Ventricular Fibrillation

Ventricular Fibrillation

Ventricular Fibrillation | Johns Hopkins Medicine

Ventricular fibrillation, or VFib, is a dangerous problem with your heart rhythm (arrhythmia). It keeps your heart from pumping blood the way it should. This is a medical emergency.

Your heart muscle has four main sections, called chambers. The bottom two chambers are called ventricles. Ventricular fibrillation happens when the electrical signals in your heart go haywire. This causes a ventricle to quiver (fibrillate) instead of pumping blood to your body.

Without medical treatment right away, VFib can cause death. In fact, it’s the most common cause of sudden cardiac death.

VFib doesn’t give you much warning. The main symptom is passing out.

But you may have symptoms of ventricular tachycardia (VT). This makes your lower heart chambers beat too fast. This can lead to VFib. Signs and symptoms of VT include:

  • Chest pain
  • Pounding or fast heartbeat
  • Dizziness
  • Nausea
  • Shortness of breath
  • Passing out

Sudden cardiac arrest (SCA) is the worst thing that can happen with VFib. The two main signs of SCA are lack of responsiveness and major breathing trouble (no breathing at all or gasping for air).

Doctors don’t know for sure what causes ventricular fibrillation. But they do know some situations have a link to it. For instance, it happens most often during or right after a heart attack. That may be because the heart’s electrical signals can become unstable when there isn’t enough blood flow.

Other things that can raise your chances of VFib include:

VFib comes on fast and needs treatment just as fast. If you get medical care right away, here’s what may happen:

  • Step 1: Cardiopulmonary resuscitation (CPR)
  • Step 2: Defibrillation
  • Step 3: Medication to make your heart rhythm stable again

You can’t completely prevent an episode of ventricular fibrillation. But there are several ways to make it less ly to happen:

  • Arrhythmia medications (drugs that help control abnormal heart rhythms)
  • Defibrillators (devices that correct abnormal heart rhythms)
  • Catheter ablation (surgery to control abnormal electrical signals)

You’ve probably seen defibrillators in action on TV, especially in medical dramas. They’re the paddles placed on a person’s chest to shock their heart into beating. This type of defibrillator is called an automated external defibrillator (AED). It can help save the life of someone in cardiac arrest.

Two other types of defibrillators can also help someone with a dangerous arrhythmia such as VFib.

Implantable cardioverter defibrillator (ICD). A surgeon places this device inside your chest or belly. When your heart rhythm isn’t normal, it gives high- or low-energy electrical shocks to get your heartbeat back to normal. (If your ventricles start to quiver, it will deliver a high-energy shock). It’s a pacemaker, but a pacemaker delivers only low-energy shocks.

Wearable cardioverter defibrillator (WCD). WCDs work much ICDs, except they’re outside the body. Wires connect sensors on your skin to a unit you wear under your clothes. WCDs can be programmed to detect a certain type of arrhythmia, such as VFib.


American Heart Association: “Ventricular Fibrillation.”

Mayo Clinic: “Ventricular fibrillation.”

Johns Hopkins Medicine: “Ventricular Fibrillation.”

National Heart, Lung, and Blood Institute: “Defibrillators,”

Merck Manual: “Ventricular Fibrillation.”

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Resuscitation After Prolonged Ventricular Fibrillation With Use of Monophasic and Biphasic Waveform Pulses for External Defibrillation

Ventricular Fibrillation | Johns Hopkins Medicine

Background—Survival after prolonged ventricular fibrillation (VF) appears severely limited by 2 major factors: (1) low defibrillation success rates and (2) persistent post-countershock myocardial dysfunction.

Biphasic (BP) waveforms may prove capable of favorably modifying these limitations.

However, they have not been rigorously tested against monophasic (MP) waveforms in clinical models of external defibrillation, particularly where rescue from prolonged VF is the general rule.

Methods and Results—We randomized 26 dogs to external countershocks with either MP or BP waveforms. Hemodynamics were assessed after shocks applied during sinus rhythm, after brief VF (>10 seconds), and after resuscitation from prolonged VF (>10 minutes). Short-term differences in percent change in left ventricular +dP/dtmax (MP −16±28%, BP +9.1±24%; P=0.

