Cardiology

Devices

General description of procedure, equipment, technique

Most implantable electronic devices (IED) are designed to treat electrophysiologic (EP) abnormalities associated with chronic left ventricular (LV) systolic dysfunction. Chronic EP substrate problems lead to increased risk for lethal arrhythmias and/or diminished LV pump efficiency. Recently, a new type of implantable device, designed to frequently monitor pulmonary artery pressures to guide medical management of symptomatic patients, was approved for use in patients with heart failure (HF). The indication for this device is to reduce hospitalizations for NYHA Class III previously hospitalized patients.

Sudden death risk is clearly reduced with appropriate neurohormonal intervention, such as beta-blockers and aldosterone antagonists. However, lethal arrhythmias still accounted for the majority of deaths in the treatment groups of clinical trials. These findings suggest that lethal arrhythmias can "escape" chronic neurohormonal suppression and must be terminated with defibrillation to improve chances of survival.

In addition to a substrate for lethal arrhythmias, intraventricular conduction delay, particularly left bundle branch block, results in intraventricular mechanical dyssynchrony , which further decreases left ventricular systolic and diastolic efficiency. Dyssynchronous left ventricular contraction alters mitral valve function, leading to worsening regurgitation and decreased forward flow.

Application of cardiac resynchronization devices (CRT) using biventricular pacemakers successfully improves heart failure symptoms, reduces the need for hospitalization, and prolongs survival. It is difficult to clearly identify the proportion of patients that respond to CRT and, in the past several years of clinical trials, it is clear that appropriate patient selection is key to ensure success. These selection criteria will be covered later in this chapter.

There are, in general, three forces that influence the prescription of an implanted electronic device in the United States. Clinical trial evidence is still the most important basis for prescribing any therapy, including device therapy.

However, regulatory decisions made by the U.S. Food and Drug Administration sometimes limit application of technologies to those patient populations perceived to be most likely to benefit, even if the population is different than those included in trials. Finally, the U.S. Center for Medicare and Medicaid Services (CMMS) issues National Coverage Decisions (NCD) that identify covered patient groups for which devices are considered appropriate. Use of IED's in populations not covered by CMMS NCD cannot be reimbursed and can be subject to fines or even criminal investigation.

These three forces increase the complexity of applying technology from clinical trials in everyday practice. They do not replace clinical judgment, but must be considered when developing a strategy for device prescription. All of these considerations will be covered in this chapter.

The following types of implanted devices intended for patients with heart failure will be covered in this chapter: Implantable cardioverter defibrillators, atrial-biventricular pacemakers to achieve cardiac resychronization therapy (CRT), and implantable hemodynamic monitoring systems. Finally, the role of wearable defibrillators will be covered. Left ventricular assist devices are considered a part of advanced therapies for American College of Cardiology/American Heart Association (ACC/AHA) stage D refractory symptomatic heart failure and are discussed in other chapters.

Implantable cardioverter defibrillators (ICD) are designed to sense potentially lethal tachyarrhythmias and terminate them by delivering two types of antiarrhythmic therapy: (1) Antitachycardia pacing is a painless intervention specific for sustained ventricular tachycardia; (2) direct current shock is reserved for ventricular fibrillation. The devices may have an atrial lead, but all have a lead implanted in the right ventricular apex for both sensing and delivering therapy. These devices also have full pacemaker capabilities and the amount of right ventricular apical pacing is an important component of post-implantation monitoring (see below).

These interventions are programmed in "tiers" of therapy as described later. Ventricular tachyarrhythmias are defined by the device based on the R–R interval sensed by the right ventricular lead, which can be programmed for individual patients to potentially avoid false detections and inappropriate shocks.

Cardiac resynchronization therapy (CRT) pacemakers are configured with an atrial lead coupled with two ventricular leads.

One of the ventricular leads is introduced transvenously through the coronary sinus to a lateral cardiac vein on the epicardium of the left ventricle. The other pacing lead is usually attached to the endocardium of the right ventricular apex.

This configuration allows sensing of atrial depolarization and simultaneous activation of the left ventricular septum and more lateral segments. In this way, CRT devices are different than ICDs in that CRT devices provide active therapy on a beat-to-beat basis, while ICDs monitor and provide therapy in the event that a potentially lethal arrhythmia is sensed. Most CRT devices combine ICD circuitry and are called "CRT-D." Biventricular pacemakers alone are called "CRT-P.

Wearable defibrillators are now available for patients who are perceived to be at risk for sudden death, but are waiting the required time to determine if ventricular function is destined to improve after diagnosis and application of neurohormonal antagonists or revascularization intervention (PCI or CABG). These devices provide immediate direct current shock for ventricular fibrillation (VF) defined, again, by the R-R interval sensed by the device. An alarm sounds when the device senses an electrical signal consistent with VF and allows the patient to disable the device if the electrical signal is noise. Otherwise, if true VF is sensed, the patient will be unconscious during the shock.

Implantable Hemodynamic Monitoring Systems currently approved for use in the United States include a microelectromechanical sensor (MEMS) that is manufactured inside a small hermetically sealed wafer that is permanently implanted in a branch of the pulmonary artery (PA) during right heart catheterization using a special over-the-wire delivery catheter. The device has nitinol loops inserted at each end of the wafer which allows the implant to auto-size to the appropriate PA branch once released into the circulation. Calibration sequences occur once the device is in the PA.

This particular implantable device has no battery or lead and is empowered by interrogation. The MEMS technology included on the implanted wafer has a capacitor and an antenna which receives radiofrequency energy from an external source.

The external RF source is an antenna imbedded in a pillow on which the patient reclines at a 45° angle to initiate the interrogation sequence. The energy emitted from the external source is reflected back to the emitting antenna at a different frequency proportional to the pressure on the capacitor. High frequency interrogation over 18 seconds allows the creation of a series of PA pressure waveforms which are captured by a bedside device and transmitted by cellular telephone to a secured website. PA pressure data then populates an Internet-based system and the information is graphically displayed for provider review.

In addition, the website is capable of automatically notifying the heart failure nurse or other provider if pressures are outside user-defined ranges. The clinical trial validating use of this device found that medication dosing based on PA pressures is superior to traditional disease management systems allowing medical therapy individualization. Most frequently, diuretic dosing was added or altered in response to pressure information, but vasodilator therapies also were altered to maintain stable pressures. In the clinical trial, pressures were uploaded daily and reviewed at least weekly by investigators.

Indications and patient selection - Implantable Electronic Devices

Indications for Implantable Cardioverter Defibrillator devices

The consensus application of ICDs for patients with cardiovascular disease can be confusing and is not limited to patients with heart failure. ICDs are implanted as part of a strategy to provide either primary or secondary prevention of sudden cardiac death.

A detailed historical database is needed in order to determine which strategy is appropriate. In general, lethal arrhythmia risk is considered to be high enough for ICD implantation if patients have experienced and survived cardiac arrest without a clear reversible cause or if they have an electrophysiologic substrate known to be associated with high risk for lethal arrhythmias.

