Pénfigo vulgar: dificultad en el diagnóstico de un tipo de dermatosis vulvar poco frecuente. Reporte de un caso / Vulgar pemphigus: Difficulty in diagnosis of a infrequent vulvar dermatoses. A case report

Resumen ANTECEDENTES: las alteraciones cutáneas de la vulva suponen un motivo frecuente de consulta a ginecólogos y dermatólogos. Los síntomas suelen ser imprecisos, con prurito y ardor, por lo que las pacientes tardan en acudir a consultar al médico. OBJETIVO: exponer un caso poco frecuente de pénfigo vulgar vulvar; además, revisar la incidencia, manifestaciones clínicas, diagnóstico y estrategias de tratamiento. CASO CLÍNICO: paciente de 86 años de edad que acudió a consulta por la aparición de lesiones vulvares ulceradas y ardorosas de dos meses de evolución. Se obtuvo una biopsia para el estudio histológico, cuyo resultado fue acantólisis y formación de una vesícula intraepidérmica suprabasal, sin evidencia de disqueratosis o necrosis. Se prescribieron corticoesteroides por vía tópica y oral durante un mes. Después de ese lapso se realizó un estudio de control, esta vez de una lesión más reciente, que evidenció infiltrado inflamatorio linfoplasmocitario con aislados eosinófilos, sin permeación del epitelio. La inmunofluorescencia directa reportó depósitos intercelulares de IgG en todo el espesor de la epidermis y de C3 en los estratos suprabasales, con lo que se confirmó el diagnóstico de pénfigo vulgar. CONCLUSIONES: para establecer el diagnóstico de las dermatosis vulvares poco frecuentes es importante efectuar una correcta correlación clínico-patológica, pues la mayor parte de estas enfermedades se manifiestan casi de forma idéntica.

Abstract BACKGROUND: The skin diseases of the vulva are a frequent reason for consultation with both gynecologists and dermatologists. The clinical symptoms are usually vague as pruritus or stinging and patients usually consult later. OBJECTIVE: To document a case of vulgaris vulvar pemphigus, and review the incidence, clinical presentation, diagnostic strategies and treatment. CLINCAL CASE: An 86-year-old patient who came to medical service for ulcerated and burning vulvar lesions of two months of progression. A biopsy was obtained for the histological study, which resulted in acantholysis and suprabasal intraepidermal vesicle, without evidence of dyskeratosis or necrosis. We prescribe topical and oral corticosteroids during a month. Posteriorly, a control study was performed of the most recent lesion that evidenced lymphoplasmacytic inflammatory infiltrate with eosinophilic isolates, without epithelial permeation. Direct immunofluorescence test reported intercellular deposits, IgG throughout the thickness of the epidermis, and C3 in the suprabasal stratum, thus confirming the diagnosis of pemphigus vulgaris. CONCLUSIONS: For correct diagnosis it is essential the clinic-pathological correlation, because many of these diseases manifest themselves almost identically.

Muerte súbita recuperada en un consumidor de cocaína / Aborted sudden death in a cocaine consumer

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Prognostic and therapeutic implications of dipyridamole stress cardiovascular magnetic resonance on the basis of the ischaemic cascade.