03) and left ventricular −dP/dtmax (MP −37±26%, BP −18±20%; P=0.05) were present after rescue from brief VF, with BP animals exhibiting less countershock-induced dysfunction. After prolonged VF, the BP group had lower mean defibrillation thresholds (107±57 versus 172±88 J for MP, P=0.04) and significantly shorter resuscitation times (397±73.7 versus 488±74.

3 seconds for MP, P=0.03).

Conclusions—External defibrillation is more efficacious with BP countershocks than with MP countershocks. The lower defibrillation thresholds and shorter resuscitation times associated with BP waveform defibrillation may improve survival after prolonged VF arrest.


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Ventricular Tachycardia

Ventricular Fibrillation | Johns Hopkins Medicine

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Ventricular tachycardia (VT or V-tach) is a type of abnormal heart rhythm, or arrhythmia. It occurs when the lower chamber of the heart beats too fast to pump well and the body doesn't receive enough oxygenated blood.

A normal heartbeat begins with an electrical impulse from the sinus node, a small area in the heart's right atrium (right upper chamber). Ventricular tachycardia begins in the lower chambers (ventricles) and is quite fast.

When it lasts only a few seconds, ventricular tachycardia may cause no problems. But when sustained, ventricular tachycardia can lower the blood pressure, resulting in syncope (fainting) or lightheadedness.

Ventricular tachycardia can also lead to ventricular fibrillation (a life-threatening arrhythmia) and cardiac arrest.

Structural Heart Disease

Ventricular tachycardia most often occurs when the heart muscle has been damaged and scar tissue creates abnormal electrical pathways in the ventricles. Causes include:

  • Heart attack
  • Cardiomyopathy or heart failure
  • Myocarditis
  • Heart valve disease

Idiopathic Ventricular Tachycardia

Sometimes, people with no known heart disease can develop ventricular tachycardia, often due to an irritable focus — when cells outside the sinus node start generating an electrical impulse automatically on their own. This form of ventricular tachycardia is easier to address and is usually not life threatening.

What are the symptoms of ventricular tachycardia?

When ventricular tachycardia lasts a short time, there may be no symptoms except palpitations — a fluttering in the chest. But ventricular tachycardia lasting more than 30 seconds may cause more severe symptoms:

  • Chest pain
  • Dizziness
  • Fainting (syncope)
  • Shortness of breath
  • Cardiac arrest

How is ventricular tachycardia treated?

  • Radiofrequency ablation: a minimally invasive procedure to destroy the cells that cause ventricular tachycardia; less effective when there is structural heart disease
  • Implantable cardioverter defibrillator (ICD): an implanted device that delivers an electrical pulse to the heart to reset a dangerously irregular heartbeat
  • Medication: A number of antiarrhythmic medications are used to prevent ventricular tachycardia. These include:
    • Sotolol
    • Flecainide
    • Propafenone
    • Amiodarone

Learn more about arrhythmias or visit the Johns Hopkins Electrophysiology and Arrhythmia Service.

The victim of an unexpected ventricular fibrillation, James Cromwell was saved by the intervention of Johns Hopkins electrophysiologists. But the initial approach wasn’t enough to comfortably control his severe condition. So doctors tried something new: they tracked down the patch of heart cells causing the extra beats and destroyed them.


Dynamic Analysis of Cardiac Rhythms for Discriminating Atrial Fibrillation From Lethal Ventricular Arrhythmias | Circulation: Arrhythmia and Electrophysiology

Ventricular Fibrillation | Johns Hopkins Medicine

Implantable cardioverter-defibrillators (ICDs), the first line of therapy for preventing sudden cardiac death in high-risk patients, deliver appropriate shocks for termination of ventricular tachycardia (VT)/ventricular fibrillation.

A common shortcoming of ICDs is imperfect rhythm discrimination, resulting in the delivery of inappropriate shocks for atrial fibrillation (AF). An underexplored area for rhythm discrimination is the difference in dynamic properties between AF and VT/ventricular fibrillation.

