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  • 1
    Electronic Resource
    Electronic Resource
    Demonstration of Electrical and Anatomic Connections Between Marshall Bundles and Left Atrium in Dogs: Implications on the Generation of P Waves on Surface Electrocardiogram (2002)
    Oxford, UK : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 13 (2002), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Marshall Bundle and P Wave. Introduction: The muscle bundles within the ligament of Marshall (LOM) are electrically active. The importance of these muscle bundles (Marshall bundle [MB]) to atrial activation and the generation of the ECG P wave is unclear. Methods and Results: We used optical mapping techniques to study epicardial activation patterns in isolated perfused left atrium in four dogs. In another seven dogs, P waves were studied before and after in vivo radiofrequency (RF) ablation of the connection between coronary sinus (CS) and the LOM. Computerized mapping was performed before and after RF ablation. Optical mapping studies showed that CS pacing resulted in broad wavefronts propagating from the middle and distal LOM directly to the adjacent left atrium (LA). Serial sections showed direct connection between MB and LA near the orifice of the left superior pulmonary vein in two dogs. In vivo studies showed that MB potentials were recorded in three dogs. After ablation, the duration of P waves remained unchanged. In the other four dogs, MB potentials were not recorded. Computerized mapping showed that LA wavefronts propagated to the MB region via LA-MB connection and then excited the CS. After ablation, the activation of CS muscle sleeves is delayed, and P wave duration increased from 65.3 ± 14.9 msec to 70.5 ± 17.2 msec (P = 0.025). Conclusion: In about half of the normal dogs, MB provides an electrical conduit between LA free wall and CS. Severing MB alters the atrial activation and lengthens the P wave. MB contributes to generation of the P wave on surface ECG.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8167.2002.01283.x
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  • 2
    Electronic Resource
    Electronic Resource
    Aging-Related Increase to Inducible Atrial Fibrillation in the Rat Model (2002)
    Oxford, UK : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 13 (2002), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aging and Atrial Fibrillation. Introduction: Aging is associated with atrial interstitial fibrosis and increased incidence of atrial fibrillation (AF). We hypothesized that aged rats are suitable for study of aging-related AF and that partial atrial cellular uncoupling induced with heptanol in young rats mimics aging-related AF. Methods and Results: Interatrial conduction time and atrial response to burst atrial pacing were evaluated in 11 young (2–3 months) and 12 old (22–24 months) male rats (Fisher 344) in the Langendorff-perfused setting. At baseline, sustained (〉30 sec) atrial tachycardia (AT) and AF were induced in 10 of 12 and in 7 of 12 old rats, respectively. No such arrhythmias could be induced in the young rats. Old rats had significantly (P 〈 0.01) longer interatrial conduction time and P wave durations than the young rats. Burst pacing failed to induce AT and AF in all 11 young rats studied. The effects of heptanol 2 to 10 μM were studied in both groups. Heptanol 2 to 5 μM promoted inducible AT in all 5 young rats studied; however, when its concentration was raised to 10 μM, AT could no longer be induced in any of the 5 young rats. No AF could be induced in any of the 5 young rats at heptanol concentrations of 2 to 10 μM. In the old rats, AF could still be induced during perfusion of 2 μM heptanol. However, when its concentration was raised to 5 and 10 μM, AF could not be induced in any of the 6 old rats studied. Optical mapping using a potentiometric dye showed a periodic single wavefront of activation during AT in both groups and 2 to 4 independent wavefronts propagating in different directions during AF in the old rats. Histology revealed a significant increase in interstitial atrial fibrosis (P 〈 0.01), atrial cell size (P 〈 0.05), and heart weight in old versus young rats. Fibrosis in the old rats was highly heterogeneous. Conclusion: The rat model is suitable for study of aging-related AF. Uniform partial atrial cellular uncoupling with heptanol perfusion in the young rats, although promoting inducible AT, does not mimic aging-related AF. The results suggest that heterogeneous atrial interstitial fibrosis and atrial cell hypertrophy might contribute to the aging-related increase in atrial conduction slowing, conduction block, and inducible AF in the old rat model.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8167.2002.00801.x
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  • 3
    Electronic Resource
    Electronic Resource
