Ventricular arrhythmias in patients with bicuspid aortic valves.

INTRODUCTION: Bicuspid aortic valves (BAV) are the most common congenital heart defects and the extent of ventricular arrhythmias (VA) in patients with BAV is unclear. The objective of this study is to describe VAs and late gadolinium enhancement cardiac magnetic resonance imaging (LGE-CMR) in patients with BAV. METHODS: A total of 19 patients with BAV (18 males, age: 58 ± 13 years) were referred for VA ablation procedures. Ten patients had BAVs at the time of ablation, nine patients had prior aortic valve replacement for a BAV. All but one patient had LGE-CMR and all patients underwent programmed ventricular stimulation at the time of the ablation. RESULTS: Frequent PVCs were the targeted VAs in 17/19 patients and VT in 2/19 patients. Monomorphic ventricular tachycardia (VT) was inducible in 6 patients. A total of 15 VTs were inducible (2.5 ± 1.0 VTs per patient with a mean cycle length of 322 ± 83 msec). LGE was present in 13 patients. Patients with inducible VT had larger borderzone and core scar compared to non-inducible patients (7.8 ± 2.1 cm3 vs. 2.5 ± 3.1 cm3 and 5.1 ± 2.6 cm3 vs. 1.9 ± 3.0 cm3, p-value < .05 for both). PVCs and VTs were mapped to the periaortic valve area in 12 patients and 4 patients, respectively. The PVC burden was reduced from 27 ± 13 to 3 ± 6 (p < .001) and the ejection fraction improved from 49 ± 13% to 55 ± 9% (p = .005). CONCLUSIONS: VAs in patients with BAV often originate from the perivalvular area and patients often have LGE and inducible VT. LGE may be due to ventricular remodeling secondary to the presence of BAV and harbors the arrhythmogenic substrate for VT.

Long-term outcomes of patients with ventricular arrhythmias and negative programmed ventricular stimulation followed with implantable loop recorders: Impact of delayed-enhancement cardiac magnetic resonance imaging.

BACKGROUND: Programed ventricular stimulation (PVS) is a risk stratification tool in patients at risk for adverse arrhythmia outcomes. Patients with negative PVS may yet be at risk for adverse arrhythmia-related events, particularly in the presence of symptomatic ventricular arrhythmias (VA). OBJECTIVE: To investigate the long-term outcomes of real-world patients with symptomatic VA without indication for device therapy and negative PVS, and to examine the role of cardiac scaring on arrhythmia recurrence. METHODS: Patients with symptomatic VA, and late gadolinium enhancement cardiac magnetic resonance imaging (LGE-CMR), and negative PVS testing were included. All patients underwent placement of implantable cardiac monitors (ICM). Survival analysis was performed to investigate the impact of LGE-CMR findings on survival free from adverse arrhythmic events. RESULTS: Seventy-eight patients were included (age 60 ± 14 years, women n = 36 (46%), ejection fraction 57 ± 9%, cardiomyopathy n = 26 (33%), mitral valve prolapse [MVP] n = 9 (12%), positive LGE-CMR scar n = 49 (62%), history of syncope n = 23 (29%)) including patients with primarily premature ventricular contractions (n = 21) or nonsustained VA (n = 57). Patients were followed for 1.6 ± 1.5 years during which 14 patients (18%) experienced VA requiring treatment (n = 14) or syncope due to bradycardia (n = 2). Four/9 patients (44%) with MVP experienced VA (n = 3) or syncope (n = 1). Baseline characteristics between those with and without adverse events were similar (p > 0.05); however, the presence of cardiac scar on LGE-CMR was independently associated with an increased risk of adverse events (hazard ratio: 5.6 95% confidence interval: [1.2-27], p = 0.03, log-rank p = 0.03). CONCLUSIONS: In a real-world cohort with long-term follow-up, adverse arrhythmic outcomes occurred in 18% of patients with symptomatic VA despite negative PVS, and this risk was significantly greater in patients with positive DE-CMR scar. Long term-monitoring, including the use of ICM, may be appropriate in these patients.

Value of genotyping and scar-phenotyping for VT ablation procedures in patients with nonischemic left ventricular cardiomyopathies.

