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Biomedical subjects

D E Haines

Publications and source records attributed to D E Haines.

At least 19 recordsLinked to original sources

Electrocardiographic abnormalities after radiofrequency catheter ablation of accessory bypass tracts in the Wolff-Parkinson-White syndrome.

Repolarization abnormalities on surface electrocardiograms have been described after loss of ventricular preexcitation in some patients with the Wolff-Parkinson-White syndrome. Radiofrequency catheter ablation of overt accessory pathways provides a unique opportunity to study this phenomenon. In this study, serial electrocardiograms were obtained before and after radiofrequency ablation of manifest accessory pathways in 19 patients, of concealed accessory pathways in 6 and after radiofrequency atrioventricular nodal modification in 12. Seven patients undergoing manifest right-sided accessory pathway ablation had left superior frontal plane T-wave axis deviations after ablation (-42 +/- 13 degrees). No patient with a manifest left-sided or concealed accessory pathway, or atrioventricular nodal modification had T-wave abnormalities after ablation; however, left anterior fascicular block and incomplete right bundle branch block each occurred in 1 patient with left accessory pathway ablation. Repolarization abnormalities observed after ablation were similar to T-wave abnormalities during the absence of preexcitation before ablation and persisted up to 5 weeks after the procedure. Patients with repolarization abnormalities after ablation had significantly longer preexcited QRS durations than those without such changes, suggesting that the initial contribution of the pathway to ventricular activation is an important determinant of T-wave changes after ablation. The proposed mechanism for repolarization abnormalities after ablation is the phenomenon of T-wave "memory."

Atrioventricular Node

Does a posterior aneurysm increase the risk of endocardial resection?

The bias has been that the ideal anatomic circumstance for endocardial resection is the anterior left ventricular location. Posterior left ventricular aneurysms have been thought to be problematic to map and more difficult to close, and possibly to have a different substrate for ventricular tachycardia. To address this problem, we retrospectively reviewed the cases of 110 consecutive patients who underwent sequential endocardial resection for ventricular tachycardia between 1983 and 1991. Ninety-six patients had an anterior aneurysm, and 14 patients had a posterior aneurysm or infarct. Operative survival and 5-year survival were very similar between the two groups (p = not significant). A positive postoperative electrophysiological study was present in 11% of the anterior group versus 14% of the posterior group (p = not significant). There was a significantly greater incidence of mitral valve replacement in the posterior group, and we believe this was most likely due to frequent localization of the arrhythmia to the papillary muscle. Otherwise, patients with a posterior aneurysm or infarct had surgical results equivalent to those in patients with an anterior location. As long as there is a discrete aneurysm or infarct, endocardial resection is a safe and effective therapeutic procedure for ventricular tachycardia.

Endocardium

Thermal ablation of perfused porcine left ventricle in vitro with the neodymium-YAG laser hot tip catheter system.

Catheter ablation in the treatment of arrhythmias has been limited by the small lesion size achievable with a radiofrequency energy source. The feasibility of catheter ablation with a neodymium-yttrium-aluminum-garnet (Nd-YAG) laser hot tip catheter was tested because of the capability of achieving a high catheter-tissue contact temperature, which should result in a larger lesion. In a model of isolated perfused pig hearts, 77 endocardial lesions were produced with powers of 1 to 10 watts and peak measured temperatures of 40 degrees to 318 degrees C. Lesion size correlated with power and temperature, but the correlations were poor. High temperature lesions resulted in significant intramyocardial catheter penetration and only marginal increased lesion width. Catheter ablation with a Nd-YAG laser hot tip catheter is feasible, but carries a risk of perforation at high powers. High temperatures result in tissue dessication with a resultant fall in thermal conductivity that limits the radius of thermal injury and overall lesion size.

Animals

Adenosine and verapamil-sensitive ventricular tachycardia originating from the left ventricle: radiofrequency catheter ablation.

