Multiple coronary micro-aneurysm formation after drug-eluting stent implantation.

Although there are limited data regarding the formation of coronary artery aneurysms (CAAs) after drug-eluting stent (DES) implantation, CAAs appear to be a rare complication of coronary stenting. The exact mechanism of CAA formation is unknown, but several hypotheses have been proposed. As the use of DES increases, the clinical significance of these findings will become clearer. We report on a patient who developed multiple CAAs in 2 different locations after sirolimus-eluting stent implantation.

Marked troponin elevation after implantation of a permanent antibradycardia pacemaker.

INTRODUCTION: Transvenous insertion of endocardial leads for permanent pacing is often accompanied by minor myocardial damage, detected thanks to the high sensitivity of cardiac troponins. It is unknown whether higher troponin levels, commensurate with more severe myocardial damage, can be encountered after implantation procedures. METHODS: Over a 3-year period, 283 patients underwent an implantation of a full antibradycardia pacemaker system (pulse generator plus leads). Patients were required to have normal levels of cardiac troponin I (CTNI) on a venous blood sample taken immediately prior to elective pacemaker insertion. Post implantation CTNI levels were measured in all patients 6 hours after the procedure. Repeated samples were taken if high CTNI levels were found at 6 hours. RESULTS: Elevated CTN-I levels were found in 167 patients (59%, 95% CI: 0.53-0.64), but only 5 of them (1.8%, 95% CI=0.8 to 4.1%) had peak CTN-I levels far exceeding the range of minimal myocardial damage (i.e. CTN-I >1.5 ng/ml). Implantation of the devices was successful in all patients and we did not observe any complications. None had clinical evidence of an acute coronary event before or during the pacemaker implantation procedure and coronary angiography revealed no significant lesions in the coronary arteries. CONCLUSIONS: CTN-I elevations after pacemaker implantation may far exceed levels corresponding to minimal myocardial damage. This should be a matter of concern, especially if an early discharge is planned after pacemaker implantation.

Biochemical evidence of cardiac damage following transvenous implantation of a permanent antibradycardia pacemaker lead.

OBJECTIVES: We tested the hypothesis that transvenous permanent pacemaker lead implantation causes clinically detectable myocardial damage. BACKGROUND: Histological evidence of myocardial damage has been reported after antibradycardia pacemaker lead implantation. METHODS: We studied 30 patients undergoing implantation of a full antibradycardia pacemaker system (pulse generator plus leads) and 10 patients in whom only a generator was implanted. Blood samples for cardiac troponin-I (CTNI), CK-MB mass, and myoglobin measurement were drawn at baseline, at the end of the procedure, and at 2, 6, 12, 24, 48, and 72 hours thereafter. RESULTS: Abnormal CTNI levels were noted only in 24 of the 30 patients undergoing a full system implantation. CTNI levels were already abnormal at the end of the procedure in 16 and became so in all 24 during the next 6 hours. Peak levels were reached within 6 hours in 21 patients and were compatible with "minimal" necrosis (CTNI < 1.5 pg/mL) in 20. Maximum ventricular lead diameter and number of implanted leads were independent predictors of peak CTNI levels. CK-MB mass also increased after the procedure, but exceeded the normal range in only 10 patients. Myoglobin levels increased significantly both in patients undergoing a complete system implantation and in those where only a pulse generator was implanted. CONCLUSIONS: Transvenous insertion of endocardial leads for permanent pacing is accompanied in most patients by "minimal" myocardial damage. In this setting CTNI level kinetics are fast, characterized by early elevation and peak.

Early brain natriuretic peptide increase reflects acute myocardial ischemia in patients with ongoing chest pain.

BACKGROUND: Plasma brain natriuretic peptide levels increase during acute ischemic events. In this study we tested the diagnostic performance of brain natriuretic peptide measurements in the detection of acute myocardial ischemia. METHODS: Blood brain natriuretic peptide was measured in 101 patients with ongoing chest pain but no heart failure or an ST-segment elevation myocardial infarction on arrival at the emergency department (baseline) and at 2 and 6 h later. After diagnostic testing and 1-month follow-up for ischemia, patients were classified as either ischemic or non-ischemic. RESULTS: In the ischemic group median (25th, 75th percentiles) brain natriuretic peptide values (pg/ml) were 122 (20, 349) at baseline, 116 (36, 347) at 2 h, increasing to 148 (52, 428) at 6 h (p<0.001 vs. baseline). Non-ischemic patients had 12 (5, 32) at baseline, 9 (6, 30) at 2 h, and 13 (5, 29) at 6 h (p<0.001 vs. corresponding values of the ischemic group). Receiver operator characteristic curves were constructed for brain natriuretic peptide values at baseline 2 and 6 h and for the increase of peptide levels from baseline to 6 h. All areas under curve indicated a significant diagnostic ability for the detection of ischemia. The 6-h measurement had better diagnostic performance than baseline and 2-h measurements. The subgroup of ischemic patients without myocardial necrosis also had higher brain natriuretic peptide values and could thus be discriminated from non-ischemic subjects. CONCLUSIONS: Brain natriuretic peptide values may detect acute myocardial ischemia in patients with ongoing chest pain but without ST-segment elevation, and distinguish ischemic patients from those with pain of non-ischemic origin.