Predictors of long-term outcomes following direct percutaneous coronary intervention for acute myocardial infarction.

To determine predictors of a long-term major adverse cardiac event (MACE) in unselected patients undergoing direct percutaneous coronary intervention (PCI), 274 consecutive patients presenting within 12 hours of ST-segment elevation acute myocardial infarction (AMI) were evaluated. No patient with ST-segment elevation AMI received intravenous thrombolytic drugs. Chest pain to balloon time was 3.8 hours (range 2.5 to 6.9). percutaneous transluminal coronary angioplasty was successful in 95% of patients. Abciximab was administered to 69% of patients, stents were deployed in 53%, and 17% underwent only catheterization. In-hospital events were death (7%), abrupt closure (2%), emergent coronary artery bypass grafting (CABG) (5%), repeat PCI (3%), and recurrent myocardial infarction (1%). In patients undergoing direct PCI (n = 227), the in-hospital event rate was death 5.3%, abrupt closure 2.2%, emergency CABG 0.9%, repeat PCI 3.1%, and repeat myocardial infarction 1.3%. Median time to last follow-up or death was 20 months (range 11 to 34), and to any event, 0.3 months (range 0.03 to 24.0). Postdischarge MACE included death (5%), AMI (4%), repeat PCI (8%), CABG (9%), and stroke (0.7%). Among those undergoing direct PCI (n = 227), 10% died, 3.5% had a repeat AMI, 9% had a repeat PCI, 5% had CABG, and 1% had a stroke at long-term follow-up. At long-term follow-up, 75% were event free. Multivariate predictors were (hazard ratio [95% confidence interval (CI)]): abciximab use 0.6 (95% CI 0.43 to 0.95), Killip class 2.2 (95% CI 1.1 to 4.4), and number of narrowed coronary arteries 1.7 (95% CI 1.4 to 2.2). In this unselected consecutive series of patients presenting with ST-segment elevation AMI, direct PCI was associated with sustained long-term efficacy. Outcomes were predicted by cardiac impairment at presentation and number of narrowed coronary arteries. MACE is not related to device selection but is significantly improved with abciximab.

Incidence and angiographic predictors of side branch occlusion following high-pressure intracoronary stenting.

We evaluated the incidence, angiographic predictors, and clinical outcome of side branch occlusion (SBO) following high-pressure intracoronary stenting in 175 patients. All stent implants during a 7-month period were reviewed for the incidence of major (>1 mm) SBO. Side branches were further characterized based on side branch and index lesion morphology. Clinical events (death, myocardial infarction, and target vessel revascularization rates) were determined at 9 months. A total of 175 patients (182 lesions) had 224 major side branches covered by intracoronary stents. Of these, 43 (19%) occluded. Most SBOs (29 of 43 [67%]) occurred after poststent dilation using high-pressure inflations (15.3 +/- 3.3 atmospheres). No clinical characteristics correlated with SBO. By multivariate analysis, those side branches with >50% ostial narrowing that arose from within or just beyond the diseased portion of the parent vessel (threatened side branch morphologies) were a powerful angiographic predictor of SBO (odds ratio 40, 95% confidence interval, 14 to 130, p <0.0001). At 9-month follow-up there was no difference in combined clinical events between those patients with and without SBO. These data demonstrate that side branches with ostial stenoses in continuity with diseased parent lesions were at risk of occlusion following stenting. SBO, however, was not associated with adverse clinical outcome. These findings lend support to plaque shift ("snow plow effect") as the mechanism behind SBO following stent placement.

Primary angioplasty reduces risk of myocardial rupture compared to thrombolysis for acute myocardial infarction.

Although the mechanical complications of acute ventricular septal defect and acute mitral regurgitation are uncommon after acute myocardial infarction, these complications are associated with an extremely high morbidity and mortality. We hypothesized that the administration of thrombolytic drugs may result in hemorrhagic infarction as well as the potential for incomplete revascularization and thus may lead to an increased incidence of mechanical complications compared to primary angioplasty. Accordingly, we reviewed the data of the most contemporary thrombolytic and primary angioplasty trials and compared the incidence of mechanical complications among 36,303 patients treated with thrombolytics reported in the GUSTO trial to the incidence of mechanical complications among 1,295 patients treated with primary angioplasty obtained from the PAMI-1 and PAMI-2 trials. We found that angioplasty resulted in an overall 86% relative risk reduction in mechanical complications (2.20% vs. 0.31%, P < 0.001). In comparison to thrombolytic therapy, angioplasty resulted in an 82% decrease in acute mitral regurgitation (1.73% vs. 0.31%, P < 0.001) and a 100% decrease in acute ventricular septal defect (0.47% vs. 0.00%, P < 0.03). In conclusion, in patients with acute myocardial infarction, reperfusion with primary angioplasty is associated with less myocardial rupture and mechanical complications than thrombolytics. This finding may, in part, explain the improved prognosis observed in myocardial infarction patients treated with primary angioplasty.

