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)
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.
We describe pathological abnormalities in a 72‐year‐old male member of a family with a congenital absence of sinus rhythm and a tendency to develop atrial fibrillation at an early age, and in a 54‐year‐old female member of a family with cardiomyopathy and progressive conduction system disease manifested by first‐degree atrioventricular (AV) block, left bundle branch block, and atrial arrhythmias. Both patients died suddenly. The absence of sinus rhythm in case 1 could be explained by marked atrophy, degeneration, and isolation of the sinoatrial (SA) node. The SA node was also diseased in the member of the other family with atrial arrhythmias. Additional common features in both cases included: fatty metamorphosis and degenerative changes of the approaches to the SA node, the atrial preferential fibers, and the approaches to the AV node, a small AV node, degenerative changes of the bundle branches, and floppy AV valves. These findings show that the pathological substrate of familial supraventricular arrhythmias consists of a diffuse involvement of the entire conduction system, bearing resemblance to pathological findings in elderly subjects with acquired sick sinus syndrome.
Atrioventricular block may occasionally occur after surgical correction of truncus arteriosus. We therefore studied the conduction system by means of serial sections in five cases of truncus (one after surgical intervention) to delineate the course of the conduction system and its relationship to the ventricular septal defect and the membranous septum. In general, the ventricular septal defect is in the anterior septum, confluent with the truncus, and the atrioventricular bundle is posterior and unrelated to the rim of the ventricular septal defect. In cases in which the ventricular septal defect is anterior and separated from the membranous septum by distinct muscle, the ventricular septal defect can be surgically closed without injury to the atrioventricular bundle. If the ventricular septal defect is related to the membranous septum, the atrioventricular bundle may be close to the ventricular septal defect and susceptible to surgical injury. If muscle separates the ventricular septal defect from the membranous septum, the branching bundle is close to the ventricular septal defect and also is susceptible to surgical injury. In one operated case there was partial dissolution of the left bundle branch, and the right bundle branch was involved in surgical closure of the defect. In summary, in truncus the conduction system varies in its course and is related to the location of the ventricular septal defect and its relationship to the membranous septum. The ventricular septal defect may be close to or related to the membranous septum, and the atrioventricular bundle and the beginning of the bundle branches may be vulnerable to surgical injury.
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 has 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.
OBJECTIVES:The purpose of this study was to test the feasibility of selective elimination of ventriculoatrial (VA) conduction by limited laser photocoagulation of the atrioventricular (AV) node, and to analyze the histologic substrate of unidirectional retrograde block.BACKGROUND:Atrioventricular node reentry requires intact retrograde conduction.METHODS:Neodymium:yttrium-aluminum-garnet laser photocoagulation was performed during cardiopulmonary bypass through a right atriotomy in 15 dogs that had intact retrograde conduction before operation. Short laser pulses were delivered to an area between the coronary sinus orifice and the proximal His bundle. The end point of lasing was second-degree AV node block at a paced atrial cycle length of 250 ms.RESULTS:Complete retrograde block developed immediately in 11 of the 15 dogs (group I), while AV conduction persisted in all 11. In 4 of the 15 dogs (group II), both AV and VA conduction remained intact. During a 3-month follow-up period, retrograde conduction remained absent in all group I dogs. Retrograde block was not reversed by isoproterenol. Anterograde AV node characteristics (Wenckebach cycle length, functional refractory period, ventricular rate during atrial fibrillation) were unchanged in five dogs and modified in six. Complete AV block did not develop. In four control dogs (group III, sham operation), anterograde and retrograde AV node characteristics were unchanged. The anterograde Wenckebach cycle lengths in groups I, II and III at 3 months measured 192 +/- 15 ms, 195 +/- 6 ms and 170 +/- 22 ms, respectively, whereas the retrograde Wenckebach cycle lengths in groups II and III measured 345 +/- 62 ms and 278 +/- 25 ms, respectively. Histologic study at 3 months in cases with unidirectional VA block showed the compact part of the AV node intact with destruction of the atrial approaches and the superficial layers of the proximal end of the node on the right side.CONCLUSIONS:1) With limited laser photocoagulation of the proximal AV node area, VA conduction can be eliminated and anterograde AV node transmission maintained. 2) Destruction of the atrial approaches on the right side with preservation of the compact part of the AV node may result in unidirectional retrograde block.
