Subendocardial infarction

Cardiovascular Effects. No studies were located regarding cardiovascular effects of various forms of aluminum following intermediate- or chronic-duration oral exposure in humans. Acute-duration oral exposure to aluminum phosphide has been shown to cause tachycardia, hypotension, cardiovascular electrocardiographic abnormalities, subendocardial infarction, and transient atrial fibrillation in persons who either ingested it accidentally or in suicide attempts (Chopra et al. 1986 Khosla et al. 1988). However, toxicity was probably due to the formation of highly toxic phosphine gas rather than to aluminum exposure. 

Hendel, R. C., McSherry, B. A., and Leppo, J. A. (1990) Myocardial uptake of indium-ill-labeled antimyosin in acute subendocardial infarction clinical, histochemical and autoradiographic correlation of myocardial necrosis. J. Nucl. Med. 31,1851-1853. 

Non-ST-segment elevation A type of myocardial infarction (MI) that is limited to the subendocardial myocardium and is smaller and less extensive than an ST-segment MI. There is usually no pathologic Q-wave on the electrocardiogram in non-ST-segment elevation. 

More recent studies continue to support the unique antifibrillatory activity of bretylium. Kowey et al. [38] have shown that bretylium prevented spontaneous VF and decreased the effects on VF threshold in a feline myocardial infarction model. They attributed this beneficial effect to a decrease in the dispersion of refractoriness between normal and ischaemic regions of the heart. In contrast, clofilium (14, see below), which had little effect on dispersion of refractoriness after coronary occlusion, was unable to prevent spontaneous VF. Similar results were seen in isolated tissue studies with canine subendocardial Purkinje fibres and ventricular muscle which contained both normal and ischaemic regions [39]. In these studies bretylium caused a smaller increase in dispersion of refractoriness in subendocardial Purkinje fibres than either sotalol or clofilium. In ventricular muscle tissue, bretylium decreased dispersion while sotalol and clofilium increased dispersion of refractoriness. 

A 58-year-old man with a previous smoking history and a history of hypertension was severely biochemically hypothyroid (serum TSH 221 mU/1) and was given thyroxine, initially in a low dose (25 micrograms/day), increasing to 100 micrograms/day after 2 weeks. A month later he sustained a subendocardial myocardial infarction associated with only minor abnormalities on coronary angiography. 

Myocardial ischemia is unusual during infusion of iloprost. It mainly occurs in patients with pre-existing coronary disease, when it is ascribed to a steal phenomenon detrimental to the subendocardial tissue. As a rule it is transient and exceptionally proceeds to infarction. However, such an event has now been reported in a patient with systemic sclerosis (7). 

First predominant subendocardial compromise occurs and then, transmural and homogeneous compromise ACS with ST-segment elevation evolving to Q-wave infarction or coronary spasm (Prinzmetal angina) ... 

In theory the presence of subendocardial or transmural injury in completely opposite areas of the heart may decrease or even conceal the two injury vectors (Madias, 2006). However, in practice, this does not occur usually, because the ischaemia is usually due to occlusion of only one vessel and this does not generate equal and opposed injured areas (Rautaharju, 2006). Furthermore, with the same amount of injury in two opposite areas, it is more visible in the surface ECG of the injury area that is more close to subepicardium. In the chronic phase it is more often seen that a new vector of infarction in opposed area may cancel the Q-wave pattern of a previous infarction (see Figure 5.38). 

In summary, according to what has been discussed, it is understood that in the presence of an infarction that may affect extensive areas of the entire wall, but with predominant subendocardial compromise, one can find pathological Q waves on some occasions (Figure 5.2C) yet not on others (Figure 5.2D). 

Camacho AN, Guindo J, Bayes de Luna A. Usefulness of silent subendocardial ischemia detected by ST-segment depression in postmyocardial infarction patients as a predictor of ventricular arrhythmias. Am J Cardiol 1992 69 1243. 

By assessing the myocardium in patients with known history of coronary artery disease, subendocardial or trans-mural myocardial infarction scars may frequently be identified as hypodense areas. With further organization and healing of a sub-endocardial or trans-mural myocardial infarction, a thinning of the myocardial wall or myocardial aneurysm may take place. Due to myocardial dysfunction, or in atrial fibrillation, thrombus formation is likely to develop in the cardiac chambers and can be detected by CTA in the axial slices even more than by trans-thoracic ultrasound (Masuda et al. 1984). 

Wagner A etal. (2003) Contrast-enhanced MRl and routine single photon emission computed tomography (SPECT) perfusion imaging for detection of subendocardial myocardial infarcts an imaging study. Lancet 361 374-379 Wilson RF (1996) Assessing the severity of coronary-artery stenoses. N Engl J Med 334 1735-1737... 

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