OBJECTIVE: To determine the prognostic and therapeutic implications of stress perfusion cardiovascular magnetic resonance (CMR) on the basis of the ischaemic cascade. SETTING: Single centre study in a teaching hospital in Spain. PATIENTS: Dipyridamole stress CMR was performed on 601 patients with ischaemic chest pain and known or suspected coronary artery disease. On the basis of the ischaemic cascade, patients were categorised in C1 (no evidence of ischaemia, n = 354), C2 (isolated perfusion deficit at stress first-pass perfusion imaging, n = 181) and C3 (simultaneous perfusion deficit and inducible wall motion abnormalities, n = 66). CMR-related revascularisation (n = 102, 17%) was defined as the procedure prompted by the CMR results and carried out within the next three months. RESULTS: During a median follow-up of 553 days, 69 major adverse cardiac events (MACE), including 21 cardiac deaths, 14 non-fatal myocardial infarctions and 34 admissions for unstable angina with documented abnormal angiography were detected. In non-revascularised patients (n = 499), the MACE rate was 4% (14/340) in C1, 20% (26/128) in C2 and 39% (12/31) in C3 (adjusted p value = 0.004 vs C2 and <0.001 vs C1). CMR-related revascularisation had neutral effects in C2 (20% vs 19%, 1.1 (0.5 to 2.4), p = 0.7) but independently reduced the risk of MACE in C3 (39% vs 11%, 0.2 (0.1 to 0.7), p = 0.01). CONCLUSIONS: Dypiridamole stress CMR is able to stratify risk on the basis of the ischaemic cascade. A small group of patients with severe ischaemia-simultaneous perfusion deficit and inducible wall motion abnormalities-are at the highest risk and benefit most from MACE reduction due to revascularisation.

A multimarker risk stratification approach to non-ST elevation acute coronary syndrome: implications of troponin T, CRP, NT pro-BNP and fibrin D-dimer levels.

INTRODUCTION: Biomarkers have emerged as interesting predictors of risk in non-ST elevation acute coronary syndromes (non-ST ACS). The aim of this study was to define the utility of the combined measurement of troponin T (TnT), C-reactive protein (CRP), NT pro-brain natriuretic peptide (NT pro-BNP) and D-dimer as biomarkers to predict adverse events. METHODS: We included 358 consecutive patients admitted in two hospitals for non-ST ACS. Baseline measurements of TnT (associated with myocardial injury, positive, if > or =0.1 ng mL(-1)), CRP (a marker of inflammation), NT-proBNP (associated with left ventricular (dys)function) and fibrin D-dimer (and index of thrombogenesis) were performed. A positive CRP, NT-proBNP and D-dimer test was considered upper than the 75th percentile of our population. The risk for major events (death, new ACS, revascularization and heart failure) at 6 months' follow-up was analysed. RESULTS: Troponin T, NT pro-BNP and CRP were predictors of adverse events in the multivariate analysis [hazards ratio (HR): 2.00 (1.30-3.07), P = 0.0016; HR: 2.27 (1.47-3.50), P = 0.0002; HR: 1.90 (1.24-2.92), P = 0.0034 respectively], but not D-dimer levels [HR: 1.26 (0.79-2.02), P = 0.337). After adjusting for baseline characteristics and electrocardiographic changes, multimarker risk approach was associated with adverse events at 6 months, especially with the presence of three positive biomarkers [HR 2.80 (95%CI 1.68-4.68), P < 0.001]. When we divided patients by risk groups [Thrombolysis in Myocardial Infarction (TIMI) risk score], patients with two or three elevated biomarkers had higher event rates [HR 2.59 (95% CI 1.37-4.91), P = 0.004]. CONCLUSION: A multimarker approach based on TnT, CRP and NT-proBNP provides added information to the TIMI risk score in terms of ACS prognosis at 6 months, with a worse outcome for those with two or three elevated biomarkers.

Mapping of atrial activation patterns after inducing contiguous radiofrequency lesions: an experimental study.

