S. Singarayar

Immediate balloon deflation for prevention of persistent phrenic nerve palsy during pulmonary vein isolation by balloon cryoablation

BACKGROUNDnPersistent phrenic nerve palsy is the most frequent complication of cryoballoon ablation for atrial fibrillation and can be disabling.nnnOBJECTIVESnTo describe a technique-immediate balloon deflation (IBD)-for the prevention of persistent phrenic nerve palsy, provide data for its use, and describe in vitro simulations performed to investigate the effect of IBD on the atrium and pulmonary vein.nnnMETHODSnCryoballoon procedures for atrial fibrillation were analyzed retrospectively (n = 130). IBD was performed in patients developing phrenic nerve dysfunction (n = 22). In vitro simulations were performed by using phantoms.nnnRESULTSnNo adverse events occurred, and all patients recovered normal phrenic nerve function before leaving the procedure room. No patient developed persistent phrenic nerve palsy. The mean cryoablation time to onset of phrenic nerve dysfunction was 144 ± 64 seconds. Transient phrenic nerve dysfunction was seen more frequently with the 23-mm balloon than with the 28-mm balloon (11 of 39 cases vs 11 of 81 cases; P = .036). Balloon rewarming was faster following IBD. The time to return to 0 and 20° C was shorter in the IBD group (6.7 vs 8.9 seconds; P = .007 and 16.7 vs 37.6 seconds; P<.0001). In vitro simulations confirmed that IBD caused more rapid tissue warming (time to 0°C, 14.0 ± 3.4 seconds vs 46.0 ± 8.1; P = .0001) and is unlikely to damage the atrium or pulmonary vein.nnnCONCLUSIONSnIBD results in more rapid tissue rewarming, causes no adverse events, and appears to prevent persistent phrenic nerve palsy. Simulations suggest that IBD is unlikely to damage the atrium or pulmonary vein.

Balloon warming time is the strongest predictor of late pulmonary vein electrical reconnection following cryoballoon ablation for atrial fibrillation

BACKGROUNDnPulmonary vein isolation by cryoballoon ablation is an accepted method of treating atrial fibrillation. Little data exist regarding factors affecting late electrical reconnection of pulmonary veins following cryoballoon ablation.nnnOBJECTIVEnTo investigate factors determining pulmonary vein reconnection in patients undergoing repeat catheter ablation for recurrent atrial fibrillation following cryoballoon ablation.nnnMETHODSnFifty-one consecutive patients undergoing repeat catheter ablation for recurrent atrial fibrillation following initial cryoballoon ablation underwent retrospective assessment of initial cryoablation characteristics, including balloon and vein sizes, venogram occlusion score, balloon freezing time from 0 to -30 °C, nadir temperature, and balloon warming time from -30 to +15 °C, recorded during the initial cryoballoon procedure.nnnRESULTSnOf 199 veins assessed, 91 had reconnected (1.8 per patient). Balloon warming time (odds ratio [OR] 3.21; 95% confidence interval [CI] 2.00-5.13; P < .0001), nadir temperature (OR 1.94; 95% CI 1.42-2.66; P < .0001), vein occlusion score (OR 1.74; 95% CI 1.29-2.34; P = .0003), and balloon freezing time (OR 1.58; 95% CI 1.03-2.42; P = .037) predicted pulmonary vein reconnection. On multivariate analysis, balloon warming time (OR 3.71; 95% CI 2.2-6.24; P ≤ .0001), pulmonary vein size (OR 1.63; 95% CI 1.08-2.43; P = .020), and vein occlusion score (OR 1.48; 95% CI 1.06-2.08; P = .021) remained statistically significant independent predictors of pulmonary vein reconnection. The receiver operating characteristic for the multivariate model yielded an area under the curve of 0.82.nnnCONCLUSIONSnBalloon warming time, vein occlusion score, and pulmonary vein size predict pulmonary vein reconnection. Balloon warming time was the most important predictive factor, and the manipulation of balloon warming may be a novel therapeutic strategy for improving outcomes of cryoballoon ablation for atrial fibrillation.