We hypothesized that the higher entropy of rapid cardiac rhythms preceding ICD shocks distinguishes AF from VT/ventricular fibrillation.

Methods and Results—

In a multicenter, prospective, observational study of patients with primary prevention ICDs, 119 patients received shocks from ICDs with stored, retrievable intracardiac electrograms.

Blinded adjudication revealed shocks were delivered for VT/ventricular fibrillation (62%), AF (23%), and supraventricular tachycardia (15%). Entropy estimation of only 9 ventricular intervals before ICD shocks accurately distinguished AF (receiver operating characteristic curve area, 0.

98; 95% confidence intervals, 0.93–1.0) and outperformed contemporary ICD rhythm discrimination algorithms.


This new strategy for AF discrimination entropy estimation expands on simpler concepts of variability, performs well at fast heart rates, and has potential for broad clinical application.

Ventricular tachycardia (VT) and ventricular fibrillation (VF) are lethal cardiac arrhythmias, claiming a quarter million lives per year from sudden cardiac death (SCD).

1 Implantable cardioverter-defibrillators (ICDs), the first line of therapy for preventing SCD, deliver appropriate shocks for termination of VT/VF.

2,3 A common shortcoming of ICDs is inadequate rhythm discrimination, resulting in the delivery of inappropriate shocks for non–life-threatening arrhythmias, such as atrial fibrillation (AF).

Clinical Perspective on p 561

Even with optimal ICD programming and contemporary technological advances,4–15 about one third of ICD recipients receive inappropriate shocks for AF.

15–24 Inappropriate shocks are painful, are associated with substantial psychological stress, decrease quality of life, can initiate more dangerous arrhythmias, and may increase mortality.

15,22–25 Minimizing inappropriate shocks, while maintaining high sensitivity for detecting VT/VF, is an essential attribute of contemporary ICDs.

An underexplored opportunity for rhythm discrimination in patients with ICD is the difference in dynamic properties of AF and VT/VF.

In AF, complexities of atrial activation and decremental impulse conduction through the atrioventricular node produce a highly irregular rhythm. As a result, the time series for ventricular activation approaches white noise.

In most cases, this sharply differs from arrhythmias that arise from diseased ventricular myocardium.

One approach to characterize this distinctive difference is to measure the information entropy, a concept of uncertainty related to thermodynamic entropy.

26 In this context, entropy is fundamentally different from conventional measures of heart rate variability (HRV) in that entropy exploits information on the ordering of the times between ventricular activation and quantifies the degree to which self-similar fluctuation patterns repeat. These self-similar fluctuations are indistinguishable in moment statistics and frequency domain measures of HRV. We hypothesized that the entropy of rapid cardiac rhythms immediately preceding ICD shocks discriminates AF from VT/VF. We directly compared performances of entropy estimation with those of representative discrimination algorithms used in contemporary ICDs.

Adjudicated Rhythm Groups

The intracardiac electrogram data were drawn from a multicenter, prospective cohort of patients with dual- or single-chamber ICDs implanted for primary prevention of SCD.

We studied patients with ischemic or nonischemic heart failure, ejection fraction ≤35%, New York Heart Association class I to III symptoms, and no history of VT/VF or SCD.

Patients with secondary prevention indication, New York Heart Association class IV heart failure, permanent pacemaker, or pre-existing Class 1 indication for permanent pacemaker were not included in this cohort.

This study includes 119 consecutive patients, who received ICDs equipped with intracardiac electrogram storage that were retrieved for rhythm discrimination and analysis. The ICDs were manufactured by Medtronic (Minneapolis, MN), Boston Scientific (Natick, MA), and St. Jude Medical (St. Paul, MN).

During the implant procedure, sensing, pacing, and defibrillation thresholds were tested as per standard protocol. ICDs were programmed at the discretion of the implanting physicians. High VT/VF cutoff zones were encouraged and supraventricular tachycardia (SVT) discriminator algorithms could be enabled.

The ICDs were reprogrammed by the treating physician when considered clinically indicated (eg, hemodynamic well-tolerated VT and VT in monitor zone). The electrogram and interval data were downloaded from ICDs using proprietary software obtained from the manufacturers.

