JRSM >
Volume 95, Number 8 >
Pp. 398-400
Departments of Cardiology, London Chest and Homerton Hospitals, London, UK
Correspondence to: Dr B Chandrasekaran, Department of Medicine and Cardiology, General Hospital, Gloucester Street, St Helier, Jersey JE1 3QS, UK E-mail: badri53{at}hotmail.com
 | INTRODUCTION |
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 TOP INTRODUCTION MECHANISMSTREATMENT AND PROGNOSISCONCLUSIONREFERENCES |
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MINCA can be classified into four groups based on risk factors for IHD and angiographic findings:
| MECHANISMS |
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TOPINTRODUCTIONMECHANISMSTREATMENT AND PROGNOSISCONCLUSIONREFERENCES |
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Atheroma
Most myocardial infarctions arise from coronary artery disease.
Atheromatous plaque rupture initiates an inflammatory response in which the
resulting thrombosis and superimposed vasopasm compromise coronary perfusion.
With selective coronary angiography the proportion of MI patients with normal
or near-normal coronary arteries is between 1% and
12%5, depending on
the definition of normal—i.e. ‘no endoluminal
irregularities’ or ‘no significant (< 30%) stenosis’. In
a retrospective analysis, 1.1% with proven MI had no luminal
irregularities6.
Angiograms, of course, provide only a two-dimensional silhouette of the lumen,
and the extent of disease found post mortem often differs from that diagnosed
angiographically7.
In a patient with ‘normal’ coronary arteries, intravascular
ultrasound techniques will often reveal extraluminal
disease7; so far,
however, there have been no large studies with intravascular ultrasound in
MINCA. There are compensatory mechanisms which preserve luminal integrity even
when the internal elastic lamina is seriously
diseased8, and such
diffuse coronary disease can substantially reduce coronary blood flow in the
absence of significant stenosis on
angiography9.
Hypercoagulable states
One possible mechanism for MINCA is occlusion of the vessel lumen by
thrombus that subsequently lyses rapidly. Platelet aggregates have been shown
to cause transmural infarction and their half-life is 10-15
minutes10. The
evidence on hypercoagulable states is mixed. The risk of MI is above normal in
people with raised plasma fibrinogen and plasminogen activator inhibitor
111. However, for
most clotting abnormalities, including the most common inherited
thrombophilia, factor V Leiden, there is no consistent link with
MI11. In reports
suggesting some excess risk, this was mainly in people who had other risk
factors for coronary artery
disease12.
Lately there has been much interest in raised levels of homocysteine as a risk factor for coronary artery disease, especially in those without other risk factors, but to our knowledge no studies have been reported in MINCA patients. A raised homocysteine is thought to increase the concentrations of factor VII and thrombin13. This is an important cause to identify because it can be countered by vitamin supplementation14.
Tobacco smoking, which predisposes to coronary vasospasm and thrombosis, is one of the strongest risk factors for IHD but its contribution to MINCA is less certain. Ammann et al. found that the prevalence of smoking was the same in patients with MINCA as in those with angiographic evidence of coronary artery disease6. This was the only study in which the definition of normal angiograms was ‘no endoluminal irregularity’ and MI was confirmed by wall motion abnormalities on left ventricular angiography. Earlier studies had shown that smoking was over-represented in young males with Q-wave infarction and normal coronary arteries4.
Emboli
The role of distal emboli in the aetiology of MINCA is controversial.
Theoretically valvular heart disease, endocarditis and mural thrombosis could
predispose to embolic infarcts with subsequent recanalization of the vessel
lumen. In one study an increased incidence of mitral valve prolapse and mitral
regurgitation was found in MINCA patients, but the results are hard to
interpret because of small numbers and the frequency of minor mitral valve
prolapse in the general
population4.
Coronary endothelial dysfunction
Coronary vasospasm can produce myocardial ischaemia (as indicated by ST
elevation on a 12-lead ECG), but there is no certainty that arterial spasm
alone can cause myocardial necrosis. Syndrome X is angina with normal coronary
arteries on angiography. Although dysfunction of vascular endothelium is
thought to be a mechanism in both syndrome X and MINCA, there are important
differences between the two groups. Most patients with MINCA do not have
angina. Syndrome X patients tend to be young women. Syndrome X involves the
coronary microvasculature, whereas MINCA is associated with epicardial
vessels15. The
vasospastic disorder migraine appears to be over-represented in
MINCA6.
Certain angiotensin II type 1 receptor gene polymorphisms have been associated with an increased tendency to vasospasm in angiographically normal coronary arteries challenged with a potent vasoconstrictor16. A combination of factors including genetic predisposition and environmental agents could predispose individuals with normal coronary arteries to infarction. However, extraluminal disease may still be the primary underlying cause.
