A generic model of overall heart geometry for model based studies of electrical, mechanical, and ion-kinetics aspects of the heart

A hierarchical set of tricubic deformations is used to map generic coordinates to real world coordinates. This provides a unifying framework to compare and combine different computational models. Large-scale cellular models can now use intramural fiber orientation measured with diffusion tensor imaging. Estimated activation times of the heart can be used to compute contraction and to determine how that in turn affects the surface ECG. These computations all use different models, but they can all use the same generic coordinates

A generic model of overall heart geometry for model based studies of electrical, mechanical, and ion-kinetics aspects of the heart

A hierarchical set of tricubic deformations is used to map generic coordinates to real world coordinates. This provides a unifying framework to compare and combine different computational models. Large-scale cellular models can now use intramural fiber orientation measured with diffusion tensor imaging. Estimated activation times of the heart can be used to compute contraction and to determine how that in turn affects the surface ECG. These computations all use different models, but they can all use the same generic coordinates

Properties of unipolar electrograms recorded with a multielectrode basket catheter

In the past few years, clinical trials with multielectrocle "basket" catheters have provided unique recordings from the endocardium of intact in-situ human hearts. Analysis of these recordings is difficult because unipolar electrograms obtained from a basket catheter in the blood-filled cavity differ from those obtained by other mapping techniques such as endocardial balloons used during antiarrhythmic surgery. We investigated these differences using basket catheter recordings obtained in isolated porcine and canine hearts that could be filled with perfusion fluid and evacuated at will. The results indicated that the differences between basket and balloon recordings are largely attributable to the presence and absence of blood. Activation maps obtained in the presence and absence of blood were usually similar and only differed in a minority of cases at sites in which electrograms revealed multiple deflections. In conclusion, unipolar mapping using a basket catheter can be used with confidence for the creation of activation maps if appropriate care is taken in the interpretation of fractionated electrogram

Conversion of left ventricular endocardial positions from patient-independent co-ordinates into biplane fluoroscopic projections.

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Reduced acute myocardial ischemia–reperfusion injury in IL-6-deficient mice employing a closed-chest model

Objective and design: We examined the role of IL-6 in the temporal development of cardiac ischemia–reperfusion injury employing a closed-chest I/R model. Materials/methods: Infarction, local and systemic inflammation, neutrophil infiltration, coagulation and ST elevation/resolution were compared between wild-type (WT) and IL-6-deficient (IL-6−/−) mice after 1 h ischemia and 0, ½, 3, and 24 h reperfusion. Results: IL-6 deficiency reduced infarct size at 3 h reperfusion (28.8 ± 4.5 % WT vs 17.6 ± 2.5 % IL-6−/−), which reduction persisted and remained similar at 24 h reperfusion (25.1 ± 3.0 % WT vs 14.6 ± 4.4 % IL-6−/−). Serum Amyloid A was reduced at 24 h reperfusion only (57.5 ± 4.9 WT vs 24.8 ± 5.6 ug/ml IL-6−/− mice). Cardiac cytokines (IL-6, IL-1β and TNFα) peaked at 3 h reperfusion, but IL-1β and TNFα levels were unaffected by IL-6 deficiency. Significant neutrophil influx was only detected at 24 h reperfusion and was similar for WT and IL-6−/−. Tissue factor peaked at 24 h reperfusion, whereas fibrin/fibrinogen peaked at 3 h reperfusion and was completely resolved at 24 h reperfusion; both coagulation factors were unaltered by IL-6 deficiency. Prolonged ST elevation was observed during ischemia that completely resolved for both genotypes at early reperfusion. Conclusions: The data suggest that, in the absence of major surgical intervention, IL-6 contributes to the development of infarct size in the early phase of reperfusion; this contribution did not depend on neutrophil influx, IL-1β and TNFα, tissue factor and fibrin.Bio-Electronic

Mechanism of right precordial ST-segment elevation in structural heart disease: Excitation failure by current-to-load mismatch

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