Michael R. Chester

Differential progression of complex and smooth stenoses within the same coronary tree in men with stable coronary artery disease

OBJECTIVES We sought to compare the evolution of complex and smooth stenoses within the same coronary tree in patients with stable coronary artery disease. BACKGROUND Progression of coronary stenosis has prognostic significance and may be influenced by local and systemic factors. Stenosis morphology is a determinant of disease progression, but no previous study has systematically assessed progression of complex and smooth stenoses within the same patient. METHODS We studied 50 men with stable angina who 1) had one complex coronary stenosis and one smooth stenosis in different noninfarct-related coronary vessels at initial coronary angiography, and 2) had a second angiogram after a median interval of 9 months (range 3 to 24). Patients with lesions > or = 10 mm long, at a major branching point or with > 85% diameter reduction were not included. Coronary lesions were measured quantitatively from comparable end-diastolic frames. Stenosis morphology was determined qualitatively by two independent observers. RESULTS All patients remained in stable condition during follow-up. Progression, defined as an increase in diameter stenosis by > or = 15% was seen in only eight complex stenosis (16%) but in no smooth lesions (p < 0.01). The severity of complex stenoses changed more than that of corresponding smooth stenoses (mean +/- 1 SD 5.8 +/- 13% vs. -0.06 +/- 6%, p < 0.01). On average, the annual rate of growth was 11.4 +/- 28% and 1.5 +/- 14% for complex and smooth lesions, respectively (p < 0.01). CONCLUSIONS Few coronary stenoses progress rapidly in stable angina. Complex and smooth coronary stenoses progress at different rates within the same coronary tree. complex stenosis morphology itself is an important determinant of progression of stenosis in patients with apparently clinically stable coronary artery disease.

Differential progression of complex culprit stenoses in patients with stable and unstable angina pectoris

OBJECTIVES This study sought to compare the evolution of complex culprit stenoses in patients with stable and those with unstable angina pectoris. BACKGROUND Complex coronary stenoses are associated with adverse clinical and angiographic outcomes. However, it is not known whether the evolution of complex stenoses differs in unstable angina versus stable angina pectoris. METHODS We prospectively assessed stenosis progression in 95 patients with unstable angina whose angina stabilized with medical therapy (Group 1) and 200 patients presenting with stable angina (Group 2). After diagnostic angiography, all patients were placed on a waiting list for coronary angioplasty and restudied at 8 +/- 4 (mean +/- SD) months later. In each patient the presumed culprit stenosis was identified and classified as complex (irregular borders, overhanging edges or thrombus) or smooth (absence of complex features). Stenosis progression, as assessed by computerized angiography, was defined as > or = 20% diameter reduction or new total occlusion. RESULTS At the first angiogram, 364 stenoses > or = 50% and 383 stenoses < 50% were identified. At restudy, 36 (15%) of 236 stenoses progressed in 29 Group 1 patients and 36 (7%) of 502 stenoses in 31 Group 2 patients (p = 0.001). Forty-five (88%) of 51 stenoses > or = 50% and 6 (29%) of 21 stenoses < 50% that progressed developed to total coronary occlusion (p = 0.001). More culprit stenoses progressed in Group 1 than in Group 2 (p = 0.006), whereas progression of nonculprit stenoses was not significantly different in both groups. Culprit complex stenoses progressed more frequently in Group 1 than in Group 2 (p = 0.01). During follow-up, 3 patients died (myocardial infarction), and 51 had a nonfatal coronary event. Culprit stenoses progressed in 15 (54%) of the 28 patients with a nonfatal coronary event in Group 1 and in 9 (39%) of 23 patients in Group 2 (p = NS). Complex morphology (p < 0.001) and unstable angina at initial presentation (p < 0.01) were predictive factors for progression of culprit stenoses. CONCLUSIONS A larger proportion of culprit complex stenoses progress in unstable angina than stable angina, and this is frequently associated with recurrence of coronary events.

The natural history of unheralded complex coronary plaques

OBJECTIVES This study sought to assess the behavior of unheralded complex lesions in patients with no previous history of acute coronary ischemia. BACKGROUND Angiographically complex coronary stenoses appear to originate from plaque disruption and are associated with rapid progression early and late after acute coronary events. Complex lesions may occur without symptoms, but neither the incidence nor the behavior of these unheralded complex lesions is known. METHODS We studied 222 patients with chronic stable angina who were on a waiting list for single-vessel percutaneous transluminal coronary angioplasty of an unoccluded lesion and underwent repeat angiography immediately before the procedure as part of routine practice or shortly after a coronary event. Patients with a previous episode of myocardial infarction or unstable angina were not included. Angiograms were analyzed quantitatively and qualitatively using established methods. A change of +/- 15% stenosis severity or total coronary occlusion defined categoric change. RESULTS At first angiography, there were 52 unheralded complex target lesions (23%) and 170 smooth target stenoses (77%). Stenosis severity did not differ between complex and smooth target lesions at first and second angiography at a mean (+/- SD) interval of 7 +/- 4 months. At follow-up, seven complex lesions had progressed (14%) compared with six smooth lesions (4%, p < 0.02). Total occlusion developed in four complex lesions and one smooth lesion. Overall, complex stenoses progressed by 3 +/- 13% compared with 0.5 +/- 7% in the smooth stenoses (p = 0.15). Complex stenoses were 4.2 times more likely to progress than smooth stenoses (95% confidence interval 1.2 to 15.2 [Cornfields method]). Clinical events developed in seven patients. One complex lesion regressed and became smooth, and three smooth stenoses became complex at follow-up. CONCLUSIONS Morphologically complex stenosis can develop without an episode of acute coronary ischemia and are relatively common in patients awaiting single-vessel angioplasty. Our study demonstrates that like their clinically heralded counterparts, these unheralded complex stenoses are at higher risk of progression than smooth stenoses.

Complex stenosis morphology predicts late reocclusion during follow-up after myocardial infarction in patients with patent infarct–related coronary arteries☆☆☆★★★♢

BACKGROUND Whether angiographic morphology of infarct-related residual stenoses continues to affect prognosis after discharge is not known. METHODS We studied 175 patients after their myocardial infarction who required nonurgent coronary angioplasty for residual myocardial ischemia. The findings at diagnostic coronary angiography were compared with those before angioplasty (mean of 7 months later). Infarct-related stenoses were classified as complex or smooth. Stenosis progression was defined as >0.5 mm diameter reduction. RESULTS One hundred twenty-one (69%) infarct-related stenoses were complex. At restudy, total occlusion was found in 41 (35%) of the infarct-related complex stenoses compared with 7 (13%) smooth stenoses (P = .001). Reocclusion occurred in 16 (55%) of 29 complex infarct-related stenoses with thrombus, compared with 25 (28%) of 88 without thrombus (P = .01). During follow-up, 46 patients (26%) had cardiac events. Of these, 70% had complex lesions at study entry compared with 30% smooth (P < .05). CONCLUSIONS Residual angiographically complex stenoses after an uncomplicated myocardial infarction are associated with a greater risk of reocclusion and may predispose to coronary events at follow-up.