Late elimination of challenging idiopathic ventricular arrhythmias originating from left ventricular summit by anatomical ablation.

Ablation of premature ventricular complexes (PVCs) originating from left ventricular outflow tract (LVOT)/left ventricular summit (LVS) is challenging with considerable rate of failure. Recently, in a novel approach to ablation of these arrythmias, application of radiofrequency energy to anatomically opposite sites of presumed origin of arrythmia, has been associated with moderate procedure success. Although late elimination of PVCs that are persistent following an ablation procedure has been previously reported, this observation has not been studied sufficiently. In this report, firstly, we present three cases of lately eliminated LVS PVCs, then, we discuss possible mechanism of this observation and conclude that after an initial failed attempt of anatomic ablation, operators may choose a period of watchful waiting before attempting a redo procedure.

Effect of radiofrequency on epicardial myocardium after ablation of ventricular arrhythmias from within coronary sinus.

BACKGROUND: Radiofrequency (RF) ablation of idiopathic ventricular arrhythmias (IVA) from the coronary venous system (CVS) has been increasingly performed, but real effect of ablation lesions from CVS on epicardial myocardium has not been studied. OBJECTIVE: To compare effects of RF delivered inside the distal CVS during ablation of IVAs originating from left ventricular summit (LVS) with IVAs ablated from right ventricular outflow tract (RVOT) using cardiac magnetic resonance imaging (CMRI). METHODS: Twenty consecutive patients with IVAs who underwent acutely successful RF ablation at initial appropriate sites, i.e., distal CVS (Group 1, n = 10) or RVOT (Group 2; n = 10) were enrolled. Detailed contrast-enhanced CMRI of each patient was performed 3 months later. Presence and location of scars, distance of CVS to epicardial ventricular myocardium were measured and analyzed. RESULTS: Group 1 consisted of 10 and Group 2 consisted of 10 patients. Three months after the ablation, only three patients in Group 1 had detectable late gadolinium enhancement (LGE) on CMRI while nine out of 10 patients in Group 2 had evident LGE on CMRI (P: 0.02). The mean distance of distal CVS to epicardial anterobasal myocardium was measured to be 8.8 ± 1.6 mm in Group 1. In three cases that had detectable scar on superior anterobasal LV epicardium, the mean distance was 7.4 ± 1.1 mm. CONCLUSIONS: RF delivery inside the CVS is less likely to produce detectable LGE on CMRI compared to RVOT. This may partially explain less than ideal long-term results after ablation of LVS IVAs from within the great cardiac vein/anterior interventricular vein.

Evaluation of acute infection-induced endothelial dysfunction and its potential mediators.

OBJECTIVES: Inflammation plays an important role in the pathophysiology of atherosclerosis. Some studies suggest a link between chronic infections, an inflammatory state, and endothelial dysfunction. However, data related to acute infections are scant. We have investigated: (i) the effect of acute infection on endothelial function; (ii) the role of potential mediators of endothelial dysfunction. METHODS: Forty patients 40 years old with acute infection (mean age 53.9 +/- 8.8 years), without coronary artery disease or its equivalents were enrolled. Endothelial function and blood levels of high sensitive C-reactive protein, interleukin-6, tumour necrosis factor-a, high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), apolipoprotein-A1 (Apo-A1) and apolipoprotein-B100 (Apo-B100) were assessed in the acute infection phase and 1 month after recovery. Endothelial function was evaluated by brachial artery flow-mediated vasodilation (FMD). RESULTS: The intraclass correlation coefficients for intra- and interobserver agreement for FMD measurements were 0.98 (95% CI: 0.95-0.99) and 0.93 (95% CI: 0.83-0.97), respectively. FMD improved significantly 1 month after recovery (P < 0.001). Compared to the levels at 1 month, inflammatory markers, LDL cholesterol, LDL/HDL ratio, Apo-B100 and Apo-B100/Apo-A1 ratio were significantly higher. However, HDL and apo-A1 were significantly lower in the phase of acute infection. Change in FMD from baseline to 1 month after recovery correlated significantly only with the change in Apo-A1 (r = 0.35, P = 0.027). CONCLUSIONS: Acute infection causes transient endothelial dysfunction. It increases inflammatory markers and generates an atherogenic lipid profile. Among the parameters evaluated, only the change in Apo-A1 level was associated with acute infection-induced endothelial dysfunction.