The entropy calculations were performed offline as described below.

After each shock or after death, all available information, including electrograms before the shock, was reviewed by a committee of ≥3 board-certified clinical cardiac electrophysiologists.

The committee blindly adjudicated the type of arrhythmia eliciting the shock (eg, VT, VF, SVT, and AF) and whether the shock was appropriate or inappropriate. An inappropriate shock was defined as an episode that started with a shock not delivered for VT or VF and ended when sinus rhythm was detected.

If a patient received repetitive inappropriate shocks for the same rhythm, only the electrogram responsible for the first shock was analyzed. Causes of inappropriate shocks were categorized as SVT (including sinus tachycardia), AF (including atrial flutter), or artifact.

Although the categorization of atrial flutter as AF diminished performance estimates, it reflects the common clinical situation in which these arrhythmias often coexist in the same patient populations and share underlying substrates, mechanisms, and management strategies.

The study was approved by the institutional review boards of the participating centers (Johns Hopkins University, University of Maryland, Washington Hospital Center, and Virginia Commonwealth University). All patients provided written informed consent.

Entropy Estimation

We optimized the sample entropy27,28 measure and developed the coefficient of sample entropy (COSEn)29 for the specific purpose of AF discrimination in electrograms at all heart rates using very short time series of ventricular activation.

An illustration of the COSEn calculation is provided in the Methods in the online-only Data Supplement. Briefly, sample entropy is the conditional probability that 2 short templates of length m that match within an arbitrary tolerance r will continue to match at the next point m+1.

Mathematically expressed, SampEn=ln(A/B), where A denotes ΣAi (total number of matches of length m+1) and B denotes ΣBi (total number of matches of length m+1 and m), in a series of n consecutive intervals, x1, x2,…,xn, where the record may be as short as n=9. By allowing r to vary for sufficient matches and confident entropy estimation, conversion of the final probability to a density by dividing by the matching region volume, and correcting for the mean heart rate, the optimized sample entropy estimate was defined as COSEn. Un approximate entropy,26 frequency domain measures, or geometric measures, such as Poincaré plots,30 COSEn is accurate in very short time series.

AF Discrimination

For each patient, entropy analysis was performed only for the episode resulting in the first shock. The adjudicated ICD shock rhythms were considered the gold standard for rhythm diagnosis and compared with AF discrimination entropy estimation. Entropy values higher than a threshold (COSEn>−1.

20) for 9 consecutive ventricular activation intervals preceding a shock were classified as AF. This threshold was preselected in a prior Holter database29 such that the proportion of AF misclassified as non-AF was equal to the proportion of non-AF misclassified as AF.

31 Entropy estimation was also performed on all the electrograms, and intervals of the stored event and analysis of >9 consecutive intervals did not alter the accuracy of detection.

The diagnostic performance of entropy estimation was compared with that of standard metrics of heart rate, HRV, and stability calculated from the same 9 intervals. The heart rate was determined from the mean interval.

The coefficient of variation (SD of the intervals divided by the mean) is a common measure of HRV.

Stability, another measure of variability, is indexed as the trimmed range (ie, next-to-longest minus next-to-shortest intervals, and therefore, large values indicate less stable rhythms).

Statistical Analysis

Continuous variables were compared using t test and categorical variables were compared using χ2 test. The ability of entropy, stability, HRV, and heart rate to discriminate AF was evaluated using the receiver operating characteristic curve area.

We also calculated the sensitivity, specificity, lihood ratios, and predictive probabilities for detecting AF for standard cutoffs of each metric (COSEn≥−1.20; stability≥30 ms; HRV≥0.10; heart rate190 beats per minute. The entropy values consistently indicated AF.

Figure 2. Atrial fibrillation (AF) discrimination. A, Representative examples of AF and ventricular tachycardia (VT) with identical average heart rates (180 beats per minute) and stabilities (30 ms).

These values are similar to the discrimination thresholds used in routine clinical practice. The ventricular activation intervals measured at the right ventricular lead are plotted >3 seconds preceding implantable cardioverter-defibrillators shocks in 2 patients.