A ventricular tachycardia (VT) with right bundle branch block (RBBB) QRS morphology and left axis originating from the inferoapical segment of the left ventricle is described in a 49-year-old man without structural heart disease. This VT could be initiated during isoproterenol infusion and was terminated with intravenous administration of adenosine and verapamil. Radiofrequency ablation eliminated the tachycardia. Previous reports have suggested reentry as the mechanism for a verapamil-sensitive VT with this ECG morphology, while cAMP-mediated triggered activity has been proposed as a mechanism for VTs sensitive to adenosine. The latter more typically arise in the right ventricular outflow tract. The electrophysiological and electropharmacological characteristics of the tachycardia in this patient suggest that this VT morphology is not specific for a mechanism but rather for the location of the site of origin.

Adenosine

Failure of a second and third generation implantable cardioverter defibrillator to sense ventricular tachycardia: implications for fixed-gain sensing devices.

Failure to sense ventricular tachycardia and/or ventricular fibrillation by implantable cardioverter defibrillators (ICDs) is rare. We report a case in which persistent undersensing of monomorphic and polymorphic ventricular tachycardia occurred with a second and third generation ICD using fixed-gain sensing. This occurred despite adequate R wave sensing during sinus rhythm. The use of an endocardial sensing lead did not correct the problem. Failure to sense ventricular tachycardia in the third generation device with fixed-gain sensing occurred late after implantation and was discovered only at follow-up electrophysiology testing of the ICD. This problem could not be corrected by reprogramming of the device, and was not related to lead dislodgement. Placement of a new device with an automatic-gain sensing algorithm and use of previously implanted epicardial leads with better sensing characteristics provided appropriate sensing of ventricular tachyarrhythmias. The case illustrates the importance of testing the sensing of all ventricular arrhythmias in patients with fixed-gain ICD's. Follow-up electrophysiology testing and evaluation of epicardial and endocardial leads may be necessary in certain cases to ensure adequate sensing of ventricular tachyarrhythmias late after implantation.

Algorithms

The hypothalamo-cerebellar projection in the rat: origin and transmitter.

Hypothalamic neurons projecting to cerebellum were identified by retrograde tracing with wheat germ agglutinin-horseradish peroxidase (WGA-HRP) in the rat. Selective D-[3H]aspartate labelling was used to investigate whether any of these connections may use excitatory amino acids as transmitters. The WGA-HRP experiments revealed that the hypothalamo-cerebellar fibers have their main origins in the lateral, dorsal and posterior hypothalamic areas, and the tubero-mammillary nucleus, while smaller numbers of cells were observed in tuber cinereum, the anterior hypothalamic area, and the periventricular and paraventricular nuclei. After injections of D-[3H]aspartate into the cerebellar cortex, intense labelling of the olivocerebellar climbing fiber system was observed, but hypothalamic cells were not retrogradely labelled with this selective tracer. The absence of D-[3H]aspartate labelling indicates that hypothalamo-cerebellar neurons lack specific uptake mechanisms for excitatory amino acids, but it does not entirely preclude the possibility that some of these hypothalamic neurons may use such transmitters. Many cerebellar projecting cells were located in the tubero-mammillary nucleus, which is known to contain histaminergic and GABAergic neurons, and it was concluded that part of the hypothalamo-cerebellar pathways may use histamine and/or GABA as transmitters. The transmitter remains unknown for other parts of the hypothalamo-cerebellar pathways.

Afferent Pathways

The contributors to Volume 1 (1891) of The Journal of Comparative Neurology: C.L. Herrick, C.H. Turner, H.R. Pemberton, B.G. Wilder, F.W. Langdon, C.J. Herrick, C. von Kupffer, O.S. Strong, T.B. Stowell.