The association of elevated white blood cell count and C-reactive protein with endothelial dysfunction in cardiac syndrome X.

BACKGROUND: The aim of the study is to evaluate the association of inflammatory markers with endothelial function in syndrome X. METHODS: The study population consisted of 59 prospectively enrolled patients (28 women and 31 men; mean age, 50.29 +/- 6.48 years) and 51 healty control subjects (18 women and 33 men; mean age, 51.04 +/- 7.25 years). High-sensitive CRP (hs-CRP), white blood cell (WBC) count and its subtypes [neutrophil (N), lymphocyte (L) and monocyte (M)] were measured in each subject. Endothelial function was assessed with the brachial artery flow-mediated dilatation (FMD) technique. RESULTS: WBC counts and hs-CRP levels were significantly higher in patients who had syndrome X than in control subjects (7.53 +/- 1.52 x 10(9) cells/L versus 6.21 +/- 1.17 x 10(9) cells/L, P = 0.0001, and 3.11 +/- 0.63 mg/L versus 2.68 +/- 0.76 mg/L, P = 0.002, respectively). Neutrophil count and N/L ratio was significantly increased in syndrome X when compared with the control subjects (5.14 +/- 1.10 x 10(9) cells/L versus 4.11 +/- 0.76 x 10(9) cells/L, P = 0.0001 and 2.75 +/- 1.06 versus 2.37 +/- 0.65, P = 0.02, repectively). Other subtype counts were similar between the groups. FMD was impaired significantly in patients who had syndrome X in comparison with the control subjects (5.71 +/- 4.08% versus 16.02 +/- 4.13%, P = 0.0001). There was a significant correlation between hs-CRP levels and FMD measurements (r = -0.44; P = 0.0001). Furthermore, the correlation between WBC count and FMD measurements were also significant (r = -0.48; P = 0.0001). CONCLUSIONS: The present study showed that hs-CRP and WBC count were higher in patients with syndrome X than in control subjects. Furthermore, endothelial function was impaired significantly in patients with syndrome X.The increased levels of hs-CRP and WBC count may suggest that these markers may be used in clinical practice for the assessment of the inflammatory status of the endothelium in syndrome X.

Defibrillation testing and early neurologic outcome.

During implantable cardioverter-defibrillator (ICD) implantation, ventricular defibrillation testing (DFT) is considered a standard procedure. This procedure often requires multiple ventricular fibrillation (VF) inductions. These repeated short episodes of circulatory arrest with global cerebral ischemia may cause neurological damage. In the present study, patients undergoing initial ICD implantation and limited induction of VF for defibrillation safety margin testing were evaluated for pre- and postoperative cognitive and neurologic functions. In addition, the serum neuron specific enolase (NSE) level, which is a biochemical marker of cerebral injury, was evaluated. The study was performed on 16 patients undergoing initial elective transvenous insertion of an ICD. A neurologic examination and cognitive assessment tests were performed 24 to 48 hours before and after ICD. NSE was determined before (NSE 1) and at the end of the surgery (NSE 2), as well as 2 hours (NSE 3), 24 hours (NSE 4), and 48 hours (NSE 5) after implantation. A total of 29 internal shocks (average, 1.8 +/- 0.4) with energy ranging from 14 to 41 J (mean, 20 +/- 5; median, 20 J ) were delivered in the ICD group patients. In one patient, 3 external (50, 200 and 360 J) shocks were required for fast VT induced during ICD lead positioning. The mean duration of VF was 10 +/- 4 seconds and the mean cumulative time in VF was 16 +/- 5 seconds. The mean recovery time between VFs was 5.3 +/- 0.6 minutes. NSE levels were not different from the baseline at any time point in the patients of the group that completed the 48-hour observation period (P > 0.05). The patients did not report any new neurological symptoms after ICD implantation, and repeat examination after the procedure showed no abnormal findings other than those detected in the previous one. There were no statistically significant differences between the preoperative and postoperative scores obtained in the cognitive assessment. Single or two VF inductions and the brief arrest of cerebral circulation during ICD implantation are not associated with permanent neurological injury. However, further studies are needed to confirm this finding.