INTRODUCTION: Variants of cardiomyopathy genes in patients with nonischemic cardiomyopathy (NICM) generate various phenotypes of cardiac scar and delayed enhancement cardiac magnetic resonance (DE-CMR) imaging which may impact ventricular tachycardia (VT) management. METHODS: The objective was to compare the findings of cardiomyopathy genetic testing on DE-CMR imaging and long-term outcomes among patients with NICM undergoing VT ablation procedures. Image phenotyping and genotyping were performed in a consecutive series of patients referred for VT ablation and correlated to survival free of VT. Scar depth index (SDI) (% of scar at 0-3 mm, 3-5 mm and >5 mm projected on the closest endocardial surface) was determined. RESULTS: Forty-three patients were included (11 women, 55 ± 14 years, ejection fraction (EF) 45 ± 16%) and were followed for 3.4 ± 2.9 years. Pathogenic variants (PV) were identified in 16 patients (37%) in the following genes: LMNA (n = 5), TTN (n = 5), DSP (n = 2), AMLS1 (n = 1), MYBPC3 (n = 1), PLN (n = 1), and SCN5A (n = 1). A ring-like septal scar (RLSS) pattern was more often seen in patients with pathogenic variants (66% vs 15%, p = .001). RLSS was associated with deeper seated scars (SDI >5 mm 30.6 ± 22.6% vs 12.4 ± 16.2%, p = .005), and increased VT recurrence (HR 5.7 95% CI[1.8-18.4], p = .003). After adjustment for age, sex, EF, and total scar burden, the presence of a PV remained independently associated with worse outcomes (HR 4.7 95% CI[1.22-18.0], p = .02). CONCLUSIONS: Preprocedural genotyping and scar phenotyping is beneficial to identify patients with a favorable procedural outcome. Some PVs are associated with an intramural, deeper seated scar phenotype and have an increase of VT recurrence after ablation.

Incidental left atrial appendage isolation after catheter ablation of persistent atrial fibrillation: Mechanisms and long-term risk of thromboembolism.

INTRODUCTION: Incidental left atrial appendage (LAA) isolation may occur during radiofrequency ablation of persistent atrial fibrillation (AF). The study aims to describe the mechanisms and long-term thromboembolic risk related to incidental LAA isolation. METHODS: Patients who experienced incidental LAA isolation after AF ablation were included. Culprit sites where ablation resulted in LAA isolation were identified. Thromboembolic risk despite oral anticoagulation (OAC) was compared to that in a propensity-matched control group without LAA isolation. RESULTS: Forty-one patients with LAA isolation, and 82 matched patients without LAA isolation were included. The patient age, ejection fraction, LA diameter, and CHA2 DS2 -VASc score were 64 ± 11 years, 55 ± 12%, 45.0 ± 7 mm and 2.62 ± 1.5, respectively. Culprit sites included the LAA base, mitral isthmus, inferior LA, Bachmann's bundle, coronary sinus, and Marshall vein. After 4.2 ± 3.6 years follow-up, thromboembolism occurred in 7 of 41 patients (17%) with LAA isolation versus 3 of 82 patients (4%) without isolation (log rank p < .009, HR 5.14, 95% CI [1.32-19.94], p = .02). Patients with and without thromboembolism had similar CHA2 DS2 -VASc scores (2.65 ± 1.3 vs. 2.71 ± 0.76, p = .89). Thromboembolism occurred during noncompliance with or temporary discontinuation of OAC in four of the seven patients. CONCLUSIONS: Incidental LAA isolation may occur during ablation of atrial arrhythmias in the vicinity of, or even at sites remote from the appendage. Patients with incidental LAA isolation had higher rates of thromboembolism compared to patients without isolation. Since thromboembolism may occur despite prescription for OAC, the risks of LAA isolation must be weighed against clinical benefit and appendage occlusion devices should be considered in vulnerable patients.

Comparison of warfarin with direct oral anticoagulants for thromboembolic prophylaxis after catheter ablation of ventricular tachycardia.

