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.

Predictors for very late stent thrombosis after drug-eluting stent implantation in diabetic patients.

AIMS: Despite encouraging results with drug-eluting stents (DES) reported in diabetic patients, the long-term safety is unknown because of very late stent thrombosis (VLST). We investigated the incidence, risk factors and clinical manifestations of VLST in diabetic patients treated with DES, during long-term clinical follow-up. METHODS AND RESULTS: A total of 610 consecutive diabetic patients underwent PCI with DES. Dual antiplatelet treatment (APLT) for 12 months received 93%, more than 12 months 72% and statin treatment 93% of patients. Clinical follow-up of at least 12 months post DES implantation was obtained in 597/610 (98%) patients. The incidence of VLST was 1.8%, and 1.7% of patients developed stent thrombosis (ST) up to 12 months. All patients with VLST presented with sudden cardiac death and 82% were on dual APLT at the time of the event. In a multivariate model the only predictor for VLST (HR: 20.58, 95% CI 5.17-81.90, p < 0.001) and overall ST (HR: 4.38, 95% CI 1.73-11.10, p = 0.002) was ejection fraction < 40%. CONCLUSIONS: The incidence of ST in diabetic patients undergoing PCI with DES and receiving dual APLT is low at long-term clinical follow-up. The only predictor for VLST and overall ST was depressed left ventricular systolic function.

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.