We scanned the Holter ECGs from the THEW database to identify the recordings with 30-min epochs that were meeting the selection criteria described above. At least one epoch could be found in 97 LQT-1 recordings and in 154 recordings from healthy individuals. An additional 28 records were excluded from healthy individuals and 52 records in LQT-1 subjects because: 1) they did not include enough valid QT intervals due to the low signal quality or/and, 2) the correlation between detected QT and RR values was lower than 0.3.
In the LQT-1 cohort (N=97, age 23±16 years) were 40 men and 57 women, 49 of them were on beta blocker therapy (20 men and 29 women), 48 were off beta blocker (20 men and 28 women). In the healthy cohort, we identified 154 healthy subjects, age: 36±14 yrs, including 73 women (47%).
The average QTc, RR, GainL, GainF, and τ values are reported in for the healthy vs. the LQT-1 patients off beta-blocker. Also, we report their values between genders for both the control and the LQT-1 groups excluding the patients on beta-blockers. Finally, we evaluated whether the QT-RR dynamic coupling is different between controls and LQT-1 patients with a concealed form of the syndrome or namely a range of normal QTc interval duration (370<QTc<430 ms). This group includes 98 recordings from healthy individuals (age 36±14 years, 44 men), and 24 ECGs from LQT-1 patients (age 21±16 years, 16 men).
Values of the ECG measurements and the QT static and dynamic parameters in healthy and LQT-1 patients off beta-blocker
The control group had a significantly weaker (p<0.000001) fast gain (0.03±0.01) than slow gain (0.18±0.07) which is consistent with a normal hysteresis i.e. the long term response to heart rate changes is larger than the immediate response.16
All investigated ECG parameters were statistically different between the LQT-1 and the control groups. The LQT-1 patients had lower heart (RR: 453±35 vs. 384±26 ms, p<0.00001), prolonged QTc interval, and a shorter time adaptation (122±44 vs. 172±92 beats, P<0.00001). This was associated with an increased fast (GainF
: 0.03±0.01 vs. 0.05±0.02, p<0.00001) and slow gains (GainL
: 0.18±0.07 vs. 0.22±0.06, p<0.00001). Interestingly, the gender differences in GainL
(higher in women: 0.19±0.07 vs. 0.17±0.06, p<0.01) and τ values (longer in men: 186±109 vs. 156±65 beats, p<0.05) in healthy were not present in LQT-1 patients. Indeed, LQT-1 women and LQT-1 men presented a similar short time adaptation (119±41 vs. 125±48 beats, p=NS) combined with a strong slow gain (0.23±0.07 vs. 0.21±0.06, p=NS). Finally, the comparison of the characteristics of the QT-RR dynamic coupling for controls and LQT-1 patients with QTc interval in normal ranges, i.e. 370<QTc<430 ms, suggested that the intrinsic QT adaptation is abnormal event in patients with normal QTc interval. Indeed in this subgroup of individuals, the trends toward higher fast gain (0.037±0.01 vs. 0.030±0.01, p=0.02) and shorter time adaptation constant (116±45 vs. 167±67, p<0.001) was still strong.
The analysis of the set of recordings of LQT-1 patient on and off beta-blockers was implemented yet it did not show any difference. We explained this result by the lack of enough RR variation in patients on beta-blockers.
The curves describing the QT interval variation following an abrupt change in heart rate for the healthy, LQT1 and concealed LQT1 and healthy (QTc <370,430> ms) are in . The mean levels of QT parameters from were used at the simulation. It shows that the QT duration during increased heart rate in controls is significantly shorter than n LQT-1 patients, not looking on nearly similar QTc in concealed groups.
Figure 2 The curves describing the QT interval variation following an abrupt change in heart rate for the healthy, LQT-1 patients, LQT-1 patients with concealed QTc prolongation (LQT1C), and healthy subject (QTc <370,430> ms, HealthyC). It shows (more ...)