INTRODUCTION: Thromboembolic events after catheter ablation of ventricular tachycardia (VT) can result in significant morbidity. Thromboembolic prophylaxis after catheter ablation can be achieved by the use of antiplatelet agents, vitamin K antagonists, or direct oral anticoagulants (DOACs). The relative safety and efficacy of these modes of prophylaxis are uncertain. We sought to compare the outcomes of patients who received warfarin or DOACs for thromboembolic prophylaxis after catheter ablation of VT. METHODS AND RESULTS: Anticoagulation with DOACS was started after left ventricular VT ablation in a series of 42 consecutive patients with structural heart disease (67 ± 11 years, 3 women, ejection fraction 32 ± 14%). Duration of hospital stay, bleeding episodes, and thromboembolic events were compared to a historic consecutive group of patients (n = 38, 65 ± 13 years, 14 women, ejection fraction 36 ± 13%) in whom anticoagulation with a formerly described protocol of heparin and vitamin K antagonist was used after VT ablation procedures. Hospital stay was significantly shorter in the group where DOACs were used as compared to vitamin K antagonists (3.3 ± 1.8 vs. 5.0 ± 2.5 days postablation; p = 0.001) without an increase of bleeding or thromboembolic events. CONCLUSION: Anticoagulation with DOACs is safe and shortens hospital stay in patients with structural heart disease undergoing left ventricular VT ablation procedures.

Three-dimensional-guided and ICE-guided transseptal puncture for cardiac ablations: A propensity score match study.

INTRODUCTION: Transseptal puncture (TSP) is routinely performed for left atrial ablation procedures. The use of a three-dimensional (3D) mapping system or intracardiac echocardiography (ICE) is useful in localizing the fossa ovalis and reducing fluoroscopy use. We aimed to compare the safety and efficacy between 3D mapping system-guided TSP and ICE-guided TSP techniques. METHODS: We conducted a prospective observational study of patients undergoing TSP for left atrial catheter ablation procedures (mostly atrial fibrillation ablation). Propensity scoring was used to match patients undergoing 3D-guided TSP with patients undergoing ICE-guided TSP. Logistic regression was used to compare the clinical data, procedural data, fluoroscopy time, success rate, and complications between the groups. RESULTS: Sixty-five patients underwent 3D-guided TSP, and 151 propensity score-matched patients underwent ICE-guided TSP. The TSP success rate was 100% in both the 3D-guided and ICE-guided groups. Median needle time was 4.00 min (interquartile range [IQR]: 2.57-5.08) in patients with 3D-guided TSP compared to 4.02 min (IQR: 2.83-6.95) in those with ICE-guided TSP (p = .22). Mean fluoroscopy time was 0.2 min (IQR: 0.1-0.4) in patients with 3D-guided TSP compared to 1.2 min (IQR: 0.7-2.2) in those with ICE-guided TSP (p < .001). There were no complications related to TSP in both group. CONCLUSIONS: Three-dimensional mapping-guided TSP is as safe and effective as ICE-guided TSP without additional cost.

Late gadolinium enhancement cardiac magnetic resonance imaging of ablation lesions after postinfarction ventricular tachycardia ablation: Implications for ventricular tachycardia recurrence.

BACKGROUND: Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) imaging distinguishes between intrinsic postinfarction scar and radiofrequency ablation lesion related scar (dark core lesions [DCLs]) in patients with prior ventricular tachycardia (VT) ablation procedures. OBJECTIVE: To combine LGE-CMR and electroanatomic mapping data to describe the relationship between DCLs and recurrent VT among patients undergoing repeat ablations for postinfarction VT. METHODS: Consecutive patients with repeat ablation for postinfarct VT with LGE-CMR before the repeat procedures were studied. Prior ablation procedures and implantable cardiac defibrillator electrograms were analyzed to determine new versus previously documented VT. DCLs were identified on preprocedure LGE-CMR and registered to electroanatomic maps. A control group of patients undergoing repeat ablation procedures without imaging was included. RESULTS: Nineteen study patients and 14 control patients were followed for 2.6 (1.6-5.6) years (31 [94%] men, age 65.8 ± 8.4 years, ejection fraction 24.7 ± 10.3, p > 0.10 for all). DCLs corresponded to unexcitable tissue during repeat procedures (area 22.4 ± 15.1 vs. 22.9 ± 16.8 cm3 , correlation coefficient = .93). Most VT target sites (39/50 [78%]) were in close proximity (<1 cm) to DCLs. Most DCL related VTs 32/39 (82%) were new VTs. Patients with LGE-CMR imaging incorporated into their ablation procedures had improved 24-month survival from VT (64% vs. 38%, log rank p < 0.02). CONCLUSION: LGE-MRI can identify prior ablation lesions corresponding to nonexcitable tissue during repeat ablation procedures for postinfarction VT. VT target sites are often located in close proximity to the DCL area that may function as a fixed border for reentry circuits. Registration of DCL from prior ablation may facilitate repeat ablation procedures.

