ST-segment elevation in non-atherosclerotic coronaries: a brief overview

Abstract

The most common, clinically significant cause of ST elevation is an angiographically demonstrable occlusive disease due to atherosclerotic changes in coronary artery. Often, a patient presenting with non-specific complaints and ST-segment elevation on the electrocardiogram, is sent for a cardiac catheterization only to see no luminal stenosis on the angiogram. This clinical review is intended to inform emergency medicine physicians and internists about the conditions in which ST-segment elevation is accompanied with no atherosclerotic lesion on coronary angiography. These situations make a diverse array of conditions ranging from anomalous coronaries to anatomically normal coronaries with varied degrees of myocardial injury. These conditions are briefly reviewed in this article.

Squamous Cell Carcinoma Metastatic to the Heart Mimicking ST-Elevation Myocardial Infarction

“…The differential diagnosis for ST-elevation includes STEMI, aortic dissection, pulmonary embolism, stress (takotsubo) cardiomyopathy, pericarditis with or without effusion, myocarditis, hypercalcemia, hyperkalemia, coronary vasospasm, coronary artery dissection, left ventricular aneurysm, left ventricular hypertrophy, the Brugada syndrome, left bundle branch block, early repolarization, early post-cardioversion, intracranial hemorrhage, and rarely, tumor invasion of the heart 3,4,5,6 .…”

“…Intracranial hemorrhage or stress (takotsubo) cardiomyopathy can also present with ST-elevations, theorized to be the result of increased catecholamines. Left ventricular hypertrophy, a sequela of poorly controlled hypertension, can also lead to J point elevations mimicking STEMI 3,4 .…”

Medical emergencies: atrial fibrillation and myocardial infarction

“…The classical definition of STEMI also mandates that these changes persist for > 20 min. For a review of all causes (ischaemic and non-ischaemic) and patterns of ST segment elevation see [57] New onset left BBB Development of pathological Q waves (indicative of infarction) [28] Notes The J-point (the point where the QRS complex joins the ST segment) is used to determine the magnitude of the ST elevation J-point elevation in men decreases with increasing age; however, this is not observed in women, in whom J-point elevation is less than in men Contiguous leads means lead groups such as anterior leads (V 1 -V 6 ), inferior leads (II, III and aVF), or lateral ⁄ apical leads (I, aVL, V 5 -V 6 ). Supplemental leads maybe very informative such as V 3 R and V 4 R (which reflect the free wall of the right ventricle) and V 7 -V 9 (which reflect the inferobasal area of the left ventricle) For further detailed discussion see [28,57,58] UA, unstable angina; NSTEMI, non-ST elevation myocardial infarction; STEMI, ST elevation myocardial infarction; BBB, bundle branch block.…”

“…It is clear from continuous ST segment monitoring that episodic myocardial ischaemia is very prevalent in ICU patients and largely ignored [56]. Periodic 12-lead ECG misses the vast majority of transient ischaemic events and is additionally confounded by difficulties with interpretation; a trace unchanged from baseline does not exclude myocardial ischaemia or infarction, and ST segment or T wave changes suggestive of ischaemia or infarction occur in their absence due to other causes [57,58]. In summary, in the peri-operative and ICU settings there is a reasonable case for automated, continuous ST segment monitoring using 6 to 12-lead ECG, but the positive and negative predictive values of detecting changes for myocardial ischaemia and infarction are undetermined and no consensus exists on optimal management.…”

Blunted temporal activity of microvascular perfusion heterogeneity in metabolic syndrome: a new attractor for peripheral vascular disease?

“…Although underrepresented to date, this is an exceedingly important area of investigation, since a growing body of evidence suggests that an increasing number of human subjects are afflicted with the symptomology of PVD in the absence of overt plaque/lesion development (12,19,31,44,45).…”