CASE REPORT

It is Myocardial Infarction with Non-Obstructive

Coronary Arteries: A Myth or Reality?
Kashif Bin Naeem, Abdalla Alhajiri

Consultant Cardiologist, Al Baraha Hospital, Ministry of Health, Dubai, UAE

ABSTRACT

Acute myocardial infarction (AMI) is often associated with obstructed coronary arteries. However, recently, the occurrence of
non-obstructive coronary arteries on angiogram in a patient with AMI has puzzled many physicians. To put forward the myth into
reality, such cases have been coined into the term myocardial infarction with non-obstructive coronary arteries. It is not uncommon,
is more frequent in younger women, is associated with fewer traditional risk factors, and usually presents with non-ST elevation
myocardial infarction. However, due to its variable prognosis and diverse etiology, the condition continues to be a conundrum for
many across the world. We report a case where a 63-year-old male presented with non-ST elevation myocardial infarction based on
the Universal Definition of Myocardial Infarction. However, a subsequent coronary angiogram did not reveal obstructive coronary
artery disease. We present the diagnostic and management dilemma for such cases and review the literature.

Key words: Myocardial infarction with non-obstructive coronary arteries, coronary angiogram, non-ST elevation myocardial
infarction, plaque rupture

INTRODUCTION traditional risk factors, and usually presents with non-ST

elevation myocardial infarction. The variable prognosis, at

T
he occurrence of acute myocardial infarction (AMI) times comparable to AMI with CAD, and paucity of data to
without significant coronary artery disease (CAD) has guide appropriate treatment may lead physicians to either
been reported almost 80 years ago.[1] Many have since falsely reassure patients or avoid digging into the etiology.
then considered it a myth with unexplained occurrence. Since Hence, we considered it prudent to report such a case as it
the profoundly common use of coronary angiography in AMI happened to us and explore the related evidence.
over the past few decades, the condition has been reported on a
regular basis where patients fulfilling the criteria for AMI turn CASE REPORT
up having non-obstructive coronary arteries. This eventually
prompted the elders of the field to recognize it as a unique A 63-year-old diabetic male presented to our center with the
entity. Hence, the name myocardial infarction with non- complaints of typical anginal chest pains for few days. The pain
obstructive coronary arteries (MINOCA) came into being. was substernal, brought on by exertion, and relieved by the rest.
The reason behind ignoring the entity primarily relates to the He denied any shortness of breath, palpitations, presyncope,
inability to understand the underlying pathophysiology, to or syncope. He was diabetic and controlled on insulin therapy.
develop the diagnostic criteria, and to formulate a management He was a non-smoker and had no history of hypertension,
algorithm. It is definitely not uncommon and found in about hyperlipidemia, or family history of premature coronary heart
6% of AMI patients; however, there is a large variability in its disease. He had documented a history of allergy to aspirin. His
reported prevalence that ranges between 3.5% and 15%.[2] It blood pressure was 130/70 mmHg and pulse 64/min, regular.
is more frequent in younger women, is associated with fewer Cardiovascular and chest examination was unremarkable.

Address for correspondence:

Kashif Bin Naeem, Consultant Cardiologist, Al Baraha Hospital, Ministry of Health, Dubai, UAE.
Mobile: +971-569443145. E-mail: 
https://doi.org/10.33309/2639-8265.010205 www.asclepiusopen.com
© 2018 The Author(s). This open access article is distributed under a Creative Commons Attribution (CC-BY) 4.0 license.