Subclavian vein pacing and venous pressure waveform measurement for phrenic nerve monitoring during cryoballoon ablation of atrial fibrillation

AIMSnThe phrenic nerves may be damaged during catheter ablation of atrial fibrillation. Phrenic nerve function is routinely monitored during ablation by stimulating the right phrenic nerve from a site in the superior vena cava (SVC) and manually assessing the strength of diaphragmatic contraction. However the optimal stimulation site, method of assessing diaphragmatic contraction, and techniques for monitoring the left phrenic nerve have not been established. We assessed novel techniques to monitor phrenic nerve function during cryoablation procedures.nnnMETHODS AND RESULTSnPacing threshold and stability of phrenic nerve capture were assessed when pacing from the SVC, left and right subclavian veins. Femoral venous pressure waveforms were used to monitor the strength of diaphragmatic contraction. Stable capture of the left phrenic nerve by stimulation in the left subclavian vein was achieved in 96 of 100 patients, with a median capture threshold of 2.5 mA [inter-quartile range (IQR) 1.4-5.0 mA]. Stimulation of the right phrenic nerve from the subclavian vein was superior to stimulation from the SVC with lower pacing thresholds (1.8 mA IQR 1.4-3.3 vs. 6.0 mA IQR 3.4-8.0, P < 0.001). Venous pressure waveforms were obtained in all patients and attenuation of the waveform was always observed prior to onset of phrenic nerve palsy.nnnCONCLUSIONnThe left phrenic nerve can be stimulated from the left subclavian vein. The subclavian veins are the optimal sites for phrenic nerve stimulation. Monitoring the femoral venous pressure waveform is a novel technique for detecting impending phrenic nerve damage.

Improving the diagnosis of LV non-compaction with cardiac magnetic resonance imaging

BACKGROUNDnCurrent diagnostic criteria for left ventricular non-compaction (LVNC) poorly correlate with clinical outcomes. We aimed to develop a cardiac magnetic resonance (CMR) based semi-automated technique for quantification of non-compacted (NC) and compacted (C) masses and to ascertain their relationships to global and regional LV function.nnnMETHODSnWe analysed CMR data from 30 adults with isolated LVNC and 20 controls. NC and C masses were measured using relative signal intensities of myocardium and blood pool. Global and regional LVNC masses was calculated and correlated with both global and regional LV systolic function as well as occurrence of arrhythmia.nnnRESULTSnLVNC patients had significantly higher end-systolic (ES) and end-diastolic (ED) NC:C ratios compared to controls (ES 0.21 [SD 0.09] vs. 0.12 [SD 0.02], p<0.001; ED 0.39 [SD 0.08] vs. 0.26 [SD 0.05], p<0.001). NC:C ratios correlated inversely with global ejection fraction, with a stronger correlation in ES vs. ED (r=-0.58, p<0.001 vs. r=-0.30, p=0.03). ES basal, mid and apical NC:C ratios also showed a significant inverse correlation with global LV ejection fraction (ES basal r=-0.29, p=0.04; mid-ventricular r=-0.50, p<0.001 and apical r=-0.71, p<0.001). Upon ROC testing, an ES NC:C ratio of 0.16 had a sensitivity of 70% and a specificity of 95% for detection of significant LVNC. Patients with sustained ventricular tachycardia had a significantly higher ES NC:C ratio (0.31 [SD 0.18] vs. 0.20 [SD 0.06], p=0.02).nnnCONCLUSIONSnThe NC:C ratio derived from relative signal intensities of myocardium and blood pool improves the ability to detect clinically relevant NC compared to previous CMR techniques.

Impact of new task force criteria in the diagnosis of arrhythmogenic right ventricular cardiomyopathy

BACKGROUNDnArrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy that can lead to sudden cardiac death. The diagnostic criterion has recently been revised and through the use of cardiac magnetic resonance (CMR) imaging this study aimed to assess the clinical impact of comparing the original 1994 task force (TF) criterion to the revised 2010 criterion.nnnMETHODSnWe evaluated 173 consecutive CMR scans of patients referred with clinical suspicion of ARVC between 2008 and 2011. We then compared the prevalence of major and minor CMR criteria by applying the two criteria.nnnRESULTSnUsing the 1994 TF criterion, 13 (7.5%) patients had definite, 11 (6.4%) had borderline, and 39 (22.5%) had possible ARVC. Using the 2010 TF criterion, 10 (5.8%) patients had definite, 1 had borderline, and 7 had (0.04%) possible ARVC. With the 1994 criterion, 81 patients satisfied CMR criterion, of which 36 (44%) had major and 45 (56%) had minor criteria. Upon reclassification with the revised criterion, 61 of the 81 patients were not assigned any criteria, even though many patients had significant risk factors. The negative predictive values (NPV) for both CMR criteria were 100% but the positive predictive values (PPV) for combined CMR major or minor criteria improved from 23% to 55%.nnnCONCLUSIONSnRevision of the criterion has enhanced the diagnostic capabilities of CMR but has resulted in a large cohort of patients not classified. In these patients, there is presently no official consensus on imaging or clinical strategy for surveillance of the evolution of pathology over time.

