Abstract Background Accelerated idioventricular rhythm (AIVR) is known as reperfusion arrhythmia in the setting of acute myocardial infarction (AMI). In healthy individuals, it is usually considered to be benign. Alternating bundle branch block (ABBB) often progresses to complete atrioventricular block requiring permanent pacemaker implantation. We report a case of delayed appearance of AIVR following myocardial infarction (MI) in combination with ABBB as precursor of sudden cardiac arrest due to ventricular fibrillation (VF). Case summary A 62-year-old male with pre-existing left bundle branch block (LBBB) was admitted with an acute non-ST segment elevation MI. He underwent successful percutaneous coronary intervention (PCI) of a subtotal proximal left anterior descending artery (LAD) stenosis. Before and after PCI the electrocardiogram (ECG) demonstrated sinus rhythm with LBBB. The patient was discharged 5 days after PCI, left ventricular function at this time was moderately reduced (ejection fraction of 40%). After another 5 days, the patient was admitted for elective cardiac rehabilitation. At this time, the ECG demonstrated an AIVR with right bundle branch block morphology. Due to ABBB, the patient was scheduled for permanent pacemaker implantation. Before pacemaker implantation could take place, the patient developed a sudden cardiac arrest due to VF and was successfully resuscitated. A follow-up coronary angiography revealed no novel lesions. A cardiac resynchronization therapy defibrillator was implanted for secondary prevention of sudden cardiac death. Discussion Delayed occurrence of AIVR in combination with ABBB following AMI could be a predictor of sudden cardiac death. These patients are probably at high risk for malignant ventricular arrhythmias.

Atrial fibrillation (AF) and coronary artery disease (CAD) may be encountered coincidently in a large portion of patients. However, data on coronary artery calcium burden in such patients are lacking. Thus, we sought to determine the value of cardiac computed tomography (CCT) in patients presenting with new-onset AF associated with an intermediate pretest probability for CAD admitted to a chest pain unit (CPU).

Background: About 10% of patients admitted to a chest pain unit (CPU) exhibit atrial fibrillation (AF).Hypothesis: To determine whether calcium scores (CS) are superior over common risk scores for coronary artery disease (CAD) in patients presenting with atypical chest pain, newly diagnosed AF, and intermediate pretest probability for CAD within the CPU.Methods: In 73 subjects, CS was related to the following risk scores: Global Registry of Acute Coronary Events (GRACE) score, including a new model of a frequency-normalized approach; Thrombolysis In Myocardial Infarction score; European Society of Cardiology Systematic Coronary Risk Evaluation (SCORE); Framingham risk score; and Prospective Cardiovascular Munster Study score. Revascularization rates during index stay were assessed.Results: Median CS was 77 (interquartile range, 1-270), with higher values in men and the left anterior descending artery. Only the modified GRACE (rho = 0.27; P = 0.02) and the SCORE (rho = 0.39; P < 0.005) were significantly correlated with CS, whereas the GRACE (tau = 0.21; P = 0.04) and modified GRACE (tau = 0.23; P = 0.02) scores were significantly correlated with percentile groups. Only the CS significantly discriminated between those with and without stenosis (P < 0.01).Conclusions: Apart from modified GRACE score, overall correlations between risk scores and calcium burden, as well as revascularization rates during index stay, were low. By contrast, the determination of CS may be used as an additional surrogate marker in risk stratification in AF patients with intermediate pretest likelihood for CAD admitted to a CPU.

