Effect of continuous quality improvement analysis on the delivery of primary percutaneous transluminal coronary angioplasty for acute myocardial infarction.

A successful primary percutaneous transluminal coronary angioplasty (PTCA) program requires a learning process whereby the efficiency of the cardiac catheterization laboratory to deliver prompt intervention can be refined. The purpose of this study was to (1) quantify this learning process in terms of shortening the time to reperfusion, (2) examine the changes in strategy that allowed for this, and (3) determine if expedited reperfusion by primary PTCA improved patient outcomes. A database of all primary PTCA procedures was established in February 1, 1994. Continuous quality assurance analysis was performed, and program modifications introduced as needed. Patients were separated into early (group A = February 1, 1994 through January 31, 1995) and late (group B1 = February 1, 1995 through June 31, 1995, and group B2 = July 1, 1995 through December 31, 1995) cohorts. Time intervals to certain treatment landmarks were compared among groups. In-hospital outcomes were tabulated. Fifty-two consecutive patients were included (group A = 19, group B1 = 17, group B2 = 16). Time intervals shortened significantly (group A vs group B1 vs group B2) with the time from hospital presentation to first balloon inflation decreasing progressively (from 205 to 119 to 97 minutes; p <0.001). Most of this decrease was obtained by shortening the time from hospital presentation to xylocaine administration (158 to 85 to 72 minutes; p <0.005), although the time from xylocaine to first balloon inflation also decreased (from 47 to 33 to 24 minutes; p <0.005). Parallel decreases for in-hospital mortality (26% vs 0%; p = 0.004), adverse events (47% vs 18%; p = 0.05), and length of hospital stay (13.3 +/- 13.7 vs 8.4 +/- 4.4 days; p = NS) were demonstrated for groups A versus B1 and B2. A learning effect following initiation of a primary PTCA program is demonstrated in which reperfusion was more rapidly achieved as the result of procedural changes directed by quality improvement analysis with a concurrent improvement in in-hospital outcomes.

Percutaneous treatment of protected and unprotected left main coronary stenoses with new devices: immediate angiographic results and intermediate-term follow-up.

OBJECTIVES: We sought to evaluate the immediate angiographic results and intermediate-term follow-up after percutaneous treatment of left main coronary stenoses in the new device era. BACKGROUND: Historically, balloon angioplasty of left main coronary stenoses has been associated with high procedural morbidity and poor long-term results. It is not clear whether new devices are more effective in this anatomic setting. METHODS: Between July 1993 and July 1995, we performed initial left main coronary interventions on 46 patients (mean age 67 +/- 12 years, 26% women). Quantitative angiography was available for 42 of 46 interventions, and clinical follow-up was obtained for all patients at 1 month, 6 months and 1 year after initial revascularization. RESULTS: Most interventions (42 of 46) were performed in patients with "protected" coronary stenoses to the left coronary system owing to the presence of one or more patent left main coronary grafts. Seventy-seven percent of screened patients were deemed unsuitable for repeat coronary artery bypass surgery. Procedures performed included stenting in 73% of patients (alone in 30% and after rotational atherectomy in 43%), rotational atherectomy in 58% (alone in 15% and before stenting in 43%), directional atherectomy in 4% and angioplasty alone in 7%. Initial procedural success was achieved in all interventions, with no deaths, myocardial infarctions (creatine kinase, MB fraction > 50 IU/liter) or emergent bypass surgery. Follow-up data to date (median duration 9 months, range 6 to 19) demonstrate a 98% overall survival rate and a 6-month event-free survival rate of 78% (six target vessel revascularizations [TVRs], four non-TVRs). CONCLUSIONS: Treatment of protected left main coronary artery stenoses can be accomplished safely and effectively with new device technology. Intermediate-term follow-up demonstrates an acceptably low rate of death, myocardial infarction or repeat revascularization at 6 months and 1 year.

Stent jail: a minimum-security prison.