    Modulation of QT Interval by Cardiac Sympathetic Nerve Sprouting and the Mechanisms of Ventricular Arrhythmia in a Canine Model of Sudden Cardiac Death (2001)
    Oxford, UK : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 12 (2001), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: QT Interval and Sudden Cardiac Death. Introduction: We previously reported that there is a high incidence of sudden cardiac death (SCD) in dogs with myocardial infarction (MI), complete AV block (CAVB), and nerve growth factor (NGF) infusion to the left stellate ganglion (LSG). Whether or not QT interval prolongation underlines the mechanism of SCD was unclear. Methods and Results: We analyzed QT intervals in three groups of dogs. All dogs had CAVB and MI. The LSG group (n = 9) and right stellate ganglion (RSG) group (n = 6) received NGF infusion via the osmotic pumps over a 5-week period to LSG and RSG, respectively. The control group (n = 6) received no NGF. The dogs either died suddenly or were sacrificed within 2 to 3 months after MI. Heart rhythm and QT and RR intervals were monitored using implantable cardioverter defibrillator ECG recordings. There was a time-dependent increase of QTc intervals in the LSG group and a time-dependent decrease of QTc intervals in the RSG group. At the end of NGF infusion, QTc intervals in the LSG group (408 ± 41 msec) were significantly longer than those in the control (350 ± 41 msec; P 〈 0.05) and RSG groups (294 ± 23 msec; P 〈 0.01). In the LSG group, 4 of 9 dogs died of SCD. There was no SCD in either the RSG or control group. Immunocytochemical staining showed NGF infusion to LSG and RSG resulted in left and right ventricular sympathetic nerve sprouting and hyperinnervation, respectively. Conclusion: NGF infusion to the LSG in dogs with MI and CAVB resulted in increased QT interval and incidence of ventricular tachycardia, ventricular fibrillation, and SCD, whereas NGF infusion to the RSG shortened QT interval and reduced the incidence of ventricular tachycardia. These findings indicate that QT interval prolongation is causally related to the occurrence of ventricular arrhythmia in dogs with nerve sprouting, MI, and CAVB.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8167.2001.01068.x
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  • 4
    Electronic Resource
    Electronic Resource
    Marshall Bundle and the Valve of Vieussens (2003)
    350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 14 (2003), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8167.2003.03245.x
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  • 5
    Electronic Resource
    Electronic Resource
    Low-Affinity Nerve Growth Factor Receptor p75NTR Immunoreactivity in the Myocardium with Sympathetic Hyperinnervation (2004)
    350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 15 (2004), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Introduction: We previously demonstrated the relationship between sympathetic nerve density in myocardium and the occurrences of ventricular arrhythmia. Nerve growth factor (NGF) regulates myocardial sympathetic innervation. However, it is unclear whether the NGF high-affinity receptor tyrosine kinase A (TrkA) and the NGF low-affinity receptor p75NTR are altered in the state of sympathetic hyperinnervation in the heart. The aim of this study was to determine the density and location of TrkA and p75NTR in canine ventricles with sympathetic hyperinnervation. Methods and Results: Myocardial sympathetic hyperinnervation was induced by local infusion of NGF into myocardium or left stellate ganglia, or chronic subthreshold electric stimulation to the left stellate ganglia. The results showed that TrkA immunoreactivity was absent in the myocardium. Low-affinity receptor p75NTR immunoreactivity was present in axons, Schwann cells, and interstitial cells of sympathetic nerves, as well as in interstitial cells of the myocardium. The density of p75NTR immunolabeled myocardial interstitial cells at the NGF infusion site was lower than that at the site remote from NGF infusion, yet the sympathetic nerve density was higher at the infusion site than the remote area. The density of p75NTR also was lower in the myocardium with high sympathetic nerve density, induced by NGF infusion or chronic electric stimulation of the left stellate ganglia, compared to control groups. Conclusion: The data indicate that p75NTR may be the main NGF receptor in the myocardium, and p75NTR immunopositive interstitial cells may have a role in regulating sympathetic nerve growth in canine heart. (J Cardiovasc Electrophysiol, Vol. 15, pp. 430-437, April 2004)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8167.2004.03517.x
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  • 6
    Electronic Resource
    Electronic Resource
    Mesenchymal Stem Cell Injection Induces Cardiac Nerve Sprouting and Increased Tenascin Expression in a Swine Model of Myocardial Infarction (2003)
