Contractile function was reduced with increasing pacing frequency indicated by significant 'freq' main effects (P<0.001 in Table 4).
In both groups, diastolic sarcomere length shortened as pacing frequency increased, i.e., there was a lack of full relaxation with increasing pacing frequency.
In one study in patients with atrial fibrillation and absent intrinsic AV conduction, a decrease in optimal VV delay with increasing pacing rate was noted [ 55].
As seen in Figure 5F, diastolic sarcomere length was reduced with increasing pacing frequency in both groups and significantly more so in the HG without Zn2+.
Shortening of APD with increasing pacing frequency is a well-known response of cardiac muscle (2, 26), and shortening of CaT duration has also been observed (38).
Most notably, a reduction in diastolic sarcomere length with increasing pacing frequencies, i.e., incomplete relaxation, was more pronounced in the HG compared to controls, but was normalized with extracellular Zn2+ application.
Diastolic sarcomere length shortened with increasing pacing frequency in both HG and nonHG (note 'freq' main effect P<0.001 in Table 4), but significantly more so in the HG compared to nonHG (indicated by HG×freq interaction P=0.005 in Table 4).
There were also significant 'HG×freq' interactions for peak shortening and maximum shortening velocity (P<0.01 in Table 4) suggesting that the HG group was more susceptible to the reduction in contractile function with increasing pacing frequency.
Most notably, a reduction in diastolic sarcomere length with increasing pacing frequencies, i.e., incomplete relaxation, was more pronounced in the HG compared to controls, but was normalized with extracellular Zn2+ application, implicating that the detrimental effect of HG on cardiomyocyte Ca2+ regulation can be amelioration by Zn2+[ 60].
