Images in cardiovascular medicine. Early differential resolution of right and left ventricular obliteration in Löffler endocarditis after chemotherapy and anticoagulation.
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Biomedical subjects
Publications and source records attributed to Jerónimo Farré.
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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.
An 82-year-old female was admitted to the coronary care unit with an anterior wall myocardial infarction and cardiogenic shock. She was in chronic atrial fibrillation without oral anticoagulation. Coronary angiography showed occlusion of the left main coronary artery which originated together with a normal right coronary artery from the right sinus of Valsalva. The advanced age, the presence of chronic atrial fibrillation not anticoagulated and the normal appearance of the remaining coronary arteries suggested a thromboembolic origin. Transthoracic echocardiography showed an abrupt interruption of the myocardial wall, in the apical portion of the interventricular septum, not communicating with the pericardial sac or right ventricular cavity suggesting the presence of an incomplete contained rupture of the myocardial wall at this location. She died in cardiogenic shock due to the extensive left ventricular damage.
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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. METHODS AND RESULTS: We examined the isthmic area in 30 heart specimens by dissection, histology, and scanning electron microscopy. This area was bordered anteriorly by the hinge of the tricuspid valve and posteriorly by the orifice of the inferior caval vein. With the heart in attitudinal orientation, we identified and measured the lengths of three levels of isthmus: paraseptal (24 +/- 4 mm), central (19 +/- 4 mm), and inferolateral (30 +/- 3 mm). Comparing the three levels, the central isthmus had the thinnest muscular wall and the paraseptal isthmus the thickest wall. At all three levels, the anterior part was consistently muscular whereas the posterior part was composed of mainly fibro-fatty tissue in 63% of hearts. The right coronary artery was less than 4 mm from the endocardial surface of the inferolateral isthmus in 47% of hearts. Inferior extensions of the atrioventricular node were present in the paraseptal isthmus in 10% of hearts, at 1-3 mm from the endocardial surface. CONCLUSIONS: The thinner wall and shorter length of the central isthmus together with its distance from the right coronary artery, and nonassociation with the atrioventricular node or its arterial supply, should make it the preferred site for linear radiofrequency ablation.
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. METHODS AND RESULTS: We examined by gross dissection the courses of the right and left phrenic nerves in 19 cadavers. Measurements were made of the minimal and maximal distances of the nerves to the superior caval vein, superior cavoatrial junction, right pulmonary veins, and coronary veins. Histologic studies were carried out on tissues from six cavaders. Tracing the course of the right phrenic nerve revealed its close proximity to the superior caval vein (minimum 0.3 +/- 0.5 mm) and the right superior pulmonary vein (minimum 2.1 +/- 0.4 mm). The anterior wall of the right superior pulmonary vein was <2 mm from the right phrenic nerve in 32% of specimens. The left phrenic nerve passed over the obtuse cardiac margin and the left obtuse marginal vein and artery in 79% of specimens. In the remaining specimens, its course was anterosuperior, passing over the main stem of the left coronary artery or the anterior descending artery and great cardiac vein. CONCLUSIONS: The right phrenic nerve is at risk when ablations are carried out in the superior caval vein and the right superior pulmonary vein. The left phrenic nerve is vulnerable during lead implantation into the great cardiac and left obtuse marginal veins.
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OBJECTIVES: The aim of this study was to analyze modifications in the plasma protein map during an acute coronary syndrome (ACS) using proteomics. BACKGROUND: Proteomics is a new technology that allows the detection and identification of several proteins at a given time in a sample. METHODS: Plasma from 19 patients, 11 with acute myocardial infarction (AMI) and 8 with unstable angina (UA), was investigated. The control group included nine age-matched volunteers. RESULTS: In two-dimensional electrophoresis using a pH range of 4 to 7, constant differences were found in at least four different areas within the plasma protein map. In area 1, we identified the presence of seven alpha(1)-antitrypsin (AAT) isoforms in plasma from control subjects. alpha(1)-antitrypsin isoform 1 was undetectable in plasma from UA and AMI patients. The AAT isoforms 5, 6, and 7 were reduced in plasma from AMI patients when compared with UA patients. Three fibrinogen gamma chain isoforms were identified in area 2. Fibrinogen gamma chain isoforms 1 and 2 were increased in AMI patients with respect to UA patients. Five apolipoprotein A-I isoforms were identified in area 3. All of them were reduced in plasma from AMI patients with respect to UA patients. In area 4, the gamma-immunoglobulin heavy chains were detected and were found increased in plasma from ACS patients. CONCLUSIONS: Plasma proteomic analysis makes it possible to develop a map of the protein isoforms that are expressed in plasma during an ACS.