The conduction system was studied by serial section in three patients with intractable supraventricular tachycardias originating from the atrioventricular (AV) junction who died suddenly. The three patients were a 6 month old girl (Case 1), a 5 month old boy (Case 2) and a 22 year old woman (Case 3). The latter had a pacemaker inserted after surgical ablation of the AV node. The heart was hypertrophied and enlarged in all.In Case 1, the AV node was partly within the central fibrous body and there was a left-sided AV bundle with acute necrosis in the summit of the ventricular septum, adjacent to the AV node and bundle. In Case 2, the coronary sinus was displaced cranially close to the central fibrous body, resulting in abnormality of the latter, with entrapment, distortion and division of the AV node and bundle into two distinct components within the central fibrous body. In Case 3, a left-sided AV node was connected to the atrial septum. The right AV node was completely interrupted by sutures and the penetrating and branching bundle and bundle branches were markedly fibrosed. In addition, the atrial septum and summit of the ventricular septum showed marked inflammatory reaction with fibrosis, which was more marked on the right ventricular side.Histologic examination of the conduction system in all three cases demonstrated congenital abnormalities of the AV junction that may be related to the tachycardia. These findings emphasize the need to carefully evaluate the atrial septum and AV junctional area, including the coronary sinus, before ablative procedures are undertaken. Finally, these anomalies at the AV junctional area may be elusive on clinical evaluation, but have important implications for ablative procedures performed from the right-sided approach.
The purpose of this study was to test the feasibility of neodymiumyttrium-aluminum-garnet (Nd-YAG) laser photocoagulation of the atrioventricular (AV) node to control the ventricular rate during rapid atrial rhythms without creating AV block. In 12 dogs on normothermic cardiopulmonary bypass, short laser pulses were delivered to an area between the coronary sinus orifice and the site of the most proximally recorded His deflection until second degree AV block occurred at a paced atrial rate of 200 beats/min.Long-term effects on AV node function were followed up for 3 months. Three animals developed chronic high grade AV block. In nine animals with preserved 1:1 conduction, the mean (+/-SEM) critical atrial cycle length resulting in AV node Wenckebach periodicity increased from 183 +/- 6 to 261 +/- 24 ms (+43%), the mean RR interval during induced atrial fibrillation increased from 248 +/- 14 to 330 +/- 27 ms (+32%) and the shortest RR interval during atrial fibrillation increased from 215 +/- 11 to 275 +/- 20 ms (+28%). Laser effects were not reversed by isoproterenol infusion. Histologic examination of the irradiated area showed fibrotic changes in the AV node and fatty metamorphosis.This study suggests that 1) graded Nd-YAG laser photocoagulation of the AV node region in dogs results in long-term modification of anterograde AV node transmission properties; 2) 1:1 conduction during sinus rhythm usually remains preserved, but ventricular rate during rapid atrial rhythms is chronically reduced; and 3) progression to high grade AV block occurs in a minority of animals. Laser modification of the AV node could become a form of nonpharmacologic heart rate control in patients with disabling atrial tachyarrhythmias.
The heart and conduction system were studied in a 412-year-old boy with Kawasaki disease who died suddenly in the early phase of illness. Severe perivasculitis, neuritis, pancarditis, and involvement of all parts of the specialized conduction system were found. The boy's brother, born a year later, at the age of 12 months had relapsing Kawasaki disease. He received intravenous gamma globulin and recovered.