The concept of a truly innovative "neurology" journal germinated in the mind of Clarence Luther Herrick and then flowered, in March of 1891, as the first issue of Volume 1 of The Journal of Comparative Neurology. The other parts appeared in June, October, and December of the same year. The contributors to this volume, and their affiliations, were: C.L. Herrick (University of Cincinnati-UC), C.H. Turner (UC), B.G. Wilder (Cornell), F.W. Langdon (Miami Medical College, Cincinnati), C.J. Herrick (UC) H.R. Pemberton (Princeton), T.B. Stowell (State Normal and Training School, Potsdam), and O.S. Strong of Columbia who translated a large paper by Carl von Kupffer, the famous German anatomist. In 1890-91 some of these scientists (e.g., Wilder, Langdon, Stowell, von Kupffer) were well known and had already made notable contributions in their chosen fields. However, several were students (e.g., Turner, C.J. Herrick, Pemberton, Strong), most of whom would make important contributions in later years. The founder of JCN, Clarence Luther Herrick, by 1891 had an excellent reputation in geology and natural science and had already established a successful scientific journal. Based on the totality of their contributions, the authors of the papers that made up Volume 1 of JCN were a unique group. Textbooks that went through several editions came from Wilder, C.J. Herrick, and Strong; the latter is currently going into its 9th edition. Structures were named in recognition of the original descriptions by von Kupffer and C.L. Herrick, a type of insect behavior recognized Turner's discovery, and after their deaths several had university buildings, one a scientific club, and one a research award, named in their honor. There were also interesting and important links between these nine men. Turner and C.J. Herrick were students of C.L. Herrick, and Stowell served as a member of the Association of American Anatomists nomenclature committee which was chaired by Wilder. C.J. Herrick became a student (for his Ph.D.) of Strong's, and Strong became an associate editor of JCN under C.J. Herrick. Of the nine, two practiced medicine; Langdon in an academic setting, Pemberton in private practice. The lives of the nine scientists whose work made up Volume 1 of JCN are reviewed. Many of these individuals were notable, not only for their work in the first volume of JCN, but for their larger and enduring contributions in the biomedical sciences.

Anatomy, Comparative

On the question of a subdural space.

The structure of the meninges, with particular attention to the architecture of the inner portions of the dura mater and the arachnoid mater, has been reviewed in reference to the probable existence of a "subdural" space. The dura is composed of fibroblasts and large amounts of extracellular collagen. The innermost part of the dura is formed by the dural border cell layer. This layer is characterized by flattened cells with sinuous processes, extracellular spaces containing an amorphous material, and the presence of junctions between its cells. The dural border cell layer is continuous with the inner (meningeal) portions of the dura and may be attached to the underlying arachnoid by an occasional cell junction. The arachnoid consists of an outer part, the arachnoid barrier cell layer, and an inner portion, the arachnoid trabeculae which bridge the subarachnoid space. Arachnoid barrier cells are electron-lucent, closely apposed to each other, and joined by many cell junctions; in this layer there is little extracellular space and essentially no intercellular material. Arachnoid trabecular cells cross the subarachnoid space in a random manner, have extracellular collagen associated with their flattened processes, and form structures of variable shapes and sizes. There is no evidence of an intervening space between the arachnoid barrier cell layer and the dural border cell layer that would correlate with what has been called the subdural space. When a tissue space is created in this general area of the meninges it is the result of tissue damage and represents, in most instances, a cleaving open of the dural border cell layer. In this situation, extracellular spaces in the dural border cell layer are enlarged, cell junctions are separated, and it is probable that cell membranes are damaged. A survey of reports describing the morphology of the inner and outer capsule of so-called subdural hematomas in humans reveals that dural border cells are found in both parts of the capsule. Also, experimental infusion of blood into this portion of the meninges in animals frequently dissects open the dural border cell layer. These data support the view that what has been called a subdural hematoma is most frequently a lesion found within the layer formed by dural border cells. It is suggested that the so-called subdural space is not a "potential" space since the creation of a cleft in this area of the meninges is the result of tissue damage. In this respect it shares no similarities with legitimate potential spaces (i.e., serous cavities) found at other locations in the body.(ABSTRACT TRUNCATED AT 400 WORDS)

Arachnoid

Evidence of an x zone in lobule V of the squirrel monkey (Saimiri sciureus) cerebellum: the distribution of corticonuclear fibers.