Anatomy of the proximal septal vein in patients with focal intramural ventricular arrhythmias.

BACKGROUND: Focal ventricular arrhythmias (VAs) originating from the intramural myocardium of the basal septum are difficult to localize and ablate. Proximal septal veins emptying into the great cardiac vein can reach close to the origin of intramural arrhythmias. OBJECTIVE: To assess characteristics of proximal septal coronary veins in patients with intramural VAs. METHODS AND RESULTS: Among 84 consecutive patients with intramural VAs, 29 patients (age 60 ± 11years, 16 males, ejection fraction 47 ± 13%) underwent preprocedural cardiac computed tomographic angiography (CTA). In 14 of these patients, the intramural site of origin (SOO) was identified with multipolar catheters. The intramural SOO could not be accessed with mapping catheters in the other 15 patients while mapping the coronary venous system. The CTA identified sizable proximal septal veins in all patients in whom the SOO could be accessed with mapping catheters. In the patients in whom the intramural SOO was not identified, the proximal septal veins were often either small (<2 mm at the branching site) or non-existent (n = 9, p = .001). The proximal septal veins in patients in whom the SOO was identified were larger than in the patients in whom the SOO could not be identified (3.0 ± 0.6 mm vs. 2.1 ± 0.9 mm, p = .01). CONCLUSIONS: Preprocedural imaging with CTAs can be beneficial in identifying the anatomy of proximal septal coronary veins that allow adequate mapping of patients with suspected intramural VAs.

Intramural mapping of intramural septal ventricular arrhythmias.

BACKGROUND: Intramural ventricular arrhythmias (VAs) can originate in patients with or without structural heart disease. Electrogram (EGM) recordings from intramural sources of VA have not been described thoroughly. OBJECTIVE: We hypothesized that the presence of scar may be linked to the site of origin (SOO) of focal, intramural VAs. METHODS: In a series of 21 patients (age: 55 ± 11 years, 12 women, mean ejection fraction 43 ± 14%) in whom the SOO of intramural VAs was identified, we analyzed bipolar EGM characteristics at the SOO and compared the findings with the endocardial breakout site. The patients were from a pool of 86 patients with intramural VAs referred for ablation. RESULTS: In 16/21 patients intramural scarring was detected by cardiac magnetic resonance (CMR) imaging In patients in whom the intramural SOO was reached, intramural bipolar EGMs showed a lower voltage and had broader EGMs compared to the endocardial breakout sites (0.97 ± 0.56 vs. 2.28 ± 0.15 mV, p = .001; and 122.3 ± 31.6 vs. 96.5 ± 26.3 ms, p < .01). All intramural sampled sites at the SOO had either low voltage or broad abnormal EGMs. The activation time was significantly earlier at the intramural SOO than at breakout sites (-36.2 ± 11.8 vs. -23.2 ± 9.1 ms, p < .0001). CONCLUSIONS: Sites of origin of intramural VAs with scar by CMR display EGM characteristics of scarring, supporting that scar tissue localizes to the SOO of intramural outflow tract arrhythmias in some patients. Scarring identified by CMR may be helpful in planning ablation procedures in patients with suspected intramural VAs.

Association between biventricular pacing and incidence of ventricular arrhythmias in the early post-operative period after left ventricular assist device implantation.

INTRODUCTION: Cardiac resynchronization therapy (CRT) and left ventricular assist devices (LVAD) improve outcomes in heart failure patients. Early ventricular arrhythmias (VA) are common after LVAD and are associated with increased mortality. The association between left ventricular pacing (LVP) with CRT and VAs in the early post-LVAD period remains unclear. METHODS: This was a retrospective study of all patients undergoing LVAD implantation from 1/2016 to 12/2019. Patients were divided into those with CRT and active LVP (CRT-LVP) immediately post-LVAD implant versus those without CRT-LVP. Implantable cardiac defibrillator electrograms were reviewed and early VAs were defined as sustained ventricular tachycardia (VT)/ventricular fibrillation occurring within 30 days of LVAD implantation. RESULTS: Of 186 included patients (mean age 53 years, 75% male, mean body mass index 28), 72 had CRT devices, 63 of whom had LV pacing enabled after LVAD implant (CRT-LVP group). Patients with CRT-LVP were more likely to have VA in the early postoperative period (21% vs. 4%; p = .0001). All 9 patients with CRT in whom LVP was disabled had no early VA. Among those with early VA, patients with CRT-LVP were more likely to have monomorphic VT (77% vs. 40%; p = .07). In multiple logistic regression, CRT-LVP pacing remained an independent predictor of early VA after adjustment for history of VA and AF. CONCLUSIONS: Patients with CRT-LVP after LVAD implant had a higher incidence of early VA (specifically monomorphic VT). Epicardial LV pacing may be proarrhythmic in the early postoperative period after LVAD.

