| 1. |
- Odenstedt, Jacob, 1968, et al.
(författare)
-
Distorted T-vector loop and increased heart rate are associated with ventricular fibrillation in a porcine ischemia-reperfusion model
- 2009
-
Ingår i: Journal of Electrocardiology. - : Elsevier BV. - 0022-0736 .- 1532-8430. ; 42:3, s. 267-73
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The ventricular repolarization (VR) response to short-lasting coronary occlusion has been characterized by 3-dimensional vectorcardiography during angioplasty in humans; the T-vector loop becomes distorted (increased T(avplan)) and more circular (decreased T(eigenvalue)), but these changes have not been related to ventricular arrhythmias. PURPOSE: The VR response was therefore explored in a porcine ischemia-reperfusion model and compared in pigs with (n = 16) vs without (n = 17) ventricular fibrillation (VF). METHODS: Different aspects of VR were evaluated at baseline, at maximum ischemia, before reperfusion and at the subsequent ST maximum, after 1 hour of reperfusion, and before VF. Three aspects of the VR response were assessed: the ST-segment, the T-vector angles, and the T-vector loop morphology. RESULTS: All parameters changed significantly from baseline during ischemia and/or reperfusion. The early changes were similar to those previously observed in humans during angioplasty. The VF episodes were preceded by a significantly exaggerated T-loop distortion (increased T(avplan)) and increased heart rate. CONCLUSION: Aggravated T-loop distortion might, in this porcine ischemia-reperfusion model, reflect aspects of VR relevant to arrhythmogenesis.
|
|
| 2. |
- Odenstedt, Jacob, 1968
(författare)
-
Porcine myocardial ischemia-reperfusion studies on cardioprotection, ventricular arrhythmia and electrophysiology
- 2009
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Background: Coronary artery disease is the primary cause of death in adults in the industrialised world and ventricular fibrillation associated with myocardial ischemia is the main cause of sudden cardiac death. Restoration of blood flow and preservation of myocardial integrity throughout ischemia and reperfusion is essential to improve clinical outcome. Alteration in calcium handling and its consequences are central features of these events. Sympathico-vagal imbalance and electrophysiological alterations are important predisposing factors for malign ventricular arrhythmia and sudden cardiac death. Aims: To investigate whether ultra-short acting calcium antagonism or spinal cord stimulation (SCS) could reduce myocardial ischemia and infarct size in a porcine closed-chest model. Furthermore, the feasibility of endocardial electromechanical mapping for defining myocardial viability during acute infarction was evaluated. Finally, non-invasive electrophysiological characteristics of ischemia-reperfusion and the occurrence of ventricular arrhythmias were investigated as well as the effects of SCS on these measures and events. Methods: Myocardial infarction was induced by 45 minute coronary occlusion in closed-chest landrace pigs. An ultra-short acting calcium antagonist, clevidipine, was administered into the myocardium at risk. Myocardial viability was assessed by Evans Blue, tetrazolium and endocardial electromechanical mapping and the correlation between these methods was investigated. Three-dimensional vectorcardiography was continuously recorded, analysed offline with regard to depolarisation and repolarisation parameters, and later correlated to myocardial ischemia and ventricular arrhythmia. In a second series of experiments, the effects of SCS were investigated with regards to haemodynamics, infarct size, ventricular arrhythmia and electrophysiology. Results: Clevidipine did not reduce infarct size. Electrical and mechanical activities were both impaired within the infarct zone, but the precision of electromechanical mapping to identify an infarct was poor, and due to intersegmental variability and arrhythmia. All T vector loop parameters changed in response to ischemia. Ventricular arrhythmia was more prevalent during proximal left anterior descending coronary artery occlusion, which was associated with more pronounced electrophysiological alterations. In the SCS group, ventricular arrhythmia occurred less frequently in association with signs of less ischemia and electrical alterations. SCS did not reduce infarct size. Conclusions: Infarct size was neither reduced by ultra-short acting calcium antagonism nor by SCS, but the latter seemed to have cardioprotective properties as it reduced the occurrence of ventricular arrhythmia. Endocardial electromechanical mapping was not feasible for acute myocardial viability assessment.
|
|
