Rihal, Charanjit S.

Background— American College of Cardiology/American Heart Association guidelines recommend a door-to-balloon time (DTB) <90 minutes for nontransferred patients with ST-elevation myocardial infarction (STEMI) who undergo primary percutaneous coronary intervention. Systems of care to achieve and sustain this DTB performance over several years have not been previously reported. Methods and Results— The Mayo Clinic STEMI protocol was implemented in April 2004 and included activation of the cardiac catheterization laboratory by the emergency medicine physician; a single call system to activate the catheterization laboratory; catheterization laboratory staff arrival within 20 to 30 minutes of activation; and real-time performance feedback within 24 to 48 hours. Data were collected on nontransferred STEMI patients. The preimplementation group (June 2002 to March 2004) comprised 96 patients with a median DTB of 97 (interquartile range, 82, 130) minutes, and 40% had a DTB <90 minutes. The postimplementation group (May 2004 to March 2008) comprised 322 patients with a median DTB of 67 (interquartile range, 55, 82) minutes, and 81% had a DTB <90 minutes. Postimplementation DTB was significantly shorter than preimplementation DTB ( P <0.001). In the 4-year follow-up after protocol implementation, the DTB performance remained stable over time ( P =0.41). Conclusions— The Mayo Clinic STEMI protocol implemented strategies to reduce DTB for nontransferred patients with STEMI. DTB was significantly reduced, and the results were sustained over the 4-year follow-up period. Our experience demonstrates the effectiveness and durability of process changes targeting timeliness of primary percutaneous coronary intervention.

A significant proportion of patients with ST-elevation myocardial infarction have persistent impairment of microvascular blood flow despite successful reperfusion of epicardial vessels. Microvascular dysfunction has been associated with larger infarct size, increased predisposition to ventricular arrhythmias, heart failure, cardiogenic shock, recurrent myocardial infarction, and death. It remains unclear whether this association is of direct mechanistic significance or whether the microcirculatory injury is an epiphenomenon and a manifestation of greater ischemic insult to the myocardium. Although several potential mechanisms have been proposed for the microvascular dysfunction, distal microembolization during mechanical reperfusion is likely to be an important contributor. Consequently, there has been increasing interest in the concept of adjunctive mechanical thrombectomy to improve outcomes in primary percutaneous coronary intervention. Until recently, randomized trials of thrombectomy and distal protection devices during primary percutaneous coronary intervention have provided conflicting results with no definitive evidence for efficacy. The recently published Thrombus Aspiration During Percutaneous Coronary Intervention in Acute Myocardial Infarction Study has rekindled the interest in this area. This trial is the largest randomized study of a thrombectomy device published to date and demonstrates that adjunctive treatment with aspiration thrombectomy during primary percutaneous coronary intervention improves surrogate and clinical end points. The aim of the present report is to review the evidence to date on the role of mechanical thrombectomy and embolic protection in native coronary arteries during primary percutaneous coronary intervention.

Background— Myonecrosis after percutaneous coronary intervention (PCI) has been correlated with a worse prognosis, but controversy exists about the clinical significance and potential mechanisms for the association. The aim of this study was to evaluate the relative impact of preprocedural and postprocedural cardiac troponin T (cTnT) levels on survival rate after PCI. Methods and Results— We evaluated 5487 patients from the Mayo Clinic registry who required nonemergency PCI, and we examined the relationship between periprocedural cTnT levels, with the 99th percentile cutoff value used for normal (<0.01 ng/mL), and outcomes. The patients were divided into 3 groups: normal preprocedural and postprocedural cTnT levels (no myonecrosis), normal preprocedural but elevated postprocedural cTnT levels (PCI-related myonecrosis), and abnormal preprocedural cTnT. The 30-day death rates were 0.1%, 0.6%, and 2.3%, respectively, in the 3 groups. In a multivariable model, an abnormal pre-PCI cTnT level (hazard ratio 9.66 [2.30–40.57]; P =0.002), and PCI-related myonecrosis (4.71 [1.02–21.83]; P =0.048) were independent predictors of 30-day mortality. Over a median follow-up of 28 months, an abnormal pre-PCI cTnT level (hazard ratio 1.79 [1.35–2.39]; P <0.001) independently predicted death, but the occurrence of PCI-related myonecrosis did not. A postprocedural elevation in creatine kinase MB fraction was not an independent predictor of long-term risk of death (0.912 [0.70–1.19]; P =0.5). Conclusions— A preprocedural cTnT level >0.01 is a powerful independent predictor of prognosis after PCI and is of greater prognostic significance than the postprocedural biomarker levels. PCI-related myonecrosis occurs frequently and predicts short-term but not long-term risk of death.