The distribution of corticonuclear fibers to medial-most parts of the posterior interposed nucleus (NIP) from lateral areas of the vermis was studied in the squirrel monkey (Saimiri sciureus), using a silver impregnation method. The origin and course of degenerated fibers were studied in serial sections. The distribution pattern of corticonuclear fibers from a series of small well localized lesions placed in the vermis and paravermal cortex of lobule V is compatible with the interpretation that an x zone is present in Saimiri. A comparison of the positions of lesions and the trajectory of fibers arising therein suggests that corticonuclear input to medial-most parts of the NIP originated from a narrow cortical area (about 0.5-0.7 mm wide) located between a cortical area projecting into the medial cerebellar nucleus (the A zone) and a laterally adjacent area (the B zone) which related to the lateral vestibular nucleus. This NIP-projecting cortical area, located about 1.7 mm to 2.5 mm off the midline in lobule V, is interpreted as the x zone in this primate; it extends from lobule IV into lobule VI in squirrel monkey. Corticonuclear fibers of zone x in this primate form a comparatively small terminal field in the medial-most portions of NIP. This contrasts with the distribution of corticonuclear fibers of the C2 zone which consistently distribute to terminal fields that are shifted into more central areas of NIP. There appears to be no overlap of the corticonuclear terminal fields in the NIP for zone x versus the C2 zone. These results were correlated with data from the literature on the distribution of olivocerebellar fibers to the x zone and the C2 zone and the arrangement of cerebellar nucleoolivary projections into the inferior olive from the NIP. The x zone and the C2 zone both receive input from the contralateral medial accessory olive (MAO), both zones project into the NIP, and the NIP projects into those regions of the MAO which, in turn, project to these respective cortical zones and into the NIP. This suggest that the x zone is a component of the NIP-MAO circuit. Furthermore the proposed function of the x zone would support the view that this sagittal strip may have a more extensive rostrocaudal distribution in primates as compared to the cat.

Animals

The influence of preoperative shock on outcome in sequential endocardial resection for ventricular tachycardia.

Sequential endocardial resection was used in 92 consecutive patients to treat ventricular tachycardia. All patients had coronary artery disease with previous myocardial infarction. All patients had repeated cycles of mapping and resection of arrhythmogenic foci in the normothermic beating heart until ventricular tachycardia was no longer inducible. Eighty-six patients (93%) survived to hospital discharge. The survival rate in patients normotensive at the time of operation was 98% and in patients in shock at the time of operation, 43%. By Cox regression analysis, preoperative shock was the significant predictor (p less than 0.001) of operative mortality. Seventy-four of the 86 operative survivors (86%) had no sustained ventricular tachycardia at initial postoperative electrophysiologic study when receiving no antiarrhythmic drugs. Eighty-three of the 86 operative survivors (97%) had no sustained ventricular tachycardia at final postoperative electrophysiologic study when using antiarrhythmic drugs as needed. After a median follow-up of 21 months (range 1 to 79 months) there were 4 sudden cardiac deaths, 12 other cardiac deaths, and 3 noncardiac deaths. There were no documented nonfatal episodes of sustained monomorphic ventricular tachycardia after hospital discharge. Use of the sequential endocardial resection technique is effective in curing ventricular tachycardia with low operative morbidity and mortality.

Adult

Neuronal connections between the cerebellar nuclei and hypothalamus in Macaca fascicularis: cerebello-visceral circuits.

