Saroja Bharati

Cardiac conduction system involvement in sudden death of obese young people

Involvement of the conduction system in the sudden death of obese young people has not been documented in the literature. We therefore studied the conduction system by serial section examination in 7 subjects, 5 obese and 2 mild to moderately obese, who died suddenly at ages 6, 11, 14, 16, 20, 30, and 32 years of age (5 males, 4 black and 1 white; two females, 1 black and 1 white). Three had a history of sleep apnea. The heart was hypertrophied and enlarged in 6; all 6 had a distinct ventricular septal bulge and epicardial coronary arteries were normal. All had focal mononuclear cells in and around the sinoatrial node and/or its approaches, with marked fat throughout the conduction system in 3, fibrosis of the atrioventricular (AV) bundle and/or the left bundle branch in 5, and the branching bundle sandwiched between the bulbar muscle and the summit of the ventricular septum in 5 (2 with left-sided bundle, 1 with loop formation, and 1 with a markedly fragmented bundle). The AV node was partly within the central fibrous body and/or the atrial septum in 6 patients; focal mononuclear cells were present to a varying degree, with focal fibrosis of the ventricular septum in 6 patients, arteriolosclerosis in 4, and myocardial disarray in 3. The mild to moderately obese patients demonstrated lesser amounts of fat with more fibrosis when compared with the markedly obese. In summary, there are significant pathologic findings in the conduction system in the sudden death of obese young people.(ABSTRACT TRUNCATED AT 250 WORDS)

Three-Dimensional Transesophageal Echocardiography of Atrial Septal Defect: A Qualitative and Quantitative Anatomic Study

BACKGROUND Real-time three-dimensional (3D) transesophageal echocardiography (TEE) was used to analyze atrial septal defect (ASD) with 4 goals: (1) to determine feasibility, (2) to analyze the accuracy of qualitative and quantitative data, (3) to assess strengths and weaknesses of the available modes of 3D TEE, and (4) to provide 3D transesophageal echocardiographic reference images. METHODS Sixty-five patients with ASDs (age, 5-64 years; weight, 20-114 kg; body surface area, 0.8-2.4 m(2)) underwent 3D TEE during catheter intervention or surgery. Three-dimensional transesophageal echocardiographic formats included live 3D, 3D zoom, and full-volume 3D modes. Qualitative and quantitative analysis of the 3D data was compared with two-dimensional echocardiographic data and intraoperative inspection. RESULTS Diagnostic-quality 3D TEE was successfully performed in all 65 patients. Fifty had secundum ASDs and 15 had other ASD types (seven sinus venosus, six primum, one common atrium, and one coronary sinus ASD). ASD type and location were correctly diagnosed in all patients. ASD shape and orientation were confirmed in 21 patients at surgery. Quantitative analysis of ASDs successfully demonstrated rims and changes in dimensions from systole to diastole. Live 3D mode had the highest volume rate, the best transgastric views, and the best views during device deployment but was limited by small sector size. Three-dimensional zoom mode allowed precropped live 3D images but was limited by slow volume rate. Full-volume mode had the best views of large defects and surrounding anatomy. However, it was limited by stitch artifact and required postacquisition cropping. CONCLUSIONS Three-dimensional TEE is feasible and accurate. Each of the 3D transesophageal echocardiographic modalities has strengths and limitations.

Histopathological study following catheter guided radiofrequency current ablation of the slow pathway in a patient with atrioventricular nodal reentrant tachycardia

The present study examined histological changes induced by catheter guided radiofrequency current in a patient with AV nodal reentrant tachycardia who underwent cardiac transplantation 1 week after ablation of the slow pathway. During the electrophysiology study AV nodal conduction curves were discontinuous and AV nodal reentry was induced. At the conclusion of the procedure there was no evidence of slow pathway function. Histological sections from the explanted heart demonstrated a sharply demarcated atrial lesion (5 × 5 × 4 mm) extending from the septal portion of the tricuspid annulus to the posterior border of the AV node. The lesion did not encompass the compact AV node. These observations support the hypothesis that the slow pathway is comprised of atrial approaches to the AV node and is distinct from the compact AV node.

