INDICATIONS¹

The OPTIMIZER Smart Mini System, which delivers CCM™ therapy, is indicated to improve 6 minute hall walk, quality of life, and functional status of NYHA Class III heart failure patients who remain symptomatic despite guideline directed medical therapy, who are not indicated for  CRT, and have a left ventricular ejection fraction ranging from 25% to 45%.

The OPTIMIZER Smart Mini system delivers non-excitatory CCM™ signals to the heart and has no pacemaker or ICD functions.

 CONTRAINDICATIONS AND PRECAUTIONS

Use of the OPTIMIZER Smart Mini system is contraindicated in:

1. Patients with a mechanical tricuspid valve
2. Patients in whom vascular access for implantation of the leads cannot be obtained

WARNINGS

Potential Complications of Device Implantation

Just like any surgical procedure, implantation of an OPTIMIZER Smart Mini IPG is associated with a certain risk. Complications of IPG implantation reported in the literature include, but are not limited to: arrhythmias induced by the IPG, including life-threatening arrhythmias (e.g. ventricular fibrillation), infection, skin necrosis, device migration, hematoma formation, seroma and histotoxic reactions (also see: Potential Adverse Effects, Section 6).

Programming high sensitivities (i.e. sensitivity settings less than 2 mV) may increase the system’s susceptibility to electromagnetic interference, which could either inhibit or trigger signal delivery.

Acute and chronic complications reported in the literature include, but are not limited to: lead fracture, lead displacement, ventricular perforation, and rare cases of pericardial tamponade. Perforation of the ventricular wall can induce direct stimulation of the phrenic nerve or the diaphragm. An impedance change demonstrated on a check-up can be indicative of lead fracture, lead displacement, or perforation (also see: Potential Adverse Effects, Section 6).

In very rare cases (<1%), transvenous lead placement can also lead to venous thrombosis and subsequent SVC syndrome.

Loss of sensing shortly after implant can be the result of lead displacement. In addition, loss of CCM™ signal delivery could be due to a lead fracture.

Atrial and Ventricular Arrhythmias Potentially Caused by Lead Implantation

As noted above, the use of transvenous leads may lead to arrhythmias, some of which may be life-threatening such as ventricular fibrillation and ventricular tachycardia. The use of screw-in leads such as those used for CCM™ signal delivery also have the potential of causing conduction disturbances such as bundle branch block. These can be minimized by performing the implant with the use of fluoroscopic guidance, ensuring that the leads are in appropriate position prior to fixation and by limiting the number of lead manipulations. Please read and follow all directions of the original Physician Manual for the leads that you intend to use to minimize adverse events connected to lead implantation.

Ventricular Arrhythmias Potentially Caused by CCM™ Signals

CCM™ signals are of greater strength than that of typical pacing pulses and are thus capable of eliciting activation of cardiac tissue when delivered outside of the absolute refractory period. CCM™ signals delivered outside of the ventricular absolute refractory period thus have the potential of causing signal-induced arrhythmias (some of which may be life-threatening, such as ventricular fibrillation and tachycardia). For this reason, it is imperative that CCM™ signal delivery parameters be chosen carefully. Most importantly, the various settings related to conditions that inhibit CCM™ signal delivery (e.g. Long AV Delay, Short AV Delay, LS Alert Window, refractory periods, and IEGM sensitivities) must be selected to allow delivery of CCM™ signals only on normally conducted (e.g. non-arrhythmic) beats, but inhibit them on beats of suspected ectopic or premature origin.

In addition, CCM™ signals may cause changes in the electrical conduction of tissue. For this reason, the delivery of CCM™ signals to the ventricular septum has the potential of causing bundle branch block that could lead to bradycardia. Through similar mechanisms, CCM™-induced changes in the electrical conduction of the myocardium have the potential of inducing tissue refractoriness that may facilitate the induction of reentrant tachyrrhythmias. It is recommended that the patient’s rhythm be monitored carefully for changes in rhythm when CCM™ signals are delivered during lead implantation, as well as during first activation of the OPTIMIZER Smart Mini IPG and subsequent follow-up visits. Changes in ventricular rhythm caused by the delivery of CCM™ signals may require relocating the leads, as well as reprogramming the CCM™ delay and amplitude to settings that do not cause changes in the patient’s ventricular rhythm.

Atrial Arrhythmias Potentially Caused by CCM™ Signals

Atrial and supraventricular arrhythmias could theoretically be initiated when CCM™-induced ventricular activity is conducted retrograde to the atria, resulting in premature atrial depolarization. The OPTIMIZER Smart Mini IPG may sense the ventricular activation resulting from the retrograde-induced atrial event and deliver CCM™ as programmed. In addition, strong CCM™ signals delivered through leads implanted in basal position close to the atria have the potential of directly stimulating the atria. If CCM™ delivery causes atrial activation through either of these mechanisms, and the atrial signal is then conducted to the ventricles, the cycle may develop into a condition similar to pacemaker-mediated tachycardia (PMT).

The main variables that may have an impact on CCM™ events leading to atrial activation are the location of lead placement on the right ventricular septum, CCM™ amplitude, and CCM™ delay. To prevent the occurrence of atrial arrhythmias due to CCM™ signal delivery, it is recommended that basal lead implant locations be avoided. The potential for direct atrial activation by CCM™ signals can be tested during the implant by delivering the strongest possible CCM™ signal 20 to 30 ms longer than the LS-CCM delay with which the IPG will be ultimately programmed, as long as this delay places the CCM™ signal, including its 40 ms balancing phase, completely within the ventricular absolute refractory period, and monitoring for atrial activations. In such a case, the delay should be programmed to a longer value and lack of atrial activation confirmed. Besides proper lead location and CCM™ parameter programming, the “Atrial Tachycardia Rate” must be programmed to a sufficiently low value as a protective measure against atrial arrhythmias that could be induced by CCM™ signal delivery.