Atrial Fibrillation Resulting from Superior Vena Cava Drivers Addressed with Cryoballoon Ablation: Late Reconnection at the Site of Phrenic Nerve Pacing Catheter

Introduction Cryoballoon ablation is now an established approach for achieving pulmonary vein (PV) isolation, as part of the management of drug-refractory symptomatic atrial fibrillation (AF). More recently, the technique has been utilized for successful isolation of the superior vena cava (SVC). We present a case highlighting a potential pitfall affecting the durability of SVC isolation using the cryoballoon.

Serious postoperative syncope

In November, 2008, an arrest call was made for a 69-yearold woman after a syncopal episode in a rural hospital. The patient had had an elective right total hip replacement a day earlier. The syncope occurred when she mobilised with a physiotherapist. She regained full consciousness within seconds, but her blood pressure was unrecordable. She denied chest pain or discomfort, palpitation, dizziness, or dyspnoea. She had a history of treated hyper cholesterolaemia. Physical examination was unremarkable. The initial 12-lead electrocardiograms (ECGs), done within the fi rst 15 min, showed sinus rhythm at 89 beats per min with 1 mm ST depression in V5 compared with the preoperative ECG (fi gure A). Nursing staff noted that she had self-administered a 6 mg bolus of morphine-based patient-controlled analgesia (PCA) before mobilising. On the basis of the initial clinical assessment, her syncope was attributed to either hypovolaemia or morphineinduced hypotension, especially in view of her good response to fl uid resuscitation. However, a repeat ECG 30 min later showed widespread ischaemic changes (fi gure B), although the patient still remained asymptomatic and haemodynamically stable. Troponin I and creatine kinase concentrations were high (0·14 μg/L and 429 U/L, respectively; normal renal function). She was started on aspirin and a heparin infusion. Her PCA was stopped, and she started complaining of chest pain 4 h later, although there were no new ECG changes, and the pain was relieved by glyceryl trinitrate. The PCA was resumed, and the patient remained free of chest pain overnight (29 mg morphine used). The next morning, troponin I and creatine kinase concentrations were higher (6·14 μg/L and 1042 U/L, respectively). An echocardiogram done in the early afternoon showed many areas of cardiac akinesia. She subsequently developed cardiogenic shock requiring a dobutamine infusion while awaiting transfer to a tertiary hospital. On arrival there, her systolic blood pressure was 60 mm Hg (on inotropes) and a coronary angiogram showed severe left main stenosis and triple-vessel disease. A balloon pump was inserted and the left main lesion stented. Subsequently, her condition stabilised and she underwent coronary bypass surgery 7 days later. She made an uneventful recovery and remained well when we last contacted her in January, 2009. PCA has become a common standard for postoperative pain management since its introduction in 1971. On the basis of a study of postoperative myocardial infarction after non-cardiac surgery, we estimate the incidence of painless postoperative myocardial infarction to be 5%. The authors of that study suggested that such cases might be related to postoperative use of opioid analgesia. Our case demonstrates the initial masking of chest pain until the removal of PCA. A change from self-administered to medically controlled morphine in this patient might have allowed symptomatic detection of sustained ischaemia with the postoperative pain still controlled. Of note, there is concern over intravenous morphine use in acute coronary syndromes and the recommendation for its use has been downgraded in the new ACC/AHA guideline. It has been reported that 56% of postoperative myocardial infarctions may manifest as hypotension, pulmonary oedema, or atrial fi brillation; chest pain may be absent. These manifestations can be attributed to common postoperative complications and managed accordingly, especially in patients who have had major surgery without obvious initial ECG changes or chest pain. Therefore, care should be taken to exclude ischaemia in postoperative patients who have abnormal cardiovascular symptoms or signs, especially those using PCA or being given large amounts of opioid-based analgesia.