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Local inflammation within the coronary arteries is involved in the pathogenesis of acute coronary syndrome. However, the contribution of a systemic inflammatory response to the pathogenesis of this syndrome has not been well characterized. Accordingly, we investigated systemic inflammatory responses in patients with acute coronary syndrome.A total of 83 patients with ischemic heart disease (15 with stable exertional angina and 68 with acute coronary syndrome) were studied. The luminol-dependent chemiluminescence (CL) response of polymorphonuclear leukocytes (PMNs), which reflects their ability to generate oxygen species, was used as a marker for PMN activation. Soluble interleukin-2 receptor (sIL-2R) levels were measured to assess T-lymphocyte activation.CL counts of whole blood from patients with acute coronary syndrome were twice those of patients with stable angina (2.38 +/- 0.22 vs 1.10 +/- 0.17 x 10(6) counts, P0.05). A comparison of CL counts between patients with unstable angina and those with acute myocardial infarction revealed no significant differences. T-lymphocyte activity, measured by serum sIL-2R, was significantly lower in patients with acute coronary syndrome than those with stable angina (214.3 +/- 11.5 vs. 358.3 +/- 115.7 U/ml, P0.05).This investigation shows that there is a systemic increase in PMN activity and a decrease in T-lymphocyte activity in patients with acute coronary syndrome. This contrasts with the pattern of cellular activation seen at sites of local inflammation within atherosclerotic plaques, suggesting that two independent inflammatory processes (local and systemic) may be involved in the pathogenesis of this syndrome.

The relationship between ST reelevation at reperfusion and the occurrence of late potentials (LPS) in 35 patients with a first anterior infarction who had single vessel disease was investigated. All patients underwent a successful primary angioplasty and had a patent infarct related artery confirmed angiographically 4 weeks later. Patients were classified into groups based on changes in the ST level at reperfusion: patients with ST reelevation (group A, n = 22) and patients without ST reelevation (group B, n = 13). Signal-averaged ECG was performed 4 weeks after primary angioplasty to detect LPS. Cineventriculography was performed to measure left ventricular ejection fraction (LVEF) and evaluate regional wall motion of the infarct area (SD/chords). LPS were present in eight of the 22 group A patients (36%) and in none of the 13 group B patients (P < 0.05). Left ventricular function was impaired in patients in group A compared with patients in group B (LVEF: 5 1 +/- 12 vs 63 +/- 10, P < 0.01; SD/chords: -2.7 +/- 0.9 vs -1.9 +/- 1.1, P < 0.05). These data suggest that ST reelevation and myocardial damage at reperfusion are associated with the occurrence of LPS in patients with successfully recanalized infarct related arteries after acute anterior infarction.

A saline-jet aspiration thrombectomy (JAT) catheter was used in a patient with acute myocardial infarction. A right coronary arteriogram showed complete thrombotic occlusion at the proximal segment. With this catheter the thrombus was removed without complications in 5 sec. The patient underwent percutaneous transluminal coronary angioplasty and placement of a Palmaz-Schatz stent after successful thrombectomy. Thrombectomy with a JAT catheter was very useful in this patient.

We conducted a prospective observational study to assess the effectiveness of "transradial primary stenting" in 33 patients with acute myocardial infarction, along with acute risk stratification and accelerated patient care. With use of adequate inclusion and exclusion criteria, the radial artery can be used as an access site for catheterization, and transradial primary stenting can be performed rapidly and successfully by trained coronary interventionalists.

We evaluated the therapeutic efficacy of cilostazol, a novel potent inhibitor of phosphodiesterase, for the prevention of stent thrombosis following implantation of a Palmaz-Schatz stent guided by angiographic visual estimation alone in 71 patients with 84 lesions. Patients received 81 mg of aspirin 3 times daily and 100 mg of cilostozol twice daily after angiographic confirmation of optimal Palmaz-Schatz stent implantation. Of the 84 vessels stented, 65 (77%) were classified as type B2 or C lesions according to the modified American Heart Association/American College of Cardiology classification, and 51 (61%) were3.0 mm in diameter. Multiple stents were used in 26 patients (31%). The final balloon inflation pressure was 18.3 +/- 1.5 atm. The balloon-to-vessel ratio was 1.18 +/- 0.16. No patient received heparin or warfarin after the procedure. There were no deaths, Q-wave myocardial infarctions, in- or out-of-hospital stent thrombosis, coronary bypass surgery, or serious side effects such as neutropenia and/or liver dysfunction during the 1-month follow-up period. These results indicate that cilostazol was a safe and effective antiplatelet agent with minimum side effects after Palmaz-Schatz stent implantation.

The purpose of this study was to investigate the significance of ST re-elevation at reperfusion using strict criteria for patient inclusion and exclusion. Twenty-nine patients who had a first anterior infarction with single-vessel disease, successful recanalization by intracoronary thrombolysis (ICT) with urokinase, and an angiographically confirmed patent infarct-related artery after 4 weeks, were divided into three groups according to the deviation of the ST segment at reperfusion: Group A, 10 patients with sustained ST re-elevation; Group B, 10 patients with transient ST re-elevation; and Group C, 9 patients with ST reduction. Left ventricular (LV) function was evaluated from cineventriculograms performed in the 30 degrees right anterior projection 4 weeks after ICT. LV ejection fraction and regional wall motion of the infarct area, evaluated by the centerline method (SD/chords), were significantly lower in Group A (44 +/- 10%, -3.2 +/- 0.4) than in Group B (61 +/- 9%, -1.9 +/- 0.7) and Group C (60 +/- 5%, -2.0 +/- 0.4) (p0.01). Peak creatine kinase (CK) activity was significantly higher in Group A (5848 +/- 2112 IU) than in Group B (2485 +/- 1254 IU) and Group C (1889 +/- 1525 IU) (p0.05). These data suggest that a sustained ST re-elevation at reperfusion was strongly associated with marked LV dysfunction and higher peak CK activity. It was concluded that sustained, not transient, ST re-elevation associated with successful reperfusion indicates extensive myocardial damage.