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Pathobiology, not angiography, should guide managementin acute coronary syndrome/non–ST-segment elevation myocardial infarction

The non-interventionist’s perspective

^* Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio, USA

View larger version (162K): [in a new window]   Figure 1 Angiogram of complex lesion of right coronary artery. Several features make this artery difficult to evaluate by angiography. The lesion is complex with a bulbous projection that is difficult to quantitate. In addition, there is uncertainty regarding which segment to consider normal for comparative purposes.

View larger version (131K): [in a new window]   Figure 2 Coronary remodeling concealing extensive disease. Intravascular ultrasound cross-sections from four sites (A, B, C, and D) are shown. At each site, there is extensive atherosclerosis, but without luminal encroachment. Comparing lumen size from the least diseased segment, D, to the most diseased segments, A and B, there is no change in lumen size.

View larger version (70K): [in a new window]   Figure 3 Diffuse disease masquerading as a normal artery. Two sites, A and B, are shown by intravascular ultrasound. At both sites, a diffuse, concentric and symmetrical plaque involves the entire vessel circumference, giving the false appearance of a normal artery.

View larger version (93K): [in a new window]   Figure 4 Positive remodeling in a ruptured plaque. A ruptured plaque (right) is shown, along with a relatively normal adjacent reference segment (left). In the right panel, an interruption of the fibrous cap can be seen with exposure of the underlying lipid core. Compared with the normal reference segment, the external elastic membrane (EEM) area is considerably larger in the segment with plaque rupture than in the adjacent normal reference segment.

View larger version (92K): [in a new window]   Figure 5 The non-stenotic lesion as culprit. A patient with unstable angina was examined by coronary angiography and intravascular ultrasound (IVUS). The right coronary angiogram (far left, top panel) shows a right coronary artery lesion that was subsequently stented (far left, bottom panel). The IVUS examination of the mildly diseased left circumflex (middle panel) reveals a site (black arrow) that by IVUS (far right panel) shows a fresh plaque rupture (cavity from 12 to 2 o’clock).

View larger version (101K): [in a new window]   Figure 6 Coronary disease in a 33-year-old transplant donor. The left anterior descending (left) and circumflex (right) show significant atherosclerosis in a previously asymptomatic young man who was a transplant donor after a motor vehicle accident.

View larger version (19K): [in a new window]   Figure 7 Prevalence of coronary disease in transplant donors. These data demonstrate an aggressive increase in the likelihood of an atheroma of at least 0.5 mm in thickness in individuals as young as 13 years of age. yrs. = years. Tuzcu EM, Kapadia SR, Tutar E, et al High prevalence of coronary atherosclerosis in asymptomatic teenagers and young adults: evidence from intravascular ultrasound. Circulation 2001;103:2705–10. Adapted with permission from Lippincott, Williams, and Wilkins.

View larger version (97K): [in a new window]   Figure 8 Plaque rupture by intravascular ultrasound (IVUS). Two adjacent sites in the coronary artery of a patient with an acute myocardial infarction are shown. In the right panel, the IVUS catheter is in a small lumen separated by a fibrous cap from a large lipid core. In this example, the lipid core is no longer present, and there is blood flow through the center of this atherosclerotic plaque. In the left panel, rupture of the fibrous cap can be seen at approximately 12 o’clock, and the underlying lipid core has apparently escaped after plaque rupture.

View larger version (104K): [in a new window]   Figure 9 Stable and vulnerable coronary atheromata. In the left panel, a lesion with a thick fibrous core and small lipid core is illustrated. The right panel shows a lesion in a different patient with a thin fibrous cap and a large lipid core. The left hand plaque might be termed "stable" and the right hand plaque "vulnerable" based on pathological criteria.