Transmural changes in mast cell density in rat heart after infarct induction in vivo

The cardiac distribution of mast cells was investigated after the induction of acute myocardial infarction in the rat. The left anterior descending coronary artery (LAD) was occluded by ligation in the infarct group, whereas in sham rats only a superficial ligature was placed beside the LAD. Rats of both groups were killed at 4, 7, 14, 21, 35, and 85 days following surgery. Hearts were excised and formalin-fixed. Mast cell densities were monitored in subepicardial and subendocardial layers of the left ventricle (LV) in 6 microns thick toluidine blue-stained cross-sections. In control (non-operated) animals, mast cell densities were comparable in the LV subepicardial and subendocardial layers (1.5-2.0 cells per mm2). Following infarction, the mast cell density at the subepicardial site of the infarction gradually increased, reaching a maximum of 25 cells per mm2 on day 21, while a non-significant increase was observed at the subendocardial site. In the non-infarcted regions, the mast cell density increased transiently to reach a maximum of 7 cells per mm2 on day 35 in the subepicardial layer. Again, changes in mast cell density in the subendocardial layer were non-significant. In the sham group, a gradual increase to 9 cells per mm2 on day 21 and a subsequent decrease to 5 cells per mm2 on day 85 were observed in the subepicardial layers. These findings indicate a massive accumulation of mast cells in the subepicardial layers of the infarcted region and a small but significant effect of the surgical procedure on cardiac mast cell deposition, especially in the outer layers of the left ventricl

Opportunities for Optimization of Biventricular Pacing Using an Implanted Hemodynamic Monitor

PURPOSE: Optimization of pacing parameters such as AV delay is important in heart failure (HF) patients treated with cardiac resynchronization therapy (CRT). We hypothesized, that an implantable hemodynamic monitor (IHM) might be helpful in identifying the optimal AV-delay. METHODS:10 patients with HF, successfully treated by CRT were also implanted with an IHM that continuously records heart rate, activity, RV pressures and an estimation of the pulmonary artery diastolic pressure (ePAD). First, AV delays were optimized by echo, then different AV-delays (50-190 ms) were randomly programmed using steps of 20 ms. RESULTS: Using the IHM, a U-shaped curve was obtained with an optimal AV delay slightly longer as compared with echo. Shortening the AV interval resulted in increased ePAD values. CONCLUSIONS: In future, CRT optimization may be guided by hemodynamic sensors recording basic cardiovascular measures during daily activities of living. 1