    350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 14 (2003), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Introduction: Mesenchymal stem cell (MSC) transplantation is a promising technique to improve cardiac function. Whether MSC can increase cardiac nerve density and contribute to the improved cardiac function is unclear. Methods and Results: Anterior wall myocardial infarction was created in 16 swine. One month later, 6 swine were given MSC and fresh bone marrow (BM) into infarcted myocardium (MSC group). Four swine were given fresh BM only (BM group), and 6 swine were given culture media (MI-only group). The swine were sacrificed 95.8 ± 3.5 days after MI. Six normal swine were used as control. Immunocytochemical staining was performed using antibodies against growth-associated protein 43 (GAP43), tyrosine hydroxylase (TH), and three subtypes of tenascin (R, C, and X). Five fields per slide were counted for nerve density. The results show the following. (1) There were more GAP43-positive nerves in the MSC group than in the BM, MI-only, or Control group (P 〈 0.0001). TH staining showed higher nerve densities in the MSC group than in the MI-only (P 〈 0.01) or Control group (P 〈 0.0001) in the atria. (2) There were more sympathetic (TH-positive) nerves in myocardium distant from infarct than in the peri-infarct area (P 〈 0.05). (3) Optical intensity and color analyses showed significantly higher tenascin R and tenascin C expression in the MSC and BM groups than in the MI-only or Control group (P 〈 0.01). Conclusion: MSC injected with BM into swine infarct results in overexpression of cardiac tenascin, increased the magnitude of cardiac nerve sprouting in both atria and ventricles, and increased the magnitude of atrial sympathetic hyperinnervation 2 months after injection. (J Cardiovasc Electrophysiol, Vol. 14, pp. 841-848, August 2003)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8167.2003.03124.x
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  • 7
    Electronic Resource
    Electronic Resource
    Relation Between Cellular Repolarization Characteristics and Critical Mass for Human Ventricular Fibrillation (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 10 (1999), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Critical Mass for Human Ventricular Fibrillation. Introduction: The critical mass for human ventricular fibrillation (VF) and its electrical determinants are unclear. The goal of this study was to evaluate the relationship between repolarization characteristics and critical mass for VF in diseased human cardiac tissues. Methods and Results: Fight native hearts from transplant recipients were studied. The right ventricle was immediately excised, then perfused (n = 6) or superfused (n = 2) with Tyrode's solution at 36° C. The action potential duration (APD) restitution curve was determined by an S1-S2 method. Programmed stimulation and burst pacing were used to induce VF. In 3 of 8 tissues, 10 μM cromakalim, au ATP-sensitive potassium channel opener, was added to the perfusate and the stimulation protocol repeated. Results show that, at baseline, VF did not occur either spontaneously or during rewarming, and it could not he induced by aggressive electrical stimulation in any tissue. The mean APD at 90% depolarization (APD90) at a cycle length of 600 msec was 227 ± 49 msec, and the mean slope of the APD restitution curve was 0.22 ± 0.08. Among the six tissues perfused, five were not treated with any antiarrhythmic agent. The weight of these five heart samples averaged 111 ± 23 g (range 85 to 138). However, after cromakalim infusion, sustained VF (〉 30 min in duration) was consistently induced. As compared with baseline in the same tissues, cromakalim shortened the APD90 from 243 ± 32 msec to 55 ± 18 msec (P 〈 0.001) and increased the maximum slope of the APD restitution curve from 0.24 ± 0.11 to 1.43 ± 0.10 (P 〈 0.01). Conclusion: At baseline, the critical mass for VF in diseased human hearts in vitro is 〉 111 g. However, the critical mass for VF can vary, as it can he reduced by shortening APD and increasing the slope of the APD restitution curve.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1999.tb00280.x
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  • 8
    Electronic Resource
    Electronic Resource
    Induction of Atrial Fibrillation and Nerve Sprouting by Prolonged Left Atrial Pacing in Dogs (2003)
    350 Main Street , Malden , MA 02148-5018 , U.S.A . : Blackwell Publishing