Cocaine use has been linked with MI in the absence of coronary artery disease. The proposed aetiology is increased myocardial oxygen demand and paradoxical coronary vasospasm and thrombosis as a result of alpha-adrenergic action17. The likelihood of MI and further complications is further increased by smoking, concomitant alcohol intoxication and the presence of coronary heart disease17. Cocaine use is an important cause to identify because beta-blockers are contraindicated (the alpha-vasoconstrictor actions of catecholamines are left unopposed). There have been no prospective studies of cocaine use by MINCA patients.
Dissection
Aortic dissection and spontaneous coronary artery dissection can result in
an MI with little evidence of coronary artery disease. If aortic dissection is
suspected a chest CT or transoesophageal echo is indicated to exclude the
diagnosis since thrombolysis will be contraindicated. Spontaneous coronary
dissection can be managed safely by stenting.
Inflammation
Mediators of acute inflammation are thought to have a key role in acute
coronary syndromes; indeed, markers of inflammation can be used for risk
stratification. Whether the inflammatory response is the primary trigger or
secondary to plaque rupture is unclear. Some investigators have linked
specific infective agents with acute coronary syndromes—Chlamydia
pneumoniae, cytomegalovirus, Helicobacter
pylori—suggesting that they might destabilize atheromatous
plaques18. However,
the retrospective series of Ammann et
al.6 (21
patients with MINCA) did not show significantly higher antibody titres to
those organisms than patients with MI and abnormal coronaries—though
they did have a higher incidence of febrile episodes and upper respiratory
tract infections before the infarction.
Myocardial infarction with normal coronary arteries has been reported in the context of systemic lupus erythematosus (without evident vasculitis19) and in myocarditis20. Myocarditis was confirmed by endomyocardial biopsy in two individuals with MINCA preceded by a viral infection20. Myocarditis can mimic MI and endomyocardial biopsy combined with immunohistochemical analysis can be helpful in identification. Angelini et al.21 reported 12 patients (8 male) with MI confirmed by ECG changes, cardiac enzyme rises and wall motion abnormalities on echocardiography who were subsequently found to have normal coronary arteries on angiography. Endomyocardial biopsy yielded evidence of myocarditis in 11. There were no distinguishing clinical features to suggest myocarditis: only 6 patients gave a history of previous viral illness; ECGs showed regional changes and only 3 patients had a global decrease in left ventricular function on admission. These patients were young (average 29 years old) and most had no risk factors for IHD. Viral serology was not performed in all the patients and had a low yield.
| TREATMENT AND PROGNOSIS |
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TOPINTRODUCTIONMECHANISMSTREATMENT AND PROGNOSISCONCLUSIONREFERENCES |
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If absolutely normal coronary arteries are identified and a regional wall abnormality has confirmed MI, then a search for an underlying clotting disorder is reasonable though unlikely to be fruitful. If an inherited thrombophilia is identified, anticoagulation must be considered. In what circumstances should endocardial biopsy be performed? The argument for biopsy is strongest in young patients with no risk factors for IHD (group 1) and without other identifiable cause. However, the procedure carries risks, and in most cases myocarditis is self-limiting, not requiring special treatment. Thus, the main argument for confirming myocarditis is avoidance of unnecessary treatment.
In groups 1 and 2, with an identifiable cause absent, underlying coronary artery disease is the most likely aetiology. Treatments include aspirin, a beta-blocker, a statin and an angiotensin converting-enzyme (ACE) inhibitor. Hypertension and diabetes should be well controlled and smoking should be discouraged. In group 2 some clinicians have advocated the use of calcium channel blockers, to relieve or prevent vasospasm. There is no evidence that this improves outcome. The prognosis in groups 1 and 2 is more favourable than in age and sex matched individuals with identifiable coronary artery disease: in a mean follow-up of nearly 5 years in 21 such patients there were no deaths or major cardiac events6.
Groups 3 and 4, who have identifiable coronary artery disease on coronary angiography, should likewise be treated with aspirin, a beta-blocker, a statin, an ACE inhibitor and risk factor modification. Their worse prognosis (annual death rate 1.5% and major recurrence rate 2.7%) justifies a more rigorous approach to blood pressure, cholesterol and glycaemia.
| CONCLUSION |
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TOPINTRODUCTIONMECHANISMSTREATMENT AND PROGNOSISCONCLUSIONREFERENCES |
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| REFERENCES |
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TOPINTRODUCTIONMECHANISMSTREATMENT AND PROGNOSISCONCLUSIONREFERENCES |
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e
F, et al. Myocarditis mimicking acute myocardial infarction: role of
endomyocardial biopsy in the differential diagnosis.
Heart2000; 84:245
-50
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