Cell-free DNA levels in acute myocardial infarction patients during hospitalization.

OBJECTIVES: The objectives of this study were to investigate cell-free DNA daily concentration changes following an acute myocardial infarction (AMI) and to assess any correlations with complications during hospitalization. METHODS AND RESULTS: Serial cell-free DNA level determinations were performed by quantitative Real-Time PCR in 47 AMI patients once daily during hospitalization (235 samples) and once in 100 healthy subjects. Cell-free DNA concentrations are significantly higher in patients throughout hospitalization compared to healthy subject levels (2.644 (SE 0.0952) vs. 1.519 (SE 0.0566), P < 0.001). The median maximum cell-free DNA concentration was 3.5-fold higher (Mann Whitney P = 0.0035) in 20/47 patients with complicated post AMI course--group I--(1719.7, range 117.32-4996212.1 GenEq/ml plasma) compared with 27/47 patients without complications--group II--(492.9, range 56.43-4715.15 GenEq/ml plasma). Substantial differences exist between cell-free DNA concentrations measured on t(pre) (the day before the complication) and t(c) (the day the complication occurred) as well as t(post) (the day after the complication) in group I whereby cell-free DNA rises significantly in t(c) and remains elevated in t(post) (t(pre) vs. t(c), 2.445 vs. 2.965, P = 0.0171 and t(pre) vs. t(post) 2.445 vs. 2.913, P = 0.023). CONCLUSIONS: Cell-free DNA concentrations were elevated in AMI patients compared to healthy control subjects, rise significantly when complications occur and have a potential clinical value in monitoring patient progress during hospitalization.

Infective endocarditis in an adult patient with CHARGE association: a case report.

A case of an adult patient with CHARGE association complicated with infective endocarditis is presented.

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.

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.