Granulocytic sarcoma, or chloroma, is an uncommon presentation of acute leukemia. Cardiac involvement is very rare and usually diagnosed at autopsy. We present a case that discloses the essential role of transesophageal echocardiography for its in vivo diagnosis. The principal features with this imaging technique are finely described.
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INTRODUCTION AND OBJECTIVES: Tako-tsubo-like transient left ventricular apical ballooning has been described in Japan, but few cases have been reported in Western countries. We report one of the first series outside Japan, which provides new information on the coronary anatomy of this disorder. PATIENTS AND METHODS: From January 1998 to February 2003 we observed 11 patients with a clinical suspicion of acute myocardial infarction, normal coronary arteries, and transient tako-tsubo-like systolic left ventricular apical ballooning. We compared the coronary artery anatomy in these 11 patients with that in 44 controls matched for age and sex: 22 with normal coronary arteries and 22 with acute myocardial infarction related with an obstructive thrombus in the left anterior descending coronary artery. RESULTS: As in Japanese patients, tako-tsubo syndrome in Caucasian patients frequently occurs in women in their seventh or eighth decades of life, and is usually preceded by emotional or physical stress. The left anterior descending in our patients with tako-tsubo syndrome was longer overall, and its recurrent diaphragmatic segment was longer, than in controls. To compare these groups we designed a measure termed recurrent segment index (left anterior descending recurrent segment length/total left anterior descending length x 100). In tako-tsubo syndrome this index was 22.3 (1.5)%, vs 10.9 (6.7)% in normal controls (P<.001), and 11.3 (7.7)% in acute myocardial infarction patients (P<.001). Patients with acute myocardial infarction and a high recurrent segment index (> or =16%) had ventriculographic findings of systolic apical ballooning identical to those in patients with tako-tsubo syndrome. CONCLUSIONS: All our patients with tako-tsubo syndrome had a left anterior descending with a long recurrent segment. The identical ventriculographic findings in patients with tako-tsubo syndrome and those with acute myocardial infarction with a long recurrent segment may be due to a common etiology.
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. CONCLUSIONS: 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.
BACKGROUND: Pulmonary vein isolation with radiofrequency catheter ablation techniques is used to prevent recurrences of human atrial fibrillation. Visualization of the architecture at the venoatrial junction could be crucial for these ablative techniques. Our study assesses the potential for intravascular ultrasound to provide this information. METHODS AND RESULTS: We retrieved 32 pulmonary veins from 8 patients dying from noncardiac causes. We obtained cross-sectional intravascular ultrasound (IVUS) images with a 3.2F, 30-MHz ultrasound catheter at intervals on each vein. Histological cross-sections at the intervals allowed comparisons with ultrasonic images. The pulmonary venous wall at the venoatrial junction revealed a 3-layered ultrasonic pattern. The inner echogenic layer represents both endothelium and connective tissue of the media (mean maximal thickness, 1.4+/-0.3 mm). The middle hypoechogenic stratum corresponds to the sleeves of left atrial myocardium surrounding the external aspect of the venous media. This layer was thickest at the venoatrial junction (mean maximal thickness, 2.6+/-0.8 mm) and decreased toward the lung hilum. The outer echodense layer corresponds to fibro-fatty adventitial tissue (mean maximal thickness, 2.15+/-0.36 mm). We found a close agreement among the IVUS and histological measurements for maximal luminal diameter (mean difference, -0.12+/-1.3 mm) and maximal muscular thickness (mean difference, 0.17+/-0.13 mm) using the Bland and Altman method. CONCLUSIONS: Our experimental study demonstrates for the first time that IVUS images of the pulmonary veins can provide information on the distal limits and thickness of the myocardial sleeves and can be a valuable tool to help accurate targeting during ablative procedures.
The aim was to analyze whether pericardial tissue expresses endothelial NO synthase (eNOS) protein and to determine the presence of cytosolic proteins that bind to eNOS mRNA. The effect of aspirin on the above-mentioned parameters was also analyzed. eNOS protein was expressed in pericardial tissue from male guinea pigs. Escherichia coli lipopolysaccharide (LPS, 10 microgram/mL) and Staphylococcus aureus endotoxin (SA, 10 microgram/mL) reduced eNOS protein expression and shortened the half-life of the eNOS messenger. Under basal conditions, cytosolic extracts from pericardial samples bound to the 3'-untranslated region (3'-UTR) of eNOS mRNA, which was enhanced by LPS and SA. Proteinase K fully prevented the binding of cytosolic pericardial extracts to 3'-UTR of eNOS mRNA, suggesting the involvement of proteins that were further characterized as 60- and 51-kDa proteins. Aspirin (1 to 10 mmol/L) restored eNOS expression in either LPS- and SA-stimulated pericardial samples and reduced the binding activity of the pericardial cytosolic proteins to 3'-UTR of eNOS mRNA. Indomethacin also reduced the downregulation of eNOS by LPS and diminished the binding activity of the cytosolic proteins, although higher doses of indomethacin than of aspirin were needed to improve these parameters. In conclusion, eNOS protein is expressed in guinea pig pericardial tissue. LPS and SA stimulate the binding activity of pericardial cytosolic proteins to 3'-UTR of eNOS mRNA and reduce eNOS protein expression. High doses of aspirin and indomethacin protect eNOS protein expression and reduce the binding activity of the cytosolic proteins to 3'-UTR of eNOS mRNA, suggesting an inverse association between the presence of these cytosolic proteins and eNOS expression.
