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  • Title: [Experimental subendocardial anterolateral infarctions].
    Author: Medrano GA, de Micheli A.
    Journal: Arch Inst Cardiol Mex; 1989; 59(4):353-60. PubMed ID: 2818092.
    Abstract:
    Epicardial and thoracic unipolar tracings were recorded in 44 dog hearts after chemical necrosis had been produced on the anterior face of the free left ventricular wall by intramural injection of 96 percent alcohol. The damaged area was transmural (22 cases), intramural (10 cases) or localized in the interior half of the left ventricular wall. The last is commonly described as subendocardial necrosis (12 cases). Generally, direct leads recorded QrS complexes, with the R wave delayed according to the degree of damage to the myocardial muscle. These complexes were registered in at least one of the direct or semi-direct leads when myocardial necrosis was transmural or subendocardial in the interior half of the wall. Nevertheless, a small subendocardial (3 mm or less) or intramural necrosis created tiny Q waves, somewhat slurred but of normal duration, followed by R waves of low voltage. These signs alone are not diagnostic of myocardial necrosis. However, the presence of these Q waves in V2 and V3 only, or from V2 to V4 with greater voltage than in V5 and V6, implies the existence of non-transmural necrosis. The same applies when polyphasic ventricular morphologies are recorded in two intermediate precordial leads in absence of intraventricular conduction disturbances. These can mask the manifestation of transmural myocardial necrosis. Electrophysiologic data are sufficient to establish diagnosis if the infarcted area involves a substantial part of the thickness of the ventricular wall. However, in cases of small subendocardial or intramural necrosis, there are not always signs of dead tissue. At the same time, if the extension of transmural necrosis is more longitudinal than transverse, there is less probability of recording QS complexes in the precordial leads.
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