Background: Initial catheter-based renal sympathetic denervation (RSD) studies demonstrated promising results in showing a significant reduction of blood pressure, while recent data were less successful. As an alternative approach, the objective of this study was to evaluate the feasibility of using magnetic resonance-guided high-intensity focused ultrasound (MRgHIFU) to perform RSD in a porcine model.Methods: An intravascular fiber optic temperature probe was used to confirm energy delivery during MRgHIFU. This technique was evaluated both in a vascular phantom and in a normotensive pig model. Five animals underwent unilateral RSD using MRgHIFU, and both safety and efficacy were assessed. MRI was used to evaluate the acoustic window, target sonications, monitor the near-field treatment region using MR thermometry imaging, and assess the status of tissues post-procedure. An intravascular fiber optic temperature probe verified energy delivery. Animals were sacrificed 6 to 9 days post-treatment, and pathological analysis was performed. The norepinephrine present in the kidney medulla was assessed post-mortem.Results: All animals tolerated the procedure well with no observed complications. The fiber optic temperature probe placed in the target renal artery confirmed energy delivery during MRgHIFU, measuring larger temperature rises when the MRgHIFU beam location was focused closer to the tip of the probe. Following ablation, a significant reduction (p = 0.04) of cross-sectional area of nerve bundles between the treated and untreated renal arteries was observed in all of the animals with treated nerves presenting increased cellular infiltrate and fibrosis. A reduction of norepinephrine (p = 0.14) in the kidney medulla tissue was also observed. There was no indication of tissue damage in arterial walls.Conclusions: Performing renal denervation non-invasively with MRgHIFU was shown to be both safe and effective as determined by norepinephrine levels in a porcine model. This approach may be a promising alternative to catheter-based strategies.

Optimal pharmacotherapy is essential to realize the bestoutcomes in patients undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI). In this regard, effectively restoring reperfusion and maintaining the patency of the infarct artery after stenting requires a balance between the haemorrhagic risks and the ischaemic benefits of anticoagulant and antiplatelet agents. Over the last three decades, as the principal device used for primary PCI has evolved from balloon angioplasty to bare metal stents to drug-eluting stents, parallel advances have occurred in antithrombotic and antiplatelet regimens, from unfractionated heparin (UFH) alone, toUFHplus a glycoprotein IIb/IIIa inhibitor (GPI), to bivalirudin with provisional (bailout) GPI use, and from ticlopidine and clopidogrel to prasugrel and ticagrelor (on a background of aspirin). Given the time, complexity, and costs of performing appropriately powered randomized trials, clinical practice has progressed faster than the evidence base required to inform optimal drug and device usage for all possible drug and device permutations. Unfractionated heparin, a heterogeneous mixture of polysaccharides of varying chain lengths, while familiar and inexpensive, has numerous shortcomings, which become most clinically apparent in acute coronary syndromes (ACS). Unfractionated heparin has an indirect mechanism of action (binding to and activation of antithrombin III, the amount of which varies in disease states) and has limited activity against clot-bound thrombin. Non-specific protein and cellular binding of UFH results in variable biological activity and can result in heparin-induced thrombocytopenia and thrombosis. Moreover, UFHbinds to the glycoprotein IIb/IIIa receptor, thereby paradoxically activating platelets. Kastrati and colleagues elegantly demonstrated that, despite pre-treatment with aspirin and clopidogrel, myocardial infarction rates in non-STEMI are substantially reduced after PCI with abciximab. Meta-analysis of eight randomized trials in 3949 patients with STEMI undergoing PCI demonstrated that the addiion of abciximab to UFH reduced the 30 day odds of re-infarction by 37% (P , 0.001) and the 6–12 month odds of mortality by 28% (P 1⁄4 0.01). In the largest such study, CADILLAC, 30 day stent thrombosis was also reduced with abciximab plus UFH vs. UFH alone (P 1⁄4 0.01). These benefits more than offset the increased rates of bleeding and thrombocytopenia that may occur with GPI. As such, aspirin, clopidogrel, and UFH plus GPI became the preferred regimento supportprimary PCI inSTEMI, used in .90%ofpatients in the USA and in the majority of patients in Europe. This regimen remained the standard for more than a decade until challenged by the direct thrombin inhibitor bivalirudin, a rapidly reversible agent (half-life 25 min), which overcomes many of the limitations of UFH. Specifically, bivalirudin does not require antithrombin III for activation, is able to inhibit fibrin-found thrombin, has predictable biological activity and dosing, does not cause thrombocytopenia or activate platelets, and indeed, blocks both collagenand thrombin-induced platelet activation. A series of multicentre randomized PCI trials across the spectrum of coronary artery disease has demonstrated that in comparison to UFH plus GPI, bivalirudin with provisional GPI use results in similar rates of composite ischaemic events,with 40–50% reductions inmajorbleedingand thrombocytopenia. 12 The EuroMax trial confirmed that the bleeding benefits of bivalirudinarepresent inpatients treatedwith radial aswell as femoral access, which is not surprising given that the majority of major bleeding events after PCI in ACS are not access site related. Morevoer, in the largest randomized primary PCI trial to date, anticoagulation with bivalirudin in comparison to UFH plus GPI resulted in reduced cardiac and all-cause mortality at 30 days, benefits which were sustained to 3 years, reflecting both haematological and nonhematological benefits of bivalirudin. As a result, in many countries bivalirudin has supplanted UFH plus GPI as the preferred regimen to support primary PCI in STEMI. How can the results with bivalirudin be improved further? One glaring deficiency of bivalirudin monotherapy in primary PCI during STEMI (which has not been observed in other settings) was first noted in the HORIZONS-AMI trial, and subsequently confirmed in EuroMax; stent thrombosis, occurring within the first 4 h after the