OBJECTIVES: To analyze the differences in the nitric oxide (NO) forming system between neutrophils obtained from patients during unstable angina (UA) and during acute myocardial infarction (AMI). BACKGROUND: Neutrophils are involved in the regulation of thrombus formation through the release of active substances such as NO. Acute myocardial infarction is the result of an occlusive thrombus; unstable angina is attributed to intermittent thrombus formation. METHODS: We studied 49 patients admitted to hospital within 24 h after the onset of chest pain: 31 experienced AMI and 18 experienced UA. Acute myocardial infarction was defined as CK greater than two-fold the upper limit of normal value of biochemical laboratory, with CK-MB >10% total CK. Unstable angina was defined as transient ST segment changes without significant increases in CK and CK-MB. RESULTS: The amount of NO generated by neutrophils from AMI patients was significantly higher than that generated by neutrophils from UA patients. Neutrophils from UA and AMI patients showed low levels of endothelial-like NO synthase protein expression and a marked expression of the inducible NO synthase (iNOS) isoform. Although neutrophils from patients during acute coronary syndromes generated high amounts of NO, they did not demonstrate an increased ability to stimulate cyclic guanosine monophosphate (cGMP) synthesis in platelets. This lack of activity to release NO by neutrophils from patients during AMI was unrelated to a defect in the platelet cGMP-forming system; sodium nitroprusside, an exogenous NO donor, similarly increased cGMP levels in platelets from AMI patients and healthy donors. CONCLUSIONS: Neutrophils from patients during AMI and UA showed an increased production of NO and a marked expression of the iNOS isoform. However, NO released from these neutrophils showed a deficient functionality. These findings could have clinical implications because they show differences in thrombus growth in patients with UA versus patients with AMI.
INTRODUCTION AND OBJECTIVES: In our laboratory, we recently obtained evidence that cultured bovine endothelial cells contain cytosolic proteins that form complexes with the 3'-unstranslated region of endothelial nitric oxide synthase (eNOS) mRNA and are associated with its destabilization. The aim of this study was to determine the presence of such proteins and the level of eNOS expression in hypercholesterolemic rabbits as an in vivo model of endothelial dysfunction. METHODS AND RESULTS: Endothelium-dependent relaxation in response to acetylcholine was reduced in aortic segments from hypercholesterolemic rabbits compared with controls. Treatment of hypercholesterolemic rabbits with simvastatin (25 mg/kg body weight/day) restored endothelium-dependent relaxation. Aortic eNOS expression was reduced in hypercholesterolemic rabbits and was accompanied by enhanced binding activity of a 60-KDa cytosolic protein and reduced stability of eNOS mRNA. Simvastatin treatment upregulated eNOS expression and reduced the interaction of cytosolic protein with the 3'-untranslated region of eNOS mRNA. CONCLUSIONS: These results demonstrate the presence of a 60-KDa protein that binds to eNOS mRNA and reduces eNOS expression in the vascular wall.
The understanding of cardiac anatomy is crucial for the interventional arrhythmologist. In spite of the introduction of several nonfluroscopic navigational tools, some of them capable of reconstructing a computer-based surrogate of the endocardial surface of the heart cavities, simple fluoroscopy with or without the aid of angiographic techniques is still the most widely used method to guide mapping and ablation procedures. In some instances, fluoroscopic and angiographic methods have no possible replacement to unravel certain arrhythmologically useful anatomic landmarks. New interpretations of cardiac architecture show the need to challenge some traditional anatomic views, like the concept of septums within the heart. The fluoroscopic anatomy also needs to be reconsidered in the light of the new attitudinally oriented nomenclature. This article presents an overview of the fluoroscopic anatomy of the heart. When pertinent, some anatomical concepts are discussed in more detail like the triangle of Koch, the pyramidal space, and the interatrial groove. In the sections on the atria and on the ventricles, the authors focus on the anatomic information that is relevant for mapping and ablation from a fluoroscopic viewpoint, providing some hints on how best to depict the morphological features from the stance of the interventional arrhythmologist. The Visible Human Slice and Surface Server using data sets from the Visible Human Male and Female Project, has been used to facilitate the understanding of the fluoroscopic anatomy.