A comparison of clinical outcomes and cost of radiofrequency catheter ablation for atrial fibrillation with monitored anesthesia care versus general anesthesia.

INTRODUCTION: Monitored anesthesia care (MAC) or general anesthesia (GA) can be used during catheter ablation (CA) of atrial fibrillation (AF). However, each approach may have advantages and disadvantages with variability in operator preferences. The optimal approach has not been well established. The purpose of this study was to compare procedural efficacy, safety, clinical outcomes, and cost of CA for AF performed with MAC versus GA. METHODS: The study population consisted of 810 consecutive patients (mean age: 63 ± 10 years, paroxysmal AF: 48%) who underwent a first CA for AF. All patients completed a preprocedural evaluation by the anesthesiologists. Among the 810 patients, MAC was used in 534 (66%) and GA in 276 (34%). Ten patients (1.5%) had to convert to GA during the CA. RESULTS: Although the total anesthesia care was longer with GA particularly in patients with persistent AF, CA was shorter by 5 min with GA than MAC (p < 0.01). Prevalence of perioperative complications was similar between the two groups (4% vs. 4%, p = 0.89). There was no atrioesophageal fistula with either approach. GA was associated with a small, ~7% increase in total charges due to longer anesthesia care. During 43 ± 17 months of follow-up after a single ablation procedure, 271/534 patients (51%) in the MAC and 129/276 (47%) patients in the GA groups were in sinus rhythm without concomitant antiarrhythmic drug therapy (p = 0.28). CONCLUSION: With the participation of an anesthesiologist, and proper preoperative assessment, CA of AF using GA or MAC has similar efficacy and safety.

Spontaneous coronary artery dissection is infrequent in individuals with heritable thoracic aortic disease despite partially shared genetic susceptibility.

Spontaneous coronary artery dissection (SCAD) is a potential precipitant of myocardial infarction and sudden death for which the etiology is poorly understood. Mendelian vascular and connective tissue disorders underlying thoracic aortic disease (TAD), have been reported in ~5% of individuals with SCAD. We therefore hypothesized that patients with TAD are at elevated risk for SCAD. We queried registries enrolling patients with TAD to define the incidence of SCAD. Of 7568 individuals enrolled, 11 (0.15%) were found to have SCAD. Of the sequenced cases (9/11), pathogenic variants were identified (N = 9), including COL3A1 (N = 3), FBN1 (N = 2), TGFBR2 (N = 2), TGFBR1 (N = 1), and PRKG1 (N = 1). Individuals with SCAD had an increased frequency of iliac artery dissection (25.0% vs. 5.1%, p = 0.047). The prevalence of SCAD among individuals with TAD is low. The identification of pathogenic variants in genes previously described in individuals with SCAD, particularly those underlying vascular Ehlers-Danlos, Marfan syndrome, and Loeys-Dietz syndrome, is consistent with prior reports from clinical SCAD series. Further research is needed to identify specific genetic influences on SCAD risk.

Diagnosis, significance, and management of ventricular thrombi in patients referred for VT ablation.

