Myocardial Ischemia

This section is dedicated to a discussion on the spectrum of ischemic heart disease and the associated electrocardiographic changes.

This will be a large section that includes discussions on:

• Pathobiology of cardiac ischemia: including the following topics:

  • An overview of normal coronary and myocardial anatomy and physiology, as it pertains to ischemic heart disease, such as:

    • The different layers of the myocardium.

    • The configuration of the coronary arteries with respect to the myocardium and how the subendocardium becomes the watershed area. 

    • The difference in the action potential morphologies in the various myocardial layers, and how these contribute to the normal transmural dispersion of repolarization.

    • The factors involved in the balance of cardiac oxygen supply and demand, including: heart rate and diastolic filling time, coronary perfusion pressure (i.e. diastolic blood pressure, left ventricular end-diastolic pressure), arterial oxygen content, coronary artery patency, wall tension (i.e. Laplace's law), and contractility.

    • The parts of the heart more susceptible to ischemic damage (i.e. the left anterior fascicle, the posteromedial papillary muscle) and the parts more resistant (i.e. the right ventricle, the left posterior fascicle), and why.

  • An overview of the spectrum of ischemic heart disease, from stable coronary disease (which can range from mild disease to triple-vessel or left main disease wherein collateralization can occur) to acute coronary syndromes (such as unstable angina, NSTEMI, and STEMI). We will discuss here the pathobiology of normal atherosclerotic disease.

  • An overview of the pathophysiology of acute ischemia. This involves the following topics:

    • The difference between subendocardial ischemia (i.e. NSTEMI) versus transmural ischemia (i.e. STEMI).

    • The mechanisms of acute coronary blockage, such as plaque rupture, erosion, embolism, aneurysm, dissection, and spasm. We will also discuss how secondary factors (such as elevated LVEDP from ischemia-induced impaired relaxation, or tachycardia) can exacerbate ischemic damage.

    • The electrophysiology of injury currents.

    • The normal evolution of damage to a cardiomyocyte subject to ischemia that is not corrected (starting at edema and progressing to cellular rupture, inflammation, and fibrosis). We will also cover other possible natural histories for myocardial cells exposed to ischemia, such as: hibernation, stunning, and ischemic pre-conditioning. 

    • The effects of reperfusion on ischemic cells, from arrhythmias (i.e. PVCs, AIVR) to changes in contractile function.

  • An overview of the electrical complications of cardiac ischemia, including:

    • Sinus bradycardia and/or AV block due to high vagal tone from irritation of the cardiac branches of the vagus nerve and the Bezold-Jaarisch reflex, especially with inferior infarcts.

    • Atrial arrhythmias, especially atrial fibrillation.

    • Ventricular arrhythmias, such as polymorphic VT and ischemic VF in the acute stages, and monomorphic scar-reentrant VT in the later stages.

    • Various conduction disorders either due to direct ischemic damage or damage related to structural adaptations to ischemic damage (i.e. LV dilatation). Specifically, we will highlight AV blocks and how infranodal and intranodal blocks tend to be associated with infarcts of different vascular territories.

  • An overview of the mechanical or structural complications of cardiac ischemia, such as:

    • Ventricular remodelling, which can start as hypokinesis and LV dilatation and progress to aneurysm formation.

    • Pump failure due to reduced left ventricular systolic function that can precipitate heart failure or cardiogenic shock.

    • Acute right ventricular dysfunction leading to acute right heart failure and preload-dependent shock.

    • LV thrombus, especially in the context of apical akinesis in anterior infarcts, leading to an elevated risk of strokes and other embolic phenomena.

    • Acute ventricular septal defect.

    • Acute papillary muscle rupture leading to ischemic mitral regurgitation. Worse with inferior infarcts due to posteromedial papillary muscle having a single blood supply.

    • Free wall rupture leading to either pseudoaneurysm formation or cardiac tamponade.

    • Early and late post-MI pericarditis.