High resolution mapping techniques are used to analyze the changes in atrial activation patterns produced by contiguous RF induced lesions. In 12 Langendorff-perfused rabbit hearts, left atrial activation maps were obtained before and after RF induction of epicardial lesions following a triple-phase sequential protocol: (phase 1) three separate lesions positioned vertically in the central zone of the left atrial wall; (phase 2) the addition of two lesions located between the central lesion and the upper and lower lesions; and (phase 3) the placement of four additional lesions between those induced in the previous phases. In six additional experiments a pathological analysis of the individual RF lesions was performed. In phase 1 (lesion diameter = 2.8+/-0.2 mm, gap between lesions = 3+/-0.8 mm), the activation process bordered the lesions line in two (250-ms cycles) and four experiments (100-ms cycles). In phase 2, activation bordered the lesions line in eight (250-ms cycles, P < 0.01 vs control) and nine experiments (100-ms cycles, P < 0.001), and in phase 3 this occurred in all experiments except one (both cycles, P < 0.001 vs control). In the experiments with conduction block, the increment of the interval between activation times proximal and distal to the lesions showed a significant correlation to the length of the lesions (r = 0.68, P < 0.05, 100-ms cycle). In two (17%) experiments, sustained regular tachycardias were induced with reentrant activation patterns around the lesions line. In conclusion, in this acute model, atrial RF lesions with intact tissue gaps of 3 mm between them interrupt conduction occasionally, and conduction block may be frequency dependent. Lesion overlap is required to achieve complete conduction block lines. Tachycardias with reentrant activation patterns around a lesions line may be induced.

[Epicardial mapping of reentrant activation during ventricular fibrillation. An experimental study]. / Cartografía epicárdica de la activación reentrante durante la fibrilación ventricular. Estudio experimental.

INTRODUCTION AND OBJECTIVES: High-resolution epicardial mapping was used in an experimental model to analyze reentrant activation during ventricular fibrillation. METHODS: In 30 isolated Langendorff-perfused rabbit hearts, recordings were made of ventricular fibrillation activity using an epicardial multiple electrode. In the activation maps with reentrant activation patterns, determinations were made of the number of consecutive rotations, the maximum length of the central core, the area encompassed by the core and two electrodes surrounding it, and the cycle defined by reentrant activation. RESULTS: Most of the activation maps analyzed showed complex patterns with two or more wave fronts that either collided or remained separated by functional block lines (514 maps, 86%). In 112 maps (19%) activation patterns compatible with epicardial breakthrough of the depolarization process were observed. Reentrant activity was recorded in 42 maps (7%) - the maximum number of consecutive rotations being 3 (mean = 1.3 +/- 0.5). The maximum length of the central core ranged from 3 to 7 mm (mean = 5 +/- 1 mm), while the area encompassed by the central core plus two electrodes surrounding it ranged from 35 to 55 mm2 (mean = 45 +/- 6 mm2). The reentrant cycle length (mean = 47 +/- 8 ms) showed a linear relation to the maximum length of the central core reentry (cycle = 4.52 x length + 24.6; r = 0.7; p < 0.0001). CONCLUSIONS: a) Epicardial mapping allowed the identification of reentrant activation patterns during ventricular fibrillation in the experimental model used; b) the reentrant activity detected is infrequent and unstable, and c) a linear relation exists between the duration of the cycles defined by reentrant activity and the maximum length of central core reentry.

[Determinants of contractile reserve in the infarction area. A quantitative study using dobutamine in contrast left ventriculography]. / Determinantes de la reserva contráctil en la zona del infarto. Estudio cuantitativo mediante ventriculografía de contraste con dobutamina.

AIM: The aim of this study was to relate the contractile reserve in infarction segments to the dysfunction at rest and to the residual coronary stenosis. METHODS: The study group consisted of 95 patients with a first myocardial infarction. Contrast left ventricular at baseline and after dobutamine infusion at 7.5 microg/kg/min and coronary angiograms were performed. The centerline method was used to quantify the extent of dysfunction (percentage of chords with dysfunction in the territory of the infarction artery) and its maximum severity (maximum units of standard deviation [SD] below the normal wall motion reference). Reduction of dysfunction extent with dobutamine was measured. RESULTS: On increasing baseline dysfunction severity, both the magnitude of the response to dobutamine ( 2 SD 3 SD 4 SD +/- 5 SD [n = 15] = 9+/-13%, > 5 SD [n = 13] = 3+/-4%, p = 0,0001), and the number of patients with a significant (> or =15%) positive response ( 2 SD 3 SD 4 SD 5 SD = 0%, p<0,0001) decreased. There were no differences in dobutamine improvement among the subgroups with (n = 84) or without (n = 11) significant stenosis in the infarction artery (18+/-15 vs. 16 +/-18%), or between the subgroups with a patent (n = 76, 18+/-19%) or occluded (n = 19, 11+/-11%) artery. CONCLUSIONS: Dobutamine response is related to dysfunction severity in the infarction area: when the severity is 5 (high negative response prevalence), dobutamine testing does not seem indicate. The existence of residual coronary stenosis does not attenuate contractile reserve at low dobutamine doses.