For patients with symptomatic heart failure (NYHA Class II-III) and no history of malignant arrhythmias, risk for sudden death is stratified based on the persistence of left ventricular systolic dysfunction despite the application of appropriate medical therapies. The key part of this concept is "persistent." Appropriate medical therapies or revascularization may lead to improved left ventricular systolic function, which may move the patient into a lower sudden cardiac death risk assessment, removing the need for an implantable device.

Several questions should be answered before consideration of an ICD prescription:

1. What is the ejection fraction (EF)? In general, LVEF <35% represents high enough risk to consider primary prevention ICD recommendation.

2. What is the etiology of left ventricular systolic dysfunction? Patients with ischemic heart disease should be assessed for revascularization potential and time should be allowed after revascularization to determine long-term sudden death risk. Patients with nonischemic etiologies may respond to medical therapies with an improvement in LVEF as well. Most clinical trials excluded patients with "reversible" non-ischemic dilated cardiomyopathy, such as peripartum, tachycardia induced or acute myocarditis.

3. When was left ventricular dysfunction first discovered? Timing is based on objective assessment of left ventricular function and not symptoms of heart failure.

4. When was the last documented myocardial infarction, if ischemic heart disease is present? Generally, elevated troponin with documented obstructive coronary artery disease is needed. Sometimes patients present with small troponin elevations that may represent "troponin leak" from ventricular stress, but may be documented in the medical record as an "acute myocardial infarction," even if the patient does not have obstructive coronary artery disease. Acute myocardial infarction, for purposes of timing implantation of an ICD, should be limited to elevated troponin in the presence of significant obstructive coronary artery disease. Significant debate continues about inappropriate use of ICD's because medical records reflect "myocardial infarction" with minor troponin leak and no coronary artery disease.

5. If ischemic heart disease is present, when was the last intervention? For most situations, 3 months should be allowed following coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI) to see if ventricular function improves before ICD recommendation.

6. Is there a reversible cause for the potentially lethal arrhythmias? Electrolyte abnormalities, illicit drug use, trauma, myocardial infarction, or revascularizable ischemia represent some of the reversible causes of potentially lethal arrhythmias. Confusion arises when patients with "out of the hospital" cardiac arrest survive with defibrillation and/or CPR and have mildly elevated troponin levels. Many times the medical records initially reflect "acute myocardial infarction," but upon investigation the patient's coronary arteries are normal and the troponin leak is not considered myocardial infarction. This is especially important if the hospitalization is coded and billed as a "myocardial infarction" since CMMS NCD only considers billing codes when assessing appropriate use criteria. Many times coding information is not available to implanting physicians, which may lead to ICD use that does not meet NCD qualifications. Therefore, it is important to clarify if an elevated troponin meets criteria for myocardial infarction or is present only because of defibrillation or other ventricular stress.

7. Currently, how symptomatic is the patient? Patients with NYHA Class IV, ACC/AHA stage D refractory heart failure are NOT considered candidates for ICD implantation. These patients usually die from progressive pump failure and not sudden death. Furthermore, defibrillation does not change the long-term prognosis for these patients. Completely asymptomatic patients are underrepresented in clinical trials and may not benefit from ICD implantation. Therefore, a complete historical evaluation of symptoms, even using more objective criteria such as metabolic stress testing or results from 6-minute hall walk tests are required to appropriately recommend ICD therapy.

Indications for ICD use for secondary prevention of sudden cardiac death (SCD) are fairly straightforward and focus on patients regardless of their heart failure status:

1. Patients who survive out of the hospital cardiac arrest not associated with a reversible cause, such as acute myocardial infarction (class I, level of evidence A).

2. Patients with sustained (documented longer than 30 seconds), hemodynamically stable or unstable ventricular tachycardia (VT) and structural heart disease (class I, level of evidence B).

3. Patients with syncope of unknown etiology who have sustained hemodynamically significant VT or ventricular fibrillation (VF) induced during electrophysiologic (EP) testing (class I, Level of evidence B).

4. Patients with normal or near normal left ventricular function and spontaneous sustained VT (class IIa, level of evidence C).

Patients with arrhythmogenic genetic syndromes represent a unique group at risk for lethal arrhythmias in that they have electrophysiologic heart disease, but usually preserved left ventricular function. They include the following conditions:

1. Patients with long-Q–T syndrome who have syncope and/or VT while on beta-blocker therapy (class IIa, level of evidence B).

2. Patients with Brugada syndrome and syncope or documented VT (class IIa, level of evidence C).

3. Patients with long-Q–T syndrome and risk factors for SCD (class IIb, level of evidence C).

Most (approximately 95%) patients with spontaneous ventricular arrhythmias suffering outpatient cardiac arrest do not survive, which severely limits a secondary prevention approach to sudden death prevention. Therefore, a number of clinical trials were designed to stratify risk for sudden death in patients with no history of ventricular arrhythmias to guide ICD use before cardiac arrest occurs.

Primary prevention of SCD is supported by a very rich database and focuses on several groups of patients that are at high enough long-term SCD risk to warrant ICD implantation without a history of sustained arrhythmias:

1. Patients with a previous myocardial infarction and symptomatic (NYHA Class II-III) heart failure associated with persistent left ventricular systolic dysfunction (LVEF <35%) who are at least 40 days post-MI (class I, level of evidence A).

2. Patients who are at least 40 days post-MI and have an LVEF less than 30% in NYHA functional class I (asymptomatic) (class I, level of evidence A).

3. Patients with nonischemic cardiomyopathy and LVEF <35% with NYHA Class II-III symptoms despite maximal medical therapy (class I, level of evidence B). For most situations this includes patients who do not have a CRT indication. Medical therapy should be maximized and continued for at least 9 months before permanent ICD implantation. Patients enrolled in a FDA-approved clinical trial are exempt from the 9 month rule if the trial's protocol provides for less time on medical management before enrolment.

4. Patients with nonsustained VT associated with previous MI coupled with LVEF <40% and inducible VF or VT at EP study (class I, level of evidence B).

5. Patients with NYHA Class IV heart failure if deemed in need of CRT, LVEF <35%

6. Patients with hypertrophic cardiomyopathy or arrhythmogenic right ventricular dysplasia coupled with at least 1 risk factor for sudden death (class IIa, level of evidence C) or unexplained syncope.

7. Nonhospitalized patients awaiting cardiac transplantation (class IIa, level of evidence C).

8. Patients with cardiac sarcoidosis, giant cell myocarditis or Chagas disease (class IIa, level of evidence C).

Situations in which there are less data supporting use of ICDs, but it is reasonable to consider ICD use for primary SCD prevention are:

1. NYHA Class I patients with nonischemic cardiomyopathy (LVEF <35%) (class IIb, level of evidence C).

2. Patients with syncope and structural heart disease in whom invasive and noninvasive investigations failed to define a cause (class IIb, level of evidence C).

3. Patients with ventricular noncompaction or those with a familial cardiomyopathy associated with SCD (class IIb, level of evidence C).

Indications for Cardiac Resynchronization Therapy devices

Cardiac resynchronization therapy devices are indicated to correct interventricular mechanical dyssynchrony associated with interventricular conduction delays, particularly left bundle branch block (LBBB). QRS duration on a resting surface electrocardiogram (ECG) continues to be the test of choice to determine eligibility for CRT recommendations. Using other modalities, such as mechanical dyssynchrony on echocardiography, are not supported by clinical trial evidence.

