José Angel Cabrera

ANATOMY OF THE LEFT ATRIUM : IMPLICATIONS FOR RADIOFREQUENCY ABLATION OF ATRIAL FIBRILLATION

Anatomy of the Left Atrium. Introduction: The feasibility of treating atrial fibrillation with radiofrequency ablation has revived interest in the structure of the left atrium, a chamber that has been neglected in many textbooks of anatomy.

Mapping and ablation of ventricular fibrillation associated with long-QT and Brugada syndromes.

Background—The long-QT and Brugada syndromes are important substrates of malignant ventricular arrhythmia. The feasibility of mapping and ablation of ventricular arrhythmias in these conditions has not been reported. Methods and Results—Seven patients (4 men; age, 38±7 years; 4 with long-QT and 3 with Brugada syndrome) with episodes of ventricular fibrillation or polymorphic ventricular tachycardia and frequent isolated or repetitive premature beats were studied. These premature beats were observed to trigger ventricular arrhythmias and were localized by mapping the earliest endocardial activity. In 4 patients, premature beats originated from the peripheral right (1 Brugada) or left (3 long-QT) Purkinje conducting system and were associated with variable Purkinje-to-muscle conduction times (30 to 110 ms). In the remaining 3 patients, premature beats originated from the right ventricular outflow tract, being 25 to 40 ms ahead of the QRS. The accuracy of mapping was confirmed by acute elimination of premature beats after 12±6 minutes of radiofrequency applications. During a follow-up of 17±17 months using ambulatory monitoring and defibrillator memory interrogation, no patients had recurrence of symptomatic ventricular arrhythmia but 1 had persistent premature beats. Conclusion—Triggers from the Purkinje arborization or the right ventricular outflow tract have a crucial role in initiating ventricular fibrillation associated with the long-QT and Brugada syndromes. These can be eliminated by focal radiofrequency ablation.

Anatomic Relations Between the Esophagus and Left Atrium and Relevance for Ablation of Atrial Fibrillation

Background—Esophageal injury is a potential complication after intraoperative or percutaneous transcatheter ablation of the posterior aspect of the left atrium. Understanding the spatial relations between the esophagus and the left atrium is essential to reduce risks. Methods and Results—We examined by gross dissection the course of the esophagus in 15 cadavers. We measured the minimal distance of the esophageal wall to the endocardium of the left atrium with histological studies in 12 specimens. To measure the transmural thickness of the atrial wall, we sectioned another 30 human heart specimens in the sagittal plane at 3 different regions of the left atrium. The esophagus follows a variable course along the posterior aspect of the left atrium; its wall was <5 mm from the endocardium in 40% of specimens. The posterior left atrial wall has a variable thickness, being thickest adjacent to the coronary sinus and thinnest more superiorly. Behind is a layer of fibrous pericardium and fibrofatty tissue of irregular thickness that contains esophageal arteries of 0.4±0.2-mm external diameters. Conclusions—The nonuniform thickness of the posterior left atrial wall and the variable fibrofatty layer between the wall and the esophagus are risk factors that must be considered during ablation procedure. Esophageal arteries and vagus nerve plexus on the anterior surface of the esophagus may be affected by ablative procedures.

How close are the phrenic nerves to cardiac structures? Implications for cardiac interventionalists.

Background: Phrenic nerve injury is a recognized complication following cardiac intervention or surgery. With increasing use of transcatheter procedures to treat drug‐refractory arrhythmias, clarification of the spatial relationships between the phrenic nerves and important cardiac structures is essential to reduce risks.

Effect of Early Metoprolol on Infarct Size in ST-Segment–Elevation Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Intervention The Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction (METOCARD-CNIC) Trial