Journal of Clinical Cardiology and Diagnostics  •  Vol 1  •  Issue 2  •  2018 11

 Naeem and Alhajiri

Electrocardiography (ECG) showed sinus rhythm, normal DISCUSSION

axis, mild ST-segment elevation V1-3, inferolateral T-wave
inversions with mild ST-segment depression, and bifid p We believe that our case with MINOCA is just a drop in the
wave in V1 [Figure 1]. Laboratory tests revealed raised ocean of natural occurrences that puzzle science and therefore
serial troponin-I levels, 0.08/0.1 ng/ml (abnormal >0.05 ng/ inspire researchers. DeWood et al. demonstrated, in his early
ml as per our laboratory criteria). Creatinine was 88 umol/L, AMI coronary angiography studies, that ST-segment elevation
hemoglobin 14.6 g/dL, glycated hemoglobin 7.1%, and myocardial infarction was more frequently associated with
low-density lipoprotein 1.8 mmol/L. 2-D transthoracic occluded coronary artery compared to non-ST elevation
echocardiography showed left ventricular (LV) hypertrophy, myocardial infarction.[5,6] Overall, >90% had angiographic
normal wall motion, LV ejection fraction 72%, impaired evidence of obstructive CAD, underscoring the importance
relaxation, normal valves in structure and function, no pericardial of the atherosclerotic process in the pathogenesis of AMI.
effusion, no masses, and normal pulmonary pressures. Still, it is fascinating that about 10% had no significant CAD
on coronary angiography.
He was diagnosed as non-ST elevation myocardial
infarction, based on the Universal Definition of Myocardial Several large AMI registries have confirmed the incidence of
Infarction.[3] Global Registry Of Acute Coronary Events risk 1–13% of AMIs that occurred in the absence of obstructive
score[4] predicted in-hospital mortality of 2.2% and 3.5% CAD.[7,8] This sparked an array of questions including the
risk of death at 1 year. He was treated with clopidogrel (no mechanism of myocardial damage, patient characteristics,
aspirin as he had allergy to aspirin), atorvastatin, bisoprolol, and management strategies for such cases. This led the
perindopril, and subcutaneous enoxaparin. He was also clinical researchers to design the diagnosis of MINOCA.
commenced on intravenous tirofiban (glycoprotein 2b3a
inhibitor) due to high risk. He was then transferred to a Only recently, the European Society of Cardiology (ESC)
tertiary center for coronary angiogram. He was not found working group position paper[9] has provided the diagnostic
to have any significant CAD [Figure 2]. Cardiac magnetic criteria for MINOCA that comprises of (a) AMI criteria as
resonance imaging (CMRI) was performed to exclude other per the Third Universal Definition of Myocardial Infarction,
causes of myocardial injury that was normal. He became (b) non-obstructive CAD on angiography, and, (c) no clinically
pain fee and was subsequently discharged on clopidogrel, overt specific cause for the acute presentation. On dissecting
atorvastatin, bisoprolol, and perindopril. The patient will be the definition, we found out that it has very wisely mentioned
followed in the outpatient cardiology clinic. the steps to follow. The initial clinical diagnosis of AMI takes
precedence and involves considering the symptoms, rise/fall
of troponin values, ECG, and echocardiography features,
as per the definition of myocardial infarction.[3] Once the
diagnosis has been made, almost everyone undergoes coronary
angiography. The skill of radial approach has alleviated major
bleeding concerns that have made angiography popular. The
ESC diagnostic criteria[9] have clearly defined obstructive
CAD as coronary artery stenosis ≥50% in any potential
infarct-related artery. This includes both patients with normal
coronary arteries (no stenosis <30%) and mild coronary
stenosis (stenosis >30% but <50%). The third segment of the
Figure 1: Electrocardiography showed sinus rhythm, normal diagnostic criteria means that, at the time of angiography, the
axis, mild ST-segment elevation V1-3, inferolateral T-wave cause and thus a specific diagnosis for the clinical presentation
inversions with mild ST-segment depression, and bifid p wave are not apparent. Accordingly, there is a need for further
in V1 evaluation. Importantly, MINOCA is a “working diagnosis”
and should prompt the physician to investigate underlying
causes, analogous to heart failure.

MINOCA has many possible etiologies and pathogenic

mechanisms. Therefore, the key principle in the management
of this syndrome is to clarify the underlying mechanism to
achieve patient-specific treatment. Scalone et al.[10] provided
a b c a framework to diagnose the underlying mechanism of
Figure 2: Coronary angiogram showing the left and right myocardial injury. Clinical history, ECG, cardiac enzymes,
coronary systems a)Left Anterior Descending Artery b)Left echocardiography, coronary angiography, and LV angiography
Circumflex Artery c)Right Coronary Artery represent the first-level diagnostic investigations. In particular,