This study tested the feasibility of neodymium:YAG laser photocoagulation of selected sinus node areas to depress sinus rate responsiveness. In 14 open-chest dogs, origin of the sinus impulse (O point) was electrically mapped from the epicardium before and during isoproterenol infusion. Epicardial laser photocoagulation was applied to the O point observed during isoproterenol infusion and stepwise to remapped new O points until a 30 +/- 5% decrease in heart rate occurred. Long-term effects were assessed by Holter monitoring and electropharmacologic testing preoperatively and up to 10 weeks or 6 months. Mean (+/- SEM) percent decreases were observed at 10 weeks in the following parameters: average 24-hour heart rate, 17.4 +/- 5.0%; maximum heart rate on Holter, 30.5 +/- 3.5%; heart rate during pharmacologic autonomic blockade, 32.7 +/- 3.5%; and maximum heart rate on isoproterenol, 23.1 +/- 4.6% (all p less than 0.01). Curves with pacemaker recovery time plotted against control cycle length remained unchanged. Holter monitoring did not show excessive bradycardic episodes even after administration of propranolol. In three control dogs (sham operation), sinus node function remained unchanged. Histologic study of the irradiated area showed replacement by inflammatory cells, fibrosis, and cartilage formation with surrounding normal cells and occasional cells resembling pacemaker-like cells at the caudal end of the sinoatrial node. This study suggests that 1) map-guided graded laser photocoagulation of sinus node regions showing earliest activation during catecholamine stimulation successfully limits maximum heart rates without causing significant bradycardia, 2) the effects are long lasting, and 3) the remaining pacemaker behaves like the sinus node. Laser modification of sinus node function could become a form of nonpharmacologic heart rate control in patients with coronary artery disease undergoing surgery and in the syndrome of inappropriate sinus tachycardia.
Pacing and Clinical ElectrophysiologyVolume 12, Issue 6 p. 879-882 The Morphology of the AV Junction and its Significance in Catheter Ablation SAROJA BHARATI, Corresponding Author SAROJA BHARATI Congenital Heart and Conduction System Center, Heart Institute for Children of the Christ Hospital and Medical Center, Oak Lawn, Illinois and the Department of Pathology, RushPreshyterian-St. Luke's Medical Center, of Rush University, Chicago, IllinoisAddress for reprints: Saroja Bharati, M.D., Congenital Heart and Conductions System Center, 11745 Southwest Highway, Palos Heights, Illinois 60463.Search for more papers by this authorMAURICE LEV, MAURICE LEV Congenital Heart and Conduction System Center, Heart Institute for Children of the Christ Hospital and Medical Center, Oak Lawn, Illinois and the Department of Pathology, RushPreshyterian-St. Luke's Medical Center, of Rush University, Chicago, IllinoisSearch for more papers by this author SAROJA BHARATI, Corresponding Author SAROJA BHARATI Congenital Heart and Conduction System Center, Heart Institute for Children of the Christ Hospital and Medical Center, Oak Lawn, Illinois and the Department of Pathology, RushPreshyterian-St. Luke's Medical Center, of Rush University, Chicago, IllinoisAddress for reprints: Saroja Bharati, M.D., Congenital Heart and Conductions System Center, 11745 Southwest Highway, Palos Heights, Illinois 60463.Search for more papers by this authorMAURICE LEV, MAURICE LEV Congenital Heart and Conduction System Center, Heart Institute for Children of the Christ Hospital and Medical Center, Oak Lawn, Illinois and the Department of Pathology, RushPreshyterian-St. Luke's Medical Center, of Rush University, Chicago, IllinoisSearch for more papers by this author First published: June 1989 https://doi.org/10.1111/j.1540-8159.1989.tb05023.xCitations: 12 Aided by grant HL 30558–06 from Ihe National Institutes of Health. National Heart, Lung and Blood Institute, Bethesda, Maryland. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume12, Issue6June 1989Pages 879-882 RelatedInformation