Lijia Chen

Rapid Angiographic Progression of Coronary Artery Disease in Patients With Angina Pectoris The Role of Complex Stenosis Morphology

BACKGROUNDnRapid disease progression commonly underlies acute coronary events, and complex stenosis morphology may play a role in this phenomenon.nnnMETHODS AND RESULTSnWe studied the role of complex stenosis morphology in rapid disease progression in 94 consecutive patients awaiting routine coronary angioplasty. Coronary arteriography was repeated at 8 +/- 3 months follow-up, immediately preceding angioplasty (68 patients) or after an acute coronary event (26 patients). Disease progression of 217 stenoses, of which 79 (36%) were complex and 138 (64%) were smooth, was assessed by computerized angiography. At presentation, 63 patients had stable angina pectoris and 31 had unstable angina that settled rapidly with medical therapy. At follow-up, 23 patients (24%) had progression of preexisting stenoses and 71 (76%) had no progression. Patients with progression were younger (55 +/- 12 years) than those without (58 +/- 9 years) but did not differ with regard to risk factors, previous myocardial infarction, or severity and extent of coronary disease. Twenty-three lesions (11%) progressed, 15 to total occlusion (11 complex and 4 smooth; 65%). Progression occurred in 17 of the 79 complex stenoses (22%) and in 6 of the 138 smooth lesions (4%) (P = .002). Mean stenosis diameter reduction was also significantly greater in complex than in smooth lesions (11.6% versus 3.9% change; P < .001). Acute coronary events occurred in 57% of patients with progression compared with 18% of those without progression (P < .001) and were more frequent in patients who presented with unstable angina (P = .002).nnnCONCLUSIONSnRapid stenosis progression is not uncommon, and complex stenoses are at risk more than smooth lesions.

Angiographic Stenosis Progression and Coronary Events in Patients With ‘Stabilized’ Unstable Angina

BACKGROUNDnRecent studies suggest that angiographically complex coronary stenoses are associated with an adverse short-term outcome. It is not known, however, if this applies to unstable angina patients who stabilize on medical therapy.nnnMETHODS AND RESULTSnWe prospectively studied 85 consecutive patients with unstable angina who stabilized on medical therapy but were found to require angioplasty for treatment of obstructive coronary disease. Angiography was carried out at admission, and patients were restudied 8 +/- 4 months (mean +/- SD) after the first angiogram. Ischemia-related stenoses were identified and classified as complex (irregular borders, overhanging edges, or thrombus) or smooth (absence of complex features). Stenosis progression (> or = 20% diameter reduction or new total occlusion) was assessed by automated edge detection. At initial angiography, there were 198 stenoses (> or = 50%, 102), of which 85 (54 complex and 31 smooth) were ischemia related. At restudy, 21 ischemia-related stenoses and 8 non-ischemia-related stenoses progressed (25% versus 7%, P = .001). Seventeen of the 21 ischemia-related stenoses that progressed developed into total occlusion compared with 3 of the 8 non-ischemia-related stenoses (P = .02). Changes in average stenosis severity and in absolute stenosis diameter were significantly larger in ischemia-related stenoses than in non-ischemia-related stenoses (P = .03). Eighteen (34%) complex stenoses progressed, compared with 3 (10%) smooth lesions (P = .02). During follow-up, 1 patient died (myocardial infarction) and 25 patients had nonfatal coronary events that were associated with progression of ischemia-related stenoses in 14 (56%).nnnCONCLUSIONSnIn unstable angina patients who stabilize medically, subsequent short-term stenosis progression and coronary events are common. The unstable coronary lesion (particularly complex stenoses) is often not stabilized and will continue to progress over the ensuing months.

