Critical analysis of autoregressive and fast Fourier transform markers of cardiovascular variability in rats and humans

The autonomic nervous system plays an important role in physiological and pathological conditions, and has been extensively evaluated by parametric and non-parametric spectral analysis. To compare the results obtained with fast Fourier transform (FFT) and the autoregressive (AR) method, we performed a comprehensive comparative study using data from humans and rats during pharmacological blockade (in rats), a postural test (in humans), and in the hypertensive state (in both humans and rats). Although postural hypotension in humans induced an increase in normalized low-frequency (LFnu) of systolic blood pressure, the increase in the ratio was detected only by AR. In rats, AR and FFT analysis did not agree for LFnu and high frequency (HFnu) under basal conditions and after vagal blockade. The increase in the LF/HF ratio of the pulse interval, induced by methylatropine, was detected only by FFT. In hypertensive patients, changes in LF and HF for systolic blood pressure were observed only by AR; FFT was able to detect the reduction in both blood pressure variance and total power. In hypertensive rats, AR presented different values of variance and total power for systolic blood pressure. Moreover, AR and FFT presented discordant results for LF, LFnu, HF, LF/HF ratio, and total power for pulse interval. We provide evidence for disagreement in 23 percent of the indices of blood pressure and heart rate variability in humans and 67 percent discordance in rats when these variables are evaluated by AR and FFT under physiological and pathological conditions. The overall disagreement between AR and FFT in this study was 43 percent.

Critical analysis of autoregressive and fast Fourier transform markers of cardiovascular variability in rats and humans.

The autonomic nervous system plays an important role in physiological and pathological conditions, and has been extensively evaluated by parametric and non-parametric spectral analysis. To compare the results obtained with fast Fourier transform (FFT) and the autoregressive (AR) method, we performed a comprehensive comparative study using data from humans and rats during pharmacological blockade (in rats), a postural test (in humans), and in the hypertensive state (in both humans and rats). Although postural hypotension in humans induced an increase in normalized low-frequency (LFnu) of systolic blood pressure, the increase in the ratio was detected only by AR. In rats, AR and FFT analysis did not agree for LFnu and high frequency (HFnu) under basal conditions and after vagal blockade. The increase in the LF/HF ratio of the pulse interval, induced by methylatropine, was detected only by FFT. In hypertensive patients, changes in LF and HF for systolic blood pressure were observed only by AR; FFT was able to detect the reduction in both blood pressure variance and total power. In hypertensive rats, AR presented different values of variance and total power for systolic blood pressure. Moreover, AR and FFT presented discordant results for LF, LFnu, HF, LF/HF ratio, and total power for pulse interval. We provide evidence for disagreement in 23% of the indices of blood pressure and heart rate variability in humans and 67% discordance in rats when these variables are evaluated by AR and FFT under physiological and pathological conditions. The overall disagreement between AR and FFT in this study was 43%.

Second-degree atrioventricular heart block after doxapram administration.

Doxapram, a respiratory stimulant, is used to treat idiopathic apnea of prematurity. The side effects reported are minimal. We present three cases of second-degree atrioventricular block caused by QT interval prolongation associated with doxapram administration. All three infants returned to normal sinus rhythm after doxapram administration was stopped.

Induction of in vitro heart block is not restricted to affinity purified anti-52 kDa Ro/SSA antibody from mothers of children with neonatal lupus.