Treatment of no-reflow in degenerated saphenous vein graft interventions: comparison of intracoronary verapamil and nitroglycerin.

No-flow has been reported after 10-15% of percutaneous interventions on degenerated saphenous vein grafts. In this prospective study of 36 degenerated saphenous vein graft lesions (32 patients), no-flow (TIMI flow < 3 in the absence of a significant lesion or dissection) occurred in 15/36 (42%) lesions. A total of 32 episodes of no-flow occurred after angioscopy (n = 14), extraction atherectomy (n = 10), balloon angioplasty (n = 2) or stent implantation (n = 6). Intragraft nitroglycerin (100-300 micrograms) alone resulted in no improvement in TIMI flow in the setting of no-reflow (TIMI flow 1.2 +/- 0.6 to 1.4 +/- 0.8, P = NS). Intragraft verapamil (100-500 micrograms) resulted in improvement in flow in all 32 episodes (TIMI flow 1.4 +/- 0.8 before, to 2.8 +/- 0.5 after verapamil, P < 0.001). Although verapamil increased TIMI flow after all episodes of no-reflow, two (6.3%) had persistent no-reflow (TIMI 1) despite verapamil, associated with non-Q wave myocardial infarction. In conclusion, treatment of no-reflow with verapamil during degenerated vein graft interventions was associated with reestablishment of TIMI 3 flow in 88% of cases. In contrast, intragraft nitroglycerin alone was ineffective for reversing no-reflow.

Enhanced coronary vasoconstrictive response to serotonin subsides after removal of dietary cholesterol in atherosclerotic monkeys.

Constriction in response to serotonin is enhanced in the coronary arteries of atherosclerotic monkeys. The main objective of the present study was to determine whether abnormal responses to serotonin in atherosclerosis are reversed following removal of dietary cholesterol. In addition, we examined the effect of an atherogenic diet and reduction in dietary cholesterol on vascular responses to activation of ATP-sensitive K+ channels with aprikalim. Diameters of small coronary arteries were measured on the epicardial surface of the left ventricle in vivo by using stroboscopic illumination synchronized to the heart cycle to visually freeze the motion of the heart. Diameters were measured with a microscope-video system during topical application of two vasoconstrictor agonists, serotonin and the thromboxane mimetic U46619, and the vasodilator agonists aprikalim and nitroprusside. Responses were compared in normal (n = 9), atherosclerotic (n = 14; high-cholesterol diet), and regression (n = 8; high-cholesterol diet followed by normal diet) monkeys. Constriction of coronary arteries in response to serotonin was enhanced in monkeys on an atherogenic diet and was normal in regression monkeys. Vasoconstriction in response to U46619 and vasodilation in response to nitroprusside and aprikalim were not altered by atherosclerosis. Thus, abnormal vascular responses to serotonin in small coronary arteries of atherosclerotic monkeys without morphological evidence of disease can be reversed to normal by reducing dietary cholesterol.

Transcatheter embolization of an internal mammary artery bypass graft sidebranch causing coronary steal syndrome.

We describe a 66-yr-old man with angina after internal mammary artery-coronary bypass grafting due to coronary artery steal by a sidebranch of the mammary artery. Myocardial ischemia was successfully treated by transcatheter embolization of the sidebranch.

Functional improvement precedes structural regression of atherosclerosis.

BACKGROUND: Vasoconstrictor responses to serotonin are augmented in monkeys with diet-induced atherosclerosis and improve after 18 months of normal diet. We tested the hypothesis that functional improvement may occur early during regression, before evidence of structural improvement. METHODS AND RESULTS: Responses of the iliac artery to serotonin were measured by quantitative angiography and a Doppler flow probe in several groups of monkeys: (1) normal monkeys, (2) monkeys fed an atherogenic diet for 2 years (atherosclerotic), and (3) monkeys fed an atherogenic diet for 2 years (preregression) followed by a normal diet for 4, 8, or 12 months (regression). In normal monkeys, serotonin produced minimal constriction of the iliac artery, and blood flow to the legs increased. In atherosclerotic monkeys, there was pronounced constriction of the iliac artery, and blood flow to the legs decreased markedly. After 4 months of regression diet, four of eight monkeys demonstrated marked reduction in hyperresponsiveness to serotonin angiographically, and by 8 months, six of eight monkeys had significant improvement. After regression, serotonin produced minimal changes in flow. There was no reduction in intimal area (ie, atherosclerotic lesion) in iliac arteries from regression monkeys compared with atherosclerotic monkeys, but there was a marked reduction in cholesteryl ester in arteries from regression monkeys. CONCLUSIONS: Abnormal vasoconstrictor responses to serotonin usually return to or toward normal within a few months during regression of atherosclerosis. Functional improvement occurs in conjunction with early resorption of lipid from the arterial wall and occurs before detectable changes in mass of the atherosclerotic lesion.