The effect of high-dose aspirin pre-treatment on the incidence of myonecrosis following elective coronary stenting.

BACKGROUND: Inadequate platelet response to aspirin is associated with increased incidence of peri-procedural myonecrosis. Antiplatelet activity of aspirin can be improved by increasing the dose. High-dose aspirin pre-treatment, therefore, may reduce the incidence of myonecrosis post stenting. METHODS AND RESULTS: Two-hundred patients taking 75-325 mg daily doses of aspirin for at least 2 weeks were randomized for addition or no addition of 500 mg aspirin before elective coronary stenting (aspirin 500 group, n=100 and control group, n=100). Primary endpoint was the occurrence of peri-procedural myonecrosis defined as creatine kinase-myocardial band (CK-MB) elevation of >1x upper limits of normal (ULN). Aspirin 500 patients were significantly younger and more likely to have family history of coronary artery disease, but less likely to have received statins than controls. Elevation of CK-MB was observed in 29% of aspirin 500 patients and 15% of controls (p=0.017). The incidence of non-Q wave myocardial infarction (CK-MB elevation of >3xULN) tended to be higher in the aspirin 500 group than in the control group (5% versus 0%, p=0.059). Multivariate analysis identified baseline aspirin dose (OR: 1.006; 95% CI: 1.002-1.010; p=0.004), aspirin 500 mg treatment (OR: 2.5; 95% CI: 1.2-5.5; p=0.021) and baseline CK-MB level (OR: 1.4; 95% CI: 1.1-1.7; p=0.012) as independent predictors of CK-MB elevation after coronary stenting. CONCLUSION: For patients taking daily low-dose aspirin therapy, supplementation with high-dose aspirin before elective coronary stenting does not reduce, but may increase the incidence of peri-procedural myonecrosis.

Effect of transvenous cardiac resynchronization therapy device implantation on cardiac troponin I release.

BACKGROUND: Pacemaker and implantable cardioverter defibrillator (ICD) implantation increases cardiac troponin I (cTnI) levels which indicates myocardial injury. During implantation of a cardiac resynchronization therapy (CRT) device, balloon inflation for coronary sinus (CS) venogram, cannulation of CS side branch, and electrode advancement may interfere with CS drainage and, hence, may decrease the washout of toxic metabolites from the heart. Thus, CRT implantation may further increase cTnI levels. In this study, we investigated the effects of CRT implantation on cTnI release. METHODS: We included 10 patients (mean age = 57 +/- 15 years) in whom a successful transvenous CRT system was implanted (CRT group). Twenty patients (mean age = 65 +/- 10 years) who underwent a transvenous pacemaker or ICD implantation were included as the control group. Blood samples for cTnI were drawn at baseline and at six, 12, 18, and 24 hours thereafter. RESULTS: Baseline median cTnI levels were similar in CRT and control groups (0.03 ng/mL vs 0.02 ng/mL, respectively; P = 0.1). Postoperative cTnI levels during 24 hours were significantly higher in the CRT group (P < 0.05) by two-way repeated measures of analysis of variance. Post hoc analysis revealed that cTnI levels were higher at the 6th, 12th, 18th, and 24th hours compared to baseline levels (P < 0.001, P < 0.001, P < 0.01, and P < 0.01, respectively). There was a significant difference in the area under the curves (AUCs) of cTnI measurements (1.79 hr.ng/mL in the CRT group and 0.78 hr.ng/mL in the control group, P < 0.05). CONCLUSION: Postoperative cTnI levels were higher after CRT implantation than simple pacemaker/ICD implantation. This may be due to CS manipulation during CRT implantation.