Unfortunately, clinical trials evaluating CRT in heart failure patients are inconsistent in defining QRS duration and type of intraventricular conduction delay (IVCD) on the ECG as entry criteria. The shortest QRS duration was 120 msec in the MIRACLE Trial and COMPANION. CARE-HF also used 120 msec, but further quantified dyssynchrony in patients between 120 and 150 msec using echo-based markers of dyssynchrony (septal to posterior wall motion delay >130 msec). MADIT-II-CRT examined CRT use in asymptomatic or minimally symptomatic (NYHA Class I-II) participants with a QRS duration >130 msec.

Initial randomized prospective clinical trials demonstrated functional improvement in very symptomatic patients with NYHA Class III or IV heart failure and IVCD treated with CRT. Subsequent trials were performed in less ill patients with left ventricular systolic dysfunction, NYHA Class I and II symptoms, and demonstrated improvement in ventricular function and geometry along with significant mortality benefit with CRT.

These trials included all types of IVCD, but post-hoc, hypothesis generating analyses by the USFDA suggested that most CRT benefit in less symptomatic patients was found in those with left bundle branch block (LBBB). Based on retrospective ad-hoc analyses, the FDA approved CRT for NYHA Class I-II patients with LBBB, and a QRS duration >130 msec for those who were already receiving appropriate medical therapies.

Other studies with non-LBBB conduction delay and QRS duration between 120 and 150 msec may not benefit from CRT. In fact, there is some evidence to suggest these patients may be harmed by CRT. Another group of patients who are underrepresented in clinical trials are those with persistent atrial fibrillation. It is still unclear if the lack of atrio-ventricular synchrony dampens the benefit of CRT. Certainly, rapid ventricular response to atrial fibrillation can compete with biventricular pacing delivery, thus decreasing the effectiveness of the intervention.

This regulatory decision constrains application of CRT to less ill patients in the United States. Other countries, likely, will have different regulatory decisions.

Patients who may benefit from CRT:

1. Patients with any etiology of left ventricular systolic dysfunction (LVEF <35%) that has persisted for more than 3 months despite maximal guideline directed medical therapy and revascularization strategies, when appropriate. These clinical features coupled with sinus rhythm, NYHA Class II, III, or ambulatory class IV symptoms and prolonged interventricular conduction due to LBBB with QRS duration >150 msec on a 12-lead ECG have the highest level of consensus recommendation for CRT (Class I, level of evidence A, level of evidence B for NYHA Class II).

2. Patients with NYHA Class II, III, or ambulatory class IV symptoms accompanied by LVEF ≤35%, sinus rhythm, LBBB, and QRS duration between 120 and 149 msec may benefit with a Class IIa, level of evidence B indication.

3. CRT may be useful for those with LVEF ≤35%, sinus rhythm, non-LBBB pattern with QRS duration ≥150 msec and NYHA Class II, III, or ambulatory class IV symptoms on guideline directed medical therapy (Class IIa, level of evidence A for NYHA class III and IV; level of evidence B for NYHA class II).

4. Patients with permanent atrial fibrillation may benefit from CRT with NYHA Class III and ambulatory Class IV symptoms, LVEF ≤35%, who require ventricular pacing or rate control (AVN ablation or medications), which will assure near 100% ventricular pacing (Class IIa, level of evidence B). The European Society of Cardiology recommendations also include less symptomatic patients (NYHA Class II) and QRS duration ≥120 msec.

5. CRT is NOT recommended for patients with NYHA Class I or II symptoms and non-LBBB pattern with QRS duration less than 150 msec (Class III, level of evidence B).

6. CRT is NOT recommended for patients with QRS duration less than 120 msec.

7. CRT is NOT indicated for patients whose comorbidities and/or frailty limit survival with good functional capacity to less than 1 year (Class III, level of evidence C).

Special patient populations not yet reflected in consensus recommendations:

A large prospective clinical trial examined a very important hypothesis concerning right ventricular apical pacing and patients with depressed LVEF (≤50%). Clinical evidence suggested that RV apical pacing >40% in patients with LV dysfunction is associated with worsening LV function and worse clinical outcomes. It was hypothesized that biventricular pacing in these patients, predominantly those with high grade AV block and Class I or II indications for standard pacing, would fare better in the long run with biventricular pacing. Indeed the trial found biventricular pacing to be a superior means to provide ventricular rate support in the presence of severe AV nodal disease. The trial results led to USFDA approval of biventricular pacing to individuals with a Class I or II indication for pacing due to bradyarrhythmias and AV node dysfunction with LVEF <50%.

Patients with chronic kidney disease or end-stage renal failure requiring dialysis were not included in clinical trials evaluating either ICD or CRT efficacy. This should be considered carefully as patients with end-stage renal disease tend to die from non-arrhythmic causes that would not be prevented by an implanted device.

Indications for CRT-ICD combination devices

1. Any ICD indication as listed above.

2. Patients with NYHA ambulatory Class IV heart failure symptoms may benefit from an ICD if they are also a CRT candidate, whereas NYHA Class IV (stage D) patients are usually not considered ICD candidates.

How do I determine the need for an implanted device in my heart failure patient?

Patients with symptoms of left ventricular dysfunction should be evaluated with an imaging technique to measure the LVEF. Appropriate testing should be performed to determine the etiology of left ventricular dysfunction clarifying if coronary artery disease is present or absent.

Appropriate neurohormonal intervention, including angiotensin-converting enzyme inhibition or angiotensin receptor blockers, beta-blocker therapy and, when appropriate, aldosterone antagonism or nitrate/hydralazine therapies, are then applied. The time-course for ventricular recovery is based on one of two general etiologies: Ischemic or nonischemic cardiomyopathy.

1. Ischemic left ventricular dysfunction due to acute myocardial infarction without revascularization - 40 days is allowed for medical therapies to effect an improvement in ventricular function.

2. Ischemic left ventricular dysfunction due to acute myocardial infarction with revascularization - 90 days is allowed for revascularization coupled with medical therapies to effect a change in ventricular function.

3. Nonischemic left ventricular dysfunction - 9 months is allowed for medical therapy to effect an improvement in ventricular function unless enrolled in a FDA approved device trial.

Most of these waiting times are determined by reimbursement National Coverage Decisions from the Centers for Medicare and Medicaid Services. Scant data is available to fully document the appropriate time from the initial diagnosis of heart failure to implantation of a cardiac therapy device.

Most clinical trials required patients to have established heart failure syndromes for at least 3 months before implantation of CRT devices, however no NCD exists for CRT pacemakers. Although still unclear, it appears that the same NCD waiting periods used for ICD's apply to CRT-D devices. Clearer data exists for ICDs after myocardial infarction in which one trial demonstrated no benefit and possible harm when ICDs were implanted immediately following myocardial infarction (from 0-40 days). These data support a waiting period for ICDs in relation to myocardial infarction.

What do I do while waiting for ventricular function to improve?

Patients with left ventricular systolic dysfunction who find themselves in the "waiting period" for ICD implantation are not at low risk for sudden death. They may, however, experience significant improvement in left ventricular function such that their long-term sudden death risks are low. So what do we do with those who are waiting to see if they will recover?

