defibrillators

“It’s tough to make predictions, especially about the future”
Yogi Berra

Sudden death is just that: sudden, fulminant and without warning. This is a reality for some patients with a compromised left systolic ventricular function, in particular those with left ventricular ejection fractions of less than 35%¹. Given the advent of improving acute, and chronic heart failure treatment, many of these patients with see an improvement in the vital metric referred to as “EF.” For patients who fail to improve and continue to be considered a “high risk for sudden death,” a primary implantable cardioverter defibrillator (ICD) implant can be offered to mitigate the risk of a sudden cardiac death. Nevertheless, there exist strict ICD implant guidelines as proposed by ACC/HRS and a waiting period is often necessary to meet implant criteria. With that being said, it is a well-known fact that despite undergoing medical uptitration, and recovering from revascularization, at risk patients may still succumb to fatal ventricular arrhythmia².

How often does this really occur? That is the fundamental question. The logical follow-up is to identify to whom and when exactly is a potentially fatal ventricular tachycardia or fibrillation (VT/VF) event going to occur? Knowing the answers to these questions would imply successfully predicting the future.

Out of these concerns arose the wearable cardiac defibrillator (WCD), or more commonly known as the “lifevest”³. In essence, the device which resembles a military “flak jacket” has the capability to detect and treat sustained VT/VF with an external shock. Presumably, life-saving therapy could be delivered quickly and improve the likelihood of survival. The system also permits the patient to defer therapy if still conscious. The reasoning being that a non-hemodynamically collapsing rhythm may terminate spontaneously forgoing a shock, which is a uniformly painful experience. No system is perfect, and common complaints leading to patients’ refusal to wear the device is the anxiety associated with wearing the system. Additionally, the WCD can be cumbersome to wear, provoke excess warmth and will cause frequent alarming if not well-fitted. In my experience, the alarming has lead patients to discontinue its use.

Over the last several years, I have observed a minority of WCD-prescribed patients successfully resuscitated by the Lifevest. However, I have also observed “no events” in the overwhelming majority who never experience any VT/VF and “graduate” to no device; the remainder will ultimately receive an ICD implant. A common management issue encountered in clinical practice is the “protection” of a post-myocardial infarction patient with an EF of 35% or less. The patient will often be the recipient of a percutaneous intervention, or even surgical

revascularization. Notably, the ICD implant guidelines recommend a “waiting period” of ninety days to permit improvement in the EF while maximal medical therapy is employed. Recently at the ACC in Orlando, the results of VEST were presented. The VEST study posed the question of whether the WCD can improve survival in the aforementioned patients using a randomized controlled trial⁴. Over 13,000 patients were screened, and just over 2300 were enrolled in 2:1 fashion: WCD vs optimal therapy only. The duration of follow-up was ninety days.

The results were underwhelming. In fact, there was no statistical difference in the primary outcome of sudden cardiac death VT/VF death: 1.6% for the study group, and 2.4% for the control group. Would a longer study period have made a difference? Were the subjects who expired too sick and prone to lethal electrical storms? A careful subanalysis may provide clues to these questions. Oddly enough, and perhaps the result of a wishful interpretation, the secondary endpoint of “all-cause mortality” was in favor of the WCD (3.1% vs 4.9%). The device is designed to treat VT/VF, and simply cannot defend against the myriad of other mechanisms of death – motor vehicle accidents, septic shock, cancer, sinkhole, shark attack etc. How these were adjudicated is unclear. Personally, I would interpret these results cautiously. Perhaps it is nothing more than a coin toss as to whether the WCD has any benefit in this population.

Undoubtedly for some patients the WCD has provided life-saving therapy. However, these patients appear to be relatively few and far in between. Rather than a broad use of the Lifevest system, further studies should focus on identifying clinical, imaging or electrophysiological features which better define who truly is at high risk for a sudden arrhythmic death, at least in the short-term. For now, accurately predicting sudden death continues to be elusive.