Background— The clinical efficacy of alcohol septal ablation for drug-refractory hypertrophic cardiomyopathy remains unclear. This study examines the outcome of alcohol septal ablation performed at a tertiary hypertrophic cardiomyopathy referral center. Methods and Results— Among 601 patients with severely symptomatic obstructive hypertrophic cardiomyopathy referred for alcohol septal ablation or myectomy from 1998 to 2006, 138 patients (median age, 64 years; 39% men) chose to undergo ablation. Procedural complications included death in 1.4%, sustained ventricular arrhythmias in 3%, tamponade in 3%, and pacemaker implantation in 20%. This rate was higher than a combined complication rate of 5% in age- and gender-matched patients who had undergone septal myectomy at Mayo Clinic ( P <0.0001). Four-year survival free of all mortality was 88.0% (95% confidence interval, 79.4 to 97.5%), which was similar to that of the age- and gender-matched patients who had undergone myectomy ( P =0.18). Six patients had documented ventricular arrhythmias after ablation, 4 of whom had successful intervention. Four-year survival free of death and severe New York Heart Association class III/IV symptoms after septal ablation was 76.4%, and 71 patients (51%) became asymptomatic. Myectomy patients ≤65 years of age had significantly better survival free of death and severe symptoms ( P =0.01). Conclusions— Alcohol septal ablation is an efficacious procedure if performed in an experienced institution and may resolve symptoms in a subset of patients with obstructive hypertrophic cardiomyopathy. However, the procedural complication rate exceeds that of myectomy. Patients ≤65 years of age have better symptom resolution with myectomy. No impairment in short-term survival was noted in this nonrandomized study, but the long-term outcome remains unknown.

Despite percutaneous intervention after an acute coronary syndrome, patients remain at high risk for recurrent events in the first year. Prior studies have shown that a plaque rupture can occur not only at a single culprit lesion site but also in other atherosclerotic plaques throughout the coronary vasculature in patients with stable angina, silent myocardial ischemia, and during acute coronary syndromes. A 71-year-old man who presented with exertional angina and who had a successful stent in a culprit right coronary artery is described in this article. After 4 weeks, he represented with accelerated angina. A prior lesion in the obtuse marginal artery, remote from the site of the index lesion, had progressed from a 30% to 90% stenosis. This case report demonstrates the systemic nature of acute coronary syndromes, highlights the inherent instability of coronary artery disease, and supports the notion of aggressive secondary prevention in these patients.

In vitro and animal studies suggest that oxidative stress is associated with endothelial dysfunction. We tested whether local oxidative stress and nitric oxide (NO) bioavailability in the coronary circulation is associated with coronary endothelial dysfunction in humans. Blood samples were obtained simultaneously from the left main coronary artery and the coronary sinus for measurement of F2-isoprostanes, myeloperoxidase, nitrotyrosine, and superoxide dismutase in 20 patients without significant coronary disease. Afterward, coronary blood flow and the vascular response to intracoronary acetylcholine and N G -monomethyl- L -arginine (L-NMMA) were assessed. The gradient of isoprostanes between the arterial levels and coronary sinus correlated with the change in coronary artery diameter in response to acetylcholine ( r =−0.79, P <0.0001). Isoprostanes net production across the left anterior descending artery territory correlated with a decrease in superoxide dismutase activity ( r =0.66, P =0.002) and decrease in coronary artery diameter in response to L-NMMA (r s =0.48, P <0.05). Myeloperoxidase and nitrotyrosine gradients were similar in patients with endothelial dysfunction and controls. The effect of L-NMMA was similar in both groups. We conclude that coronary endothelial dysfunction in humans is characterized by local enhancement of oxidative stress without a decrease in basal NO release. This study supports the hypothesis that local oxidative stress has a role in reduction of NO bioavailability in humans with coronary endothelial dysfunction.