Alteration of ventricular fibrillation by flecainide, verapamil, and sotalol: an experimental study.

BACKGROUND: The purpose of this study was to determine whether the myocardial electrophysiological properties are useful for predicting changes in the ventricular fibrillatory pattern. METHODS AND RESULTS: Thirty-two Langendorff-perfused rabbit hearts were used to record ventricular fibrillatory activity with an epicardial multiple electrode. Under control conditions and after flecainide, verapamil, or d,l-sotalol, the dominant frequency (FrD), type of activation maps, conduction velocity, functional refractory period, and wavelength (WL) of excitation were determined during ventricular fibrillation (VF). Flecainide (1.9+/-0.3 versus 2.4+/-0.6 cm, P<0. 05) and sotalol (2.1+/-0.3 versus 2.5+/-0.5 cm, P<0.05) prolonged WL and diminished FrD during VF, whereas verapamil (2.0+/-0.2 versus 1. 7+/-0.2 cm, P<0.001) shortened WL and increased FrD. Simple linear regression revealed an inverse relation between FrD and the functional refractory period (r=0.66, P<0.0001), a direct relation with respect to conduction velocity (r=0.33, P<0.01), and an inverse relation with respect to WL estimated during VF (r=0.49, P<0.0001). By stepwise multiple regression, the functional refractory periods were the only predictors of FrD. Flecainide and sotalol increased the circuit size of the reentrant activations, whereas verapamil decreased it. The 3 drugs significantly reduced the percentages of more complex activation maps during VF. CONCLUSIONS: The activation frequency is inversely related to WL during VF, although a closer relation is observed with the functional refractory period. Despite the diverging effects of verapamil versus flecainide and sotalol on the activation frequency, WL, and size of the reentrant circuits, all 3 drugs reduce activation pattern complexity during VF.

Opposite effects of myocardial stretch and verapamil on the complexity of the ventricular fibrillatory pattern: an experimental study.

An experimental model is used to analyze the effects of ventricular stretching and verapamil on the activation patterns during VF. Ten Langendorff-perfused rabbit hearts were used to record VF activity with an epicardial multiple electrode before, during, and after stretching with an intraventricular balloon, under both control conditions and during verapamil (Vp) infusion (0.4-0.8 mumol). The analyzed parameters were dominant frequency (FrD) spectral analysis, the median (MN) of the VF intervals, and the type of activation maps during VF (I = one wavelet without block lines, II = two simultaneous wavelets with block lines, III = three or more wavelets with block lines). Stretch accelerates VF (FrD: 22.8 +/- 6.4 vs 15.2 +/- 1.0 Hz, P < 0.01; MN: 48 +/- 13 vs 68 +/- 6 ms, P < 0.01). On fitting the FrD time changes to an exponential model after applying and suppressing stretch, the time constants (stretch: 101.2 +/- 19.6 s; stretch suppression: 97.8 +/- 33.2 s) do not differ significantly. Stretching induces a significant variation in the complexity of the VF activation maps with type III increments and type I and II decrements (control: I = 17.5%, II = 50.5%, III = 32%; stretch: I = 7%, II = 36.5%, III = 56.5%, P < 0.001). Vp accelerates VF (FrD: 20.9 +/- 1.9 Hz, P < 0.001 vs control; MN: 50 +/- 5 ms, P < 0.001 vs control) and diminishes activation maps complexity (I = 25.5%, II = 60.5%, III = 14%, P < 0.001 vs control). On applying stretch during Vp perfusion, the fibrillatory process is not accelerated to any greater degree. However, type I and II map decrements and type III increments are recorded, though reaching percentages similar to control (I = 16.5%, II = 53%, III = 30.5%, NS vs control). The following conclusions were found: (1) myocardial stretching accelerates VF and increases the complexity of the VF activation pattern; (2) time changes in the FrD of VF during and upon suppressing stretch fit an exponential model with similar time constants; and (3) although stretching and verapamil accelerate the VF process, they exert opposite effects upon the complexity of the fibrillatory pattern.

