Acute myocardial infarction in a patient with coronary artery aneurysm and Crohn's disease.

Crohn's disease is a chronic inflammatory disorder of unknown cause involving the gastrointestinal tract. Complications from the cardiovascular system seem to be uncommon in patients with Crohn's disease. We present a case of a 37-year-old man with a known history of Crohn's disease, who was admitted to our hospital with acute myocardial infarction. An aneurysm of a totally occluded circumflex coronary artery was revealed during the attempt at primary intervention. The artery was successfully opened and the aneurysm was sealed with the use of 2 covered stents.

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.

Effect of high doses of magnesium on converting ibutilide to a safe and more effective agent.

Ibutilide is a class III antiarrhythmic agent indicated for cardioversion of atrial fibrillation and atrial flutter to sinus rhythm (SR). The most serious complication of ibutilide is torsades de pointes (TdP). Magnesium has been successfully used for the treatment of TdP, but its use as a prophylactic agent for this arrhythmia has not yet been established. The present study investigated whether high dose of magnesium would increase the safety and efficacy of ibutilide administration. A total of 476 patients with atrial fibrillation or atrial flutter who were candidates for conversion to SR were divided into 2 groups. Group A consisted of 229 patients who received ibutilide to convert atrial fibrillation or atrial flutter to SR. Group B consisted of 247 patients who received an intravenous infusion of 5 g of magnesium sulfate for 1 hour followed by the administration of ibutilide. Then, another 5 g of magnesium were infused for 2 additional hours. Of the patients in groups A and B, 154 (67.3%) and 189 (76.5%), respectively, were converted to SR (p = 0.033). Ventricular arrhythmias (sustained, nonsustained ventricular tachycardia, and TdP) occurred significantly more often in group A than in group B (7.4% vs 1.2%, respectively, p = 0.002). TdP developed in 8 patients (3.5%) in group A and in none (0%) in group B (p = 0.009). The administration of magnesium (despite the high doses used) was well tolerated. In conclusion, the administration of high doses of magnesium probably makes ibutilide a much safer agent, and magnesium increased the conversion efficacy of ibutilide.

Cell-free DNA levels as a prognostic marker in acute myocardial infarction.

Cell-free DNA that originates from cell death, circulates in peripheral blood. There are indications that the infarcted myocardium contributes to an increase of cell-free DNA levels. Our aims were to quantify levels of cell-free DNA in patients with acute myocardial infarction (AMI) and examine their correlation with myocardial markers and with postinfarction (PI) clinical course. Thirteen patients (age 57 +/- 16 year) admitted with AMI and who underwent thrombolysis with reteplase within 6 h from the onset of chest pain were studied. PB samples were collected on admission and for 5 consecutive days. Creatine kinase (CK) and troponin I (TnI) were measured on admission and every 8 h for 3 consecutive days. Clinical events were recorded throughout the hospitalization period. Cell-free DNA levels were also measured in 30 healthy controls. Log-transformed mean (+/-SE) of maximum free DNA values in patients higher than controls (6873 +/- 357 g.e./mL verses 4112 +/- 234 g.e./mL, P < 0.0001). Log-transformed maximum values of CK and TnI were correlated with log-transformed free DNA values of first (r = 0.62, P = 0.02/r = 0.68, P = 0.01) and second (r = 0.57, P = 0.04/r = 0.72, P = 0.0053) PI day. Nine patients (group A) had an uncomplicated PI clinical course and four patients (group B) had recorded events (three with angina and one death). Free DNA levels on the second PI day were higher in group B than group A (1298.0 +/- 796.0 g.e./mL verses 244.6 +/- 257.7 g.e./mL, P = 0.003). In conclusion, free DNA levels are significantly higher in patients with AMI than in controls and may play a role in the prognosis of these patients.

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.

Radiation doses to patients and cardiologists from permanent cardiac pacemaker implantation procedures.

BACKGROUND: The purpose of this study was to determine the patient and cardiologist doses during the implantation of permanent cardiac pacemakers under fluoroscopic control. METHODS: For 55 procedures concerning three different types of pacemakers (DDD, VDD, and VVI), the dose-area product (DAP) meter readings and fluoroscopy times were recorded. From these data, the dose to the operating cardiologist was estimated. RESULTS: The median values of DAP and fluoroscopy time for all the procedures monitored were 11.4 Gycm(2) and 6.6 minute, respectively. For the 22 DDD, 21 VDD, and 12 VVI pacemakers implanted, the respective DAP median values were 14.7, 9.9, and 7.3 Gycm(2) and the respective median fluoroscopy times were 8.4, 5, and 2.9 minutes. The median doses to the hands, chest, eyes, and legs of the cardiologist conducting the manipulations were estimated to 0.21, 0.06, 0.03, and 0.11 mGy, respectively, per procedure. CONCLUSIONS: Compared to the existing literature, the median DAP value of this study is almost identical to the 11.2 Gycm(2) reported from a sample of 627 patients in 17 different x-ray rooms, whereas the fluoroscopy times are within the range of values reported by other authors. Concerning the cardiologist exposure, the estimated values indicate that the implantation of pacemakers is a procedure that does not involve a severe risk, especially if it is taken into account that lead aprons and collars are routinely used.

Adenosine stress myocardial perfusion tomographic imaging in patients with significant aortic stenosis.

BACKGROUND: Myocardial perfusion scintigraphy has been used by some investigators for the diagnosis of coronary artery disease (CAD) in patients with mild, moderate, and moderate to severe aortic stenosis, with various results. The aim of this study was to assess the safety and diagnostic accuracy of adenosine stress myocardial perfusion scintigraphy (adenosine single photon emission computed tomography [Ad-SPECT]) for the detection of CAD in patients with significant aortic stenosis. METHODS AND RESULT: The study included 75 patients with significant aortic stenosis (maximal instantaneous aortic valve gradient >80 mm Hg [range, 81-149 mm Hg] and aortic valve area <0.75 cm2). All patients underwent Ad-SPECT after a 6-minute infusion of adenosine (140 microg/kg body weight per minute). At the third minute of adenosine infusion, a bolus of 3 mCi thallium 201 was injected, and SPECT acquisition was obtained immediately after completion of adenosine infusion. Coronary angiography was performed in all patients. No major complications during adenosine infusion were observed. All unpleasant symptoms lasted for only a few seconds and did not necessitate cessation of the test. Concerning the angiographically diagnosed CAD, we found that Ad-SPECT showed a sensitivity of 88.6%, a specificity of 72.5%, a positive predictive value of 73.8%, a negative predictive value of 87.8%, and a diagnostic accuracy of 80%. CONCLUSIONS: Ad-SPECT is a moderately accurate method for detecting the presence or absence of CAD in patients with severe aortic stenosis. However, further modification of this method is required before it can supplant cardiac catheterization in the preoperative evaluation of patients with severe aortic stenosis.