The purpose of this study was to identify the basic pattern of interconnections between the cerebellar nuclei and hypothalamus in Macaca fascicularis. The distribution of retrogradely labeled cells and anterogradely filled cerebellofugal axons in the hypothalamus of M. fascicularis was investigated after pressure injections of a horseradish peroxidase mixture (HRP + WGA-HRP) in the cerebellar nuclei. Following injections in the lateral, anterior, and posterior interposed cerebellar nuclei retrogradely labeled cells were present in the following areas (greatest to least concentration): lateral and dorsal hypothalamic areas, dorsomedial nucleus, griseum periventriculare hypothalami, supramammillary and tuberomammillary nuclei, posterior hypothalamic area, ventromedial nucleus and periventricular hypothalamus, around the medial mammillary nucleus, lateral mammillary nucleus, and infundibular nucleus. Cell labeling was bilateral with an ipsilateral preponderance. In these same experiments anterogradely labeled cerebellar efferent fibers terminated in the contralateral posterior, dorsal and lateral hypothalamic areas, and the dorsomedial nucleus. In these regions retrogradely labeled hypothalamic cells were occasionally found in areas that also contained anterogradely filled cerebellar axons. This suggests a partial reciprocity in this system. In addition, sparse numbers of labeled cerebellar fibers recross in the hypothalamus to distribute to homologous areas ipsilateral to the injection site. Subsequent to an injection in the medial cerebellar nucleus (NM), cell labeling was present in more rostral hypothalamic levels including the lateral and dorsal hypothalamic areas, the dorsomedial nucleus, around or in fascicles of the column of the fornix, and in the periventricular hypothalamic area. Although no fastigiohypothalamic fibers were seen in this study, on the basis of information available from the literature it is likely that such a connection exists in primates. In summary, hypothalamic projections to NM originated mainly from rostral to midhypothalamic levels, whereas those projections to the lateral three cerebellar nuclei came from mid and more caudal levels. The existence of direct hypothalamic projections to cerebellar nuclei in M. fascicularis and of cerebellofugal projection to some hypothalamic centers indicates that circuitry is present through which the cerebellum may influence visceral functions. Furthermore, the fact that projections to NM versus the other cerebellar nuclei originate from somewhat different regions of the hypothalamus would suggest that the visceral functions modulated by each pathway is not the same.

Animals

Sustained intraatrial reentrant tachycardia: clinical, electrocardiographic and electrophysiologic characteristics and long-term follow-up.

Although intraatrial reentry has been traditionally listed as a mechanism for supraventricular tachycardia, few reports describing the clinical features of this arrhythmia exist. Nineteen patients with a clinical history of sustained supraventricular tachycardia were diagnosed as having intraatrial reentrant tachycardia. Seventeen (89%) patients of the 19 had underlying structural heart disease and 17 had echocardiographic evidence of atrial enlargement; the mean left ventricular ejection fraction was 51 +/- 16%. A history of concomitant atrial fibrillation or flutter was present in 13 patients (68%). The mean atrial cycle length during tachycardia was 326 +/- 57 ms (range 260 to 460). Fourteen patients had 1:1 atrioventricular (AV) conduction during tachycardia, of whom 50% had an RP'/RR' ratio greater than 0.5. Intravenous adenosine (dose range 37.5 to 150 micrograms/kg) and verapamil (dose range 5 to 10 mg) had no effect on atrial tachycardia cycle length in 13 of 14 and 9 of 9 patients, respectively, despite induction of second degree AV block. Type 1a antiarrhythmic drugs achieved long-term suppression of intraatrial reentrant tachycardia in only 6 patients, whereas amiodarone (326 +/- 145 mg/day) was successful in 11 patients during a 32 +/- 20 month follow-up period. The remaining two patients and one patient who later developed amiodarone toxicity either progressed to (n = 1) or had (n = 2) catheter-induced high grade AV block and were treated with long-term ventricular pacing. It is concluded that intraatrial reentrant tachycardia is often associated with structural heart disease, particularly of types that cause atrial abnormalities, but left ventricular dysfunction is not a requisite finding. Other arrhythmias are frequently observed in these patients. This arrhythmia responds poorly to type 1a antiarrhythmic drugs, but is effectively treated with amiodarone. Catheter ablation of the AV junction offers a therapeutic option for patients who are refractory to medical therapy.

