Circulation. 2015; 131:861–870
23. Tamis-Holland JE, Jneid H, Reynolds HR, et al.; American Heart Association Interventional Cardiovascular Care Committee of the Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Epidemiology and Prevention; Council on Quality of Care and Outcomes Research. Contemporary diagnosis and management of patients with myocardial infarction in the absence of obstructive coronary artery disease
: a scientific statement from the American Heart Association. Circulation. 2019; 139:e891–e908
24. Jánosi A, Ferenci T, Kőszegi Z, et al. [Myocardial infarction without obstructive coronary artery disease
(MINOCA) - prevalence and prognosis]. Orv Hetil. 2019; 160:1791–1797
25. Ishii M, Kaikita K, Sakamoto K, et al.; JROAD Investigators. Characteristics and in-hospital mortality of patients with myocardial infarction in the absence of obstructive coronary artery disease
in super-aging society. Int J Cardiol. 2020; 301:108–113
26. Hausvater A, Pasupathy S, Tornvall P, et al. ST-segment elevation and cardiac magnetic resonance imaging findings in myocardial infarction with non-obstructive coronary arteries. Int J Cardiol. 2019; 287:128–131
27. Poku N, Noble S. Myocardial infarction with non obstructive coronary arteries (MINOCA): a whole new ball game. Expert Rev Cardiovasc Ther. 2017; 15:7–14
28. Choo EH, Chang K, Lee KY, et al.; KAMIR-NIH Investigators. Prognosis and predictors of mortality in patients suffering myocardial infarction with non-obstructive coronary arteries. J Am Heart Assoc. 2019; 8:e011990
29. Pelliccia F, Pasceri V, Niccoli G, et al. Predictors of mortality in myocardial infarction and nonobstructed coronary arteries: a systematic review and meta-regression. Am J Med. 2020; 133:73–83.e4
30. Falk E, Nakano M, Bentzon JF, et al. Update on acute coronary syndromes: the pathologists’ view. Eur Heart J. 2013; 34:719–728
31. Libby P, Pasterkamp G. Requiem for the ‘vulnerable plaque’. Eur Heart J. 2015; 36:2984–2987
32. Matthews SD, Frishman WH. A Review of the clinical utility of intravascular ultrasound and optical coherence tomography in the assessment and treatment of coronary artery disease
. Cardiol Rev. 2017; 25:68–76
33. Hung MJ, Hu P, Hung MY. Coronary artery spasm: review and update. Int J Med Sci. 2014; 11:1161–1171
34. Beltrame JF, Psaltis PJ. The forgotten vascular layer in the forgotten coronary disorder. J Am Coll Cardiol. 2018; 71:426–428
35. Ciliberti G, Seshasai SRK, Ambrosio G, et al. Safety of intracoronary provocative testing for the diagnosis of coronary artery spasm. Int J Cardiol. 2017; 244:77–83
36. Beltrame JF, Crea F, Kaski JC, et al. International standardization of diagnostic criteria for vasospastic angina. Eur Heart J. 2017; 38:2565–2568
37. Bereczky Z, Balogh L, Bagoly Z. Inherited thrombophilia and the risk of myocardial infarction: current evidence and uncertainties. Kardiol Pol. 2019; 77:419–429
38. Löffler AI, Bourque JM. Coronary microvascular dysfunction, microvascular angina, and management. Curr Cardiol Rep. 2016; 18:1
39. Campisi R, Marengo FD. Coronary microvascular dysfunction in women with nonobstructive ischemic heart disease as assessed by positron emission tomography. Cardiovasc Diagn Ther. 2017; 7:196–205
40. Lebrun S, Bond RM. Spontaneous coronary artery dissection (SCAD): The underdiagnosed cardiac condition that plagues women. Trends Cardiovasc Med. 2018; 28:340–345
41. Bullock-Palmer RP, Shaw LJ, Gulati M. Emerging misunderstood presentations of cardiovascular disease in young women. Clin Cardiol. 2019; 42:476–483
42. Tweet MS, Hayes SN, Pitta SR, et al. Clinical features, management, and prognosis of spontaneous coronary artery dissection. Circulation. 2012; 126:579–588
43. Mihatov N, Januzzi JL Jr, Gaggin HK. Type 2 myocardial infarction due to supply-demand mismatch. Trends Cardiovasc Med. 2017; 27:408–417
44. Blankstein R, Shaw LJ, Chandrashekhar Y. The promise of imaging in MINOCA. JACC Cardiovasc Imaging. 2019; 12:2100–2102
45. Collste O, Sörensson P, Frick M, et al. Myocardial infarction with normal coronary arteries is common and associated with normal findings on cardiovascular magnetic resonance imaging: results from the Stockholm Myocardial Infarction with Normal Coronaries study. J Intern Med. 2013; 273:189–196
46. Bezerra HG, Attizzani GF, Sirbu V, et al. Optical coherence tomography versus intravascular ultrasound to evaluate coronary artery disease
and percutaneous coronary intervention. JACC Cardiovasc Interv. 2013; 6:228–236
47. Opolski MP, Spiewak M, Marczak M, et al. Mechanisms of myocardial infarction in patients with nonobstructive coronary artery disease
: results from the optical coherence tomography study. JACC Cardiovasc Imaging. 2019; 1211 Pt 12210–2221
48. Reynolds HR, Srichai MB, Iqbal SN, et al. Mechanisms of myocardial infarction in women without angiographically obstructive coronary artery disease
. Circulation. 2011; 124:1414–1425
49. Kim HO, Kim CJ, Kurihara O, et al. Angiographic features of patients with coronary plaque erosion. Int J Cardiol. 2019; 288:12–16
50. Montone RA, Niccoli G, Fracassi F, et al. Patients with acute myocardial infarction and non-obstructive coronary arteries: safety and prognostic relevance of invasive coronary provocative tests. Eur Heart J. 2018; 39:91–98
51. Y-Hassan S. Most of the patients classified under “Myocardial infarction with non-obstructive coronary arteries (MI-NOCA)” have either no MI or no NOCA. Int J Cardiol. 2019; 294:54
52. Hausvater A, Reynolds HR. Response to most of the patients classified under “Myocardial infarction with non-obstructive coronary arteries (MI-NOCA)” have either no MI or no NOCA. Int J Cardiol. 2019; 297:17
53. Tornvall P, Brolin EB, Caidahl K, et al. The value of a new cardiac magnetic resonance imaging protocol in myocardial infarction with non-obstructive coronary arteries (MINOCA) - a case-control study using historical controls from a previous study with similar inclusion criteria. BMC Cardiovasc Disord. 2017; 17:199