The relationship between periprocedural myocardial infarction and subsequent target vessel revascularization following percutaneous coronary revascularization: insights from the EPIC trial. Evaluation of IIb/IIIa platelet receptor antagonist 7E3 in Preventing Ischemic Complications.

OBJECTIVES: We sought to determine whether periprocedural myocardial infarction complicating percutaneous coronary revascularization is associated with subsequent clinical restenosis, as judged by the need for target vessel revascularization. BACKGROUND: Although myocardial enzyme elevation following angioplasty is associated with increased late mortality, its effect on subsequent clinical restenosis, as assessed by the need for late target vessel revascularization (TVR), is unknown. METHODS: Serial myocardial enzyme determinations were performed on 2,099 patients who underwent angioplasty or atherectomy in the Evaluation of IIb/IIIa platelet receptor antagonist 7E3 in Preventing Ischemic Complications (EPIC) trial. Thirty-day survivors were prospectively followed for three years for adverse clinical events including death and need for TVR. RESULTS: Within the study population, periprocedural creatine kinase (CK) elevation was a predictor of late mortality. Among patients with elevated CK, however, a paradoxical decrease in the need for late TVR was present. This relationship became progressively more profound as the magnitude of CK release increased. Late TVR occurred in 29.8% of patients with no CK elevation, 24.8% with CK elevation to >3 times normal, and 16.9% with >10 times elevation (hazard ratio 0.51, 95% CI 0.29, 0.91). CONCLUSIONS: In the EPIC study, patients with periprocedural MI were less likely to develop clinical restenosis as measured by the need for TVR. Mechanistically, although it is unlikely that CK elevation prevents vascular renarrowing per se, myocardial necrosis impairs the clinical manifestation of restenosis, thereby reducing the need for ischemia-driven TVR. This novel finding 1) highlights the potential discordance between angiographic and clinical measures of restenosis, and 2) has implications for clinical trials, as therapies that reduce periprocedural MI may be associated with a perceived excess of restenosis when measured by the need for TVR.

Prevention of in-stent restenosis.

Despite the favourable impact of stent implantation on restenosis rates for selected lesion types, in-stent restenosis remains a commonly encountered and difficult to manage entity. Histologically, in-stent restenosis appears to derive almost exclusively from neointimal hyperplasia, which appears to be more abundant following stent implantation than balloon angioplasty. The most powerful predictors of in-stent restenosis include the presence of diabetes, greater lesion length, small vessel caliber, and inadequate stent expansion. Several strategies have been proposed as a means to reduce the incidence of in-stent restenosis. Perhaps the most important among these relates to a strategy of provisional stent use, whereby stenting is undertaken only if suboptimal results are achieved following balloon angioplasty. Recent data from the EPILOG and EPILOG-stent trials suggest that the use of IIb/IIIa receptor antagonists may enhance the strategy of provisional stenting. When stents are used, adequate deployment is essential. The ability of adjunct IVUS imaging to guide proper balloon sizing during stent implantation and consequently reduce the risk of restenosis is currently the subject of randomized trials. Based on preliminary study results, intravascular radiation appears to hold great potential as a means to inhibit neointimal hyperplasia and consequently reduce the occurrence of in-stent restenosis, and large scale safety and efficacy trials are in progress. Other pharmacologic- and device-oriented strategies are likewise undergoing evaluation. In conclusion, while the availability of coronary stents has without question improved the safety and efficacy of coronary angioplasty, it remains critical that we continue to determine in an objective manner how and when best to use these devices.

Clinical implications of silent versus symptomatic exercise-induced myocardial ischemia in patients with stable coronary disease.

OBJECTIVES: This study was undertaken to better understand the functional and prognostic significance of silent relative to symptomatic ischemia. BACKGROUND: Previous studies have reached conflicting conclusions as to whether painless ischemia identified during noninvasive cardiac testing is related to a lesser extent of myocardial ischemia or a different prognosis than ischemia accompanied by angina, or both. METHODS: Nine hundred thirty-six clinically stable patients 1 to 6 months after an acute coronary event, either myocardial infarction or unstable angina, underwent ambulatory monitoring, exercise treadmill testing and stress thallium-201 scintigraphy. They were then followed up prospectively for a mean of 23 months for recurrent cardiac events (cardiac death, nonfatal myocardial infarction or unstable angina). RESULTS: Compared with patients with symptomatic ischemia during testing (n = 125), those with silent ischemia (n = 378) demonstrated less severe and extensive reversible defects on stress thallium scintigraphy (p = 0.0008), less functional impairment during treadmill testing manifested by longer exercise duration (640 +/- 173 vs. 529 +/- 190 s, p = 0.002) and longer time to ST segment depression (530 +/- 215 vs. 419 +/- 205 s, p = 0.0001) and less frequent ST segment depression during ambulatory monitoring (9% vs. 19%, p = 0.005). Patients with symptomatic ischemia had a significantly (p = 0.004) increased number of subsequent recurrent cardiac events (28.8%) versus those with silent (18.0%) or no (17.3%) ischemia. Adverse outcomes were especially concentrated in the subgroup with symptomatic ischemia and poor exercise tolerance. The difference in cardiac event rates between patients with silent versus symptomatic ischemia persisted after adjustment for baseline clinical characteristics by Cox regression analysis. CONCLUSIONS: Patients with painless ischemia during exercise testing 1 to 6 months after recovery from a coronary event have less jeopardized ischemic myocardium and fewer recurrent cardiac events than patients with symptomatic ischemia.

The development of valvular strands during thrombolytic therapy detected by transesophageal echocardiography.

A case report of a patient who had valvular strands while undergoing treatment with thrombolytic therapy for prosthetic mitral valve thrombosis is presented. The development of valvular strands during thrombolytic therapy provides unique evidence supporting a thrombotic/fibrotic origin to this relatively common finding on transesophageal echocardiography.

Relation between activated clotting time during angioplasty and abrupt closure.

BACKGROUND: The purpose of this study was to determine whether the degree of heparin anticoagulation during coronary angioplasty, as measured by the activated clotting time, is related to the risk of abrupt vessel closure. METHODS AND RESULTS: Sixty-two cases of in- and out-of-laboratory abrupt closure in patients in whom intraprocedure activated clotting times were measured were identified from a population of 1290 consecutive patients who underwent non-emergency coronary angioplasty. This group was compared with a matched control population of 124 patients who did not experience abrupt closure. Relative to the control population, patients who experienced abrupt closure had significantly lower initial (median, 350 seconds [25th to 75th percentile, 309 to 401 seconds] versus 380 seconds [335 to 423 seconds], P = .004) and minimum (345 seconds [287 to 387 seconds] versus 370 seconds [321 to 417 seconds], P = .014) activated clotting times. Higher activated clotting times were not associated with an increased likelihood of major bleeding complications. Within this population, a strong inverse linear relation existed between the activated clotting time and the probability of abrupt closure. CONCLUSIONS: This study demonstrates a significant inverse relation between the degree of anticoagulation during angioplasty and the risk of abrupt closure. A minimum target activated clotting time could not be identified; rather, the higher the intensity of anticoagulation, the lower the risk of abrupt closure.