Many health care providers now offer patients wearable defibrillatorsto provide sudden death prevention during the waiting period. This approach lacks rigorous clinical trial evidence, but is low risk and appears effective. Long-term adherence to wearing the device is difficult, especially if the patient is requested to wear the vest for months. Frequent reassessment of ventricular function is recommended so the wearable defibrillator can be discontinued if LVEF recovers beyond 35%.

Arrhythmia discrimination is reasonable with wearable defibrillators and an alarm sounds before shock to allow the patient to disable the device if they are not hemodynamically compromised. Patients who develop a treatable arrhythmia during the waiting period, as long as reversible causes are not found, become secondary prevention candidates and ICD therapy is indicated. Wearable defibrillators do not treat sustained ventricular tachycardia, but may monitor it so a secondary ICD indication may be met even if shock is not required.

What do I tell the patient about an ICD recommendation?

ICDs reduce the chances of dying suddenly. Patients should be asked if they want to avoid that possibility. Most, of course, do want to avoid dying suddenly, but they should understand the goals of ICD use with the following points emphasized:

Instruction to the patient must include what an ICD will NOT do:

1. Does not improve left ventricular systolic dysfunction

2. Does not reduce the need for hospitalization and will not make them feel better

3. Might give them an inappropriate shock and that the shock hurts

4. Sometimes shocks can produce a significant anxiety disorder with avoidance of activities associated with the shock. This anxiety disorder can be life-changing and disabling requiring medical and psychiatric therapies.

Patients should know about things they CANNOT do after ICD implantation:

  1. 1. MRI scanning

  2. 2. Arc-welding, or working in close proximity with external devices that produce a periodic electrical impulse

  3. 3. Patients should be given a balanced representation of lead failure/fracture possibility and the need for revision due to ineffective lead placement or malfunction. The need for extraction of the system in case of pocket erosion or persistent bacteremia should be fully explained. Finally, patients should be provided with a general idea of how long the battery lasts and how the battery will be replaced.

What do I tell the patient about CRT recommendation?

Patients should know that most clinical trials usually evaluated clinical improvement 6 months after implantation. Subsequent follow-up studies demonstrate a continued improvement and benefit for several years following implant compared to patients without CRT. Therefore, patients should be aware that the benefit may not be immediate and possibly 30% of patients do not improve despite CRT.

Finally, up to 10% of patients cannot have transvenous left ventricular lead placement. This requires epicardial left ventricular lead placement from a transthoracic surgical approach to complete the system.

This approach is associated with longer healing, recovery, and clinical response times. Patients should know of this possibility and should have an idea what they want to have done to them prior to device implantation. If epicardial lead placement is required and acceptable to the patient, then an incomplete device with transvenous right-sided leads and a pulse generator can be implanted with subsequent plans for LV lead placement.

A significant debate exists about defining what is a clinical response to CRT. To date, however, most still cite Abraham and colleagues from the MIRACLE trial in which 70% of patients had improved clinical composite scores at 6 months. Over 15 definitions of "response" are the subject of clinical studies adding to the difficulty of providing patients with a realistic expectation for post-CRT life.

When one considers preventing worsening heart failure as a success, "maintenance of stability" suggests that over 80% of patients "respond" to the therapy.

It is probably most reasonable to explain to patients that they are very likely to feel better with CRT and the chances of success (symptom improvement or maintaining stability) are over 80%.

What can clinicians and patients reasonably expect from most (approximately 80%) patients who receive CRT?

1. Reduction of heart failure symptoms or no worsening of symptoms

2. Improved left ventricular systolic function with reduced left ventricular dimensions

3. Improved mitral valve function and associated increase in forward flow

4. Prolonged survival

5. Long-term improved survival and functional status

What should I do before recommending CRT?

1. Ensure maximal medical therapy is established for at least 3 months. This includes attempting to use maximal doses of beta-blockers and angiotensin intervention indicated by clinical trial evidence. Maximal doses in the "forced titration" studies using beta-blockers aimed for 25 mg twice daily of carvedilol, 200 mg daily of metoprolol succinate and 10 mg daily of bisoprolol. Also, clinical trial evidence suggests that higher ACE inhibitor dose improves important clinical outcomes. Of course, dose must be individualized and is mostly limited by hypotension when combination drugs are used.

2. Assess patient's exertional capacity (e.g., 6-minute hall walk, metabolic stress test) to establish a baseline if possible. This can serve to monitor clinical improvement in functional capacity post-CRT.

3. Ensure that the patient has optimal volume.

4. Advanced imaging for patients who are at risk for vascular abnormalities is reasonable. Patients with previous cardiac surgery, valve replacement, or chest radiation may have venous anatomy that is difficult to access percutaneously, which makes left ventricular lead delivery impossible. Imaging such as cardiac magnetic resonance imaging or computerized tomography angiography may help provide a map for the implanter.

5. The left ventricular ejection fraction should be assessed at least 3 months following institution or uptitration of heart failure medical therapy.

6. Some evidence exists suggesting that biomarker assessment prior to CRT implantation may predict response to the intervention. Specifically galectin-3 levels and possibly brain natriuretic peptide (BNP) may serve to predict the benefit from CRT. No consensus exists about this approach, however.

Contraindications

When not to recommend ICD implantation

As mentioned, ICD therapy should not be recommended in the following situations (class III, level of evidence C):

1. Patients who do not have a reasonable expectation of survival for 1 year, even if they meet other ICD implantation indications.

2. Patients with incessant VT or VF

3. Patients with significant psychiatric illness that may be worsened by device implantation or that precludes follow-up.

4. Patients with syncope who do nothave inducible VT or structural heart disease

5. Patients in whom VT/VF is treatable with surgical or catheter ablation

6. Patients with VT/VF due to conditions that are completely reversible (i.e., drugs, electrolyte imbalance, acute myocardial infarction or trauma).

Implantable Hemodynamic Monitoring Systems

Most patients with heart failure become more symptomatic because of either exogenous fluid accumulation or endogenous fluid redistribution. Both of these events result in increased pulmonary artery pressure, which can be thought of as the "lesion" of heart failure symptoms. This is reflected in registry studies demonstrating that over 90% of patients presenting for heart failure hospitalization have evidence for excess volume. Excess volume exerts excess pressure.

A large database now exists supporting the hypothesis that elevated filling pressures portend high risk for subsequent hospitalization. Additionally, it is clear from clinical research that decreasing pressures with medical therapies reduce subsequent risk for hospitalization. Preventing hospitalization in patients with heart failure is important from a variety of perspectives. Allowing patients to congest and decompensate to the point of needing hospitalization to resolve their clinical problem leads to worsening neurohormonal activation, ventricular wall stress, endomyocardial ischemia, and troponin elevation thus worsening ventricular function. Furthermore, the risks of death in a heart failure hospitalization approach 25% and even higher in patients with low perfusion and renal insufficiency.

Disease management of patients with chronic symptomatic heart failure includes multiple obtaining and interpreting a multiplicity of data points, including daily measured weights and patient symptoms, and frequent face-to-face encounters to reinforce education goals or possibly detect changes in volume early enough to avoid hospitalization.