Adenosine

Observations on electrode-tissue interface temperature and effect on electrical impedance during radiofrequency ablation of ventricular myocardium.

The purpose of this study was to correlate changes in electrical impedance with the electrode-tissue interface temperature and to characterize the associated events occurring at the catheter tip electrode. In a canine model, lesions were created in vitro (n = 49) and in vivo (n = 31) and radiofrequency power settings were varied. Electrode-tissue interface temperature, delivered current, and voltage were recorded, and impedance was calculated. A sudden rise in electrical impedance was seen in only two of 17 ablations in vitro and in one of 16 ablations in vivo with a peak electrode-tissue interface temperature of less than 100 degrees C compared with 29 of 32 ablations in vitro (p = 0.0001) and 12 of 15 ablations in vivo with a temperature of more than 100 degrees C (p = 0.0001). This phenomenon was associated with the observation of boiling and popping at the tip in in vitro preparations and tissue avulsion and thrombus formation on the catheter tip in in vivo studies. The lesion size was directly proportional to the peak temperature for all ablations but not to the peak power, current, or voltage during radiofrequency catheter ablation in the heart. Maintaining electrode-tissue interface temperature at less than 100 degrees C during radiofrequency catheter ablation in the heart may avoid the complications associated with the sudden rise in electrical impedance.

Animals

Electrode radius predicts lesion radius during radiofrequency energy heating. Validation of a proposed thermodynamic model.

Myocardial heating by transcatheter delivery of radiofrequency (RF) energy has been proposed as an effective means of arrhythmia ablation. A thermodynamic model describing the radial temperature gradient at steady state during RF-induced heating is proposed. If one assumes that RF power output is adjusted to maintain a constant electrode-tissue interface temperature at all times, then this thermodynamic model predicts that the radius of the RF-induced lesion will be directly proportional to the electrode radius. A total of 76 RF-induced lesions were created in a model of isolated canine right ventricular free wall perfused and superfused with oxygenated Krebs-Henseleit buffer. Electrode radius was varied between 0.75 and 2.25 mm. RF energy (500 kHz) was delivered for 90 seconds, and the power output was adjusted to maintain a constant electrode-tissue interface temperature of 60 degrees C. A strong linear correlation was observed between electrode radius and lesion radius in two dimensions: transverse (p = 0.0001, r = 0.85) and transmural (p = 0.0001, r = 0.89). With these data, the temperature correlation with irreversible myocardial injury in this model was calculated at 46.6-48.8 degrees C. Therefore, the proposed thermodynamic model closely predicts the observed relation between electrode radius and lesion size during RF myocardial heating.

Animals

Operative risks of the implantable defibrillator versus endocardial resection.

Both map-guided endocardial resection (ER) and the automatic implantable cardioverter defibrillator (AICD) are currently used for surgical treatment of patients who have sustained ventricular tachyarrhythmias. Some authors have preferred AICD implant due to a lower published operative mortality rate. To determine if there is a discrepancy in mortality rates between the two techniques, we analyzed hospital survival in 46 patients undergoing ER and in 44 patients undergoing AICD implantation during the same 3-year period. Two ER patients (4%) died before hospital discharge. Two patients (4%) died after AICD implantation. At predischarge electrophysiologic study five patients (11%) had inducible ventricular tachycardia and received antiarrhythmic drug therapy after ER. In contrast 35 of 42 patients surviving AICD placement received chronic long-term antiarrhythmic therapy (p less than 0.05 compared to ER). Our experience shows that ER and AICD placement may be carried out with similar procedure-related mortality and morbidity rates. Lower operative risks should not be a reason for choosing the AICD over ER for surgical treatment of ventricular tachyarrhythmias. The AICD may actually improve the results of ER by offering an alternative to ventriculotomy in poor-risk surgical candidates.

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