Ablation of residual potentials along the circumferential line reduces acute pulmonary vein reconnection.

INTRODUCTION: Acute pulmonary vein (PV) reconnection is frequently encountered in patients undergoing PV isolation (PVI) procedure for the treatment of atrial fibrillation. In this study, we investigated whether the identification and ablation of residual potentials (RPs), after the initial achievement of PVI, reduces acute PV reconnection rate. METHODS: Following PVI in 160 patients, mapping along the ablation line was performed to identify RPs, defined as bipolar amplitude ≥0.2 mV or 0.1-0.19 mV combined with a negative component of the unipolar electrogram. Ipsilateral PV sets with RPs were randomized to either no further ablation (Group B) or to additional ablation of the identified RPs (Group C). The primary study endpoint was spontaneous or adenosine-mediated acute PV reconnection after a 30-min waiting period and was also evaluated in ipsilateral PV sets without RPs (Group A). RESULTS: After isolation of 287 PV pairs, 135 had no RPs (Group A), whereas the remaining PV pairs were randomized to either Group B (n = 75) or Group C (n = 77). Ablation of RPs resulted in a reduction of spontaneous or adenosine-mediated PV reconnection rate (16.9% in Group C vs 48.0% in Group B; p < 0.001). Group A was associated with a significantly lower percentage of acute PV reconnection as compared to Group B (5.9% vs 48.0%; p < 0.001) and Group C (5.9% vs 16.9%; p = 0.016). CONCLUSION: After PVI achievement, the absence of RPs along the circumferential line is associated with a low likelihood of acute PV reconnection rate. Ablation of RPs significantly reduces spontaneous or adenosine-mediated acute PV reconnection rate.

Possible role of circulating endothelial cells in patients after acute myocardial infarction.

Acute myocardial infarction (AMI) occurs as a result of insufficient myocardial perfusion leading to cell necrosis. This is most commonly due to the obstruction of the coronary artery by ruptured atherosclerotic plaque and thrombosis. Damaged ischemic and necrotic myocardial cells release pro-inflammatory substances in tissue and plasma, leading to a systemic inflammatory response. Profound systemic inflammatory response during ischemia/reperfusion injury causes disruption of endothelial glycocalyx and detachment of endothelial cells that express von Willebrant factor (vWF). We hypothesize that circulating vWF+ endothelial cells could act as antigen presenting cells which interact with T and NK cells directly, by cell to cell contact and indirectly by cytokine and chemokine secretion, leading to the immune response towards inflammation. Analyzing the frequency, phenotype and pro-inflammatory substances produced in circulating vWF positive (+) cells in patients with AMI could be beneficial to determine the severity of the pro-inflammatory response, according to the level of endothelial dysfunction in the early period of AMI. To evaluate these hypotheses, we suggest to determine frequency, phenotype, and ability of cytokine/chemokine production in circulating vWF+ endothelial cells by simultaneous surface and intracellular cell staining, and flow cytometry analysis. Secretion of pro-inflammatory cytokines and chemokines, pro-atherogenic substances and the components of glycocalyx might be measured in supernatants of magnetically separated or sorted vWF+ endothelial cells, as well as in the serum of a patient with acute AMI by enzyme linked-immunoassay tests. The interaction of increasing concentrations of isolated circulating vWF+ endothelial cells and cognate T and NK cells might be investigated by lymphocyte proliferation rate, cytotoxic mediators' expression, and cytokine production. If our hypothesis is correct, characterization of circulating vWF+ endothelial cells could grant us greater insight into their role in pathophysiology of AMI and the degree of myocardial damage.

Correlation between immunological-inflammatory markers and endothelial disfunction in the early stage of coronary heart disease.

Classical risk factors for endothelial dysfunction (ED), such as age, gender, total cholesterol, high-density lipoprotein cholesterol, systolic blood pressure, and smoking history are utilised for the Framingham score and Systemic Coronary Risk Estimation (SCORE) for evaluation of the 10-year cardiovascular risk in routine practice. Nonetheless, pro-inflammatory mediators are deeply involved in the initiation and the progression of ED and coronary artery disease (CAD), and act additionally or independently of metabolic factors before clinical manifestations of the disease appear. C-reactive protein, a marker of intimal thickening of the myeloid-related protein 8/14 heterodimer, monocyte chemotactic protein 1, interleukin-15, the cytotoxic mediator, granulysin, and the matrix metalloproteinase 9 could be valuable, single, fast, and non-invasive laboratory tools for ED deterioration degree assessment. We propose to investigate the impact of pro-inflammatory biomarkers on ED, measured by previously established clinical methods in patients with yet undiagnosed CAD and at medium risk for an acute coronary event. It could be useful to measure and correlate the concentration of particular inflammatory markers in peripheral blood samples and the results of the Framingham and SCORE charts, multi-slice computed tomography coronary angiography, echocardiography, brachial artery flow-mediated dilatation, carotid-femoral pulse wave velocity, ankle-brachial index, carotid wall thickening, myocardial perfusion scintigraphy, and particularly, cardiac magnetic resonance imaging. The goal would be that the degree of correlation between particular inflammatory markers and the results of some methods for the assessment of ED or cardiac ischaemic imaging could be emphasised and pro-inflammatory markers positioned in the pathogenetic algorithm of CAD.