    Pacing and clinical electrophysiology 26 (2003), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The authors hypothesized that rapid electrical stimulation can induce nerve sprouting in canine atria, and that LA pacing is more effective than RA pacing in inducing sustained AF. Chronic rapid (20 Hz) LA epicardial pacing was performed in six dogs. Sustained AF (〉48 hours) was induced within 23 ± 8 days, which was much faster than that with RA endocardial pacing using the same protocol (139 ± 84 days, P 〈 0.05). Nerves were identified by immunocytochemical techniques. In all dogs, growth-associated protein 43-positive (sprouting) nerve density was highest near the pacing site, and the rapid LA pacing resulted in differential nerve sprouting among the LA, left superior pulmonary vein (LSPV), interatrial septum (IAS), and RA (5521 ± 1496, 3154 ± 2355, 3953 ± 1164, 1559 ± 1077 μm2/mm2, respectively, P = 0.0032). Tyrosine hydroxylase-positive (sympathetic) nerve density were not significantly different among groups (2726 ± 1165, 1586 ± 558, 2156 ± 1741, 1509 ± 1242 μm2/mm2, respectively). The nerves were inhomogeneously distributed. LA epicardial pacing induced sustained AF much faster than RA endocardial pacing and rapid electrical stimulation can induce inhomogeneous nerve sprouting near the pacing site. (PACE 2003; 26:2247–2252)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8159.2003.00355.x
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  • 9
    Electronic Resource
    Electronic Resource
    Brown adipose tissue in cancer patients: Possible cause of cancer-induced cachexia (1986)
    Springer
    Journal of cancer research and clinical oncology 111 (1986), S. 82-85 
    Details
    ISSN: 1432-1335
    Keywords: Brown adipose tissue ; Cachexia ; Cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cachexia is a common manifestation of advanced cancer and frequently contributes to physical disability and mortality. An increased metabolic rate has been suggested to be one of the causes of cancer-induced cachexia, although the mechanisms producing this hypermetabolism remain unclear. The presence and activation of brown adipose tissue, a highly thermogenic tissue, may result in a hypermetabolic state and be partially responsible for weight loss in cancer patients. To investigate this hypothesis, we examined necropsy samples of peri-adrenal tissues using light microscopy to identify the prevalence of brown adipose tissue in 25 cachectic patients who died from cancer and 15 age-matched subjects who died from other illnesses. Brown adipose tissue was observed in 20 of the cancer patients (80%) compared to 2 of the age-matched subjects (13%). Therefore, our preliminary results indicate that a high prevalence of brown adipose tissue is associated with cancer-induced cachexia and may reflect an abnormal mechanism responsible for profound energy expenditure and weight loss.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00402783
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  • 10
    Electronic Resource
    Electronic Resource
    Cooling System Permits Effective Transcutaneous Ultrasound Clot Lysis In Vivo Without Skin Damage (1998)
    Springer
    Journal of thrombosis and thrombolysis 6 (1998), S. 125-131 
    Details
    ISSN: 1573-742X
    Keywords: clot dissolution ; ultrasound ; cooling system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous in vivo studies have shown that transcutaneous ultrasound enhances clot dissolution in the presence of either streptokinase or microbubbles. However, ultrasound-induced skin damage has been a major drawback. The objective was to evaluate the effect of a cooling system to prevent the skin damage that has heretofore been associated with transcutaneous low-frequency, high-intensity ultrasound clot dissolution. After thrombi were induced in both iliofemoral arteries in 15 rabbits, streptokinase (25,000 U/kg) was given intravenously and dodecafluoropentane was injected slowly (2 mL/15 min) through an infusion catheter into the abdominal aorta. One iliofemoral artery was randomized to receive ultrasound treatment, and the contralateral artery was treated as a control (receiving streptokinase and dodecafluoropentane alone). In six rabbits (group 1), the skin below the ultrasound transducer was protected by the use of a balloon cooling system, and in the other nine rabbits (group 2), ultrasound was used without a cooling system. Seven of nine (78%) arteries treated without the cooling system, and six of six (100%) arteries treated with the cooling system were angiographically recanalized after ultrasound + streptokinase + dodecafluoropentane treatment. Thermal damage was present in the skin and soft tissues of all nine rabbits treated without a cooling system. However, the skin and soft tissues were grossly and histologically normal in the six rabbits in which the transcutaneous ultrasound was used with the cooling system. Low-frequency, high-intensity ultrasound energy can be delivered transcutaneously for clot dissolution without concomitant tissue damage when coupled with the use of a cooling system to prevent thermal injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1008801605451
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