Echocardiographic Diagnosis and Prognosis of Fetal Left Ventricular Noncompaction

BACKGROUND Left ventricular noncompaction (LVNC) has rarely been described in the fetus. METHODS The presence of associated congenital heart disease and rhythm disturbance was identified and the presence of heart failure was assessed using the cardiovascular profile score in all fetuses with LVNC presenting from January 1999 to July 2010. The left ventricle was divided into 12 segments-four segments each at the base, midpapillary, and apical regions-in the short-axis view to calculate the noncompaction/compaction ratio for each segment. RESULTS Of 24 fetuses with LVNC included in the study, 22 had significant congenital heart disease, and 15 had complete heart block. Of the 16 patients with adequate follow-up and not electively terminated, 12 (81%) died or progressed to heart transplantation. The average noncompaction/compaction ratios were 2.02 in patients who died or underwent heart transplantation and 1.67 in survivors (P = .2034). Fifty-seven of 93 measured segments (61%) of the left ventricle in the patients who died or underwent heart transplantation had noncompaction/compaction ratios ≥ 2 compared with five of 17 measured segments (29%) in survivors (P = .0837). The average cardiovascular profile score was 6. The apical region had greater involvement of noncompaction than the midpapillary and basal regions, with ratios of 2.27, 2.14, and 1.10, respectively (P = .00035). CONCLUSIONS Fetuses with LVNC have a poor prognosis that may be related to associated congenital heart disease, increased segmental involvement of noncompaction, and complete heart block and can be predicted by the cardiovascular profile score.

The pathologic changes in the conduction system beyond the age of ninety.

The conduction systems of two women who were 92 and 91 years of age, respectively, were examined by serial section. The first patient had sick sinus syndrome for more than 20 years, and the second patient had intermittent complete AV block that alternated with normal sinus rhythm for 12 years before her death. Both patients had severe coronary artery disease and had pacemakers and were doing well. The conduction systems in both revealed fatty metamorphosis in the approaches to the SA and AV nodes, the SA node, the AV node, and the atria with fibrotic changes in the ventricular septum, the AV bundle, and the bundle branches. Patient 1 had normal SA nodal artery and patient 2 had extensive vascularization of the AV node. As the heart ages, fatty replacement of the atria affect the SA and AV nodes, and fibrotic changes of the ventricular septum affect the AV bundle and the bundle branches. Adequate collateral anastomosis to the conduction system may prevent the development of permanent complete AV block in the elderly.

Conduction system findings in sudden death in young adults with a history of bronchial asthma

OBJECTIVES This study was conducted to determine whether there are any pathologic changes in the conduction system when death occurs suddenly in young adults with a history of bronchial asthma. BACKGROUND There is a worldwide increase in sudden death, especially in young adults with a history of bronchial asthma. METHODS We studied the conduction system by serial section examination in six male patients (16 to 23 years old) with a history of bronchial asthma who died suddenly. RESULTS The sinoatrial node artery was narrowed in two patients, with chronic inflammatory cells in three; it was fibrosed in one. The atrioventricular (AV) node was within the central fibrous body in three patients and isolated by fat in one. The AV bundle was markedly fragmented in five patients and fibrosed in two. The right and left bundle branches showed fat, fibrosis and disruption in five patients. Increased fibrosis on the summit of the ventricular septum with patchy fibrosis was present in five patients, and inflammatory cells in the conduction system were found in one. CONCLUSIONS 1) There are distinct pathologic findings in the conduction system of young adults with a history of bronchial asthma who die suddenly. 2) The significant findings appear to be a markedly fragmented bundle and changes in the sinoatrial node that are not found in normal healthy young adults. 3) The changes in the conduction system may create an arrhythmic event, and sudden death may occur in some persons during an altered physiologic state. 4) We hypothesize that bronchial asthma may be associated with an alteration in immune complexes that affects the conduction system in some patients.

Histopathologic changes in the heart including the conduction system after catheter ablation.

The pathology of the heart, including that of the conduction system, after various catheter techniques used to ablate the various parts of the conduction system and the myocardium, were examined histologically by serial sections. The experiments were conducted on canines. The conduction system studies included the approaches to the AV node, the AV node, the AV bundle and bundle branches, as well as, the central fibrous body, the tricuspid, mitral and aortic valves. The methods of ablation were DC shock, laser and radio frequency energy. Production of the complete AV block clinically was associated with fibrosis with or without cartilage formation of the approaches to the AV node, the AV node, the bundle and the beginning of the bundle branches in most cases. On the other hand, creation of first degree AV block was associated with fibrotic changes in the approaches to the AV node and the AV node, and second degree block with more changes to the AV node. Coronary sinus ablation resulted in necrosis and fibrosis of the coronary sinus wall with occasional thrombosis of the coronary sinus. The adjacent atrial and/ or the ventricular myocardium also showed fibrosis. Likewise, ventricular septal ablation was associated with focal areas of fibrosis of the myocardium. The conduction system was intact in both of the above experiments. In one human where complete AV block was created to manage intractable atrial fibrillation, the AV node, the bundle, and the bundle branches were fibrosed. In addition, there was a fibrosed atrio‐Hisian connection and the patient died suddenly six weeks after the ablative procedure. The surrounding structures close to the vicinity of the conduction system, such as the aortic, tricuspid, mitral valve, the central fibrous body, and the summit ventricular septum are involved to a varing degree. In summary, (1) Whatever the method of ablation may be, the end result was fibrosis with or without cartilage formation of the ablative area. (2) Congenital anomalies of the conduction system such as an atrio‐Hisian connection may remain elusive for ablative methods, and arrhythmias may presist and may cause sudden death in some cases.

