Application of the 2015 ACC/AHA/HRS guidelines for risk stratification for sudden death in adult patients with asymptomatic pre-excitation.

The management of the asymptomatic pre-excited patient largely hinges on risk stratification and individual patient considerations and choice. A high threshold to treat patients may lead to a small overall risk of death while a low threshold clearly leads to increased invasive testing and ablation with associated cost and procedural risk. A firm recommendation to uniformly assess all by electrophysiology study or, alternatively, reassure all is inappropriate and unjustified by data as reflected in the recent guideline recommendations. The use of noninvasive and invasive parameters to identify the potentially at-risk individual with surveillance for symptoms in those comfortable with this approach or ablation for those choosing this alternative for individual reasons remains the cornerstone of best practice.

Electrophysiology testing and catheter ablation are helpful when evaluating asymptomatic patients with Wolff-Parkinson-White pattern: the con perspective.

The association between asymptomatic Wolff-Parkinson-White (WPW) syndrome and sudden cardiac death (SCD) has been well documented. The inherent properties of the accessory pathway determine the risk of SCD in WPW, and catheter ablation essentially eliminates this risk. An approach to WPW syndrome is needed that incorporates the patient's individualized considerations into the decision making. Patients must understand that there is a trade-off of a small immediate risk of an invasive approach for elimination of a small lifetime risk of the natural history of asymptomatic WPW. Clinicians can minimize the invasive risk by only performing ablation for patients with at-risk pathways.

Early Repolarisation - What Should the Clinician Do?

The early repolarisation (ER) pattern is a common ECG finding. Most individuals with the ER pattern are at minimal risk for arrhythmic events. In others, ER increases the arrhythmic risk of underlying cardiac pathology. Rarely ER syndrome will manifest as a primary arrhythmogenic disorder causing ventricular fibrillation (VF). ER syndrome is defined as syncope attributed to ventricular arrhythmias or cardiac arrest attributed to ER following systematic exclusion of other etiologies. Some ECG features associated with ER portend a higher risk. However, clinically useful risk-stratifying tools to identify the asymptomatic patient at high risk are lacking. Patients with asymptomatic ER and no family history of malignant ER should be reassured. All patients with ER should continue to have modifiable cardiac risk factors addressed. Symptomatic patients should be systematically investigated, directed by symptoms.

Further evidence for the "muscle bundle" hypothesis of cavotricuspid isthmus conduction: physiological proof, with clinical implications for ablation.

INTRODUCTION: It has been suggested that the cavotricuspid isthmus (CTI) is composed of discrete muscle bundles with preferred paths of conduction. An ablation technique targeting high-voltage local electrograms (maximum voltage guided or MVG technique) has been described with the aim of preferentially targeting the muscle bundles. We hypothesized that the MVG technique could provide isthmus block even if the high voltage targets were clearly separated on different ablation lines. In contrast, conduction over a continuous sheet of muscle would require a single continuous ablation line. METHODS: Twenty-two consecutive patients (mean age 65 ± 11.7, 5 females) underwent ablation using the MVG technique on 2 noncontiguous lines in the CTI. Ablation lesions were first applied at the septal aspect of the CTI, targeting only the ventricular (anterior) aspect of the annulus. A line distinctly lateral and noncontiguous to the first was then chosen to target high voltage potentials on the atrial (posterior) aspect of the CTI. RESULTS: Complete CTI block was achieved in all study patients without complication. A mean of 7.8 ± 3.7 ablation lesions were required. Mean ablation time was 401.0 ± 414.5 seconds. CONCLUSION: Two nonoverlapping incomplete lines of ablation in the CTI consistently lead to bidirectional conduction block. This further supports the hypothesis that conduction over the CTI occurs over discrete muscle bundles. These bundles can be targeted individually for ablation without the need to ablate a continuous line over the CTI.

Treatment of asymptomatic catecholaminergic polymorphic ventricular tachycardia.

Catecholaminergic polymorphic ventricular tachycardia is a rare genetic disorder caused by mutations in genes involved in the intracellular calcium homeostasis of cardiac cells. Affected patients typically present with life-threatening ventricular arrhythmias precipitated by emotional/physical stress. The diagnosis is based on the demonstration of polymorphic or bidirectional ventricular tachycardia associated with adrenergic stress. Genetic testing can be confirmatory in some patients. Treatment for catecholaminergic polymorphic ventricular tachycardia includes medical and surgical efforts to suppress the effects of epinephrine at the myocardial level and/or modulation of calcium homeostasis. Mortality is high when untreated and sudden cardiac death may be the first manifestation of the disease. First-degree relatives of a proband should be offered genetic testing if the causal mutation is known. If the family mutation is not known, relatives should be clinically evaluated with provocative testing. In the absence of rigorous trials, prophylactic treatment of the asymptomatic catecholaminergic polymorphic ventricular tachycardia patient appears to reduce morbidity and mortality.