• ECG manifestations of ischemia: This section will go through the various manifestations of ischemia on an ECG. This includes going through:

  • The importance of the ST vector and the mechanisms behind ST and T wave changes in ischemia. 

  • We will also provide a brief discussion on what reference point to use for measurement of ST deviation - the PQ junction or the TP segment.

  • Subendocardial ischemia/infarct and NSTEMI:

    • There will be a section on the global ischemia pattern seen in left main or triple vessel disease, or sometimes in the absence of these with exertion or tachyarrhythmia. Despite aVR elevation, this is not technically a STEMI.

    • We will also go through ST depressions, and how they aren't well localizing, but how to recognize morphologies that are more suggestive of ischemic disease.

    • We will also discuss the importance of evolving T wave inversions that could be representative of NSTEMI, and how to differentiate them from Wellen's pattern, which is usually suggestive of a threatened STEMI. In this same sense, we will discuss pseudo-normalization of the T wave as a variant that can be suggestive of ischemia.

  • Transmural ischemia/infarct and STEMI:

    • We will talk about the various morphologies of ST elevation (i.e. horizontal, upsloping or "Pardee's sign", coved, downsloping, concave, convex, tombstone, sharkfin, etc.) and how to use them to estimate the likelihood of a true STEMI versus a mimic.

    • We talk about the voltage criteria required to diagnose STEMI.

    • We will cover the different manifestations of an acute anterior STEMI at different locations in the left anterior descending artery. We cover how to determine involvement of the septal perforators or diagonal arteries, how to differentiate proximal from distal LAD occlusion, and why inferior ST elevations may be seen in the context of wraparound LAD anatomy. We will also discuss the manifestations of an acute left main artery occlusion. 

    • We will also cover the manifestations of an acute inferior STEMI. We compare the presentation of a right coronary artery occlusion versus a left circumflex occlusion. We discuss how to determine involvement of the posterior and lateral walls, and thereby involvement of the posterior descending artery and posterolateral arteries respectively. We also discuss the Aslanger pattern, a phenotype of inferior STEMI combined with a global ischemia pattern that presents with an atypical ECG that isn't strictly diagnostic for STEMI.

    • We will discuss the manifestations of an impending STEMI, such as hyperacute T waves, De Winter T waves, and Wellen's syndrome. We will also discuss the miscellaneous sign of u wave inversion as a marker of ischemia.

    • We will describe how to identify a STEMI in the presence of a pre-existing bundle branch block, and why it is more difficult. We discuss the Sgarbossa criteria and the mechanistic rationale for them. We also provide a brief discussion on the predictive value of a "new RBBB" or "new LBBB" in determining the presence of ischemia. 

    • Finally, we will go through the manifestations of successful reperfusion, such as improvement in the ST elevation, Wellen's T waves, and ventricular rhythms such as PVCs or AIVR.

  • ECG manifestations of complications of ischemic heart disease:

    • We cover arrhythmic complications of ischemia such as: vagatonia in certain infarcts, atrial fibrillation and other atrial arrhythmias, ischemic VF, monomorphic VT, and complete heart block. We also discuss features of severe ischemic cardiomyopathy.

    • We will also cover ECG evidence of structural complications of ischemia, such as: atrial infarction, aneurysm formation, pericarditis, and an old infarct.

  • Pseudo-infarction patterns: We will go through the differential diagnosis of conditions that can mimic manifestations of acute coronary syndrome. For example:

    • • The differential diagnosis of Wellen's syndrome and deep T wave inversions, such as Takotsubo cardiomyopathy, pulmonary embolism, intracranial hemorrhage, and so on.

      • The differential diagnosis of hyperacute T waves, such as benign early repolarization and ventricular hypertrophy, hyperkalemia, and so on.

      • The differential diagnosis of ST elevation, such as Brugada syndrome, hyperkalemia, paced rhythms, pericarditis, myocarditis, and so on.

• Stress testing: We will also have a section outlining how to interpret ECG stress tests in the context of identifying evidence of cardiac ischemia.