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Laser revascularisation.

Abstract

Patients who present with angina pectoris due to underlying coronary artery disease which is not controlled by medical therapy, and who have disease which is not amenable to conventional forms of revascularisation, present an increasing clinical problem. Laser techniques have been introduced to improve myocardial perfusion in this group of patients. The surgical technique of transmyocardial laser revascularisation has been evaluated in this patient population. Generally, there has been a good symptomatic response in terms of improvement in angina, and in some studies an increase in exercise capacity. The technique, however, does carry significant morbidity and mortality. More recently, a catheter-based technique has been introduced--percutaneous myocardial laser revascularisation. This technique seems to improve symptoms of angina, produce an increase in exercise capacity, with a much more favourable procedural risk profile.

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BibTeXRIS

S C Clarke, P M Schofield. 2001. Laser revascularisation.. https://doi.org/10.1093/bmb%2F59.1.249

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Intravascular ultrasound analysis of infarct-related and non-infarct-related arteries in patients who presented with an acute myocardial infarction.

BACKGROUND: Previous studies have reported diffuse destabilization of atherosclerotic plaques in acute myocardial infarction (AMI). METHODS AND RESULTS: We used intravascular ultrasound (IVUS) to assess 78 coronary arteries (38 infarct-related arteries [IRAs] with culprit and nonculprit lesions and 40 non-IRAs) from 38 consecutive AMI patients. IVUS analysis included qualitative and quantitative measurements of reference and lesion external elastic membrane (EEM), lumen, and plaque plus media (P&M) area. Positive remodeling was defined as lesion/mean reference EEM >1.0. Culprit lesions were identified by a combination of ECG, wall motion abnormalities (ventriculogram or echocardiogram), scintigraphic perfusion defects, and coronary angiogram. Culprit lesions contained more thrombus (23.7% versus 3.4% in nonculprit IRA plaques and 3.1% in non-IRA plaques; P=0.0011). Culprit lesions were predominantly hypoechoic (63.2% versus 37.9% of nonculprit IRA plaques and 28.1% of non-IRA plaques; P=0.0022). Culprit lesions were longer (17.5+/-10.1, 9.8+/-4.0, and 10.3+/-5.7 mm, respectively; P<0.0001), had larger EEM area (15.0+/-6.0, 11.5+/-5.7, and 12.6+/-5.6 mm2, respectively; P=0.0353) and P&M area (13.0+/-6.0, 7.5+/-3.7, 9.3+/-4.3 mm2, respectively; P<0.0001), smaller lumens (2.0+/-0.9, 4.1+/-3.1, and 3.4+/-2.5 mm2, respectively; P=0.0009), and more positive remodeling (79.4%, 59.0%, and 50.8%, respectively; P=0.0155). The frequency of plaque rupture/dissection was greater in culprit, nonculprit IRA, and non-IRA plaques in AMI patients than in a control group of chronic stable angina patients with multivessel IVUS imaging. CONCLUSIONS: Culprit plaques have more markers of instability (thrombus, positive remodeling, and large plaque mass); however, these markers of instability are not typically found elsewhere. This suggests that the vascular event in AMI patients is determined by local pre-event lesion morphologies.

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