The ability of affinity purified anti-52 kDa Ro/SSA antibody from patients without obstetric history of neonatal lupus to cause heart block using an experimental model was investigated. IgG-enriched fractions from sera of 20 systemic lupus erythematosus (SLE) and one Sjögren's syndrome (SS) all positives for anti-Ro/SSA antibodies as detected by CIE, were perfused on isolated whole rabbit hearts. Only six (29%) samples induced A-V block, five of them presenting low anti-Ro/SSA titre. All of them recognized the 52 kDa isoform on ELISA whereas only one had a concomitant binding to the 60 kDa protein. Moreover, affinity purified antibodies from two sera previously known to induce A-V block were obtained by affinity chromatography using a column containing the full-length 52 kDa Ro/SSA fusion protein. Paired eluate and effluent devoid of anti-52 kDa activity from the same patient were individually perfused in whole hearts. The ability to cause cardiac blockade was restricted to the affinity anti-52 kDa eluates. In addition, anti-52 kDa eluates from three IgG fractions that primarily failed to induce blockade remained ineffective. The present study has added to our knowledge that affinity anti-52 kDa Ro/SSA antibodies from mothers with healthy infants are capable of causing in vitro cardiac conduction disturbances. A prospective follow up of these patients will better delineate the clinical usefulness of this experimental model.

Use of adenosine for diagnosis and treatment of tachyarrhythmias in pediatric patients.

This report reviews our experience with the use of adenosine for diagnosis and treatment of narrow QRS complex tachyarrhythmias in children. All electrocardiograms obtained since the introduction of adenosine for clinical use at one pediatric tertiary care institution during an 18-month period were reviewed, and those patients receiving adenosine were included for study. Of the 24 patients who received adenosine, the median age was 4 years; four neonates were included. Adenosine produced atrioventricular block in 21 (88%) of 24 patients. It terminated the tachyarrhythmia in 11 patients and produced atrioventricular block but did not terminate the tachyarrhythmia in 10 patients. The mechanism of the arrhythmia was known in three patients before adenosine administration. Adenosine was useful in establishing the mechanism of the tachyarrhythmia in 17 of the remaining 18 patients but was not useful in one patient, in whom the arrhythmia was successfully terminated because a good-quality electrocardiogram was not obtained during adenosine administration. Therefore the mechanism of the supraventricular tachycardia was ultimately determined for all patients in whom adenosine successfully produced atrioventricular block and had acceptable electrocardiographic tracings. Side effects were limited and transient. We conclude that adenosine was a safe and effective agent for the pharmacologic treatment of narrow QRS complex tachyarrhythmias in our patients, including those less than 1 year of age. If proper electrocardiographic recordings are performed during adenosine administration, it is also helpful in establishing the cause of the tachyarrhythmia.

[Cardiac arrhythmia with oral oxamniquine use in the schistosomiasis mansoni treatment]. / Arritmia cardíaca com uso de oxamniquine oral no tratamento de esquistossomose mansônica.

The authors report a case of a patient with schistosomiasis (S. mansoni) treated with one single dose (15 mg/kg/BWT) of oral oxamniquine who presented Mobitz type I second-degree AV block and sinus arrest with ventricular escape as a side-effect. They conclude that in spite of the safety and good activity of oxamniquine it may be a determinant of cardiotoxicity.

[Acute effects of propafenone in patients with ventricular pre-excitation]. / Efeitos agudos da propafenona em pacientes com pré-excitação ventricular.

PURPOSE: To evaluate the electrophysiological effects of intravenous propafenone in the anterograde and retrograde effective refractory period of the accessory pathways (AP), in patients with Wolff-Parkinson-White syndrome. METHODS: Forty symptomatic patients were studied. All patients were undergone to electrophysiologic study at baseline and after IV propafenone (2.0mg/kg). Drug effects were analysed according to the basal state of the anterograde and retrograde effective refractory periods of the AP > < 270ms. RESULTS: The mean anterograde and retrograde effective refractory periods of the AP were 275 +/- 76ms and 264 +/- 44ms at the control and 462 +/- 190ms and 438 +/- 184ms after drug respectively (p < 0.01 in both situations). The mean anterograde effective refractory period of the AV node was 236 +/- 40ms (control) and 276 +/- 57ms (post-drug)- p < 0.05. The mean atrial and right ventricular effective refractory period in the control were 210 +/- 23ms and 240 +/- 34ms passing to 215 +/- 24ms and 250 +/- 40 ms after drug respectively (p = ns). After drug, complete anterograde and retrograde block of the AP, occurred in 15 (42%) and 12 (35%) patients respectively. Out of 15 patients with complete anterograde block of the AP, 11 had anterograde effective refractory period of the AP > 270ms and 4, < 270ms (p < 0.02). Out of 12 patients with complete retrograde block of the AP after drug, 4 had retrograde effective refractory period > 270ms and 8, < 270ms (p: ns). CONCLUSION: Propafenone caused significant increase in the anterograde and retrograde effective refractory periods of the AP. There was a tendency of the drug to show better effectiveness in patients with anterograde effective refractory period of the AP > 270ms. This results were not seen in relation to the retrograde effective refractory period of the AP.