[Characteristics of atrial electrograms recorded in radiofrequency induced block lines in an experimental model]. / Características de los electrogramas auriculares registrados en las líneas de bloqueo producidas con radiofrecuencia en un modelo experimental.

AIM: To analyze and quantify atrial electrogram modifications following the induction of linear lesions in the atrial wall using radiofrequency ablation procedures. METHODS: An epicardial multiple electrode (221 unipolar electrodes) was used in 12 Langendorff perfused rabbit hearts to analyze atrial activation before and after radiofrequency induction of a linear lesion in the left atrial wall. After confirming the existence of conduction blockade in the lesion zone by epicardial mapping and propagation vector analysis, six electrodes each were selected in the lesioned and non-lesioned zones in all experiments, comparing the amplitude, maximum negative slope and morphology of the electrograms in both zones, before (control) and after radiofrequency delivery. RESULTS: Analysis of the reproducibility of the measurements in two consecutive cycles showed a variation of 1 +/- 5% for amplitude (NS) and 1 +/- 9% for maximum negative slope (NS). In the non-damaged zone, amplitude (105 +/- 22%) and slope (92 +/- 16%) (values normalized with respect to those recorded before radiofrequency) did not vary significantly following radiofrequency, and simple electrograms were the most frequent recordings (82 vs 83% in control; NS). Amplitude (19 +/- 7%, p < 0.001) and slope (24 +/- 11%; p < 0.001) decreased significantly in the lesion zone, as did the percentage of simple electrograms (6 vs 86% in control; p < 0,001). In this same zone the morphology could not be determined in 12% of the recordings, while multiple electrograms were obtained in 15% (vs 2% in control; p < 0.01), and the most frequent type corresponded to double electrograms (67 vs 12% in control, p < 0.001), with both components coinciding in time with atrial activation in the zones proximal and distal to the lesion line. CONCLUSIONS: Electrograms recorded directly in radiofrequency induce block lines show a significant decrease in amplitude and maximum negative slope. Double electrograms predominate in these recordings, both components of which represent activation on either side of the lesion. In a small proportion of cases simple and multiple electrograms can also be recorded in the block line.

[The activation patterns during atrial fibrillation in an experimental model]. / Patrones de activación durante la fibrilación auricular en un modelo experimental.

INTRODUCTION AND OBJECTIVES: In atrial fibrillation, along with the mechanisms of complete reentry and random activation focal activation patterns have been described which have been attributed both to propagation from the endocardium and to the existence of zones with automatic activity. The objectives of present study are to analyze and quantify the atrial activation patterns in an experimental model of atrial fibrillation. MATERIAL AND METHODS: In 11 Langendorff-perfused rabbit hearts atrial fibrillation was induced by atrial burst pacing after right atrial dilatation with an intra-atrial balloon. A multiple electrode consisting of 121 electrodes and positioned in the right atrial free wall was used to construct the activation maps corresponding to 10 segments of 100 ms in 11 different episodes of sustained atrial fibrillation (one per experiment). RESULTS: Of the 110 segments analyzed, 44 (40%) corresponded to random activation patterns. Fifteen segments (14%) corresponded to complete reentry, and in these cases the number of consecutive rotations ranged from 1 to 2.25 (mean 1.4 +/- 0.4). In 49 segments (44%) a single activation front was seen to pass through the recording area without block; alternatively, two simultaneous fronts were recorded that did not re-excite the zone activated by the other. In two segments (2%) there was a focal activation pattern without evidence of propagation from the epicardium surrounding the activated zone. CONCLUSIONS: a) in the experimental atrial fibrillation model used, random activation patterns are more frequent than complete reentry patterns; b) complete reentry can occur in areas smaller than 1 cm2, and c) focal activation during atrial fibrillation is rare.