Recently, however, it was clear from multiple prospective clinical trials testing disease management strategies that these traditional tools, even when closely monitored using telephone-based reporting systems, were not effective at reducing hospitalization needs. This, coupled with technology evolution producing very safe and reliable sensors, led to a prospective clinical trial testing the hypothesis that remotely monitoring pulmonary artery pressures may reduce the rate of hospitalizations compared to traditional disease management strategies.

This trial used a MEMS-based sensor described above, which was permanently implanted in the pulmonary artery and allowed daily uploads of patients' pressures. Providers then either uptitrated or decreased diuretic dosing, or added vasodilator therapy such as long-acting nitrates with the expressed goal of normalizing PA pressures. Once pressures were reduced as much as possible, the pressures were monitored for deviations from the new baseline. Elevations in PA pressures are known to occur as long as 21 days prior to changes in daily weights or symptom development, which are the basis for traditional management strategies.

Providers were notified of increases (or decreases) in pressures above or below patient specific levels to allow early warning of changes that may lead to worsening heart failure. This approach allowed patient individualization of diuretic therapy, which was previously unavailable from clinical trial evidence. Using this approach, treatment patients had significant reductions in hospitalizations both at 6 months following therapy, as well as longer-term (~18 months). Patient acceptance, even in the elderly, was excellent and adherence did not seem to demonstrate fatigue over time. Based on this data, the USFDA approved the device for use in patients with symptomatic heart failure with an indication to reduce the need for hospitalizations.

Who should be considered for implantable hemodynamic monitoring?

The patient population in which implantable hemodynamic monitoring is effective in preventing hospitalizations is:

1. Symptomatic heart failure without regard to ejection fraction defined as predominantly NYHA Class III either currently hospitalized for decompensated heart failure or hospitalized during the previous 12 months.

2. NYHA Class III symptoms despite maximally tolerated guideline directed medical and device therapies. According to ACC/AHA guidelines, patients with heart failure and preserved ejection fraction, defined as LVEF ≥40% have no consensus recommended therapies and tend to have a clinical course more similar to those with LVEF ≥50%. Therefore, there was no requirement for specific neurohormonal therapies for this group. The only recommendation was to maximally control volume with diuretic therapy.

3. Patients with relatively preserved renal function defined as an estimated glomerular filtration rate (MDRD formula) of greater than 25 ml/min.

4. Patients without co-morbidities that are likely to cause death in 12 months.

5. Patients likely to adhere to daily uploads of PA pressure data.

6. Patients managed in organized disease management programs characterized by an infrastructure needed to monitor pressures (see below).

7. Patients able to tolerate dual antiplatelet therapy with aspirin and clopidogrel for at least one month.

8. Patients with suitable pulmonary artery anatomy (described below).

Specific considerations for using implantable hemodynamic monitoring in patients with heart failure

The CHAMPION Trial included sites with an interest in heart failure management and organized follow-up programs. This varied significantly across all disciplines involving academic medical centers, private practice heart failure practitioners, electrophysiologists, interventional cardiologists, and general cardiologists. Consistently, the provider team consisted of specially trained nurses or nurse practitioners and physician investigators. Although pressure data were uploaded daily, investigators were asked to review the website weekly to ensure PA pressure stability or when the providers were notified by the website of a pressure deviation. The targeted artery for sensor implantation was required to be 7 mm in diameter, which excluded a small percentage of patients at the time of implantation. Part of the informed consent process should include the possibility that the patient may not have PA anatomy suitable for implantation of the sensor and this can only be determined during the implant procedure itself.

The CHAMPION protocol defined target pressures as normal values and it was assumed that higher pressures were due to excess volume. Therefore, the first recommended change in medical therapy was an intensification of diuretic therapy until pressures normalized. If the patient exhibited signs of low perfusion (e.g. hypotension or worsening renal function) during uptitration of diuretic therapy, then diuretic therapy was reduced until the low perfusion symptoms or signs resolved. If pressures were still elevated, the protocol recommended adding long-acting nitrates and/or hydralazine as tolerated by the patient's systemic pressures. Additionally, observation in the first weeks following implantation helped identify variation patterns that may represent circadian changes rather than true changes in volume. Persistently high or low pressures were considered changes in volume requiring adjustment of diuretic therapies.

What do I tell patients to expect after implantation of a hemodynamic monitor?

Patients should be chosen not only on the basis of their clinical status, but also on their ability to consistently upload pressure data. Patients must have cell phone coverage in their area and those who are otherwise non-adherent to follow-up or taking their medications are not likely to benefit from this management strategy.

Patients should be advised of their responsibility to upload pressures at least every morning. Additional uploads during the day are acceptable, but they should be made aware that uploaded data is reviewed weekly, unless specific pressures are out of the user defined ranges. This means that the patient will not be contacted if the pressures are within the normal range. Each center must determine their policy for after-hours pressure uploads, but clinical data seems clear that pressure increases may be reasonably tolerated for several days before clinical decline. Therefore, after-hours uploaded pressures information that is elevated can certainly be acted on within 24-72 hours.

Local site providers should be designated for pressure review and management, especially when after-hours information is provided. Each site, however, must develop a system for pressure review and pressure-based heart failure management. In general, sites that provide outpatient care for patients with heart failure already have personnel designated for responding to remotely acquired data. Patients should also be made aware of the team designated for managing their heart failure based on frequently assessed PA pressures. PA pressure sensors can be interrogated remotely from the patient's home, during face-to-face clinic visits and during hospitalizations.

Complications from PA pressure sensor implantation

Complications associated with the PA pressure implantation were rare (8 complications in 550 patients) without long-term consequences. In particular, no pulmonary artery thrombosis or embolization was seen during long-term follow-up. Furthermore, no pressure sensor failures occurred in the trial. A small percentage of patients could not be implanted with the device due to unsuitable anatomy found only at the time of implantation.

Implanted Therapeutic Devices as Monitors

What do I monitor after the patient has a device implantation?

Many patients with implantable therapeutic device indications will not have an indication for implantable hemodynamic monitoring. Information from implantable hemodynamic monitoring systems is superior to clinical and other device-based diagnostics in terms of preventing hospitalization. As opposed to direct filling pressure measurements from a stand-alone implantable hemodynamic monitoring system, most device manufacturers provide some level of physiologic information sensed by the implanted therapeutic device which is then portrayed in a clinically usable form. This information may be useful in monitoring heart failure patients providing an adjunct to clinical assessment.

Device-based clinical information is obtained remotely via Internet-based information systems or face-to-face with direct device interrogation. Heart failure specific information is usually segregated from electrophysiologic information, thus creating a need for providers to communicate with each other so specialty specific information is always made available for patient management.

Information available from device-based diagnostics:

1. Occurrence of sustained or nonsustained ventricular arrhythmias and subsequent treatment (defibrillation or antitachycardic pacing) if needed.

2. Atrial arrhythmia burden. Most of the time this is atrial fibrillation, but includes any atrial tachycardia. Ventricular rate response to atrial arrhythmias is often provided to monitor the effects of medical therapies in the presence of chronic atrial tachyarrhythmias. Specific information about the nature of atrial arrhythmias can be obtained from stored electrogram morphology and rhythm if an atrial lead is present. Patients with greater than 5 hours of atrial fibrillation, even if asymptomatic, are at more than two times higher stroke risk and may benefit from anticoagulation strategies. Device based

diagnostics are more sensitive in identifying paroxysmal atrial fibrillation than historical evidence.