Both post-contrast myocardial T1 and extracellular volume (ECV) measurements have been associated with diffuse interstitial fibrosis. The cardiovascular magnetic resonance (CMR) field is migrating towards ECV, because it is largely insensitive to confounders that affect post-contrast myocardial T1 . Despite the theoretical advantages of myocardial ECV over post-contrast myocardial T1 , systematic experimental studies comparing the two measurements are largely lacking. We sought to measure the temporal changes in post-contrast myocardial T1 and ECV in an established canine model with chronic atrial fibrillation. Seventeen mongrel dogs, implanted with a pacemaker to induce chronic atrial fibrillation via rapid atrial pacing, were scanned multiple times for a total of 46 CMR scans at 3T. These dogs with different disease durations (0-22 months) were part of a separate longitudinal study aimed at studying the relationship between AF and pathophysiology. In each animal, we measured native and post-contrast T1 values and hematocrit. Temporal changes in post-contrast myocardial T1 and ECV, as well as other CMR parameters, were modeled with linear mixed effect models to account for repeated measurements over disease duration. In 17 animals, post-contrast myocardial T1 decreased significantly from 872 to 698 ms (p < 0.001), which corresponds to a 24.9% relative reduction. In contrast, ECV increased from 21.0 to 22.0% (p = 0.38), which corresponds to only a 4.5% relative increase. To partially investigate this discrepancy, we quantified collagen volume fraction (CVF) in post-mortem heart tissues of six canines sacrificed at different disease durations (0-22 months). CVF quantified by histology increased from 0.9 to 1.9% (p = 0.56), which agrees better with ECV than with post-contrast myocardial T1 . This study shows that post-contrast myocardial T1 and ECV may disagree in a longitudinal canine study. A more comprehensive study, including histologic, cardiac, and renal functional analyses, is warranted to test rigorously which CMR parameter (ECV or post-contrast myocardial T1 ) agrees better with CVF.

A 67-year-old female was admitted to our hospital exhibiting chest pain and dyspnea that occurred immediately after an exercise-induced syncope. A priori the clinical symptoms, ECG ( Panel A ), and myocardial biomarkers were indicative for an acute coronary syndrome (troponin I: 7.35 ng/mL). Coronary angiogram ruled out both coronary artery disease and coronary …

Background Post-contrast cardiac T1 measurement has been reported to be correlated with interstitial fibrosis burden. However, post-contrast cardiac T1 can also be influenced by a variety of confounders, including: cardiac function, renal function, hematocrit, magnetic field strength, contrast agent type and dosage, and specific delayed imaging time after contrast agent administration. To compensate for these confounders, investigators have proposed to measure extracellular volume (ECV). Despite the advantages of ECV over cardiac T1, systematic studies comparing the two measurements are lacking [1]. The purpose of this study was to compare the effectiveness of post-contrast cardiac T1 and ECV for evaluating the temporal changes in left ventricular (LV) fibrosis in an established canine model with chronic atrial fibrillation (AF)[2].

