Influence of coronary collateral vessels on myocardial infarct size in humans. Results of phase I thrombolysis in myocardial infarction (TIMI) trial. The TIMI Investigators.

Abstract

the TIMI Investigators* Background. The influence of coronary collateral vessels on infarct size in humans remains controversial, partly because no previous study has examined the impact of collaterals present at the onset of acute myocardial infarction on infarct size.

Impact of Severity of Coronary Artery Stenosis and the Collateral Circulation on the Functional Outcome of Dyssynergic Myocardium After Revascularization in Patients With Healed Myocardial Infarction and Chronic Left Ventricular Dysfunction

“…In the latter group of patients, acute coronary occlusion results in evolutional changes in LV function that are dependent on myocardial flow after recanalization by thrombolysis or through collaterals to occluded arteries. 11,13,15 However, in our study of patients with chronic LV dysfunction, the anatomic status of the infarct-related artery may not represent the status in the critical early phase of a myocardial infarction. Coronary artery occlusion may have developed gradually, allowing for the development of adequate collateral channels that may or may not be visualized with routine angiography.…”

“…10 Significant coronary artery disease was defined as a diameter stenosis ¢50%. Collateral channels to completely occluded coronary arteries were assessed by observing the degree of opacification distal to the occlusion and was graded using the Thrombolysis in Myocardial Infarction (TIMI) trial classification 5,11 : grade 1, absent filling to the distal vessel; grade 2, minimal, in case of faint opacification of the distal vessel or visualisation of a small vessel; and grade 3, well-developed collaterals with visualization and dense opacification of the entire distal vessel. Coronary arteries were assigned to particular echocardiographic myocardial segments as previously described.…”

Insulin activates hypoxia-inducible factor-1α in human and rat vascular smooth muscle cells via phosphatidylinositol-3 kinase and mitogen-activated protein kinase pathways: impairment in insulin resistance owing to defects in insulin signalling

“…Clinical medicine shows that a successful development of collateral arteries and new capillaries in ischaemic tissues can prevent myocardial infarction and lead to limb salvage [46], whereas defective angiogenesis and arteriogenesis promote cardiovascular events [47,48]. It has been proposed that one possible reason for this kind of vascular dysfunction can be the impairment of the growth factor system involved in new vessel formation, the so-called 'growth factor dysfunction' [49].…”

Obesity is associated with impaired coronary collateral vessel development

“…3 It was found that patients with angiographically documented coronary artery disease, who develop collateral vessels, had a higher prevalence of myocardial ischaemia than those without collateral vessels, indicating that the presence of myocardial ischaemia is associated with the growth of collateral vessels. 16 The presence of adequate collateral vessels feeding the myocardial area at risk may limit the infarct size following coronary occlusion 17 and may even provide a survival benefit. 18 In our study, we found that patients with BMIZ30 kg/m 2 , who are known as 'obese' through this definition, but without overt diabetes mellitus, have reduced collateral vessel development compared to patients with BMIo25 kg/ m 2 , known as 'normal', even though the mean number of diseased vessels, degree of coronary artery stenosis, distribution of sex, mean age and duration of anginal symptoms were not significantly different between groups.…”