Shocks were delivered for AF (blue circles) and for VT (red squares). The stability of the 9 ventricular activation intervals preceding each shock was calculated as the trimmed range using the differences in the intervals indicated by the bold symbols.

Although the AF and VT were indistinguishable on the basis of stability and heart rate, the entropy of AF (−0.999) was significantly higher than that of the VT (−1.89).

B, The receiver operating characteristic (ROC) curves for discrimination of AF from supraventricular tachycardia/VT/ventricular fibrillation by heart rate, heart rate variability (HRV), stability, and entropy. The ROC area under curve (95% confidence interval) for entropy, stability, HRV, and heart rate were 0.98 (0.93–1.0), 0.91 (0.83–0.99; P


What causes ventricular fibrillation?

The cause of ventricular fibrillation is not always known but it can occurduring certain medical conditions. V-fib most commonly occurs during anacute heart attack or shortly thereafter.

When heart muscle does not getenough blood flow, it can become electrically unstable and cause dangerousheart rhythms. A heart that has been damaged by a heart attack or otherheart muscle damage is vulnerable to V-fib.

Other causes include electrolyte abnormalities such as low potassium,certain medicines, and certain genetic diseases that affect the heart's ionchannels or electrical conduction.

Who is at risk for ventricular fibrillation?

The most common risk factors are:

  • A weakened heart muscle (cardiomyopathy)
  • An acute or prior heart attack
  • Genetic diseases such as Long or Short QT syndrome, Brugada disease, or hypertrophic cardiomyopathy
  • Certain medicines that affect heart function
  • Electrolyte abnormalities

What are the symptoms of ventricular fibrillation?

Symptoms of V-fib include:

  • Near fainting or transient dizziness
  • Fainting
  • Acute shortness of breath
  • Cardiac arrest

How is ventricular fibrillation diagnosed?

To diagnose V-fib, your healthcare provider will consider:

  • Your vital signs, such as your blood pressure and pulse
  • Tests of heart function, such as an electrocardiogram
  • Your overall health and medical history
  • A description of your symptoms that you, a loved one, or a bystander provides
  • A physical exam

How is ventricular fibrillation treated?

There are 2 stages of treatment for V-fib. The first tries to stops yourV-fib immediately to restore a blood pressure and pulse. The second stagefocuses on reducing your chances of developing V-fib in the future.Treatment includes:

  • CPR. The first response to V-fib may be cardiopulmonary resuscitation (CPR). This will keep your blood moving.
  • Defibrillation. You will need this during or immediately after the V-fib. Electric shock can correct the signals that are telling your heart muscles to quiver instead of pump.
  • Medication. Your health care provider may give you drugs immediately after V-fib to help you control and prevent another episode. He or she may prescribe additional medications to control arrhythmia and reduce your risk over time.
  • Catheter ablation. This procedure uses energy to destroy small areas of your heart affected by the irregular heartbeat. This rarely used procedure for V-fib looks to eliminate electrical triggers of V-fib.
  • Left cardiac sympathetic denervation. This is a surgical procedure that might help you if you have frequent V-fib events. It is not yet commonly used and is reserved for people with uncontrolled V-fib with a genetic predisposition.

What are the complications of ventricular fibrillation?

Complications include the possibility of repeat episodes of fainting ornear fainting. V-fib can be fatal.

Can ventricular fibrillation be prevented?

Prevention focuses on diagnosing and treating the underlying medicalconditions that cause V-fib. Certain medicines can be used to reduce therisk of recurrence.

Implantable cardiac defibrillators are devices that are implanted withinthe body that can shock the heart back to normal rhythm within seconds ifV-fib is present. Although this device does not necessarily prevent V-fib,it can rapidly and automatically diagnose and treat this potentially fatalheart rhythm.

If you are at risk for V-fib, you should wear a medical ID and let friendsand loved ones know what to do in an emergency. Talk with them about whento call 911, and encourage them to learn how to use a defibrillator.

How can I manage ventricular fibrillation?

