Implantable cardiac devices are well known in the art. An implantable cardiac device may take the form of an implantable defibrillator (ICD) which treats accelerated rhythms of the heart such as fibrillation or an implantable pacemaker which maintains the heart rate above a prescribed limit, such as, for example, to treat a bradycardia. Implantable cardiac devices are also known which incorporate both a pacemaker and a defibrillator.
A pacemaker may be considered as a pacing system. The pacing system is comprised of two major components. One component is a pulse generator which generates the pacing stimulation pulses and includes the electronic circuitry and the power cell or battery. The other component is the lead, or leads, which electrically couple the pacemaker to the heart.
Pacemakers deliver pacing pulses to the heart to cause the stimulated heart chamber to contract when the patient's own intrinsic rhythm fails. To this end, pacemakers include sensing circuits that sense cardiac activity for the detection of intrinsic cardiac events such as intrinsic atrial events (P waves) and intrinsic ventricular events (R waves). By monitoring such P waves and/or R waves, the pacemaker circuits are able to determine the intrinsic rhythm of the heart and provide stimulation pacing pulses that force atrial and/or ventricular depolarizations at appropriate times in the cardiac cycle when required to help stabilize the electrical rhythm of the heart.
For defibrillation, one lead may include at least one defibrillation electrode arranged to be positioned in the right ventricle. The ICD includes an arrhythmia detector that detects for ventricular arrhythmias, such as ventricular fibrillation. When such an arrhythmia is detected, a pulse generator delivers a defibrillating shock from the defibrillation electrode in the right ventricle to the device conductive housing to terminate the arrhythmia. Alternatively, such arrhythmia terminating systems may further include another defibrillation electrode arranged to be positioned in the right atrium and electrically connected to the right ventricular defibrillation electrode. In this arrangement, the defibrillating shock is delivered from the parallel connected right ventricular and right atrial electrodes to the conductive housing.
Ventricular fibrillation is an immediately life threatening cardiac arrhythmia. It requires immediate and effective defibrillation therapy.
However, it is best to prevent ventricular fibrillation from even occurring to avoid the need for defibrillation therapy and more importantly, to prevent exposure of the patient to such a life threatening arrhythmia. Premature ventricular contractions are believed to be an initial cause of ventricular fibrillation in some patients. A premature ventricular contraction (PVC) is a spontaneous (intrinsic) ventricular event that is not preceded by a paced or sensed atrial event. In patients who have previously suffered myocardia infarcts or ischemia, PVC's are considered particularly troublesome because they can trigger ventricular fibrillation or an accelerated ventricular arrhythmia, such as ventricular tachycardia, which may then accelerate the heart into fibrillation.
In view of the above, it is generally considered best to attempt to prevent or at least minimize the occurrence of PVCs in a patient's heart. Therapies such as overdrive pacing and vagal nervous system stimulation are known to treat the occurrence of PVCs.
The administration of PVC therapy to a heart requires detection of PVCs in a useful way which both indicates the condition of the patient's heart and when PVC therapy is required if not currently in use or when increased PVC therapy aggressiveness is required if such therapy is already enabled.
The monitoring of PVC density has been investigated as such a measure. PVC density is the number of PVCs detected during a preset period of time. PVC density variability has also been investigated as a possible measure. It has been found that patients with malignant ventricular arrhythmias have striking diurnal (daily) cycles in PVC density. Moreover, such studies indicate that patients at risk for ventricular arrhythmias may have more PVC density variability than those without such risk. Unfortunately, it has also been demonstrated that there are substantial day to day natural variations in ectopic variability. As a result, it would be difficult to prove a meaningful change in PVC density simply using overall daily PVC burden or random hourly PVC density monitoring. A more sensitive and accurate monitoring method is required to assess patient ventricular arrhythmia risk and to provide more effective PVC therapy control.