AF Ablation and eGFRIntroductionChronic kidney disease (CKD) and atrial fibrillation (AF) often coexist. We studied the association of CKD with atrial fibrosis and the effect of AF ablation on kidney function.MethodsAF patients who had a pre‐ and postablation serum creatinine and who completed a late gadolinium enhancement cardiac magnetic resonance imaging (MRI; LGE‐MRI) prior to ablation were included. Estimated glomerular filtration rate (eGFR) was calculated and CKD was staged using the National Kidney Foundation guidelines. Patients with eGFR <30 mL/min/1.73 m2 were excluded. LGE‐MRI was used to quantify atrial fibrosis. Patients were followed for recurrence and change in eGFR.ResultsA total of 392 patients were included in the study. A total of 118 (30.2%) had CKD stage 1, 198 (50.4%) CKD stage 2, 56 (14.3%) CKD stage 3A, and 20 (5.1%) CKD stage 3B. Patients with advanced CKD were more likely to be male and to have cardiovascular disease. Atrial fibrosis was not significant different between included CKD stages: 15.8 ± 8.8%, 16.6 ± 12.1%, 17.1 ± 10.4%, and 16.5 ± 8.4% for CKD stage 1, 2, 3A, and 3B, respectively (P = 0.476). At a median of 115 days following ablation, eGFR increased significantly in CKD stage 2 (74 ± 9 to 80 ± 23; P = 0.04), 3A (53 ± 5 to 69 ± 24; P < 0.001), and 3B (40 ± 4 to 71 ± 28; P < 0.01) and decreased in CKD stage 1 (109 ± 18 to 82 ± 28; P < 0.001). Arrhythmia recurrence was associated with atrial fibrosis (hazard ratio [HR] = 1.04, P < 0.01) and persistent AF (HR = 1.5; P = 0.04) but not with CKD stage (HR = 0.98; P = 0.89).ConclusionsRestoring sinus rhythm with ablation leads to significant improvement of renal function in patients with chronic kidney disease.

A 79-year-old male was seen in our Department of Otorhinolaryngology for regular head and neck cancer follow-up. Initially, in 1993, a glottic laryngeal carcinoma was diagnosed, followed by tumour excision, and subsequent recurrences in 2001 and 2006. In 2009, a hypopharyngeal–oesophageal squamous cell carcinoma, with mediastinal and axillary metastases, complicated the case, followed by palliative radiotherapy (RT). A …

Introduction: Late gadolinium enhancement (LGE)-MRI can visualize and quantify the scar on the left atrium (LA) created during atrial fibrillation (AF) ablation. This study sought to assess the long-term (over 2 years) behavior of AF ablation scar. Methods: Fifty-two patients (30 male, 68±11 years) who underwent a single AF ablation were included. Patients were followed up by LGE-MRI at 3 months and long-term (over 2 years) after ablation in order to quantify the ablation scar in all pulmonary vein (PV) antra, the LA posterior wall, and the LA septum wall which were targeted during ablation procedure. Results: At long-term follow up LGE-MRI, the scar size in LIPV, RSPV, RIPV antrum, and the posterior wall significantly decreased in comparison with 3 months post-ablation (297.8±151.3 vs. 223.3±148.1 mm2, 136.7±102.0 vs. 95.7±87.6 mm2, 230.9±152.7 vs. 153.8±110.3 mm2, 826.4±365.9 vs. 609.1±325.5 mm2; p<0.01) (Table). The number of PV encircled by scar was also decreased at long-term (1.7 vs 0.7, p<0.01). During a mean 42.7±9.5 months follow up, 27 patients (52%) had AF recurrence after a single ablation procedure. Patients with AF recurrence had a significantly more decrease in the total ablation scar and also the number of PV encircled by scar when compared with those in patients without AF recurrence (647.4±689.7 vs. 299.5±479.0 mm2; p=0.04, 1.3±1.2 vs. 0.6±0.9 PV; p=0.02). Scar area at 3 months and Long-term Conclusion: Ablation lesions at 3 months as detected by LGE-MRI significantly reduced at long-term post AF ablation. The regression of ablation scar at long-term corresponded with an increased AF recurrence.