If you have had V-fib, or are at high risk for it, follow your healthcareprovider's recommendations for taking medicine to control arrhythmia. It'salso helpful to discuss other more invasive options, such as an implantabledefibrillator, or surgery, to prevent V-fib. Educate your friends andfamily about how to respond if you collapse and stop breathing.

When should I call my healthcare provider?

It is extremely important to make sure that people around you know what todo in an emergency. Someone should call 911 immediately if you experienceany of the following symptoms of V-fib:

  • Collapsing
  • Unresponsiveness
  • Loss of consciousness
  • Inability to breathe

Key points about ventricular fibrillation

  • Ventricular fibrillation is a type of arrhythmia, or irregular heartbeat, that affects your heart’s ventricles.
  • Ventricular fibrillation is life-threatening and requires immediate medical attention.
  • CPR and defibrillation can restore your heart to its normal rhythm and may be life saving.
  • Medications and cardiac procedures after an episode of ventricular fibrillation can prevent or reduce the chances of another episode.
  • An implantable cardiac defibrillator can promptly treat V-fib.
  • It is extremely important to make sure that people around you know what to do if you collapse because of ventricular fibrillation

Next steps

Tips to help you get the most from a visit to your healthcare provider:

  • Know the reason for your visit and what you want to happen.
  • Before your visit, write down questions you want answered.
  • Bring someone with you to help you ask questions and remember what your provider tells you.
  • At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also write down any new instructions your provider gives you.
  • Know why a new medicine or treatment is prescribed, and how it will help you. Also know what the side effects are.
  • Ask if your condition can be treated in other ways.
  • Know why a test or procedure is recommended and what the results could mean.
  • Know what to expect if you do not take the medicine or have the test or procedure.
  • If you have a follow-up appointment, write down the date, time, and purpose for that visit.
  • Know how you can contact your provider if you have questions.


Computer program predicts risk of deadly irregular heart beats: Predictive program projected to save lives and reduce unnecessary surgeries

Ventricular Fibrillation | Johns Hopkins Medicine

Combining a wealth of information derived from previous studies with data from more than 500 patients, an international team led by researchers from Johns Hopkins has developed a computer-based set of rules that more accurately predicts when patients with a rare heart condition might benefit — or not — from lifesaving implanted defibrillators. The new research, published online on March 27 in the European Heart Journal provides physicians with a risk prediction tool that will identify patients most ly to benefit from the protection provided by an implantable defibrillator while preventing a fifth from receiving unnecessary — and potentially risky — surgery to place the devices.

An estimated 1 in 5,000 people have arrhythmogenic right ventricular cardiomyopathy (ARVC), a complex, multigene, inherited disease of the lower heart chambers that can cause deadly arrhythmias, or irregular heartbeats.

Although rare, it's a very frequent cause of sudden death in young adults, according to the new study's leaders. The average age of diagnosis is 31, although it can emerge from adolescence through middle age.

ARVC can be effectively managed in many cases with an implantable cardioverter-defibrillator (ICD), a device that detects electrical abnormalities in heart muscle and immediately shocks the heart to re-establish normal rhythm. ICDs prevent sudden cardiac death and save lives.

But these devices come with risks and side effects, according to co-lead investigator Cynthia A. James, Ph.D., assistant professor of medicine in the Division of Cardiology and a certified genetic counselor at the Johns Hopkins University School of Medicine.

The devices may deliver inappropriate shocks when patients aren't experiencing life-threatening arrhythmias. And the ICD itself or pacemaker leads placed in the heart to deliver a shock may fail over time, necessitating replacement with surgery.

Infections brought on by these devices — and even just wearing out the device's battery with time — also require replacement, hospitalizations and expense, she adds.

“Because patients develop this condition at such a young age, they typically need several ICD replacements over the course of their lives,” adds James, who is also a member of the Precision Medicine Center for Excellence for Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) and Complex Arrhythmias, part of Johns Hopkins InHealth, the precision medicine effort at the Johns Hopkins University School of Medicine. “For ARVC patients, getting an ICD is a big decision with serious consequences.”