Efeitos agudos da propafenona em pacientes com pré-excitaçäo ventricular / Acute Effects of Propafenone in Patients with Ventricular Pré-Excitation

Objetivo - Avaliar os efeitos agudos da propafenona sobre os períodos refratários anterógrado e retrógrado de vias anômalas (VA). Métodos - Foram estudados 40 apcientes sintomáticos. Por técnica de extra-estímulos, determinaram-se os períodos refratários anterógrado e retrógrado das VA em condiçöes de controle e após 2,0mg/Kg de propafenona IV. Os resultados foram analisados em funçäo dos períodos refratários anterógrado e retrógrado das VA><270ms no controle. Resultados - Período refratário anterógrado médio da VA no controle de 275 ñ 76ms e no pós-droga de 462 ñ 190ms (p < 0,01). Período refratário retrógrado médio da VA no controle de 264 ñ 44ms, passando no pós-droga para 438 ñ 184ms (p < 0,01). Período refratário efetivo anterógrado do nódulo AV no controle de 236 ñ 40ms, passando no pós-droga para 276 ñ 47ms (p < 0,05). Período refratário efetivo atrial no controle de 210 ñ 23ms, passando para 215 ñ 24ms (p = ns). Período refratário efetivo ventricular no controle de 240 ñ 34ms, passando no pós-droga para 250 ñ 40ms (p:ns). Notou-se o aparecimento de bloqueio completo anterógrado e retrógrado da VA no pós-droga em, respectivamente, 15 e 12(42//, 35//) pacientes. Dos 15 pacientes com bloqueio anterógrado da VA no pós-droga, 11 apresentavam período refratário anterógrado da VA>270ms (p<0,02). Dos 12 pacientes com bloqueio completo retrógrado da VA no pós-droga, 4 apresentavam período refratário retrógrado da VA > 270ms e 8,<270ms (p=ns). Conclusäo - A propafenona produziu significativo aumento dos períodos refratários efetivos anterógrado e retrógrado das VA. Observou-se tendência a uma maior açäo frente a períodos refratários efetivos anterógrdos das VA>270ms. Este padräo de resposta näo foi observado em relaçäo aos períodos refratários efetivos retrógrdos da VA

Purpose - To evaluate the electrophysialogical effects of intravenous propafenone in the anterograde and retrograde effective refractory period of the accessory pathways (AP), in patients with WolffParkinson-White syndrome. Methods - Forty symptomatic patients were studied.. All patients were undergone to electrophysiologic study at baseline and after IV propafenone (2.0mg/kg). Drug effects were analysed according to the basal state of the anterograde and retrograde effective refractory periods of the AP><270ms. Results - The mean anterograde and retrograde effective refractory periods of the AP were 275±76ms and 264±44ms at the control and 462±190ms and 438±184ms after drug respectively (p<0.01 in both situations). The mean anterograde effective refractory period of the AV node was 236±40ms (control) and 276±57ms (post-drug )- p<0.05. The mean atrial and right ventricular effective refractory period in the control were 210±23ms and 240±34ms passing to 215±24ms and 250±40ms after drug respectively (p=ns). After drug, complete anterograde and retrograde block of the AP, ocurred in 15 (42°/) and 12 (35°/) patients respectively. Out of 15 patients with complete anterograde block of the AP, 11 had anterograde effective refractory period of the AP>270ms and 4,<270ms (p<0.02). Out of 12 patients with complete retrograde block of the AP after drag, 4 had retrograde effective refractory period >270ms and 8, <270ms (p:ns). Conclusion - Propafenone caused signifcant increase in the anterograde and retrograde effective refractory periods of the AP. There was a tendency of the drug to show better effectiveness in patients with anterograde effective refractory period of the AP>270ms. This results were not seen in relation to the retrograde effective refractory peried of the AP