BackgroundMagnetic resonance imaging (MRI) can visualize locations of both the ablation scar on the left atrium (LA) after atrial fibrillation (AF) ablation and epicardial fat pads (FPs) containing ganglionated plexi (GP).MethodsWe investigated 60 patients who underwent pulmonary vein antrum (PVA) isolation along with LA posterior wall and septal debulking for AF. FPs around the LA surface in well‐known GP areas (which were considered as the substitution of GP areas around the LA) were segmented from the dark‐blood MRI. Then the FP and the ablation scar image visualized by late gadolinium enhancement (LGE)‐MRI on the LA were merged together. Overlapping areas of FP and the ablation scar image were considered as the ablated FP areas containing GP. Patients underwent 24‐hour Holter monitoring after ablation for the analysis of heart rate variability.ResultsAblated FP area was significantly wider in patients without AF recurrence than those in patients with recurrence (5.6 ± 3.1 cm2 vs 4.2 ± 2.7 cm2, P = 0.03). The mean values of both percentage of differences greater than 50 ms in the RR intervals (pRR > 50) and standard deviation of RR intervals over the entire analyzed period (SDNN), which were obtained from 24‐hour Holter monitoring 1‐day post‐AF ablation, were significantly lower in patients without recurrence than those in patients with recurrence (5.8 ± 6.0% vs 14.0 ± 10.1%; P = 0.0005, 78.7 ± 32.4 ms vs 109.2 ± 43.5 ms; P = 0.005). There was a significant negative correlation between SDNN and the percentage of ablated FP area (Y = −1.3168X + 118.96, R2 = 0.1576, P = 0.003).ConclusionExtensively ablating LA covering GP areas along with PVA isolation enhanced the denervation of autonomic nerve system and seemed to improve procedural outcome in patients with AF.

AIMS:Therapeutic effectiveness of ablation of atrial fibrillation (AF) is related to cardiovascular comorbidities. We studied the relationship between left ventricular hypertrophy (LVH) and left atrial tissue structural remodelling (LA-SRM), in patients presenting for AF ablation. METHODS AND RESULTS:We identified 404 AF patients who received a late gadolinium enhancement magnetic resonance imaging (LGE-MRI) prior to catheter ablation. Left ventricular hypertrophy was defined as LV mass index >116 g/m(2) in men and >104 g/m(2) in women. One hundred and twenty-two patients were classified as the LVH group and 282 as the non-LVH group. We stratified patients into four stages based on their degree of LA-SRM (minimal, <5% fibrosis; mild, >5-20%; moderate, >20-35%; and extensive, >35%). All patients underwent catheter ablation with pulmonary vein isolation and posterior wall and septal debulking. The procedural outcome was monitored over a 1-year follow-up period. The mean LA-SRM was significantly higher in patients with LVH (19.4 ± 13.2%) than in non-LVH patients (15.3 ± 9.8%; P< 0.01). Patients with LVH generally had extensive LA-SRM (moderate and extensive stages; 38.5% of LVH group) as compared with non-LVH patients (23.1% of non-LVH group; P < 0.01). A Cox regression analysis showed that patients with LVH also had significantly higher AF recurrence rates than non-LVH patients (43.2 vs. 28%; P = 0.008) during the 1-year follow-up period post-ablation. CONCLUSION:Patients with LVH tend to have a significantly greater degree of LA-SRM, when compared with patients without LVH. Moreover, LA-SRM is a predictor for procedural success in patients undergoing AF ablation procedure.

