Rick Schreurs

48 Chapter 3 Table 2. Baseline patient characteristics Total patient no. (n) 22 ICM (n, %) 13 (59) Age (years) 67±9 LVEF (%) 29±6 Men (n, %) 20 (91) Medical history (n, %) Body-mass index (kg/m 2 ) 29±5 - Myocardial infarction 13 (59) NYHA class (n, %) - Prior AF 10 (46) - II 13 (59) - Hypertension 9 (41) - III 9 (41) - CABG 7 (32) PR-interval (ms) 261±32 - Diabetes mellitus 6 (27) P wave duration (ms) 153±22 - COPD 6 (27) PR segment (ms) 108±31 - Ischemic stroke 5 (23) QRS duration (ms) 123±19 Medication (n, %) QRS morphology (n, %) - Beta-blocking agents 19 (86) - IVCD 12 (55) - ACE-I / ARB inhibitors ( 19 (86) - Normal 8 (36) - Diuretics 18 (82) - RBBB 2 (9) - Antiarrhythmic 7 (32) - Aldosterone antagonist 5 (23) Results are presented as mean±SD or n (%). ACE-I: angiotensin-converting enzyme inhibitors, AF: atrial fibrillation, ARB: angiotensin II receptor blocker, CABG: coronary artery bypass grafting, COPD: chronic obstructive pulmonary disease, ICM: ischemic cardiomyopathy, IVCD: intraventricular conduction delay, LVEF: left ventricular ejection fraction, NYHA: New York Heart Association, PCI: percutaneous coronary intervention, RBBB: right bundle branch block. Figure 6A presents LV pressure-volume loops of a patient during BiV (left) and RV pacing (right). As compared to baseline, BiV pacing increased LV stroke volume and stroke work (width and area of the loop, respectively), with the most pronounced benefit at an AV-delay of 50% of intrinsic PR-interval. In contrast, RV pacing tended to reduce stroke volume and stroke work, particularly at shorter AV-delays. It can also be observed that peak LV pressure diminished during RV pacing. In the entire cohort of patients, BiV pacing increased QRS duration moderately, whereas a more pronounced prolongation occurred by applying RV pacing ( Table 3 ). BiV pacing at an AV-delay of 50% of intrinsic PR-interval significantly increased LV stroke volume by 34±40% ( Figure 6B ) and LV stroke work by 26±31% ( Figure 6C ), when compared to baseline. The increase in LV stroke work provided by BiV pacing coincided with slight but significant increases in LV end-diastolic pressure (on average 2 mmHg) and LV dP/dt max and largely unchanged systolic LV pressure ( Table 3 ). In contrast, restoration of the AV- delay with RV pacing did not change or even decreased stroke volume and stroke work compared to baseline ( Table 3 ). The decrease in stroke work during RV pacing at short AV-delays coincided with significant reductions in stroke volume, systolic LV pressure and LV dP/dt max ( Table 3 ).