Verapamil overdose: case report and review of the literature.

OBJECTIVE: To report the presentation and controversies regarding therapy of an 18-year-old man following a life-threatening ingestion of verapamil. CASE SUMMARY: An 18-year-old man ingested large quantities of dipyridamole, trimethoprim/sulfamethoxazole, amoxicillin, and verapamil. He presented to an outlying hospital and was initially conscious. Soon thereafter, the patient had a seizure; he required intubation, developed cardiac conduction abnormalities, and became hypotensive. The patient required pharmacologic pressors and a pacemaker for transfer to our institution. At our institution, vigorous fluid resuscitation, cardiac pacing, and careful attention to acid/base and electrolyte management provided the basis of therapy. The patient recovered without deficit and was discharged from the intensive care unit five days later. DISCUSSION: Current controversies regarding the management of verapamil overdose are reviewed. Removal of the drug by gastric lavage is a mainstay of therapy. Administration of syrup of ipecac is contraindicated. Although specific recommendations for calcium dosing in the overdose situation have not been rigorously studied, maintenance of a normal serum ionized calcium concentration is suggested. An exogenous catecholamine, rather than dopamine, may be the drug of choice for treating hypotension. Cardiopulmonary bypass provides a method for drug removal in cases of severe toxicity; however, this invasive method requires further study. Management of fluid/electrolyte, acid/base, and ventilation abnormalities is required to treat large ingestions of verapamil. Treatment guidelines for critical care clinicians are provided.

Side effects during adenosine thallium imaging with single-port or double-port infusion protocols.

The double-port infusion protocol during adenosine thallium imaging involves the use of two infusion systems, one for adenosine and one for thallium. The single-port infusion protocol, on the other hand, uses one infusion system; both adenosine and thallium are injected via a "Y" connection. This study examined the possibility that the single infusion system, by displacing a column of blood filled with adenosine, may be responsible for a greater incidence of side effects. In a parallel study, 140 patients underwent adenosine thallium imaging with the single-port system (group 1) and 140 patients underwent imaging with the double-port system (group 2). Both groups were comparable in age (67 +/- 10 years vs 64 +/- 11 years), gender (men comprised 56% of patients in group 1 and 64% in group 2), resting heart rate, and systolic blood pressure. More patients in group 1 had chest pains (57% vs 44%; p = 0.03), ST-segment depression (25% vs 9%; p = 0.005), nausea (11% vs 4%; p = 0.04), and second- or third-degree atrioventricular block (11% vs 5%; p less than 0.08) than did patients in group 2. The other side effects were similar, and peak heart rate and peak systolic blood pressure were also similar. The thallium images that used single-photon emission computed tomography were abnormal in 61% of patients in group 1 and in 65% of patients in group 2 (p = not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiotoxic effects of astemizole overdose in children.

Astemizole, a nonsedating antihistamine, caused a prolonged corrected QT interval, ventricular dysrhythmias, and atrioventricular heart block after overdose in five children. Cardiotoxic effects lasted an average of 2 1/2 days. Children poisoned with astemizole need emergent medical evaluation, a 12-lead electrocardiogram with calculation of the corrected QT interval, and continuous cardiac monitoring for 24 hours.