Background —The effect of β-blockers on infarct size when used in conjunction with primary percutaneous coronary intervention (PCI) is unknown. We hypothesize that metoprolol reduces infarct size when administered early (intravenously [i.v.] before reperfusion). Methods and Results —Patients with Killip-class ≤II anterior ST-segment elevation myocardial infarction (STEMI) undergoing PCI within 6 hours of symptoms onset were randomized to receive i.v. metoprolol (n=131) or not (control, n=139) pre-reperfusion. All patients without contraindications received oral metoprolol within 24 hours. The pre-defined primary endpoint was infarct size on magnetic resonance imaging (MRI) performed 5-7 days after STEMI. MRI was performed in 220 patients (81%). Mean (±SD) infarct size by MRI was smaller after i.v. metoprolol compared to control (25.6±15.3 vs. 32.0±22.2 grams; adjusted difference, -6.52; 95% confidence interval [CI], -11.39 to -1.78; P=0.012). In patients with pre-PCI TIMI flow grade 0/1, the adjusted treatment difference in infarct size was -8.02; 95% CI, -13.01 to -3.02; P=0.0029. Infarct size estimated by peak and area under the curve creatine-kinase release was measured in all study population and was significantly reduced by i.v. metoprolol. Left ventricular ejection fraction was higher in the i.v. metoprolol group (adjusted difference 2.67%; 95% CI, 0.09% to 5.21%; P=0.045). The composite of death, malignant ventricular arrhythmia, cardiogenic shock, atrioventricular block and reinfarction at 24 hours in the i.v. metoprolol and control groups respectively was 7.1% vs. 12.3%, p=0.21. Conclusions —In patients with anterior Killip-class ≤II STEMI undergoing primary PCI, early i.v. metoprolol before reperfusion reduced infarct size and increased LVEF with no excess of adverse events during the first 24 hours after STEMI. Clinical Trial Registration Information —ClinicalTrials.gov. Identifier: [NCT01311700][1] & EUDRACT Number 2010-019939-35. [1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT01311700&atom=%2Fcirculationaha%2Fearly%2F2013%2F09%2F03%2FCIRCULATIONAHA.113.003653.atomBackground— The effect of &bgr;-blockers on infarct size when used in conjunction with primary percutaneous coronary intervention is unknown. We hypothesize that metoprolol reduces infarct size when administered early (intravenously before reperfusion). Methods and Results— Patients with Killip class II or less anterior ST-segment–elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention within 6 hours of symptoms onset were randomized to receive intravenous metoprolol (n=131) or not (control, n=139) before reperfusion. All patients without contraindications received oral metoprolol within 24 hours. The predefined primary end point was infarct size on magnetic resonance imaging performed 5 to 7 days after STEMI. Magnetic resonance imaging was performed in 220 patients (81%). Mean±SD infarct size by magnetic resonance imaging was smaller after intravenous metoprolol compared with control (25.6±15.3 versus 32.0±22.2 g; adjusted difference, −6.52; 95% confidence interval, −11.39 to −1.78; P=0.012). In patients with pre–percutaneous coronary intervention Thrombolysis in Myocardial Infarction grade 0 to 1 flow, the adjusted treatment difference in infarct size was −8.13 (95% confidence interval, −13.10 to −3.16; P=0.0024). Infarct size estimated by peak and area under the curve creatine kinase release was measured in all study populations and was significantly reduced by intravenous metoprolol. Left ventricular ejection fraction was higher in the intravenous metoprolol group (adjusted difference, 2.67%; 95% confidence interval, 0.09–5.21; P=0.045). The composite of death, malignant ventricular arrhythmia, cardiogenic shock, atrioventricular block, and reinfarction at 24 hours in the intravenous metoprolol and control groups was 7.1% and 12.3%, respectively (P=0.21). Conclusions— In patients with anterior Killip class II or less ST-segment–elevation myocardial infarction undergoing primary percutaneous coronary intervention, early intravenous metoprolol before reperfusion reduced infarct size and increased left ventricular ejection fraction with no excess of adverse events during the first 24 hours after STEMI. Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT01311700. EUDRACT number: 2010-019939-35.

Angiographic Anatomy of the Inferior Right Atrial Isthmus in Patients With and Without History of Common Atrial Flutter

BACKGROUND Although most ablative procedures undertaken for common atrial flutter target the inferior right atrial isthmus, comparative studies of the morphology of this area are lacking. Our study examines its angiographic anatomy, making correlations with postmortem specimens, to provide a better understanding of the anatomic substrate of this arrhythmia. METHODS AND RESULTS The gross morphological features and dimensions of the area between the orifice of the inferior caval vein and the attachment of the septal leaflet of the tricuspid valve were determined from angiograms made in 23 patients with documented atrial flutter and 30 control subjects. For comparison, we studied 20 normal heart specimens. When viewed in right anterior oblique projection, 2 morphologically distinct areas were identified. In the specimens, the inferior isthmus measured a mean length of 30+/-4 mm, not significantly different from the dimensions obtained from angiograms of control subjects. The mean length of the isthmus, however, was greater in patients with common atrial flutter than those without (37+/-8 versus 28+/-6 mm). Patients with atrial flutter and structural heart disease had an even longer isthmus than those with flutter alone (39. 6+/-8 versus 33+/-7 mm). Compared with those without flutter, the atrial diameter was also larger in patients with flutter (57.6+/-9 versus 48.5+/-6 mm). Reevaluation carried out at follow-up 10+/-2 months after ablation did not show any reduction in atrial size, although contractility improved. CONCLUSIONS The inferior isthmus and right atrium in patients with common atrial flutter were significantly larger than those in a control population.