3. The amount of ventricular apical pacing, expressed as a percentage of all beats (pacing percent), is a very important parameter to monitor. Right ventricular apical pacing increases the risk for progressive ventricular dysfunction and worsening heart failure in patients with structural heart disease. Therefore, ICDs, which have full pacemaker capabilities, should be programmed and monitored to avoid right ventricular pacing. Poorer outcomes are seen in patients receiving >40% right ventricular apical pacing.

4. The amount of biventricular pacing with CRT devices should be as high as possible. One can think of CRT's "dose" as the percentage of ventricular pacing achieved. Patients with CRT devices lose significant benefit from the device if the biventricular pacing percentage drops below 95% and further decreases in benefit are seen when biventricular pacing percentages drop below 92%. Biventricular pacing percentage is monitored and reported with interrogation of the implanted device. Several electrical events can inhibit biventricular pacing, thus decreasing the percentage of biventricular pacing, including rapid ventricular response to atrial arrhythmias, frequent premature ventricular contractions, and more sustained ventricular arrhythmias. The device is inhibited if ventricular electrical activation is sensed by the device prior to programmed delivery of ventricular pacing.

5. Atrial pacing percentages may be beneficial in patients with chronotropic incompetence either naturally or created by beta-blocker therapy. Most dual chamber ICDs have software designed to provide atrial pacing, yet avoid right ventricular apical pacing. Patients with chronotropic incompetence can report symptoms of exercise intolerance or fatigue. The device lower rate limit is programmable and rate responsiveness can be tailored to patients' physiologic needs. Occasionally treadmill ECG testing is helpful to diagnose chronotropic incompetence many times guide appropriate device settings. This approach may be helpful in some patients to allow up-titration of beta-blocker therapy when heart rates limit achieving target dosing.

6. Many manufacturers provide information about average daytime and nighttime heart rates. Average heart rates many times increase as patients decompensate and can be a marker of physiologic instability.

7. Patient activity can be monitored using an accelerometer implanted in the device. The accelerometer senses body movement and considers this as a marker of activity. Not only does patient activity decline during the decompensated state, but this can provide a useful monitoring of patient adherence to activity prescription. Many times patient activity levels can become useful in direct patient education efforts and can provide a benchmark that patients can review at each office visit.

8. Heart rate variability is provided in some manufacturers' devices. This physiologic parameter can be calculated from the atrial-to-atrial (AA) depolarization interval sensed by an atrial lead or ventricular-to-ventricular (VV) activation interval sensed by the ventricular lead.

The standard deviation of the AA or VV intervals provides information about neural control of the heart. Higher heart rate variability is associated with increased vagal input to the heart characteristic of more stable cardiovascular physiology. As patients decompensate, vagal tone is physiologically withdrawn in association with sympathetic activation. The result is a progressive decrease in overall heart rate variability and worsening of cardiovascular stability.

In clinical studies, heart rate variability was more sensitive in predicting eventual heart failure decompensation and hospitalization than any other physiologic marker derived from therapeutic delivery devices. Significant changes in heart rate variability were noted nearly 3 weeks before patients developed symptoms or signs of congestion. Decline in continuously measured heart rate variability stratifies risk for near-term heart failure events while higher, stable levels portend favorable prognosis. This parameter is useful in triaging follow-up based on physiologic stratification of decompensation risks.

9. Intrathoracic impedance is measured daily by some manufacturers' devices and is thought to be a marker of "lung water," but is also associated with pulse generator pocket edema, COPD exacerbation, lead dislodgement, and pneumonia. This feature has been the subject of significant study, but no clear clinical evidence is available about the utility of monitoring intrathoracic impedance. In fact, it is clear that monitoring intrathoracic impedance using a patient alert system significantly increases health care utilization.

Studies seem to suggest, similar to heart rate variability, progressive reduction in intrathoracic impedance is associated with increased near term hospitalization risks. Although intrathoracic impedance is less sensitive than heart rate variability in predicting clinical decline, it may be useful in monitoring clinical status and changes may provide the impetus to see the patient sooner than scheduled.

10. Battery voltage is continuously measured by the device and reported at each interrogation. Voltage is generally reported in three states: Normal, elective replacement, or end of service. Monitoring battery life is good clinical practice, and pulse generator change is reasonable at the elective replacement stage of battery status. Once reached, the device at elective replacement status has sufficient battery life with full function for several months. Devices at end-of-service are not able to provide reliable service.

11. Lead impedance and pacing thresholds are usually monitored by the electrophysiologist involved in the patient's care. These parameters reflect lead integrity and effective pacing with all leads involved in the device.

Device diagnostics can be obtained remotely from telephone/Internet uplinks from the patient's homes, which should be done in heart failure patients who are considered to be at high risk for subsequent decompensation. The frequency of uploads should be based on patient status and clinical needs. Specific infrastructure coordination is also required to route diagnostic information to the providers responsible for patients' care or changes in medical therapies to maintain stability.

Alternative and/or additional clinical decisions to consider

End of life decision making

It is a truism that all patients will eventually die. They often die despite our best efforts to keep them alive or improve their quality of life. This harsh reality is difficult to discuss for many physicians with long-term relationships with their patients. This may be particularly difficult for heart failure practitioners who must bring a sense of optimism to patients who uniformly feel hopeless.

However, there will come a time in which no medical "miracle" will change the eventual course of this very serious disease. This uncomfortable situation can be made easier with an organized approach:

  1. 1.What is the patient's functional status? Are they now with NYHA Class IV refractory ACC/AHA stage D heart failure?

  2. 2.Are they candidates for a left ventricular assist device (LVAD) or transplant? Destination LVAD implantation has certainly changed the way end-stage disease is managed and opens an opportunity for mortality reduction in severely impaired patients with low-output heart failure syndromes.

  3. 3.Has the patient developed a medical problem that is likely to cause death in a year? ICD therapy is not indicated in patients with comorbid conditions that cannot be treated. What to do with the ICD for patients who develop terminal illness years after implantation is a significant dilemma for the patient. Sometimes they need guidance and education that the device programming can be changed to "turn off" ventricular arrhythmia detection to avoid termination of sudden death. This option is usually considered ethical since no active therapy is withdrawn that results in death. ICD therapy is considered a therapy to treat a specific entity (ventricular arrhythmias), which may or may not occur. The intent of ICD therapy is to avoid sudden unexpected death in patients who otherwise have significant life expectancy, usually defined as greater than 12 months. Otherwise, ICD therapy's goal of reducing mortality is ineffective in patients with refractory heart failure or terminal illnesses.

  4. 4.Has the patient opted for "Do Not Resuscitate" status? Patients need education about the status of the ICD if they opt for DNR status, since ICD discharge is not different in intent from advanced cardiac life support measures that the patient does not want. Again, they may not know that the device can be programmed to not detect potentially lethal arrhythmias.

  5. 5.Does the patient have incessant arrhythmias? For patients with incessant arrhythmias without the option of advanced therapies, turning off the ICD is a reasonable approach and can be offered in certain circumstances.