INTRODUCTION: In patients with structural heart disease presenting with ventricular tachycardia (VT), detection of ventricular thrombi and subsequent management can be challenging. This study aimed to assess the value of multimodality imaging with cardiac magnetic resonance imaging (CMR), contrast-enhanced transthoracic echocardiography (TTE), and computed tomography (CT) for thrombus detection as well as a management algorithm geared towards anticoagulation and deferred ablation for patients referred for VT ablation. METHODS AND RESULTS: A total of 154 consecutive patients referred for VT ablation underwent preprocedural multimodality imaging with CMR, CT, and TTE. In 9 patients (6%) a new ventricular thrombus was detected and anticoagulation was initiated. Thrombi were detected by CMR in nine patients, by CT in seven patients, and by TTE in two patients. Five patients eventually underwent endocardial VT ablation procedures 6.0 ± 2.0 months after initiation of anticoagulation with one patient also requiring an epicardial approach. Two patients died while on anticoagulation, unrelated to ventricular arrhythmia. Four of five patients were rendered non-inducible and no testing was performed in 1/5 patients. Areas containing left ventricular thrombi were non-excitable with pacing. Six of thirty-two inducible VTs were mapped in close vicinity of ventricular thrombi. No clinical embolic events occurred during the ablation procedures. CONCLUSIONS: Ventricular thrombus was detected in 6% of consecutive patients with structural heart disease undergoing VT ablation. CMR was the most sensitive modality, while contrast-enhanced TTE failed to detect the majority of thrombi. Anticoagulation followed by ablation can be safely and successfully performed in patients with ventricular thrombi.

The value of cardiac magnetic resonance imaging and programmed ventricular stimulation in patients with ventricular noncompaction and ventricular arrhythmias.

INTRODUCTION: Left ventricular noncompaction (LVNC) is associated with ventricular arrhythmias (VA) including premature ventricular complexes, and ventricular tachycardia (VT). The value of imaging with delayed enhancement cardiac magnetic resonance (DE-CMR) and programmed ventricular stimulation (PVS) for risk stratification in patients with VA and LVNC is unknown. The purpose of this study was to determine whether DE-CMR and PVS are beneficial for risk stratification and whether CMR helps to identify VA target sites. METHODS AND RESULTS: Consecutive patients with LVNC undergoing ablation for VAs were included, all patients had preprocedure DE-CMR. A total of 23 patients (7 women, 46 ± 14 years, ejection fraction 35 ± 14) were included and followed for 2.9 ± 2.2 years. DE-CMR scar was present in 12/23 patients (52%). PVS was performed in 20/23 patients, 8/10 patients (80%) with scar were inducible for VT compared to 0/10 (0%) patients without scar (p < .001). VA target sites in patients with scarring were located adjacent to areas of scarring in all but 1 patient and ablation was successful in 15/23 patients (65%). Patients with scar had worse survival free of VT than those without scar (log rank p = .01) and patients with inducible VT had worse survival free of VT than those who were noninducible (log rank p < .001). CONCLUSIONS: The presence of CMR defined scar in patients with LVNC was associated with inducible VT and worse outcomes. Inducibility for VT was associated with VT recurrence. Furthermore, CMR is beneficial in localizing the arrhythmogenic substrate in LVNC and therefore can aid in procedural planning.

Efficacy and tolerability of quinidine as salvage therapy for monomorphic ventricular tachycardia in patients with structural heart disease.

INTRODUCTION: Quinidine is an effective therapy for a subset of polymorphic ventricular tachycardia and ventricular fibrillation (VF) syndromes; however, the efficacy of quinidine in scar-related monomorphic ventricular tachycardia (MMVT) is unclear. METHODS AND RESULTS: Between 2009 and 2020 a single VT referral center, a total of 23 patients with MMVT and structural heart disease (age 66.7 ± 10.9, 20 males, 15 with ischemic cardiomyopathy, mean LVEF 22.2 ± 12.3%, 9 with left ventricular assist device [LVAD]) were treated with quinidine (14 quinidine gluconate; 996 ± 321 mg, 8 quinidine sulfate; 1062 ± 588 mg). Quinidine was used in combination with other antiarrhythmics (AAD) in 19 (13 also on amiodarone). All patients previously failed >1 AAD (amiodarone 100%, mexiletine 73%, sotalol 32%, other 32%) and eight had prior ablations (median of 1.5). Quinidine was initiated in the setting of VT storm despite AADs (6), inability to tolerate other AADs (4), or recurrent VT(12). Ventricular arrhythmias recurred despite quinidine in 13 (59%) patients at a median of 26 (4-240) days after quinidine initiation. In patients with recurrent MMVT, VT cycle length increased from 359 to 434 ms (p = .02). Six (27.3%) patients remained on quinidine at 1 year with recurrence of ventricular arrhythmias in all. The following adverse effects were seen: gastrointestinal side effects (6), QT prolongation (2), rash (1), thrombocytopenia (1), neurologic side effects (1). One patient discontinued due to cost. CONCLUSION: Quinidine therapy has limited tolerability and long-term efficacy when used in the management of amiodarone-refractory scar-related MMVT.