References

Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr, Drazner MH, Fonarow GC, Geraci SA, Horwich T, Januzzi JL, Johnson MR, Kasper EK, Levy WC, Masoudi FA, McBride PE, McMurray JJ, Mitchell JE, Peterson PN, Riegel B, Sam F, Stevenson LW, Tang WH, Tsai EJ, Wilkoff BL; American College of Cardiology Foundation; American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.J Am Coll Cardiol. 2013;62(16):e147-239
Zaman S. Kovoor P. Sudden cardiac death early after myocardial infarction: pathogenesis, risk stratification, and primary prevention.Circulation. 2014;129(23):2426-35
https://lifevest.zoll.com/medical-professionals/how-does-lifevest-work/
http://www.acc.org/latest-in-cardiology/clinical-trials/2018/03/09/08/06/vest

Christian Perzanowski is an electrophysiologist in Tampa, FL. His main interests are in ablation techniques for atrial fibrillation and device therapy for congestive heart failure. He reports no conflicts of interests.

Crabtree, NC

This year’s AHA Scientific Sessions in Anaheim, CA provided the cardiology community with a number of important trials. Large clinical studies have the possibility to directly impact clinical practice. In the subspecialty of electrophysiology, there was an important trial with significant relevance to physicians who implant or provide perioperative care for patients with pacemakers/ defibrillators (“EP device procedures”).

A frequent dilemma which implanting physicians face is whether or not to suspend anticoagulation prior to insertion of an EP device. Suspension of anticoagulation raises the risk of stroke for many patients and this cannot be ignored. The obvious postoperative concern is the attendant risk of pocket hematoma which is not only a painful experience for the patient, but can also dramatically increase the risk of infection. The latter is considered a potentially disastrous complication with high morbidity and mortality. In 2013, Birnie et al published the results of BRUISE-CONTROL which was a randomized controlled trial with sought to determine outcomes between continued warfarin use, and suspension of warfarin while bridging with intravenous heparin at the time of surgical implant (NEJM 2013). The results were categorically in favor of continued warfarin use. With that study, patients in the uninterrupted oral anticoagulation arm had a marked reduction of postoperative pocket hematoma (3.5% -16%). For some time, many implanting physicians had observed the benefits of continued oral anticoagulation with warfarin during device implants, however the data from this trial provided validation of this practice.

In the past several years, a group of new oral anticoagulants have emerged (NOACs). While the pharmacological mechanisms vary (e.g. factor ten, direct thrombin inhibition) the clinical effects aim to provide systemic anticoagulation. These agents have increased in popularity as an alternative to warfarin. As experience with these agents (e..g. Apibixan, Rivaroxaban, Dabigatran) grew, a determination of their effects on device implants was needed and to ascertain their risk for postoperative hematoma formation. A new trial was launched: BRUISE CONTROL-2. The clinical question was to determine any difference in the development of a hematoma subsequent to a NOAC’s uninterrupted use versus suspension of the NOAC drug two days prior to the procedure. To further add complexity to the matter, only one of these medications has a commercially available reversal agent (dabigatran), hence there is a natural apprehension of performing a procedure under the influence of anticoagulant whose effects cannot be stopped. BRUISE CONTROL-2 presented by Dr David Birnie on 11/12/17.

Surprisingly, there was no difference in pocket hematoma formation (2.1% vs 2.1%). The study was terminated due to futility. The authors concluded that either approach is reasonable. Since the study was not blinded, one might question whether the implanting physicians modified their surgical approach and perhaps could have used different methods to curtail bleeding (e.g. the use of hemostatic or antithrombotic agents introduced into the pocket).

Overall, there was a low complication rate. A size categorization of the incisional hematomas would be helpful as well: a large tension-creating hematoma clearly does not have the same clinical impact as mild swelling. In my opinion the results further validate the safety of NOAC use perioperatively. A subanalysis of how the individual agents performed would be helpful to further elucidate whether there exists a drug superiority, or better yet a BRUISE CONTROL-3 could help address this.

Christian Perzanowski is an electrophysiologist in Tampa, FL. His main interests are in ablation techniques for atrial fibrillation and device therapy for congestive heart failure.

Can Death Be Cheated? A Different Take On The Results Of The VEST Trial

What I Took Home – “BRUISES” With EP-Devices