CHARACTERIZATION OF THE UNSTABLE LESION BY ANGIOGRAPHY, ANGIOSCOPY, AND INTRAVASCULAR ULTRASOUND

doi:10.1016/S0733-8651(05)70076-X

Cardiology Clinics

Volume 17, Issue 2, 1 May 1999, Pages 295-305

https://doi.org/10.1016/S0733-8651(05)70076-X Get rights and content

Acute coronary syndromes are a spectrum of clinical presentations with various pathophysiology substrates. As such it is impossible to talk about one type of atherosclerotic lesion being solely responsible for stable or unstable angina or acute myocardial infarction. Although atherosclerosis is a diffuse disease, with the ability to image the coronary tree in vivo and perform angioplasty of a diseased segment, focus has shifted to understanding the events occurring at the site of an individual lesion responsible for a clinical syndrome. This has resulted in efforts to detect and characterize the culprit lesion in order to (1) understand the pathophysiology of coronary artery disease and (2) potentially individualize treatment with lesion-specific strategies that may improve long-term outcomes and reduce costs. It is hoped that a better understanding of lesions and mechanisms that cause acute coronary syndromes may lead to improved therapies and ultimately to preventive strategies that will save lives, by identifying those plaques that are vulnerable to disruption and thrombosis. Most of the information available regarding the characteristics of coronary culprit lesions come from studies using angiography, angioscopy, and intracoronary ultrasound. Each method carries its own advantages and limitations and has been strengthened by information derived from histopathologic studies that validate and complement their findings. Integration of knowledge from all these sources continues to help clinicians and scientists understand the processes that lead to unstable coronary syndromes.

Section snippets

WHAT HAVE WE LEARNED FROM HISTOPATHOLOGIC ANALYSES?

Before angiography became widely used, a significant amount of evidence regarding the pathogenesis of acute coronary syndromes had been accumulated from postmortem studies. The first reports date back to the beginning of the century, when pathologists described the histologic findings in patients who died of angor pectoris. The most consistent finding was that of intracoronary thrombosis with myocardial necrosis.48, 49 From then on, the term coronary thrombosis was adopted to describe the

ASSESSMENT OF CULPRIT LESIONS BY ANGIOGRAPHY

Coronary angiography was the first available method to study coronary arteries in vivo and has been the primary source of information regarding the lesions underlying coronary syndromes. Levin and Fallon³⁹ performed histopathologic correlations of angiographic lesion morphologies in autopsy studies, and reported that angiographic features of irregular borders or intraluminal lucencies correspond histologically to disrupted plaques with hemorrhage and partially occluding or recanalized thrombus,

ASSESSMENT OF CULPRIT LESIONS BY ANGIOSCOPY

Intracoronary angioscopy provides an extraordinary instrument to define in vivo the surface features of lesions causing acute coronary syndromes. It allows direct visualization of macroscopic disruption (ulcerations, tears, and fissures); lesion color; and the presence of thrombus (Fig. 3). The surface color of a plaque can provide information regarding its content and degree of instability. Thieme et al⁵⁷ performed histopathologic analysis of coronary lesions that were imaged before

ASSESSMENT OF CULPRIT LESIONS BY INTRACORONARY ULTRASOUND

Intracoronary ultrasound devices make it possible to study in vivo atherosclerotic lesions beneath their intimal surface and perform rudimentary tissue characterization as established by multiple studies with histologic correlations.5, 47, 50 Plaques with extracellular lipid or necrotic material display minimal reflectivity and typically appear as hypoechoic areas. Fibrous plaques produce echodense images that are intermediate between the media or lipid, which are hypoechoic, and the more

CONCLUSION

Newer imaging techniques, such as intracoronary angioscopy and ultrasound, have added valuable information to histopathologic and angiographic data regarding the characteristics of unstable coronary plaques. Although there has been considerable progress, we are far from having a complete view of the puzzle that is understanding of the pathophysiologic mechanisms of acute coronary syndromes and atherosclerotic plaque behavior. The culprit lesion in acute myocardial infarction seems to have a

ACKNOWLEDGMENT

The author would like to acknowledge Dr. Richard W. Nesto and Dr. James E. Muller, with whom I have exchanged ideas over the years, and whose points of view have helped me shape my own.

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The electrocardiogram (ECG) remains the most immediately accessible and widely used diagnostic tool for guiding emergency treatment strategies. The ECG recorded during acute myocardial ischemia is of diagnostic, therapeutic, and prognostic significance. In patients with myocardial ischemia as a result of decreased blood supply, the initial 12-lead ECG typically shows (1) predominant ST-segment elevation (STE) as part of STE acute coronary syndrome (STE-ACS), or (2) no predominant STE, that is, non–STE ACS (NSTE-ACS). Patients with predominant STE are classified as having either aborted myocardial infarction (MI) or ST-elevation MI (STEMI) based on the absence or presence of biomarkers of myocardial necrosis. The MI may be aborted either by spontaneous or therapeutic reperfusion of the ischemic myocardium before development of myocardial cell necrosis. NSTE-ACS patients are classified as having either unstable angina or NSTE-MI, based also on the absence or presence of biomarkers of mycardial necrosis.
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Development of vulnerable lesion may take place simultaneously at many sites of coronary vasculature, therefore causing multisite instability. The prevalence of the phenomenon in stable angina (SA) patients remains unknown.
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: Address reprint requests to: Sergio Waxman, MD, Beth Israel Deaconess Medical Center, 110 Francis Street, Suite 4B, Boston, MA 02215, e-mail: [email protected]

^*: Division of Cardiology, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, Massachusetts

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CHARACTERIZATION OF THE UNSTABLE LESION BY ANGIOGRAPHY, ANGIOSCOPY, AND INTRAVASCULAR ULTRASOUND

Section snippets

WHAT HAVE WE LEARNED FROM HISTOPATHOLOGIC ANALYSES?

ASSESSMENT OF CULPRIT LESIONS BY ANGIOGRAPHY

ASSESSMENT OF CULPRIT LESIONS BY ANGIOSCOPY

ASSESSMENT OF CULPRIT LESIONS BY INTRACORONARY ULTRASOUND

CONCLUSION

ACKNOWLEDGMENT

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Am J Cardiol

Plaque characterization of atherosclerotic coronary arteries by intravascular ultrasound

Echocardiography

Angiographic occurrence and clinical correlates of intraluminal coronary artery thrombus: Role of unstable angina

J Am Coll Cardiol

Incomplete lysis of thrombus in the moderate underlying atherosclerotic lesion during intracoronary infusion of streptokinase for acute myocardial infarction

Circulation

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Circulation