Sudden death in athletes—Conduction system: Practical approach to dissection and pertinent pathology

Sudden death does occur in athletes with or without a previous history of arrhythmias. A study of the conduction system is mandatory in these individuals after ruling out all possible causes of sudden death, both at the gross and microscopic levels, as well as toxicological examination. In this article, a brief discussion of those anatomic landmarks in the heart that may be related to the conduction system and the method of study of the conduction system is emphasized. An examination of the conduction system in 14 athletes revealed varying types of anomalies, both congenital and acquired in nature. The congenital abnormalities included abnormally developed sinoatrial (SA) and atrio-ventricular (AV) nodes and AV bundle. The acquired changes included frequent association of mononuclear cell infiltration in the approaches to the SA node and the SA node, fat and fibrosis to a varying degree in all parts of the conduction system, and focal fibrotic scar areas in the ventricular septum. It is evident that these findings were present for a long period of time while the individual was totally asymptomatic. We therefore hypothesize that during an altered physiologic state, these congenital and/or acquired changes may form a milieu for an arrhythmic event to occur and/or promote an arrhythmic event in the vulnerable conduction system, which may in turn trigger varying types of reentry mechanisms, eventually leading to ventricular tachycardia, fibrillation, and sudden death. We also hypothesize that there may be a genetic and/or an autoimmune complex associated in some vulnerable conduction systems.

Successful Percutaneous Cardiac Resynchronization Despite an Occlusive Thebesian Valve

We report the case of a patient with symptomatic heart failure referred after an unsuccessful attempt at cardiac resynchronization therapy. An occlusive Thebesian valve prevented entry into the coronary sinus ostium. Careful analysis of the patient’s cardiovascular physiology and anatomy revealed the “fortuitous” presence of a persistent left superior vena cava. Cannulation of this vessel permitted percutaneous retrograde placement of a left ventricular lead into a posterolateral cardiac venous branch resulting in successful cardiac resynchronization. This unique case provides strong evidence that thorough knowledge of cardiac embryology, anatomy, and physiology plays a pivotal role in percutaneous electromechanical intervention for drug-refractory heart failure.

Computer three-dimensional reconstruction of the atrioventricular conduction system.

The human atrioventricular conduction system (AVCS), which includes the AV node and its approaches, AV bundle (penetrating, branching, and bifurcating parts), and the bundle branches, is a curved complex structure that has not been reconstructed in three dimensions using computer technology. Microscopic slides of every 40th serial section (cut at 7 micron level) of the AVCS were digitized into 600 dots/inch color images. External outlines of each section were manually segmented using commercially available three‐dimensional rendering software (Rhinoceros). The AVCS was traced from light microscopy and superimposed onto the external outlines. To account for inherent errors in histological slide preparation, an optimization procedure was used to align external outlines of all sections. The optimal rotation and translation of each section was established by maximizing area of overlap between adjacent sections. A sequential one‐dimensional minimization algorithm was used for optimization. Rotation and translation values were then used to align external outlines and the superimposed conduction system, reconstructing the AVCS in three‐dimensions. To validate the method, the algorithm was applied to a digitized image transformed with known translations and rotations. The validation procedure demonstrated that each test image aligned in translations and to within 0.01 degree in rotations. Spatial error determined by resolution of the digitized images was ±0.5/600 inch (±21 microns). Three‐dimensional reconstruction of every 40th serial section clearly demonstrated the complex curved shape of the AVCS. Three‐dimensional reconstruction of the human and canine AVCS permits accurate pathological and electrophysiological correlation of the conduction system. (PACE 2004; 27[Pt. I]:740–748)