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 Naeem and Alhajiri

the findings of regional wall motion abnormalities at LV confirms AMI. The present and pattern of late gadolinium
angiography limited to a single epicardial coronary artery enhancement (LGE) may point toward a vascular or non-
territory identify an “epicardial pattern,” whereas wall motion vascular cause. However, 8–67% of patients with MINOCA
abnormalities extending beyond a single coronary artery have no evidence of LGE, myocardial edema, or wall motion
territory identify a “microvascular pattern.” The most common abnormalities on CMRI.
causes include coronary artery plaque disease, coronary
dissection and coronary artery spasm “epicardial causes,” and The prognosis for MINOCA is quite variable. Contemporary
coronary microvascular spasm, Takotsubo cardiomyopathy, studies evaluating the prognosis for MINOCA report a
myocarditis, and coronary thromboembolism “microvascular 12-month all-cause mortality of 4.7% (95% confidence
causes.” In our case, normal echocardiography excluded interval 2.6–6.9),[2] which is better than those with AMI
causes such as Takotsubo disease, coronary angiogram associated with obstructive CAD. Kang et al.[7] confirmed
excluded coronary dissection, and normal cardiac MRI that 12-month major adverse cardiac events in patients with
excluded myocarditis. Therefore, the most likely cause could MINOCA were comparable to patients with AMI with single
be either coronary spasm or microvascular disease. or double vessel CAD. Grodzinsky et al.[15] demonstrated
that 25% of patients with MINOCA continued to experience
Plaque rupture and plaque erosion have been identified angina 12 months after AMI, which is equivalent to the rate
in over 40% of patients with MINOCA in studies using in those with AMI associated with obstructive CAD.
intravascular ultrasound (IVUS)[11] and optical coherence
tomography (OCT). Myonecrosis in these cases is mediated Considering the guarded prognosis of patients with
by thrombosis, thromboembolism, superimposed vasospasm, MINOCA, no randomized trials have addressed the best
or a combination of these processes. Finding of plaque treatment strategy. Lindahl et al.[16] examined the associations
rupture on OCT is associated with major adverse cardiac between treatment with statins, renin-angiotensin system
events.[12] Spontaneous coronary dissection typically causes blockers, β-blockers, dual antiplatelet therapy, and long-
an AMI by means of luminal obstruction. It is more common term cardiovascular events. He performed an observational
in women, estimated to be responsible for up to 25% of all study of MINOCA patients recorded in the SWEDEHEART
ACS cases in women under 50 years of age. Prognosis is registry, where 9466 consecutive unique patients with
excellent; however, the risk of recurrence of acute events MINOCA were identified. The results indicate long-term
has been reported to be high (27% at 5 years).[13] Coronary beneficial effects of treatment with statins and angiotensin-
artery spasm reflects vascular smooth muscle hyperreactivity converting enzyme inhibitors/angiotensin receptor blockers
to endogenous or exogenous vasospastic substances. on outcome in patients with MINOCA, a trend toward a
Provocative spasm testing has demonstrated inducible spasm positive effect of β-blocker treatment, and a neutral effect of
in 27% of patients with MINOCA.[2] Vasodilators such as dual antiplatelet therapy.
nitrates and calcium antagonists provide standard treatment
with the latter shown to prevent cardiac events. Coronary CONCLUSION
thrombosis may arise from hereditary or acquired thrombotic
disorders such as Factor V Leiden mutation and Protein C MINOCA patients continue to puzzle physicians worldwide
and S deficiencies. Thrombophilia screening studies in given the many possible etiologies and pathogenic
patients with MINOCA have reported a 14% prevalence of mechanisms involved. Unfortunately, randomized trials are
these inherited disorders.[2] Coronary emboli may occur in lacking to guide diagnostic and therapeutic strategies. IVUS/
the context of atrial fibrillation and valvular heart disease. OCT during angiography, echocardiography (including
They may also arise from valvular vegetations, cardiac transesophageal), and cardiac MRI helps to evaluate these
tumors (e.g., myxoma and papillary fibroelastoma), calcified patients. It is imperative to search for etiology as treatment
valves, and iatrogenic air emboli. Takotsubo cardiomyopathy depends on the specific cause.
presents as ACS with ST-segment changes, often with a
stressful trigger. It is characterized by left ventricle mid-
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