Biomedical subjects

V López-Merino

Publications and source records attributed to V López-Merino.

At least 19 recordsLinked to original sources

PubMed2000

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.

Animals↗

PubMed2000

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.

Animals↗

PubMed1999

Wall motion of noninfarcted myocardium. Relationship to regional and global systolic function and to early and late left ventricular dilation.

We studied the wall motion of the noninfarcted area and its role in left ventricular remodeling. The study group consisted of 43 patients with a first Q-wave acute myocardial infarction and single-vessel disease. Cardiac catheterization was performed at the first week, and was repeated six months later. Left ventricular volumes, wall motion at the infarcted and noninfarcted area, ejection fraction and infarction-related artery status were quantified. Hyperkinesia was only found at the first week in 22% of cases, and at the sixth month in 26% of cases. Wall motion at the noninfarcted area correlated with wall motion at the infarcted area (one week: r=0.53 p<0.0001; six months: r=0.52 p=0.01), ejection fraction (one week: r=0.69 p<0.0001; six months: r=0.56 p=0.006), end-diastolic volume (one week: r=-0.48 p=0.002; six months: r=-0.48 p=0.02) and end-systolic volume (one week: r=-0.70 p<0.0001; six months: r=-0.64 p=0.001). The improvement of the noninfarcted area (from the first week to the sixth month) was only related to basal (one week) wall motion in this area (r=-0.58 p=0.003). We conclude that after an intermediate-large infarction, most patients exhibit a normal or hypokinetic noninfarcted area. Patients with a more depressed infarcted area show poorer contractility at the noninfarcted area. area exhibit greater progressive improvement.

Adult↗

PubMed1999

Low-dose dobutamine testing using contrast left ventriculography in the same session as coronary angiography predicts the improvement of left ventricular function after coronary angioplasty in postinfarction patients.

The role of percutaneous transluminal coronary angioplasty (PTCA) in the subacute or chronic phases of myocardial infarction remains controversial. This study investigates the usefulness of dobutamine contrast left ventriculography in a single session with coronary angiography for predicting the improvement of ventricular function after PTCA. The study group consisted of 30 patients in whom a contrast left ventricular angiogram and PTCA were performed after a first myocardial infarction. The centerline method was used to calculate dysfunction extent at baseline and its variation during dobutamine infusion at 7.5 microg/kg/min; contractile reserve was defined as a significant (> or = 15%) reduction of dysfunction extent. A second ventricular angiogram was performed 6 months later in all patients. Abnormal wall motion extent decreased at 6 months after PTCA (84+/-21% vs 70+/-29%, p = 0.0001). Wall motion improvement after PTCA correlated with the response to dobutamine (r = 0.54, p = 0.002). Ten patients showed a significant reduction (> or = 15%) of dysfunction extent at 6 months; dobutamine testing had a 80% sensitivity, 84% specificity, 67% positive predictive value, and 89% negative predictive value in detecting regional function improvement. In the subgroup of 21 patients without restenosis, both the correlation between dysfunction improvement after PTCA and response to dobutamine (r = 0.72, p = 0.0001) and the accuracy of dobutamine testing (sensitivity 88%, specificity 92%, positive predictive value 88%, and negative predictive value 92%) increased. The ejection fraction significantly increased (>5%) after PTCA in 6 patients; dobutamine testing had a 67% sensitivity, 74% specificity, 44% positive predictive value, and 88% negative predictive value in predicting the increase in the ejection fraction. In the subgroup without restenosis the improvement of the ejection fraction correlated with the response to dobutamine (r = 0.63, p = 0.007), and the sensitivity of dobutamine testing was 80%, specificity 83%, positive predictive value 67%, and negative predictive value 91%. In conclusion, dobutamine contrast left ventriculography testing in the same session as coronary angiography predicts regional function and ejection fraction improvement after PTCA in postinfarction patients, particularly when restenosis does not develop.

Aged↗

PubMed1999

Predictors of early and late ventricular remodeling after acute myocardial infarction.