Effects of angiotensin-converting enzyme inhibition on exercise-induced angina and ST segment depression in patients with microvascular angina

OBJECTIVESnThis study was conducted to test the hypothesis that angiotensin-converting enzyme inhibition may lessen myocardial ischemia in patients with microvascular angina.nnnBACKGROUNDnPatients with syndrome X (angina pectoris, positive findings on exercise testing and normal coronary arteriogram) have a reduced coronary vasodilator reserve (microvascular angina) and may show an increased sympathetic drive. Angiotensin-converting enzyme inhibition attenuates sympathetic coronary vasoconstriction in patients with coronary artery disease.nnnMETHODSnTen patients (seven women and three men, mean age [+/- SD] 53 +/- 6 years) with syndrome X and a reduced coronary flow reserve underwent a randomized, single-blind, crossover, placebo-controlled study of the effects of the angiotensin-converting enzyme inhibitor enalapril on angina and exercise-induced ST segment depression. Assessment was by symptom-limited treadmill exercise testing after 2 weeks of treatment with 10 mg/day of enalapril and after 2 weeks of placebo administration.nnnRESULTSnAll patients had positive findings on exercise testing (> or = 1 mm ST segment depression and angina) while taking placebo, whereas six patients had a positive test result (four with angina) during enalapril therapy. Total exercise duration and time to 1 mm of ST segment depression were prolonged by enalapril over those obtained with placebo (mean 779 +/- 141 vs. 690 +/- 148 s, p = 0.006 and 690 +/- 204 vs. 485 +/- 241 s, p = 0.007, respectively). The magnitude of ST segment depression was also less with enalapril than with placebo (mean 1.1 +/- 0.4 vs. 1.5 +/- 0.2 mm, p = 0.004). Heart rate and blood pressure at peak exercise and at 1 mm of ST depression were not significantly different during placebo and enalapril treatment.nnnCONCLUSIONSnAngiotensin-converting enzyme inhibition lessens exercise-induced ischemia in patients with syndrome X and microvascular angina, probably by a direct modulation of coronary microvascular tone, which results in an increased myocardial oxygen supply.

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

OBJECTIVESnWe sought to compare the evolution of complex and smooth stenoses within the same coronary tree in patients with stable coronary artery disease.nnnBACKGROUNDnProgression 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.nnnMETHODSnWe 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.nnnRESULTSnAll 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).nnnCONCLUSIONSnFew 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.

The natural history of unheralded complex coronary plaques

OBJECTIVESnThis study sought to assess the behavior of unheralded complex lesions in patients with no previous history of acute coronary ischemia.nnnBACKGROUNDnAngiographically 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.nnnMETHODSnWe 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.nnnRESULTSnAt 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.nnnCONCLUSIONSnMorphologically 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.

Rapid angiographic progression of “target” and “nontarget” stenoses in patients awaiting coronary angioplasty

OBJECTIVESnOur aim was to compare the short-term evolution of target versus nontarget stenoses in patients awaiting coronary angioplasty.nnnBACKGROUNDnCoronary angioplasty is effective therapy for angina pectoris, but coronary events occur after successful angioplasty that are caused by both restenosis and progression of mild preexisting nontarget stenoses.nnnMETHODSnWe prospectively studied 161 consecutive patients with stable angina (124 men and 37 women). After diagnostic angiography, target stenoses for angioplasty and nontarget lesions were identified. Patients were put on a routine waiting list and followed up regularly until repeat coronary arteriography was performed (mean +/- SD 7 +/- 3 months), either immediately before angioplasty (138 patients) or soon after an acute coronary event (23 patients), if one occurred. Stenosis diameter was measured by using computerized arteriography. Progression of disease was defined as > or = 20% lesion diameter reduction, new total occlusion or development of a new stenosis > or = 30%.nnnRESULTSnAt study entry, the mean diameter of target (n = 207) and nontarget (n = 184) lesions was 68 +/- 9% and 38 +/- 9%, respectively (p < 0.001). Disease progression occurred in 33 patients (20%). Seven new lesions (one total occlusion) developed. Eighteen target (9%) and 15 nontarget (8%) stenoses progressed. The power of the study to detect a difference of 1% between the risks of progression of target and nontarget stenoses with a 90% probability was < 0.1. Total occlusion developed in 15 (83%) of the 18 target and 6 (40%) of the 15 nontarget stenoses (p = 0.03). During follow-up, a myocardial infarction developed in 3 patients (2%) and unstable angina in 20 (12%). These coronary events were associated with progression of target stenoses in 10 patients and nontarget stenoses in 7 and with the development of new lesions in 1. In five patients coronary events were not associated with stenosis progression.nnnCONCLUSIONSnDespite differences in baseline severity, a similar proportion of target and nontarget lesions progressed rapidly. However, target stenoses were more likely than nontarget lesions to progress to total occlusion. Progression of nontarget stenoses may contribute to recurrence of angina and new coronary events after successful angioplasty and should be considered when developing strategies aimed at improving outcome after angioplasty.