Effect of metformin on outcomes of catheter ablation for atrial fibrillation.

BACKGROUND: Diabetes mellitus (DM) is a risk factor for atrial fibrillation (AF). The effect of antidiabetic medications on AF or the outcomes of catheter ablation (CA) has not been well described. We sought to determine whether metformin treatment is associated with a lower risk of atrial arrhythmias after CA in patients with DM and AF. METHODS AND RESULTS: A first CA was performed in 271 consecutive patients with DM and AF (age: 65 ± 9 years, women: 34%; and paroxysmal AF: 51%). At a median of 13 months after CA (interquartile range: 6-30), 100/182 patients (55%) treated with metformin remained in sinus rhythm without antiarrhythmic drug therapy, compared with 36/89 patients (40%) not receiving metformin (p = .03). There was a significant association between metformin therapy and freedom from recurrent atrial arrhythmias after CA in multivariable Cox hazards models (hazard ratio [HR]: 0.66; ±95% confidence interval [CI]: 0.44-0.98; p = .04) that adjusted for age, sex, body mass index, AF type (paroxysmal vs. nonparoxysmal), antiarrhythmic medication, obstructive sleep apnea, chronic kidney disease, coronary artery disease, left ventricular ejection fraction, and left atrial diameter. A Cox model that also incorporated other antidiabetic agents and fasting blood glucose demonstrated a similar reduction in the risk of recurrent atrial arrhythmias with metformin treatment (HR: 0.63; ±95% CI: 0.42-0.96; p = .03). CONCLUSIONS: In patients with DM, treatment with metformin appears to be independently associated with a significant reduction in the risk of recurrent atrial arrhythmias after CA for AF. Whether this effect is due to glycemic control or pleiotropic effects on electroanatomical mechanisms of AF remains to be determined.

Risk stratification in patients with nonischemic cardiomyopathy and ventricular arrhythmias based on quantification of intramural delayed enhancement on cardiac magnetic resonance imaging.

INTRODUCTION: Intramural scarring is a risk factor for sudden cardiac death. The objective of this study was to determine the value of scar quantification for risk stratification in patients with nonischemic cardiomyopathy (NICM) undergoing ablation procedures for ventricular arrhythmias (VA). METHODS AND RESULTS: Cardiac late gadolinium-enhanced magnetic resonance imaging was performed in patients with NICM referred for ablation of premature ventricular complexes or ventricular tachycardia (VT). Only patients with intramural delayed enhancement were included. Scar volume was measured and correlated with immediate and long-term outcomes. Receiver operator curves, Wilcoxon signed-rank testing, and logistic regression were used to compare patient characteristics. The study consisted of 99 patients (74 males, mean age: 59.6 [54.0-68.1] years, ejection fraction [EF]: 46.0 [35.0-60.0]%). Patients without clinical VT or inducible VT had smaller total and core scar size compared to patients with a history of VT or inducible VT (total scar 1.12 [0.74-1.79] cm3 vs 7.45 [4.16-12.21] cm3 , P < .001). A total scar volume of greater than or equal to 2.78 cm3 was associated with inducibility of VT (AUC 0.94, 95% CI [0.89-0.98], sensitivity 85%, specificity 90%). Scar volume was associated with VT inducibility independent of a prior history of VT or the preprocedure EF (adjusted OR 1.67 [1.24-2.24]/cm3 , P < .01). CONCLUSION: Quantification of scar size in patients with intramural scarring is useful for risk stratification in patients with NICM and VA independent of the EF or a prior history of VT. Scar characteristics of patients without a history of VT who have inducible VT are similar to patients with a history of VT.

Multiparametric assessment of left atrial remodeling using 18F-FDG PET/CT cardiac imaging: A pilot study.

