Chapter 6

Differential Diagnosis of Cardiac Ischemia

Jean-Jacques Goy, Jean-Christophe Stauffer, Jürg Schlaepfer and Pierre Christeler


In this chapter, we address the basic notions of the differential diagnosis of cardiac ischemia. Hypertrophic obstructive cardiomyopathy or HOCM is characterized on the electrocardiogram by Q waves in the inferior leads and negative T waves from V2 to V5 which is difficult to distinguish from classical ischemia due to coronary pathology.The electrocardiographic abnormalities of pericarditis are non specific and sometimes difficult to distinguish from ischemia. They are typically recognized by PR segment depression, present in the majority of the leads. The repolarisation abnormalities it causes are very similar to those of ischemia-lesion; primarily, the ST segment is elevated, with an inferior convexity, the so-called “camel hump” appearance. This segment progressively returns to the isoelectric line in the same time it takes for the amplitude of the T wave to fall, and in the end becomes negative. In V5, the amplitude of the ST elevation, compared to the amplitude of the T wave is > 0.25: a ratio < 0.25 favours early repolarisation. The electrical features of pericarditis are reputed to be diffuse, but in reality are not always so. Occasionally, acute pericarditis is the cause of an arrhythmia, almost always supraventricular (atrial fibrillation). However, there is never a pathological Q wave of necrosis. Moreover, the changes are generally diffuse and widespread without systemization of coronary abnormalities. The electrocardiographic features of pulmonary embolism are not specific: on the background of preexisting right bundle branch block, the Q waves in III and QS in V1 could be due to an inferior or an antero-septal infarct respectively. In the same vein, the raised ST segment in V1 could also be an antero-septal ischemia-lesion picture. Chatterjee phenomenon is a T wave inversion, often deep, which occurs after a period of abnormal ventricular activation (broad QRS), notably ventricular tachycardia, intermittent left bundle branch block or preexcitation, or even intermittent ventricular pacing. Early repolarisation causes in leads V2 to V5, a raised J-point and ST segment, as well as an increase in the amplitude of a symmetrical T wave, as would be expected for an ischemia-lesion but the J-point remains prominent and the convexity of the ST is inferior and not superior. Brugada syndrome is not a conduction abnormality but deserves a mention under the heading of right bundle branch block as it can mimic some aspects, notably changes in the terminal phase. There are 3 types of changes in V1 and V2 and rarely in V3. In all 3 types the J-point is raised at least 2 mm.

Total Pages: 116-123 (8)

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