Sección del extracto crudo de tejido atrial (ECTA) sobre la alteración de la conducción del impulso cardiaco inducida por la acepromazina en el perro / Section of raw extract of atrial tissue in alteration of conduction cardiac impulse, induced by acepromazine in dog

En trabajos anteriores demostramos que el PNA en forma de extracto crudo de tejido atrial (ECTA) tiene un efecto preventivo y supresivo sobre los trastornos del ritmo inducidos por la Acepromazina (Ac) en la rata y preventivo en las aritmias por reperfusión canina. El presente trabajo demuestra que la Ac induce en el perro alteraciones del ritmo cardiaco consistentes con una aberrancia de conducción intraventricular, evidencia electrocardiográficamente por una taquicardia con QRS ancho, la cual es revertida con el ECTA. El uso de electrogramas intraesofágicos e intracavitarios permitió identificas el origen sinusal de este trastorno de conducción a la vez que establece la relación atrioventricular 1:1 lo cual es consistente con una taquicardia supraventricular (TSV) con conducción aberrada. El registro de la PA demostro el importante deterioro hemodinamico que acompaña este trastorno electrofisiologico, el que mejora con la administración del ECTA. El presente estudio se inscribe dentro del programa de investigación para el servicio y la docencia de nuestro programa de Maestria de investigación en Ciencias Médicas

Efecto hipotensor de los agonistas dopaminergicos en la rata / Hipotensive effect of dopaminergic agonists on the rat

La Dopamina, Bromocriptina y Apomorfina producen baja de la presión arterial en la rta, pero se ignora de la presión arterial en la rata, pero se ignora si este fenómeno ocurre en el receptor presináptico de la neurona adrenérgica o en el receptor postsináptico de la musculatura lisa vascular. El presente estudio procura identificar el sitio de acción de los tres compuestos. En ratas anestesiadas con uretano ip y con repiración espontánea, se registró la presión arterial intracarotídea y el ECG (DII) antes y durante la inyección iv de Dopamina y Bromocriptina (3.12 a 25 microng/100g en ambas) y Apomorfina (0.125 a 4.0 microng/100 g). Las tres sustancias provocaron una hipotensión dosis-dependiente que fue de mayor magnitud con la Apomorfina. En el ECG de los animales que recibieron Dopamina y Apomorfina se observó bradicardía discreta y en la mayoría de los tratados con Apomorfina, bloqueo aurículo-ventricular. La Bromocriptina no afectó la frecuencia cardiaca, ni la conducción auriculo-ventricular. En una segunda etapa se destruyó la terminación adrenérgica con 6-Hidroxi-Dopamina (6-OH-DA) en dosis de 3.0 mg/100 g i.p. Dos horas después de realizado este procedimiento, se ensayaron las tres sustancias en las dosis descritas, observándose que la Dopamina elevada la presión arterial (p<0.001). La Bromocriptina no la alteraba y la Apomorfina la disminuía sensiblemente. Se concluye que el mecnismo hipotensor observado para las tres sustancias "dopaminérgicas" es de distinta naturaleza. La dopamina requiere de la integridad del receptor presináptico para producir hipotensión, mientras que el caso de...

Repercusiones del infarto experimental de la aurícula derecha sobre P, Ta y QTa / Repercusions of experimental infarction of the right atrial in P, Ta and QTa