Reduction of atrial fibrillation inducibility by radiofrequency ablation: an experimental study.

UNLABELLED: A study is made of the antifibrillatory effects of radiofrequency (RF)-induced atrial lesions using nine Langendorff-perfused rabbit hearts in which the atrial electrophysiological properties and atrial fibrillation (AF) inducibility were modified by atrial stretching. Using a multiple electrode consisting of 121 unipolar electrodes, determinations were made of the atrial refractory periods, conduction velocity, wavelength of the atrial activation process, and the inducibility of sustained AF episodes (duration over 30 s) by atrial burst pacing in four situations: (a) control; (b) following dilatation of the right atrium; (c) after adding an RF linear lesion at the cava-tricuspid annulus isthmus; and (d) after adding two RF linear lesions rounding the base of the right atrial appendage and extending from the inferior zone of the sulcus terminalis to the anterior wall of the appendage. Under control conditions, AF was not induced in any of the experiments. The wavelengths were 10.5 +/- 1.2 cm for basic cycles of 250 ms and 6.6 +/- 0.5 cm for cycles of 100 ms. Following dilatation, a significant decrease was recorded in the atrial refractory periods, conduction velocity, and wavelength, which reached values of 6.1 +/- 0.7 cm (250-ms cycle, P < 0.01), and 3.9 +/- 0.3 cm (100-ms cycle, P < 0.01); AF was induced in five cases (P < 0.05). After producing the lesion at the cava-tricuspid isthmus, the electrophysiological modifications induced by atrial dilatation persisted (wavelength = 6.2 +/- 0.6 cm (250-ms cycle) and 4.3 +/- 0.3 cm (100-ms cycle); P < 0.01 vs the control) and AF was triggered in eight cases (P < 0.0001). In turn, on adding the two lesions at the right atrial free wall and appendage, AF was induced only in one experiment (P = NS vs control), and the dilatation-induced decrease in refractoriness and wavelength was attenuated. Nevertheless, differences remained significant with respect to the controls, with the exception of the functional refractory periods determined at cycles of 100 ms. In this phase, the wavelength was 6.6 +/- 0.7 cm (250-ms cycle, P < 0.01 vs control) and 4.9 +/- 0.5 cm (100-ms cycle; P < 0.05). Atrial conduction between the zones separated by the lesions was blocked at any frequency, or selectively at rapid atrial activation frequencies. IN CONCLUSION: (a) the production of three linear lesions in the right atrium (cava-tricuspid isthmus, atrial appendage, and inferior free wall) reduces AF inducibility in the experimental model used; (b) conduction block (either absolute or frequency dependent) through the lesions, reduction in tissue mass caused by lesion creation, and possibly the attenuation of the shortening of atrial refractoriness and wavelength in the zones not separated by the lesions are implicated in the reduction of AF inducibility; and (c) the single lesion in the cava-tricuspid isthmus does not impede AF inducibility.

[Acute changes in wavelength of the process of auricular activation induced by stretching. Experimental study]. / Modificaciones agudas de la longitud de onda del proceso de activación auricular inducidas por la dilatación. Estudio experimental.

