Arrhythmia-induced Cardiomyopathies
Early haemodynamic changes are evident almost immediately after initiation of rapid ventricular rates. In a dog model of heart failure, acute onset of pacing resulted in a decrease in arterial blood pressure and cardiac output and increases in right atrial and pulmonary wedge pressure in 24 h which persisted after 3 weeks of pacing. In most animal models, changes in LV filling and contraction properties have been completed by 4–5 weeks of rapid pacing. Furthermore, pressure–volume loops using intracardial recordings have been analysed before and immediately after short-term restoration of the normal ventricular activation sequence in chronic double-chamber paced patients—by switching from a DDD—to an AAI mode). End-systolic elastance and its ratio to effective arterial elastance were improved acutely after switching to AAI mode of pacing.
Usually, patients seek medical advice only after months to years of symptomatic congestive heart failure. The time to recovery after treatment is considered to be rate- and duration dependent. During recovery, rapid clinical improvement has been demonstrated. In contrast, echocardiographic LV diastolic cavity size remains elevated with only a gradual and incomplete return towards normalization by 4 weeks of recovery. Nearly complete recovery of symptoms and LV contractility is expected within 3 months after rhythm or rate control of the tachyarrhythmia. Similar results were published in patients who underwent atrioventricular node ablation and pacemaker insertion due to AF with high ventricular rates despite optimal medical therapy. In contrast, Brignole et al. and the most recent randomized AIRCRAFT study did not confirm such significant differences in the New York Heart Association (NYHA) functional class or objective measures of cardiac function. Probably, concerns of the possible detrimental impact of RV apical pacing must be taken into account.
Two further points have to be taken into consideration. Left ventricular hypertrophy persisting after weeks of discontinuation of pacing may be attributed to post-pacing response of myocytes to hypertrophic triggers. This response may be further enhanced by persistent LV dilatation. More importantly, despite normalization of EF, persistent LV remodelling has been demonstrated (LV dimensions and volumes significantly and persistently elevated when compared with controls) with implications on duration and type of antiarrhythmic therapy.
Time Progression and Recovery
Early haemodynamic changes are evident almost immediately after initiation of rapid ventricular rates. In a dog model of heart failure, acute onset of pacing resulted in a decrease in arterial blood pressure and cardiac output and increases in right atrial and pulmonary wedge pressure in 24 h which persisted after 3 weeks of pacing. In most animal models, changes in LV filling and contraction properties have been completed by 4–5 weeks of rapid pacing. Furthermore, pressure–volume loops using intracardial recordings have been analysed before and immediately after short-term restoration of the normal ventricular activation sequence in chronic double-chamber paced patients—by switching from a DDD—to an AAI mode). End-systolic elastance and its ratio to effective arterial elastance were improved acutely after switching to AAI mode of pacing.
Usually, patients seek medical advice only after months to years of symptomatic congestive heart failure. The time to recovery after treatment is considered to be rate- and duration dependent. During recovery, rapid clinical improvement has been demonstrated. In contrast, echocardiographic LV diastolic cavity size remains elevated with only a gradual and incomplete return towards normalization by 4 weeks of recovery. Nearly complete recovery of symptoms and LV contractility is expected within 3 months after rhythm or rate control of the tachyarrhythmia. Similar results were published in patients who underwent atrioventricular node ablation and pacemaker insertion due to AF with high ventricular rates despite optimal medical therapy. In contrast, Brignole et al. and the most recent randomized AIRCRAFT study did not confirm such significant differences in the New York Heart Association (NYHA) functional class or objective measures of cardiac function. Probably, concerns of the possible detrimental impact of RV apical pacing must be taken into account.
Two further points have to be taken into consideration. Left ventricular hypertrophy persisting after weeks of discontinuation of pacing may be attributed to post-pacing response of myocytes to hypertrophic triggers. This response may be further enhanced by persistent LV dilatation. More importantly, despite normalization of EF, persistent LV remodelling has been demonstrated (LV dimensions and volumes significantly and persistently elevated when compared with controls) with implications on duration and type of antiarrhythmic therapy.