Overall, then, patients who have refractory heart failure syndromes without an option for advanced heart failure therapies, should be given the option for discontinuation of ICD detection algorithms. Patients who have opted for DNR status should be given the option for change in ICD therapy. Finally, patients who develop an untreatable comorbid terminal condition should be given the option for ICD disabling.

CRT-D devices have separate circuitry and the defibrillator component can be considered separately in the scenarios outlined above. However, withdrawal of cardiac resynchronization therapy is considered by most as a withdrawal of an active therapy that likely will actively shorten the patient’s life. This is especially true for patients who are pacemaker dependent and is unethical in most settings.

Therefore, discontinuation of CRT is probably unwarranted in most situations and must be considered by ethical committees or palliative care experts. Most patients do not realize, however, that the ICD portion of the device can be stopped while leaving the CRT portion active.

Complications and their management

What complications are associated with ICD and CRT therapies?

  1. 1.Inappropriate shocks occur in approximately 15% of patients with primary prevention ICDs. Ventricular discrimination algorithms and detection settings can many times be altered to prevent further inappropriate shocks.

  2. 2.Lead fracture or failure is a rare event, but sometimes is associated with manufacturer defects. This may produce electrical signals that appear to the device to represent lethal arrhythmias and can lead to multiple shocks or device failure to sense appropriately. Lead failure is very rare, but very news worthy and is usually the subject of public discussion. Short-term ICD lead survival is usually thought to be about 95%, but data suggest that 15% of leads may fail over a longer period (>5 years) of time. Patients should be counseled that the lead can fail and require replacement. The exact rate at which this occurs is difficult to say, but may be as many as 15% over many years of follow-up. Studies suggest that the cost-effectiveness of ICD use to prevent sudden death is still favorable even when one considers higher long-term lead failure rates.

  3. 3.Diaphragmatic stimulation occurs when the left ventricular lead of a CRT device stimulates the phrenic nerve causing uncomfortable diaphragmatic contraction. The patient may perceive this as a shock, but device interrogation fails to reflect treated ventricular arrhythmias. Patients many times report the uncomfortable sensation in certain body positions (e.g., left lateral recumbent). Changes in stimulation parameters can many times decrease this complication, but sometimes lead revision is required.

  4. 4.Infected leads. Device and lead extraction is required if patients have persistent bacteremia despite long-term antibiotic therapy. Lead extraction is a high risk procedure and should only be done in patients who have failed medical therapy and, by consensus, lead extraction should be done at designated extraction centers.

  5. 5.Pocket infection (approximately 5%) can occur immediately postimplant and many times requires system explantation with reimplantation after appropriate antibiotic therapy.

  6. 6.Pocket erosion with lead exposure is considered to be an emergent indication for lead and system removal.

Post-implantation medical management considerations

Medical management following ICD implantation is essentially the same as preimplantation, as these devices do not alter the natural history of heart failure. As mentioned earlier, appropriate beta-blocker therapy coupled with aldosterone antagonism are known to decrease risk for ventricular arrhythmias leading to sudden death.

The pharmacodynamics of these interventions are directly related to the most common mechanisms of ventricular arrhythmogenesis in heart failure and should be maximized when patients experience treatable arrhythmias. Other antiarrhythmic interventions are required when ventricular arrhythmias "escape" suppression by neurohormonal intervention.

Antiarrhythmic drug therapy is problematic and usually relies on amiodarone for arrhythmia suppression in patients with heart failure to avoid subsequent device discharge. All device discharges should be reviewed by an expert capable of determining if the arrhythmia treatment was appropriate.

Device programming can sometimes be changed to avoid treatment of hemodynamically stable VT, for example, that may self-terminate. Changes in the way a device diagnoses or treats potentially lethal arrhythmias should be directed by the implanting electrophysiologist.

Other medical therapies may be needed, such as other antiarrhythmic drugs, but this should be prescribed under close supervision in the hospital and with collaboration between heart failure specialists and electrophysiologists. For example the treatment of ventricular or atrial arrhythmias using d,l-sotalol is a common approach, but may interfere with proven beta-blocker therapies.

Furthermore, patients with very low output states that are not candidates for advanced therapies, such as LVAD or transplant, usually do not tolerate higher dose beta-blocker therapy instituted as antiarrhythmic drug intervention. Careful evaluation of the patient's arrhythmia burden should be coupled with an even more careful evaluation of the patient's heart failure status. A close collaboration between heart failure specialists and electrophysiologists is required for successful treatment of ventricular arrhythmias.

Medical management changes are more likely to occur in patients receiving a CRT device implant since this intervention modifies heart failure disease progression. CRT is expected to improve ventricular systolic and diastolic function along with decreasing functional mitral regurgitation.

The result is improved forward flow and renal perfusion. CRT also results in increased vagal heart rate control coupled with decreased sympathetic activation.

These factors attenuate the adverse neural and hormonal stimuli that result in pathologic remodelling and congestion. Therefore, diuretic adjustment is the most important medical change in the post-CRT time period.

Most patients require less diuretic dosing to maintain optimal volume status in the months after implantation. Further adjustments in neurohormonal intervention are often possible since systemic blood pressure is better supported by the improved post-CRT forward flow. This may allow tolerance of increased doses of ACE inhibitors or ARBs. Beta-blocker therapy in particular can be the focus of uptitration in most patients after CRT implantation with better systemic blood pressure and chronotropic support from the device.

Pulse generator replacement protocols

Device batteries reach a voltage threshold that allows elective replacement while all functions of the device are fully supported. The battery status terminology varies by manufacturer but commonly conveys the concept that the battery should be electively replaced. End of service represents an urgent need for pulse generator replacement as now the function of the device is compromised by low battery voltage.

Several questions should be asked at the time of device replacement:

  1. 1.What is the ejection fraction now? Has excellent medical management improved left ventricular function such that arrhythmia risk may be less now than when the device was originally implanted. This applies to ICDs, but not CRTs because improved LV function in patients with CRT devices is in large part due to the device. Withdrawal of CRT support very likely will result in worsening of LV function. Therefore, CRT device replacement is recommended even if the ejection fraction is normal (>55%). ICDs, on the other hand, may not have the same impact on mortality in patients with normalized ventricular function. Patient's should be involved in this decision making and given an opportunity to not replace the device if they would not have an indication for the device at the time of replacement.

  2. 2.What is the QRS duration now? Sometimes patients develop interventricular conduction delays over the years of ICD implantation and at the time of replacement they may have an indication for CRT, either from changes in intrinsic conduction or increased need for ventricular rate support. This must be considered when pulse generator replacement is scheduled to ensure that the proper device is implanted.

  3. 3.What is the percentage of right ventricular apical pacing? Patients with >40% ventricular pacing likely have significant conduction abnormalities and will probably require ventricular rate support long term. It is now approved by the USFDA to provide biventricular pacing support for patients with AV block and high percentage of ventricular pacing who have LVEF less than 50%. Therefore, it is reasonable to consider a CRT upgrade from ICD alone in patients with significant ventricular rate support needs.

  4. 4.What is the patient's arrhythmia history? Patients with persistent left ventricular dysfunction, but no history of treated ventricular arrhythmias should still receive a recommendation for device replacement. Patients with recovered ventricles and no history of arrhythmias should be given the option of opting-out for replacement.

