Atrial Flutter & Ventricular Tachycardia: HRS Presidents Define State of the Art
Flutter & ablationFive years ago, the relationship between atrial flutter and underlying heart disease was hazy. The prevailing notion was that atrial flutter might occur and then deteriorate into atrial fibrillation (AF). Today, electrophysiologists (EPs) recognize that flutter is its own abnormal rhythm, separate from AF, but with perhaps common origins, says Douglas Packer, MD, president of the HRS and director of heart rhythm services at the Mayo Clinic in Rochester, Minn.
Most atrial flutter seen by EPs is the result of underlying disease. It is unusual for a patient with a normal heart to have atrial flutter. "It's possible, but it is more likely that atrial flutter will occur in the setting of concomitant atrial fibrillation, so it tends to have the same risk factors such as hypertension, diabetes, hypertrophic cardiomyopathy, underlying obstructive coronary artery disease with infarction or heart failure," Packer says.
The specialty's understanding of patients with congenital heart disease also has advanced. These patients are at a substantially increased risk of developing atrial flutter, particularly those who undergo surgical correction. "Patients with congenital heart disease may do very well with the plumbing following surgery only to have increasing electrical problems later on," Packer says. Knowing this allows EPs to be better prepared to either reduce the occurrence of flutter or properly treat it following surgery.
In the setting of atrial flutter with concomitant AF, ablating the isthmus between the tricuspid valve and the inferior vena cava generally eliminates the flutter, but does not cure the AF. Consequently, it is important to monitor patients with atrial flutter to determine whether they also have AF. If not, ablation of the flutter is straightforward.
"On other hand, if a patient had several episodes of AF, even if atrial flutter had been the predominant arrhythmia, particularly in the setting of underlying disease, then we would ablate both arrhythmias in the same procedure," Packer says. "Most of the decisions regarding treatment options come down to whether there is the presence or absence of underlying disease and the presence or absence of AF in addition to flutter or vice versa."
In the past, however, EPs would have taken care of the flutter hoping that the AF would resolve itself. "We know that is not the case today, especially in the presence of underlying disease," Packer says.
Still, flutter can remain after ablating AF. There are several mechanisms for this. First, the heart has only so many ways to respond post-AF ablation. One of those manifestations is atrial flutter. Second, a gap in the linear ablation line could cause flutter and even be aggravated by the presence of that gap. "When we re-ablate, we may have to specifically localize the gap or gaps and ablate them," Packer says.
He suggests that fluoroscopy guidance may be sufficient to ablate around the pulmonary veins for AF. If flutter develops, particularly in the presence of prior ablation, 3D mapping systems help identify and localize specific gaps. "In these cases, mapping is almost mandatory," Packer says. Merging CT or MRI datasets also is particularly helpful to show the three-dimensionality of the cardiac chambers, but the images must be appropriately registered and point-to-point confirmation made.
The use of ablation as a first-line treatment for flutter is neither supported nor refuted by available guidelines, Packer says. In his opinion, however, ablative intervention is "very reasonable" for a patient with classic isthmus-dependent flutter who is highly symptomatic. One problem, however, is that EPs may not know if it is classic isthmus-dependent flutter from the ECG alone. Another problem is that flutter with coexisting AF calls for anti-arrhythmic drug therapy first, and ablation as the second choice when symptoms are persistent.
Ventricular tachycardia & devicesOne change regarding device therapy is learning to optimize treatment in patients who are being implanted with devices as a primary preventive strategy, says Bruce L. Wilkoff, MD, president-elect of the HRS and director of cardiac pacing and tachyarrhythmia devices at the Cleveland Clinic.
"Based on studies of populations, it's difficult to know how each individual will respond to implantable device therapy, especially those who have never had arrhythmias," he says.
Today, there is better understanding that inappropriate shocks can impact survival. Atrial arrhythmias, including flutter and AF, are major causes of defibrillator shocks. "Is the programming of these devices contributing to those inappropriate shocks?" Wilkoff asks.
He and his colleagues examined that question by evaluating data from about 80,000 patients remotely monitored between 2004 and 2010 who had both single- and dual-chamber cardiac resynchronization therapy (CRT) devices. (The study was presented at the 2010 HRS meeting.) They found that patients with AF had more shocks and a reduced survival. Interestingly, not all patients with AF had the same outcomes. It was dependent on how the device was programmed. "Devices that were programmed to have longer durations of detection time tended to deliver fewer shocks," Wilkoff says. "It might be possible to identify these patients and program their devices differently."
In the same study, Wilkoff et al also looked at the percentage of ventricular pacing in those with CRT devices. In the past, a device pacing 85 percent of the time was considered the norm. This study, however, showed that survival was reduced if pacing dropped below 98 percent. In fact, each subsequent drop in pacing time reduced survival further. "These types of data, which were from remotely interrogated devices, help us realize that we have to be more aggressive with rate control with CRT devices," he says.
"This is where ablation comes in," Wilkoff says. "We have to figure out what is the right strategy for virtually 100 percent AV [atrioventricular] nodal pacing. It might mean a higher drug dose is required, but ablation will probably be a stronger therapeutic candidate." To make that determination, however, the field will need a well-designed clinical trial.
Wilkoff also was involved with the PREPARE trial, which examined whether strategically chosen ventricular tachycardia (VT) or ventricular fibrillation (VF) detection and therapy parameters on implantable cardioverter-defibrillators (ICDs) could reduce the incidence of inappropriate shocks, as well as arrhythmic syncope and untreated sustained symptomatic VT/VF (J Am Coll Cardiol 2008;52:541–550).
The trial involved 700 patients with primary prevention indications for an ICD (biventricular and non-biventricular). Researchers found that programming the devices to prolong detection significantly reduced inappropriate shocks and morbidity from untreated VF/VT.
The strategies for programming the devices included detecting only fast tachycardias, detecting only sustained tachycardias, applying antitachycardia pacing as first therapy for fast VTs, employing supraventricular tachycardia discriminators and employing high-output first shock.
"Many ventricular tachycardia rhythms will self-terminate. We showed that if you wait to treat these arrhythmias, you avoid inappropriate shocks without an increase in morbidity," Wilkoff says.
Some companies are changing the default programming in the devices, but EPs need to be better educated about the importance of strategic programming, he says, especially given the emerging data that show a reduction in survival for those receiving inappropriate shocks.
As one method, Wilkoff uses remote monitoring data to track device detection rate and ensure the antitachycardia pacing is turned on. "Having access to remote data is an excellent tool to ensure consistent care across a wide spectrum of patients," Wilkoff says. "This is a great opportunity for electrophysiologists to provide leadership in terms of mining data intelligently to provide source material for evidence-based practice."