Small but significant side branches (particularly those with baseline ostial narrowing) may be further compromised by stent placement within parent vessel segments. Despite the theoretical risks associated with dilating branches in stent jail, the procedure was successfully completed in 84%, with minimal complications (mostly balloon rupture and local dissection) and no cases of balloon entrapment or deterioration of the final result achieved in the parent vessel.

Effect of anti-CD18 antibody on myocardial neutrophil accumulation and infarct size after ischemia and reperfusion in dogs.

BACKGROUND: Polymorphonuclear neutrophils (PMNs) accumulate in postischemic myocardium and may cause injury to myocardium or to vessels by production of oxygen free radicals or by release of proteases and lipases. PMN accumulation is dependent on adherence to endothelium, which is mediated by a family of glycoproteins on the PMN surface, each of which has a common beta-subunit (CD18). The purpose of this study was to determine whether an antibody (IB4) against the CD18 protein could attenuate PMN accumulation and limit myocardial infarct size. METHODS AND RESULTS: F(ab')2 fragments of a mouse monoclonal antibody to human adherence-promoting leukocyte glycoprotein (CD18) were used. Infarct size after 90 minutes of ischemia and 3 hours of reperfusion was compared in dogs with (n = 8) and without (n = 8) the anti-CD18 treatment. Myocardial PMN accumulation was assessed with 111In-labeled autologous PMNs. Anti-CD18 treatment significantly reduced the number of PMNs in the ischemic region (19,123 +/- 5,352/mg versus 5,204 +/- 927/mg in the control and treated groups, respectively; p < 0.05). In addition, the ratio of myocardial blood flow (ischemic/nonischemic wall) at 45 minutes into reperfusion was higher in the treated than in the control group (1.18 +/- 0.18 versus 0.69 +/- 0.09; p < 0.05). Nevertheless, infarct size was similar between the control and treated groups (40.5 +/- 7.4% versus 48.5 +/- 4.4% of the area at risk; p = NS). Transmural mean collateral blood flow to the ischemic myocardium was similar between the two groups, and the inverse relation between infarct size and collateral blood flow was not shifted by anti-CD18 therapy. CONCLUSIONS: Although PMN accumulation contributed to reduced postischemic microvascular perfusion, it caused insufficient additional myocardial cell death to measurably affect infarct size in this model.

Evidence against the "early protection-delayed death" hypothesis of superoxide dismutase therapy in experimental myocardial infarction. Polyethylene glycol-superoxide dismutase plus catalase does not limit myocardial infarct size in dogs.

We previously found that superoxide dismutase (SOD) did not limit myocardial infarct size after 40 or 90 minutes of ischemia and 4 days of reperfusion in dogs. Because some other studies have shown limitation of infarct size after shorter periods of reperfusion, we postulated that our negative results might be due to late reperfusion injury mediated by superoxide anions produced after excretion of SOD. To test this "early protection-delayed death" hypothesis, we have examined whether SOD, conjugated to polyethylene glycol (PEG-SOD) to prolong its circulating half-life, limited myocardial infarct size. The circumflex artery was occluded for 90 minutes followed by 4 days of reperfusion. PEG-SOD (total dose, 10,000 units/kg) and catalase (55,000 units/kg) were given during the 30 minutes before reperfusion. Plasma SOD levels in the treated group were 330 +/- 20 units/ml at the onset of reperfusion and 140 +/- 10 units/ml on day 4 (circulating half-life, 75 +/- 5 hours) versus 5 +/- 1 units/ml in controls. Histological infarct size was 37.1 +/- 4.2% of the area at risk in the treated group (n = 11) versus 44.5 +/- 6.2% in controls (n = 10) (p = NS). Infarct size and collateral blood flow were inversely related in controls; PEG-SOD and catalase did not shift this regression (p = NS by analysis of covariance). Thus, infarct size was not limited when measured after 4 days of reperfusion, even though plasma SOD exceeded 100 units/ml throughout this reperfusion period.(ABSTRACT TRUNCATED AT 250 WORDS)