This editorial refers to ‘Feasibility of real-time magnetic resonance imaging-guided electrophysiology studies in humans’ by P. Sommer et al ., on page 101 Catheter ablation using a standard fluoroscopy imaging guidance provides a cure for a plethora of cardiac arrhythmias and has become the cornerstone of arrhythmia management.1 Nevertheless, since the introduction of complex arrhythmias ablation into the electrophysiological (EP) labs, the need for more accurate imaging visualization and guidance tools has emerged. Despite the massive amount of research and financial investments into the novel ablation and imaging modalities, the outcome of complex ablation procedures has not improved, in fact it has been stable for the last decade. For example, atrial fibrillation (AF) ablation success rates are still reported to be between 40 and 80%.2–4 This dilemma, however, prompted interest in an alternative, complete ‘outside of the box’, concept. One of the imaging/ablation modalities, which has been suggested, is real-time magnetic resonance imaging (MRI)-guided interventional procedure. Cardiac MRI is considered a great tool to help detecting the anatomy, function, and viability of the myocardium.5 Moreover, MRI imaging is an ideal method to detect and quantify critical …

LV Systolic Dysfunction is Related to LA‐SRM in AF Patients Background Catheter ablation significantly improves the left ventricular (LV) function in patients with atrial fibrillation (AF) and LV systolic dysfunction. In this study, we compared the degree of left atrial structural remodeling (LA‐SRM) in patients with normal versus reduced LV ejection fraction (LVEF). We also studied the impact of LA‐SRM on LVEF improvement in patients undergoing ablation of AF. Method and Results We categorized 384 patients into 2 groups based on their cardiac function: reduced LVEF group (LVEF ≤50%; n = 105) and normal LVEF group (LVEF > 50%; n = 279). LVEF was determined prior and mean 8 ± 3 months after catheter ablation for AF. Percentage of LA‐SRM was quantified using LGE‐MRI and patients were classified into 4 groups based on the amount of structural remodeling in their LA wall: minimal ≤ 5%, mild = 5–20%, moderate = 20–35%, and extensive ≥ 35%. The average preablation LA‐SRM (21.5 ± 13.2% vs 15.4 ± 10.0%; P < 0.001) was significantly higher in reduced LVEF group than normal LVEF group. Among the 105 patients with reduced LVEF, while there was a modest 11.7 ± 8.4% average increase in LVEF following ablation, the greatest increase was seen in patients with less extensive LA‐SRM (minimal = 19.3 ± 5.1%, n = 3, P = 0.02 and mild = 16.6 ± 9.9%, n = 48, P < 0.001). Patients with moderate and extensive fibrosis had an average EF improvement of 8.7 ± 11.1% and 2.8 ± 6.4%, respectively (n = 39, P < 0.001 and n = 15, P = 0.11, respectively). Conclusion Patients with LV systolic dysfunction displayed a comparatively greater LA‐SRM than patients with normal LVEF. Patients with lesser LA‐SRM experienced a greater improvement in LVEF after catheter ablation for AF.

The lamin A/C proteins are major structural and functional components of the nuclear lamina. Mutations identified in LMNA encoding lamin A/C belong to the most frequently described causes for inherited forms of dilated cardiomyopathy (DCM). To elucidate the clinical characteristics of LMNA mutation carriers we performed genetic analysis of LMNA in 20 unrelated patients with DCM and cardiac conduction disease. In six small nuclear families heterozygous mutations in LMNA were identified. Two missense mutations led to the substitution of highly conserved amino acid residues within the rod domain of lamin A/C and four not-yet-described nonsense mutations cause the formation of predicted truncated lamin A/C missing parts of the tail domain. DCM was the most prominent clinical characteristic of the affected family members with a high degree of involvement of conduction system defects and less often accompanied by muscular dystrophy. The cardiac phenotype of the affected family members was severe and progressive with age, indicating the necessity for a genetic testing for LMNA mutations in patients with familial DCM and early onset of conduction disorders.