OBJECTIVE: An evaluation is made of the acute modifications in the wavelength of the atrial excitation process induced by atrial stretching. MATERIAL AND METHODS: In 10 isolated Langendorff-perfused rabbit hearts and using a multiple electrode the wavelength of the atrial activation process (functional refractory period x conduction velocity) was determined in the right atrium. An analysis was also made of the inducibility of rapid repetitive atrial responses after 20 episodes of atrial burst pacing. Measurements were made under control conditions, after inducing two degrees of atrial wall stretch (D1 and D2), and following the suppression of atrial dilatation. RESULTS: Under control conditions the wavelength was 72.6 +/- 7.7 mm (250 ms cycle) and 54.0 +/- 5.1 mm (100 ms cycle). In D1 (mean longitudinal increase in atrial wall length = 24 +/- 3%) the wavelength shortened, with values of 59.8 +/- 6.6 mm (250 ms cycle; p < 0.01) and 44.9 +/- 5.1 mm (100 ms cycle; p < 0.01). In D2 (mean longitudinal increase in atrial wall length = 41 +/- 4%) the wavelength also shortened significantly, with values of 41.6 +/- 2.5 mm (250 ms cycle; p < 0.01 vs control) and 29.6 +/- 2.1 mm (100 ms cycle; p < 0.01 vs control). After suppressing atrial dilatation the wavelength was 65.7 +/- 8.0 mm (250 ms cycle, NS vs control) and 47.9 +/- 5.5 mm (100 ms cycle; NS vs control). The inducibility of rapid repetitive atrial responses increased during dilatation (22 episodes with over 30 consecutive repetitive responses in D1 [p < 0.01], 50 episodes in D2 [p < 0.001] vs 5 episodes under control conditions), and diminished after suppressing atrial dilatation (0 episodes with over 30 consecutive repetitive responses; p < 0.05). CONCLUSIONS: In the experimental model used, acute atrial dilatation produced a shortening in refractoriness and a decrease in conduction velocity. Both effects shortened the wavelength of the atrial activation process, facilitating the induction of atrial arrhythmias. The effects observed reverted upon suppressing atrial dilatation.

Quantification of the modifications in the dominant frequency of ventricular fibrillation under conditions of ischemia and reperfusion: an experimental study.

The characteristics of ventricular fibrillatory signals vary as a function of the time elapsed from the onset of arrhythmia and the maneuvers used to maintain coronary perfusion. The dominant frequency (FrD) of the power spectrum of ventricular fibrillation (VF) is known to decrease after interrupting coronary perfusion, though the corresponding recovery process upon reestablishing coronary flow has not been quantified to date. With the aim of investigating the recovery of the FrD during reperfusion after a brief ischemic period, 11 isolated and perfused rabbit heart preparations were used to analyze the signals obtained with three unipolar epicardial electrodes (E1-E3) and a bipolar electrode immersed in the thermostatized organ bath (E4), following the electrical induction of VF. Recordings were made under conditions of maintained coronary perfusion (5 min), upon interrupting perfusion (15 min), and after reperfusion (5 min). FrD was determined using Welch's method. The variations in FrD were quantified during both ischemia and reperfusion, based on an exponential model deltaFrD = A exp (-t/C). During ischemia deltaFrD is the difference between FrD and the minimum value, while t is the time elapsed from the interruption of coronary perfusion. During reperfusion deltaFrD is the difference between the maximum value and FrD, while t is the time elapsed from the restoration of perfusion. A is one of the constants of the model, and C is the time constant. FrD exhibited respective initial values of 16.20 +/- 1.67, 16.03 +/- 1.38, and 16.03 +/- 1.80 Hz in the epicardial leads, and 15.09 +/- 1.07 Hz in the bipolar lead within the bath. No significant variations were observed during maintained coronary perfusion. The fit of the FrD variations to the model during ischemia and reperfusion proved significant in nine experiments. The mean time constants C obtained on fitting to the model during ischemia were as follows: E1 = 294.4 +/- 75.6, E2 = 225.7 +/- 48.5, E3 = 327.4 +/- 79.7, and E4 = 298.7 +/- 43.9 seconds. The mean values of C obtained during reperfusion, and the significance of the differences with respect to the ischemic period were: E1 = 57.5 +/- 8.4 (P < 0.01), E2 = 64.5 +/- 11.2 (P < 0.01), E3 = 80.7 +/- 13.3 (P < 0.01), and E4 = 74.9 +/- 13.6 (P < 0.0001). The time course variations of the FrD of the VF power spectrum fit an exponential model during ischemia and reperfusion. The time constants of the model during reperfusion after a brief ischemic period are significantly shorter than those obtained during ischemia.