The terminal crest: morphological features relevant to electrophysiology

Objective: To investigate the detailed anatomy of the terminal crest (crista terminalis) and its junctional regions with the pectinate muscles and intercaval area to provide the yardstick for structural normality. Design: 97 human necropsy hearts were studied from patients who were not known to have medical histories of atrial arrhythmias. The dimensions of the terminal crest were measured in width and thickness from epicardium to endocardium, at the four points known to be chosen as sites of ablation. Results: The pectinate muscles originating from the crest and extending along the wall of the appendage towards the vestibule of the tricuspid valve had a non-uniform trabecular pattern in 80% of hearts. Fine structure of the terminal crest studied using light and scanning electron microscopy consisted of much thicker and more numerous fibrous sheaths of endomysium with increasing age of the patient. 36 specimens of 45 (80%) specimens studied by electron microscopy had a predominantly uniform longitudinal arrangement of myocardial fibres within the terminal crest. In contrast, in all specimens, the junctional areas of the terminal crest with the pectinate muscles and with the intercaval area had crossing and non-uniform architecture of myofibres. Conclusions: The normal anatomy of the muscle fibres and connective tissue in the junctional area of the terminal crest/pectinate muscles and terminal crest/intercaval bundle favours non-uniform anisotropic properties.

Left Atrial Anatomy Revisited

Recent decades have seen rapid developments in arrhythmia treatment, especially the use of catheter ablation. Although the substrates of atrial fibrillation, its initiation and maintenance, remain to be fully elucidated, catheter ablation in the left atrium has become a therapeutic option for patients with this arrhythmia. With ablation techniques, various isolation lines and focal targets are deployed; the majority of these are anatomic approaches. It has been over a decade since we published our first article on the anatomy of the left atrium relevant to interventional electrophysiologists.1 Our aim then, as now, was to increase awareness of anatomic structures inside the left atrium. In this review of anatomy, we revisit the left atrium, inside as well as outside, for a better understanding of the atrial component parts and the spatial relationships of specific structures. ### Location and Atrial Walls Viewed from the frontal aspect of the chest, the left atrium is the most posteriorly situated of the cardiac chambers. Owing to the obliquity of the plane of the atrial septum and the different levels of the orifices of the mitral and tricuspid valves, the left atrial chamber is more posteriorly and superiorly situated relative to the right atrial chamber. The pulmonary veins enter the posterior part of the left atrium with the left veins located more superior than the right veins. The transverse pericardial sinus lies anterior to the left atrium, and in front of the sinus is the root of the aorta. The tracheal bifurcation, the esophagus, and descending thoracic aorta are immediately behind the pericardium overlying the posterior wall of the left atrium. Further behind is the vertebral column. Following the direction of blood flow, the atrial chamber begins at the pulmonary veno-atrial junctions and terminates at the fibro-fatty tissue plane that marks the atrioventricular junction at the mitral orifice. The walls …

Intracoronary ultrasound assessment of directional coronary atherectomy: Immediate and follow-up findings

OBJECTIVES This study was conducted to assess the relations among intracoronary ultrasound, angiographic and histologic data obtained from patients with coronary artery disease successfully treated by directional coronary atherectomy. In addition, it was designed to elucidate whether some aspects of intravascular ultrasound or pathologic findings could predict a propensity to restenosis. BACKGROUND Intracoronary ultrasound is a useful technique in guiding and assessing atherectomy. However, there is little information about the characterization of the different types of coronary plaques and the changes observed in them after resection. Furthermore, the follow-up ultrasound appearance of previously treated lesions remains undepicted. METHODS Fifty-two patients (54 +/- 10 years old) were studied. All were successfully treated by atherectomy with the aid of intracoronary ultrasound guidance. Qualitative and quantitative ultrasound and angiographic variables were derived before and after resection. Quantitative histologic morphometric information was also obtained from the specimens. In 22 patients, a follow-up echoangiographic reevaluation was performed 6 +/- 4 months later. RESULTS Echogenic plaques had a higher collagen and calcium content, whereas echolucent plaques had an increased level of fibrin, nuclei and lipids. Ultrasound plaque reduction after atherectomy was greater in echolucent (76 +/- 21%) than in echogenic plaques (60 +/- 18%; p < 0.05). That reduction correlated with the weight of the resected material (r = 0.62; p < 0.01). At follow-up study, 13 of 22 patients had angiographic and ultrasound evidence of restenosis. Most recurrent lesions had a stenotic three-layer appearance. The incidence of restenosis of primary lesions treated with atherectomy was higher in echolucent (100%) than in echogenic (33%) plaques. Similarly, a higher proportion of nuclear content in the resected material was observed in patients who developed restenosis (2.1 +/- 0.7%) than in patients who had late success after atherectomy (1.2 +/- 0.6%). CONCLUSIONS Our findings suggest that echolucent plaques are easier to resect than are echogenic plaques but frequently develop restenosis. In contrast, the resection of echogenic plaques, although often incomplete, is associated with better long-term results.

The Inferior Right Atrial Isthmus: Further Architectural Insights for Current and Coming Ablation Technologies

Background: Although linear ablation of the right atrial isthmus in patients with isthmus‐dependent atrial flutter can be highly successful, recurrences and complications occur in some patients. Our study provides further morphological details for a better understanding of the structure of the isthmus.