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

BACKGROUNDnWhether angiographic morphology of infarct-related residual stenoses continues to affect prognosis after discharge is not known.nnnMETHODSnWe 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.nnnRESULTSnOne 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).nnnCONCLUSIONSnResidual 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.

768-5 Evolution of Infarct-related Stenoses After Clinical Stabilization

The evolution of infarct-related stenoses (IRS) was prospectively studied in 106 patients (pts) with myocardial infarction (MI) after clinical stabilization. All pts underwent diagnostic angiography (6xa0±xa05 months after MI, range 1 to 25) and were put on a routine waiting list for PTCA of the IRS. Coronary angiography was repeated (8xa0±xa04 months after first angiogram) immediately preceding PTCA (79 pts) or soon after the occurrence of coronary events (MI: 6 pts, unstable angina: 21 pts). IRS was identified and classified as “complex” (irregular borders, overhanging edges, orintracoronarythrombus) or “smooth”. Stenosis progression, assessed by computerized angiography, was defined asxa0g20% diameter reduction or new total occlusion and regression as g20% decrease in severity. At initial angiography, there were 279 stenoses (≥50:138,xa0l50%:141). Of 106 IRS, 74 (70%) were complex and 32 (30%) were smooth. At restudy, 24 of 106 IRS had progressed compared with 9 of 173 non-IRS (23% vs. 5%, pxa0=xa00.001). Twenty-two of the 24 IRS and 3 of 9 of non-IRS that had progressed developed into total occlusion (92% vs. 33%, Pxa0=xa00.01). Twenty-two of 74 complex IRS progressed, compared with only 2 of 32 smooth IRS (30% vs. 6%, Pxa0=xa00.008). During follow up, coronary events occurred in 27 pts, of which 15 (56%) were associated with IRS progression. Remoulding of stenosis morphology (from complex to smooth) was found in 8 patients (resolution of thrombus or ulceration), of these 3 were associated wilh stenosis regression. Pts age, gender, coronary disease risk factors, number of diseased vessel, anti platelet and antithrombotic therapy, interval between onset of MI and diagnostic angiogram, and interval between the 2 coronary angiograms were not associated with IRS progression. Changes of percent stenosis (%) and minimal stenosis diameter (mm) in the different subgroups were as following: 1st angio (%) 2nd anglo (%) Δ (%) 1st angio (mm) 2nd angio (mm) Δ (mm) IRS 66.2xa0±xa06.6 72.8xa0±xa016.9 * 6.6xa0±xa015.8 1.15xa0±xa00.28 0.91xa0±xa00.52 * 0.24xa0±xa00.47 non-IRS 44.6xa0±xa014.5 48.0xa0±xa015.8 * 3.4xa0±xa012.2 § 1.71xa0±xa00.50 1.61xa0±xa00.53 * 0.10xa0±xa00.31 § Com IRS 66.9xa0±xa07.1 76.5xa0±xa016.3 * 9.6xa0±xa017.2 1.13xa0±xa00.28 0.79xa0±xa00.54 * 0.34xa0±xa00.51 Smo IRS 64.8xa0±xa05.3 65.5xa0±xa012.1 0.71xa0±xa010.6 † 1.18xa0±xa00.27 1.13xa0±xa00.38 0.05xa0±xa00.30 † Data are meanxa0±xa0SD. * pxa0lxa00.01 vs. 1st angio by paired t-test; § pxa0lxa00.05 vs. IRS. and † pxa0lxa00.01 vs. Com IRS by unpaired t-test. Comxa0=xa0complex. Smoxa0=xa0smooth Despite clinical stabilization, IRS are unstable and at high risk for rapid progression to total occlusion, which is usually associated with coronary events.

