Myocardial regional

For assessing viability of a non-contractile myocardial region, the non-fasting, fed patient is given an oral glucose load and resting perfusion images are... 

Myocardial infarction (MI) is caused by the acute thrombotic occlusion of a coronary artery. The myocardial region that has been cut off from its blood supply dies within a short time owing to the lack of 02 and glucose. The loss in functional muscle tissue results in reduced cardiac performance. In the infarct border zone, spontaneous pacemaker potentials may develop, leading to fatal ventricular fibrillation. The patient experiences severe pain, a feeling of annihilation, and fear of dying. 

Acute coronary syndromes most often result from a physical disruption of the fibrous cap, either frank cap fracture or superficial endothelial erosion, allowing the blood to make contact with the thrombogenic material in the lipid core or the subendothelial region of the intima. This contact initiates the formation of a thrombus, which can lead to a sudden and dramatic blockade of blood flow through the affected artery. If the thrombus is nonocclusive or transient, it may either be clinically silent or manifest as symptoms characteristic of unstable angina. Importantly, if collateral vessels have previously formed, for example, due to chronic ischemia produced by multi vessel disease, even total occlusion of one coronary artery may not lead to an acute myocardial infarction. 

Figure 4.4 Effect of a free-radical scavenger M-(2-mercaptoproplonyl)-glycine (MPG) on the recovery of contractile function following 15 min of regional ischaemia in the dog heart, (a) MPG infused 1 min before reperfusion, (b) MPG infused 1 min after reperfusion. Contractile function was assessed as changes in ventricular wall thickening measured using an ultrasonic pulsed-Doppler epicardial probe. Note The free radical scavenger MPG can reduce myocardial stunning only when present during the first minute of reperfusion. Redrawn with permission from Bolli et af. (1989).

Tait G.A., Young R.B., Wilson G.J., Steward D.J., MacGregor D.C., Myocardial pH during regional ischemia evaluation of a fiber-optic photometric probe, Am J. Physiol.Heart Circ. Physiol. 1982 243 H1027. 

F. Najjar, and D.J. Kumbhani, Intraoperative regional myocardial acidosis and reduction in long-term survival after cardiac surgery. J. Thorne. Cardiovasc. Surg. 129, 372—381 (2005). 

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. 

The ACE gene encodes two isozymes (somatic ACE isozyme and germinal ACE isozyme). ACE is a membrane-bound enzyme on the surface of vascular endothelial cells that also circulates in plasma and shows great individual variability determined by an I/D polymorphism in intron 16 of the ACE gene (ACE-I/D polymorphism). More than 160 ACE polymorphisms have been reported, 34 of which are located in coding regions, and 18 are missense mutations (606). ACE-related polymorphic variants have been associated with hypertension, atherosclerosis, stroke, left ventricular hypertrophy, chronic renal failure in IgA nephropathy, Henoch-Schonlein purpura nephritis, mechanical efficiency of skeletal muscle, intracranial aneurysms, susceptibility to myocardial infarction, diabetic nephropathy, AD, and longevity (12,606,607). 

Orotic acid or 6-methyluracil vide infra), when administered to rabbits with myocardial infarction induced by ligation of the anterior descending branch of the left coronary artery, can decrease the incidence of necrosis and increase the rate of regeneration for healthy cellular and fibrous connective tissue in the infarct region [182]. Rats with induced aortal stenosis which are treated with... 

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