“If someone is at risk of sudden cardiac death, you don't want to miss the chance of putting in a lifesaving device. But you also don't want to put it in if that risk is not worth taking,” says Hugh Calkins, M.D.

, professor of cardiology at the Johns Hopkins University School of Medicine and director of the Electrophysiology Laboratory and Arrhythmia Service at The Johns Hopkins Hospital.

“This new model can help doctors and patients decide better if an ICD is warranted on a case-by-case basis,” he adds.

The new algorithm was developed, the researchers say, because while physicians are generally in agreement that patients who experience a life-threatening arrhythmia qualify for an ICD, it's been unclear whether patients who haven't yet experienced this event should get one for prevention.

Previous studies identified several risk factors for having life-threatening arrhythmias in ARVC patients, but each study had such relatively small numbers of patients that individually they weren't useful as a comprehensive model to predict benefit from an ICD, says Calkins, who is also a member of the Precision Medicine Center for Excellence for ARVC and Complex Arrhythmias.

To address that shortcoming, James, Calkins and their colleagues pooled medical record data from 528 patients in five registries based at 14 academic medical centers in the U.S. and Europe. The group was nearly evenly split between male and female and between North America and Europe. None had yet experienced a life-threatening arrhythmia.

Then, using risk factors derived from published previous studies — including age, sex, fainting from heart-related causes, nonsustained abnormal heart rhythms, number of abnormal beats (called premature ventricular complexes) within 24 hours, and cardiac function — they developed a computer-based mathematical set of consistent rules to try to predict whether any of the 528 patients might undergo a serious arrhythmia over time.

Over nearly five years of follow-up, just over a quarter of these patients experienced a dangerous arrhythmia, and 18 patients died.

The researchers found that their model accurately accounted for which patients would have life-threatening events. No patient with a five-year, model-predicted risk of 5 percent or less had a serious arrhythmia. More than 95 percent of arrhythmias occurred in people with at least a 15 percent five-year risk.

When the researchers compared their prediction accuracy rates with outcomes using a current consensus-based ICD placement algorithm, they found that about 20.6 percent of recommended ICD placements would have ly been unnecessary.

“We believe our findings and the risk calculator we have developed have the potential to contribute to personalized medicine and to high value health care efforts emerging throughout medical care,” says Calkins.

James and Calkins say it can cost $20,000 to implant an ICD and a similar amount of money to replace the device when the battery wears out five to 10 years later.

While results of their study seem promising, the researchers caution that because they were derived from patient registries at hospitals that specialize in treating this condition, and include many patients who carry mutations in the same ARVC gene (PKP2), the results may not match those from a community-derived population or patients who carry other types of ARVC-causing mutations. The researchers plan to validate this model in other patient populations.

In conjunction with this new publication, James and Calkins add, the team has developed a free app that will allow doctors and patients to rapidly input medical data to calculate personal risk, easing the decision-making process.

“It's an important and extremely practical tool to come this research,” James says.

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Journal Reference:

  1. Julia Cadrin-Tourigny, Laurens P Bosman, Anna Nozza, Weijia Wang, Rafik Tadros, Aditya Bhonsale, Mimount Bourfiss, Annik Fortier, Øyvind H Lie, Ardan M Saguner, Anneli Svensson, Antoine Andorin, Crystal Tichnell, Brittney Murray, Katja Zeppenfeld, Maarten P van den Berg, Folkert W Asselbergs, Arthur A M Wilde, Andrew D Krahn, Mario Talajic, Lena Rivard, Stephen Chelko, Stefan L Zimmerman, Ihab R Kamel, Jane E Crosson, Daniel P Judge, Sing-Chien Yap, Jeroen F van der Heijden, Harikrishna Tandri, Jan D H Jongbloed, Marie-Claude Guertin, J Peter van Tintelen, Pyotr G Platonov, Firat Duru, Kristina H Haugaa, Paul Khairy, Richard N W Hauer, Hugh Calkins, Anneline S J M te Riele, Cynthia A James. A new prediction model for ventricular arrhythmias in arrhythmogenic right ventricular cardiomyopathy. European Heart Journal, 2019; DOI: 10.1093/eurheartj/ehz103