812-21 Angiographic Progression of Inactive Unstable Plaque versus Stable Plaque in Patients with Stable Angina

The angiographic progression of ischemia-related stenoses (IRS) and non-IRS stenoses was prospectively assessed in 256 patients (pts) with stable angina (stable symptoms for at least 3 months) using computerized angiography. IRS were categorized as inactive unstable plaque (IRS which was responsible for a previous (g3 months) episode of unstable angina) in 76 pts (Group 1) and stable plaque (IRS which was not associated with a previous acute episode) in the remaining 180 pts (Group 2.). Following diagnostic angiography, pts were put on a waiting list for PTCA and restudied (8xa0±xa03 months after first angiogram) immediately preceding PTCA (230 pts) or soon after occurrence of coronary events (MI in 9 pts, unstable angina in 17 pts). IRS were complex (irregular borders, overhanging edges or introcoronary thrombus) in 40 of 76 (55%) inactive unstable plaques and 25 of 180 (21%1 stable plaques (pxa0lxa00.001). Stenosis progression (g20% diameter reduction or new total occlusion) and coronary events occurred more frequently in Group 1 than in Group 2 (26% vs. 11%, pxa0=xa00.01 and 17% vs. 7%, pxa0=xa00.02, respectively). IRS progressed in 14 pts of Group 1 and 9 pts of Group 2 (18% vs. 5%, pxa0=xa00.001). Progression of non-IRS (15 of 404 (4%)) was similar in Groups 1 and 2 (5% vs. 5%). Pts of Group 1 were younger than patients of Group 2 (55xa0±xa08 vs. 59xa0±xa010 (years). pxa0=xa00.002). Pts gender, risk factors, multivessel disease, baseline severity of IRS were not associated with IRS progression. Multiple regression analysis showed that inactive unstable plaque, angiographic complex morphology, and coronary events independently predicted IRS progression (pxa0=xa00.03, pxa0=xa00.02, and pxa0=xa00.0001, respectively). Change of percent stenosis (%) and minimal stenosis diameter (mm) in different subgroups were as following: 1st angio (%) 2nd angio (%) Δ (%) 1st angio (mm) 2nd angio (mm) Δ (mm) IRS in G1 66.3xa0±xa06.9 72.3xa0±xa015.3 * 6.0xa0±xa014.7 1.14xa0±xa00.26 0.88xa0±xa00.49* 0.26xa0±xa00.46 IRS in G2 65.6xa0±xa017.5 66.6xa0±xa011.0 † 1.0xa0±xa09.4 § 1.14xa0±xa00.28 1.10xa0±xa00.37 * 0.04xa0±xa00.28§ non-IRS in Gl 44.3xa0±xa012.2 46.6xa0±xa013.8 * 2.3xa0±xa095 1.69xa0±xa0045 1.59xa0±xa00.48 * 0.10xa0±xa00.32 non-IRS in G2 44.1xa0±xa013.2 46.3xa0±xa012.6 * 2.2xa0±xa010.1 1.71xa0±xa00.45 1.63xa0±xa00.50 * 0.08xa0±xa00.31 Data are mean ± SD. G = Group, Angio = angiogram * pxa0lxa00.01 † pxa0lxa00.05 vs 1st angio by paired t-test § pxa0lxa00.001 vs IRS in Gl by unpaired t-test In pts with stable angina, inactive unstable plaques, and stenoses with complex morphology are predictors of rapid progression. Our results may be of clinical and pathophysiological relevance.

812-3 Angiographic Evidence for Frequent “Silent” Plaque Disruption In Patients with Stable Angina

Histopathological studies of human coronary atheroma (post mortem and atherectomy) suggest that acute coronary syndrome (ACS) may be the extreme end of a spectrum of outcomes from intimal plaque disruption and that “silent” plaque disruption is much more common in the population than would be predicted from the incidence of ACS. It is generally held that angiographic complex coronary stenoses represent previous plaque disruption. We therefore assessed the incidence of angiographic complex plaques in 295 consecutive patients (pts) presenting with moderate to severe stable angina for single vessel PTCA. Two groups were compared: pts with a previous episode of ACS and pts without previous ACS. Results There were no clinical or biochemical differences between groups. Complex stenosis severity was (mean ± 1SD) 67xa0±xa08% in both groups using quantitative coronary angiography. Angiographic morphology Clinical features Smooth Complex n p Previous ACS 35 (38%) 56 (62%) 0.0001 No previous ACS 151 (74%) 53 (26%) Conclusion There is a relatively high incidence (26%) of angiographically complex plaques in clinically stable patients with no previous clinical evidence of acute coronary syndrome. This indicates that clinically “silent” plaque disruption is common.