## 3 Results
### Changes in LVGLS during Pacing  
Significant changes in LVGLS were observed overall in response to higher-paced HRs (Figure 1). Thirty-four (76%) patients exhibited deteriorations in LVGLS equal to or greater than 10%; only one patient exhibited some degree of improvement (Figure S1). Figure 1 also documents changes in LVGLS in participants who did and who did not exhibit deterioration in response to an increasing HR. An example of patient with and without worsening of LVGLS is reported in Figure 2. The percentage of participants exhibiting LVGLS deterioration was higher among those managed with an ICD either with or without CRT, at 71% and 86%, respectively, than in participants with PM (57.1%). However, this difference did not achieve statistical significance (\(p\) = 0.28). As shown in Table 2, participants with deteriorating LVGLS were those with reduced LV function, as determined by baseline LVEF, LVGLS, and Tei index values. \begin{table}
\begin{tabular}{l c c c} \hline \hline  & \multicolumn{2}{c}{**Clinical Characteristics**} & \multicolumn{2}{c}{**Echocardiographic Characteristics**} \\ \hline Age (years) & 66 \(\pm\) 13 & LVEDV (mL) & 176 \(\pm\) 87 \\ Male, n (\%) & 36 (80\%) & LVESV (mL) & 121 \(\pm\) 76 \\ BMI (kg/m\({}^{2}\)) & 24 \(\pm\) 4 & LVEF (\%) & 36 \(\pm\) 13 \\ Ischemic cardiomyopathy, n (\%) & 19 (42\%) & LVGLS (\%) & \(-\)10.2 \(\pm\) 4.0 \\ Arterial hypertension, n (\%) & 29 (64\%) & LV Tei index & 0.64 \(\pm\) 0.23 \\ Diabetes mellitus, n (\%) & 13 (29\%) & SV (mL) & 65 \(\pm\) 16 \\ Dyslipidemia, n (\%) & 32 (71\%) & CO (L/min) & 4.2 \(\pm\) 1.1 \\ CHF, n (\%) & 39 (87\%) & CI (L/min/m\({}^{2}\)) & 2.2 \(\pm\) 0.6 \\ SAP (mmHg) & 116 \(\pm\) 21 & LVMI (g/m\({}^{2}\)) & 156 \(\pm\) 40 \\ Heart rate (bpm) & 66 \(\pm\) 7 & LAVi (mL) & 40 \(\pm\) 19 \\ LVEF \(\leq\) 40\%, n (\%) & 31 (69\%) & e’ s (cm/s) & 5.0 \(\pm\) 1.4 \\ NYHA class, n (\%) I & 7 (16\%) & e’ l (cm/s) & 6.9 \(\pm\) 2.8 \\ NYHA class, n (\%) II & 21 (46\%) & e’ m (cm/s) & 5.9 \(\pm\) 1.9 \\ NYHA class, n (\%) III & 17 (38\%) & E/e’ ratio & 13.1 \(\pm\) 5.9 \\ GFR-EPI (mL/min/1.73 m\({}^{2}\)) & 80 \(\pm\) 17 & MR (a.u.) & 2.0 \(\pm\) 0.9 \\ NT-proBNP (pg/mL) & 2879 \(\pm\) 2841 & TAPES (mm) & 18.9 \(\pm\) 3.5 \\ ACEI/ARBs, n (\%) & 22 (49\%) & RVGLS (\%) & \(-\)15.5 \(\pm\) 3.8 \\ ARNI, n (\%) & 12 (27\%) & RVfvLS & \(-\)20.9 \(\pm\) 5.2 \\ Beta-blockers, n (\%) & 42 (93\%) & CVP (mmHg) & 6.2 \(\pm\) 3.2 \\ MRA, n (\%) & 22 (49\%) & PASP (mmHg) & 36 \(\pm\) 13 \\ Loop diuretics, n (\%) & 32 (71\%) & TR (a.u.) & 1.8 \(\pm\) 1.1 \\ \hline \hline \end{tabular}  
* ACEI, inhibitors of angiotensin converting enzyme; ARB, angiotensin II receptor blockers; BMI, body mass; index; CI, cardiac index; CO, cardiac output; CVP, central venous pressure; e’, early septal mid diastolic velocity at tissue Doppler imaging; e’, early lateral midital diastolic velocity at tissue Doppler imaging; E/e’, ratio between early pulsed Doppler diastolic mitral velocity and the mean value of e’s and e’, i’, GFR-EPI, estimated glomerular, filtration rate by EPI formula; LAVi, indexed left atrial volume; LVED, left ventricular end-diastolic volume; LVESV, left ventricular end-systolic volume; LVEF, left ventricular ejection factor; LVGLS, left ventricular global longitudinal strain; LV Tei index; left ventricular Tel index; MR, mitral regurgitation, MRA, mineralocorticoid receptor antagonists; SV, stroke volume; LVMI, indexed left ventricular mass; PASP, peak pulmonary systolic pressure; RVfvRLS, right ventricular free wall longitudinal strain; RVGLS, right ventricular global longitudinal strain; SAP: systolic arterial pressure; TAPSE, peak of systolic excursion of the tricuspid annulus; TR, tricuspid regurgitation.  
\end{table} 
Table 1: Clinical and echocardiographic characteristics of the study population.