BACKGROUND: Left atrial (LA) remodeling is associated with structural, electric, and metabolic LA changes. Integrated evaluation of these features in vivo is lacking. METHODS: Patients undergoing 18F-fluorodeoxyglucose (FDG) PET-CT during a hyperinsulinemic-euglycemic clamp were classified into sinus rhythm (SR), paroxysmal AF (PAF), and persistent AF (PerAF). The LA was semiautomatically segmented, and global FDG uptake was quantified using standardized uptake values (SUVmax and SUVmean) in gated, attenuation-corrected images and normalized to LA blood pool activity. Regression was used to relate FDG data to AF burden and critical patient factors. Continuous variables were compared using t-tests or Mann-Whitney tests. RESULTS: 117 patients were included (76% men, age 66.4 ± 11.0, ejection fraction (EF) 25[22-35]%) including those with SR (n = 48), PAF (n = 55), and PerAF (n = 14). Patients with any AF had increased SUVmean (2.3[1.5-2.4] vs 2.0[1.5-2.5], P = 0.006), SUVmax (4.4[2.8-6.7] vs 3.2[2.3-4.3], P < 0.001), uptake coefficient of variation (CoV) 0.28[0.22-0.40] vs 0.25[0.2-0.33], P < 0.001), and hypometabolic scar (32%[14%-53%] vs 16.5%[0%-38.5%], P = 0.01). AF burden correlated with increased SUVmean, SUVmax, CoV, and scar independent of age, gender, EF, or LA size (P < 0.03 for all). CONCLUSIONS: LA structure and metabolism can be assessed using FDG PET/CT. Greater AF burden correlates with the increased LA metabolism and scar.

Safety of regadenoson positron emission tomography stress testing in orthotopic heart transplant patients.

OBJECTIVES: We sought to determine the safety of regadenoson (REG) stress testing in patients who have undergone orthotopic heart transplantation (OHT). BACKGROUND: Routine screening for cardiac allograft vasculopathy (CAV) is necessary after OHT. Adenosine stress is contraindicated after heart transplantation due to supersensitivity in denervated hearts. Safety of regadenoson stress following OHT has not been well studied. METHODS: We retrospectively reviewed data from OHT patients (N = 123) who were referred to REG stress testing. Medical records were reviewed to determine hemodynamic and ECG response to regadenoson and to identify adverse reactions. RESULTS: No serious adverse events occurred. No life-threatening arrhythmias or hemodynamic changes occurred. Common side-effects related to regadenoson were observed, dyspnea being the most frequent (66.7%). On average the heart rate rose from 82.8 ± 12 to 95.7 ± 13.4 bpm (P < 0.001), systolic blood pressure decreased from 138.7 ± 20.9 to 115.9 ± 23.9 mmHg (P < 0.001) and mean arterial pressure decreased from 103.5 ± 14.1 to 84.72 ± 15.90 mmHg (P < 0.001) during stress protocol. There was no sustained ventricular tachycardia, ventricular fibrillation, or second-or third-degree atrioventricular block. CONCLUSION: Regadenoson stress testing appears to be well tolerated and safe in OHT patients.

Baseline and decline in device-derived activity level predict risk of death and heart failure in patients with an ICD for primary prevention.

BACKGROUND: Implanted defibrillators are capable of recording activity data based on company-specific proprietary algorithms. This study aimed to determine the prognostic significance of baseline and decline in device-derived activity level across different device companies in the real world. METHODS: We performed a retrospective cohort study of patients (n = 280) who underwent a defibrillator implantation (Boston, Medtronic, St. Jude, and Biotronik) for primary prevention at the University of Michigan from 2014 to 2016. Graphical data obtained from device interrogations were retrospectively converted to numerical data. The activity level averaged over a month from a week postimplantation was used as baseline. Subsequent weekly average activity levels (SALs) were standardized to this baseline. SAL below 59.4% was used as a threshold to group patients. All-cause mortality and death/heart failure were the primary end-points of this study. RESULTS: Fifty-six patients died in this study. On average, they experienced a 50% decline in SAL prior to death. Patients (n = 129) who dropped their SAL below threshold were more likely to be older, male, diabetic, and have more symptomatic heart failure. They also had a significantly increased risk of heart failure/death (hazard ratio [HR] 3.6, 95% confidence interval [95% CI] 2.3-5.8, P < .0001) or death (HR 4.2, 95% CI 2.2-7.7, P < .0001) compared to those who had sustained activity levels. Lower baseline activity level was also associated with significantly increased risk of heart failure/death and death. CONCLUSION: Significant decline in device-derived activity level and low baseline activity level are associated with increased mortality and heart failure in patients with an ICD for primary prevention.