Se produjo infarto auricular derecho (AD) en 18 perros, mediante infiltración subepicárdica de alcohol en la cara anterolateral, orejuela derecha y porción derecha de la banda interauricular. Se tomaron múltiples registros con papel fotográfico (VR6) y de inscripción directa (Sanborn 150) de 4 canales a velocidad de 50 y 100mm/seg.: 5 unipolares directas y 19 de superficie, incluyendo torácicas derechas y abdominales MD, ME y MI en condiciones de control, después de la infiltración y 120 minutos más tarde. Al fin de experimento se produjeron extrasístoles en AD (EAD) y bloqueo A-V para determinar, con certeza, la duración del QTa y su fin en el ST ventricular. Hubo disminución de la frecuencia cardiaca, ligero ensanchamiento del P-R y de la onda P y ritmo auricular derecho bajo (4 casos). Los cambios más significativos se observaron el las derivaciones torácicas derechas y a veces hasta V4-V5. El vector de lesión apunta hacia adelante elevando el segmento P-R en las derivaciones mencionadas y en las direchas de AD. Apareció onda Qp o complejos en W en las mismas derivaciones y en D2, D3 y a VF. Los signos tienen más valor en las torácicas sea en ritmo sinusal o AD bajo. El vector de necrosis se aleja de la AD. La onda Ta isquémica se prolongó hasta la irregularidad del ST ventricular, la que también se observaba en los trazos directos y en D2 desde los registros de control. El QT auricular corregido (QTac) se encontró prolongado a VM mayor de + 0.04 seg, siendo más largo en la AD dañada, lo

Duración del QT auricular (QTa) en condiciones normales y sus valoraciones con el daño auricular / Atrial QT (QTa) lenght in normal conditions and its value with the atrial damage

El QT auricular (QTa) fué medido en D2, en las derivaciones torácicas derechas V4R, V3R y V1 y en cinco unipolares auriculares directas en 40 perros. En 30 se produjeron además infarto auricular derecho (18 casos) e izquierdo (12) por infiltración de alcohol de 96-. Se produjeron extrasístoles auriculares y bloqueo A-V, lo que permitió medir el QTa con o sin daño miocárdico. La medición de éste, en los trazos de control se hizo hasta la irregularidad observada en la porción proximal del ST ventricular, por haberse confirmado en las extrasístoles auriculares bloqueadas y en las ondas P sinusales bloqueadas que tal protuberancia correspondía al fin de la sístole eléctrica auricular e inclusive, con P-R más largo, a la muesca terminal del QRS. El QTa corregido para la frecuencia cardiaca puede ser obtenido por la fórmula QTac = 0.32 raiz quadrada (P-P) + ou - 0.02. valores superiores a VM + 0.04 e inclusive de + 0.13 se observaron en el daño miocárdico auricular obteniéndose los valores mayores en la aurícula derecha. La formulación anterior puede dar mayor certeza para la localización del fin de la repolarización auricular normal o patológica así como localizar la zona vulnerable de las aurículas en el ST ventricular

[Mechanisms of conduction disorders in digitalis poisoning]. / Mecanismos de los trastornos del automatismo en la intoxicación digitálica.

Ever since the first papers on the mechanism of the arrhythmias of digitalis were first published, during the first two decades of this century, the issue has been a controversial one. Since the automaticity induced by digitalis intoxication has different characteristics when compared to normal automaticity, it has been suggested that probably the mechanisms for these two types of spontaneous activity are different. It has been recently proposed that the automaticity induced by digitalis intoxication could be secondary to the after potential oscillations described in isolated conducting fibers. In order to test this hypothesis we used two experimental models which allow for a careful analysis of the ectopic activity, without the interference of the sinus rhythm. These studies were done in two groups of animals: one, with electrically isolated atria, was used to analyze supraventricular arrhythmias. The other, with chromic atrioventricular block, was used to study ventricular arrhythmias. The results obtained from these experiments show: 1. High therapeutic doses of digitalis enhance the postpacing inhibition of normal pacemakers; 2. When the ectopic rhythms of digitalis intoxication appear, they show postpacing stimulation; 3. Ectopic activity shows a direct relationship with the rate of the conditioning stimulation, and both the coupling period and the number of premature beats depend on this rate. In view of the similarity between the behavior of these arrhythmias and that of the after potential oscillations, we conclude that these oscillations are responsible for the ectopic automaticity of digitalis intoxication.