  5. 5.What does the patient want? Sometimes patients change their attitudes toward the possibility of sudden death and do not want it prevented should it occur. Each patient must decide for themselves about replacement of devices and should be given permission by their doctor to consider notreplacing an implanted device, particularly an ICD. CRT device replacement is different in that it appears that improved status and left ventricular function achieved by CRT fades quickly after discontinuation. However, patients with CRT-D devices may opt only to replace the CRT portion and have a CRT-P replacement. While most patients opt for replacement of their devices, many do not know they have a choice.

What do I do when a patient receives a shock?

Patients should be given instructions about what they should do if they receive a shock. Most practitioners do not request the patient come for emergency medical attention if a shock happens once and they otherwise are feeling well. They should be instructed to upload information from their device and contact their health care team.

Patients should seek emergent care if they have persistent symptoms or if they receive more than one shock.

All patients who have a shock from their device should have the arrhythmia evaluated to make sure the shock was appropriate. Electrolytes including magnesium levels should be evaluated as soon as possible. Device programming or medications may be changed to avoid inappropriate interventions in the future. As mentioned earlier, ICDs define arrhythmias mostly based on the cycle length of successive heart beats. This definition is programmable and it is important to determine potential maximal heart rates for each patient, both from a sinus rhythm perspective or conduction of atrial arrhythmias. Electrogram analysis usually can determine if a shock is inappropriate and leads to appropriate device programming changes.

Other causes of inappropriate shocks may include lead fracture, which can lead to multiple shocks.

Tips for maximizing cardiac resynchronization therapy

Loss of ventricular pacing in CRT devices happens when conduction of atrial fibrillation or other atrial arrhythmias inhibit ventricular pacing. Additionally, a heavy burden of ventricular ectopy can inhibit the device. Maximal CRT effect is seen with >95% ventricular pacing with significant reduction in clinical benefit seen with ventricular pacing <92%. Several options are available for maximizing CRT benefit:

  1. 1.Monitor ventricular pacing and other diagnostic parameters. Many practitioners have no mechanism to obtain device diagnostics and therefore have no information about how the therapy is working. The first step is to actively monitor device function and ventricular pacing.

  2. 2.Increase the lower rate limit in patients with competing atrial fibrillation conduction. Sometimes this is just enough of an intervention to improve ventricular pacing to goal. Examining the rate of intrinsic conduction during interrogation at rest and during a 6-minute hall walk are simple ways to determine how fast atrial fibrillation is conducting at rest and during activities of daily living.

  3. 3.Maximize medical therapies targeting atrioventricular (AV) nodal conduction. Although digoxin is no longer considered a first-line medical intervention for heart failure patients, it still is a very good medical therapy to control conduction of atrial fibrillation. Also beta-blocker therapy can be maximized to control ventricular rate response.

  4. 4.Consider ablate and pace. AV nodal ablation and biventricular pacing is a reasonably well-studied approach for this very common patient population and sometimes is the only way to achieve appropriate ventricular pacing. The true impact of the "ablate and pace" approach is not established based on clinical trial evidence.

  5. 5.Treat ventricular ectopy. This approach usually involves maximizing beta-blocker therapy for patients with heart failure, but some would advocate more advanced antiarrhythmic therapy to suppress ventricular ectopy. This usually is reserved for patients with ectopy and occasional treatment for sustained ventricular arrhythmias.

  6. 6.Maximize atrioventricular pacing intervals. This has mostly relied on the Ritter method of synchronizing atrial and ventricular activation based on mitral inflow Doppler signals. Controversy exists about how or when to optimize AV intervals. All clinical trials optimized AV interval shortly after implantation, but review of the AV intervals achieved with echo-based methods revealed that most of the time the AV intervals were tightly clustered around 90 to 100 msec. Certainly AV optimization is needed for patients who are "nonresponders," but some practitioners perform this procedure should be done after each implantation.

  7. 7.Remember to adjust medical therapies. Dehydrated patients, who now do not need as much diuretic dose, will feel ill and seem to not respond to CRT. This is important because they may actually be responding quite well, but they just do not need as much diuretic support.

National Coverage Decisions from the Centers for Medicare and Medicaid Services—"appropriate use"

National Coverage Decision documents for ICD implantation can be found at www.cms.gov entering the term "ICD" in the search engine.

Other Considerations

Patients with ICDs who receive a shock for a potentially lethal arrhythmia may develop a significant anxiety-aversion disorder that will need specific therapy. Health care providers can unwittingly compound this issue by asking what the patient was doing when the shock occurred.

The obvious implication of the question is that the activity "caused" the arrhythmia. Lethal ventricular arrhythmias may be associated with exercise or activity, but mostly occur randomly and patients may avoid very important activities if they associate them with the shock. Each patient should be assessed for maladaptive anxiety after shock. Psychological counseling is many times needed and sometimes drug therapy is required.

What’s the evidence?

Daubert, JC, Saxon, L, Adamson, PB. "2012 EHRA/HRS expert consensus statement on cardiac resynchronization therapy in heart failure: implant and follow-up recommendations and management". Europace. vol. 14. 2012. pp. 1236-86.

Jessup, M, Abraham, WT, Casey, DE. "2009 focused update: ACCF/AHA guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation". Circulation. vol. 119. 2009. pp. 1977-2016.

Dickstein, K, Vardas, PE, Auricchio, A. "2010 Focused update of ESC guidelines on device therapy in heart failure: an update of the 2008 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure and the 2007 ESC guidelines for cardiac and resynchronization therapy". Europace. vol. 12. 2010. pp. 1526-36.

Hunt, SA, Abraham, WT, Chin, MH. "ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines". Circulation. vol. 112. 2005. pp. e154-235.

Epstein, AE, DiMarco, JP, Ellenbogen, KA. "ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities". Heart Rhythm. vol. 5. 2008. pp. e1-62.

Curtis, AB, Worley, SJ, Adamson, PB. "Biventricular pacing for atrioventricular block and systolic dysfunction". N Engl J Med. vol. 368. pp. 17-1585.

Abraham, WT, Adamson, PB, Bourge, RC. "Wireless pulmonary artery haemodynamic monitoring in chronic heart failure: a randomised controlled trial". Lancet. vol. 377. 2011. pp. 658-66.

(The CHAMPION Trial results outlining clinical benefit of implantable hemodynamic monitoring.)

Goldenberg, I, Kutyifa, V, Klein, HU. "Survival with cardiac-resynchronization therapy in mild heart failure". N Engl J Med. 2014.

(Long-term clinical benefit in patients treated with CRT)

Epstein, AE, DiMarco, JP, Hayes, DL. "2012 ACCF/AHA/HRS focused update incorporated into the 2008 guidelines for device based therapy of cardiac rhythm abnormalities". J Am Coll Cardiol. vol. 60. 2012. pp. 1297-1313.

(The latest updated recommendations for device management of cardiac rhythm disorders including CRT and ICD use.)

Yancy, CW, Jessup, M, Bozkurt, B. "2013 ACCF/AHA Guideline for the management of heart failure". J Am Coll Cardiol. vol. 62. 2013.

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