Acute effects of radiofrequency ablation upon atrial conduction in proximity to the lesion site.

The electrophysiological effects of RF ablation upon the areas in proximity to the lesioned zones have not yet been well characterized. An experimental model is used to investigate atrial conduction in the boundaries of RF damaged zones. In 11 isolated and perfused rabbit hearts, endocardial atrial electrograms were recorded using an 80-lead multiple electrode positioned in the left atrium. Both before and after the RF application (5 W, 8 s, 1-mm diameter unipolar epicardial electrode) in the mid-portion of the free left atrial wall, measurements were made of conduction time from the pacing zone (posterior wall of the left atrium) to three points between 7.5 and 7.9 mm distal to the damaged zone. Conduction velocity and the direction of the activation propagation vector were determined in ten groups of four electrodes positioned around the damaged zone, and at the left atrial appendage. The mean diameter (+/- SEM) of the transmural lesions produced by RF ablation and defined by macroscopic examination was 4.2 +/- 0.2 mm. The conduction times to the three points distal to the lesion site were significantly prolonged as a result of RF ablation; 7.6 +/- 0.4, 7.4 +/- 0.5, and 6.9 +/- 1.0 ms (control); and 11.3 +/- 1.0 (P < or = 0.01), 11.1 +/- 1.3 (P < 0.01), 10.6 +/- 1.4 ms (P < 0.05) (post-RF). The differences between the conduction velocities determined in the areas surrounding the lesion, before and after RF application, failed to reach statistical significance: 86.2 +/- 6.5 cm/s (control) versus 75.5 +/- 5.7 cm/s (post-RF) (NS). After RF, significant variations were only observed in the direction of impulse propagation in the proximal-inferior quadrant adjacent to the lesion site, the difference being -61 degrees +/- 18 degrees (P < 0.02). In 2 of 4 experiments in which the lesion size was increased by a second RF application (5 W, 16 s), tachycardias with activation sequence around the lesion could be induced, with cycle lengths of 56 and 50 ms, respectively. In the atrial wall, the conduction times to the regions distal to the RF lesion are significantly prolonged. No significant changes are observed in conduction velocity in the areas in proximity to the lesion. Prolonged conduction to the areas distal to the ablation site is due to the lengthened pathway traveled by the impulses in reaching these areas. Tachycardias with activation patterns that suggest reentry around the RF damaged zone may be induced.

[The assessment of cardiac involvement in a case of a thoracic injury from a firearm]. / Valoración de la afectación cardíaca en un caso de herida torácica por arma de fuego.

We report the case of a patient with a gunshot wound in the chest with a multiple small-caliber intrathoracic projectiles. The different noninvasive techniques employed to evaluate the anatomical location of these projectiles are discussed, together with their cardiac structural repercussions. The data provided by a simple chest X-ray, Computed Tomography (CT) and transthoracic echocardiography are commented on. A simple chest X-ray was unable to discern the location of the projectiles, in contrast to CT, which was able to identify both the number of projectiles and their location. The information provided was enhanced by transthoracic echocardiography, particularly in relation to those projectiles situated in anterior cardiac regions.

[Cardiac angiosarcoma]. / Angiosarcoma cardíaco.

We report a case of a 29-year-old patient with recurrent hemorrhagic pericardial effusion secondary to a right atrial mass detected by transthoracic echocardiography. A more detailed anatomic study was provided by transesophageal echocardiogram and nuclear magnetic resonance imaging. During surgery, a biopsy confirmed the diagnosis of angiosarcoma. We discuss the contribution of echocardiography and other noninvasive methods to evaluate intracardiac tumors. A brief review of treatment and prognosis is made.