BACKGROUND: The determinants of the early and late stages of the ventricular remodeling process after infarction are not well defined. HYPOTHESIS: The study was undertaken to evaluate the factors that condition the time course of left ventricular dilation during the first 6 months after infarction. METHODS: The study group consisted of 74 patients with a first intermediate-large (> or = 4 Q waves) acute myocardial infarction. Contrast left ventricular and coronary angiograms were performed at 7 +/- 1 and 175 +/- 25 days after infarction. Left ventricular volumes, regional function and infarction artery status were quantified. Percutaneous transluminal coronary angioplasty (PTCA) was performed in the early angiogram in 31 patients. RESULTS: In the early angiogram, 13 patients showed ventricular remodeling (end-diastolic volume > 90 ml/m2). A larger extent of dysfunction was the only predictor (p < 0.002) of early remodeling. At 6 months, a smaller, early end-diastolic volume (p < 0.0001) and a poorer regional function recovery (p < 0.05) were independently related to late diastolic enlargement, and a poorer regional function recovery (p < 0.0001) and a smaller, early end-systolic volume (p < 0.009) were independently related to late systolic enlargement. One patient with compared with 20 patients without early remodeling (p < 0.04) presented with late remodeling (increment of the end-diastolic volume > 20% at 6 months). In patients with early remodeling, the end-diastolic volume did not change significantly (101 +/- 13 vs. 94 +/- 22 ml/m2, NS) at 6 months; despite this, they maintained larger diastolic volumes than patients with late remodeling (81 +/- 12 ml/m2, p < 0.04) at 6 months. Infarction artery status did not influence the evolution of ventricular volumes and regional function. CONCLUSIONS: (1) A large infarct size is the main determinant of postinfarction remodeling. (2) Such infarct size-dependent ventricular dilation occurs early and does not tend to increase in late stage; in contrast, some cases of intermediate-large size infarcts without early remodeling exhibit late remodeling associated with a poor late recovery of regional function. (3) Recovery of regional function (indicating myocardial viability) rather than infarction artery status plays a role in the late ventricular remodeling process.

Aged↗

PubMed1999

ST-segment elevation on Q leads at rest and during exercise: relation with myocardial viability and left ventricular remodeling within the first 6 months after infarction.

BACKGROUND: Resting ST-segment elevation on Q leads after an acute myocardial infarction has been related to a greater infarct size. Otherwise, the relation between exercise-induced ST-segment elevation and myocardial viability is controversial. We investigated the relation between ST-segment elevation on Q leads at rest and during exercise and regional dysfunction and its evolution, contractile reserve, left ventricular dilation, and coronary patency. METHODS AND RESULTS: Exercise testing and cardiac catheterization were performed at the first week after infarction in 51 patients. The study group was divided according to the existence (in 2 or more Q leads; n = 36) or not (n = 15) of resting ST-segment elevation and according to the existence (n = 28) or not (n = 23) of exercise-induced ST-segment elevation. Left ventricular end-diastolic and end-systolic volumes (mL/m2), regional wall motion (SD/chord), contractile reserve (wall motion percentage improvement with low-dose dobutamine), and coronary patency in the culprit artery were analyzed. Cardiac catheterization was repeated at the sixth month in 35 patients; systolic recovery (wall motion percentage improvement), left ventricular volumes, and coronary patency were again evaluated. Patients with resting ST-segment elevation showed poorer wall motion (2.1 +/- 0.8 SD/chord vs 1.2 +/- 1 SD/chord, P =.002), lesser contractile reserve (17% [0% to 39%] vs 41% [4% to 92%], P =.04), greater end-systolic volume (32 +/- 15 mL/m2 vs 23 +/- 11 mL/m2, P =.04), and higher percentage of occlusion (36% vs 7%, P =.04) than did patients without ST-segment elevation. Likewise, patients with exercise-induced ST-segment elevation showed lesser contractile reserve (8% [0% to 40%] vs 35% [12% to 86%], P =.03) than did patients without exercise-induced ST-segment elevation. The only independent predictors of contractile reserve were wall motion <2 SD/chord (odds ratio [OR] 7.1, confidence interval [CI] 6.3 to 7.9, P =.01) and the absence of exercise-induced ST-segment elevation (OR 5.7, CI 4.9 to 6.5, P =. 02). There were no significant differences between patients with and those without ST-segment elevation (at rest or during exercise) in systolic recovery or left ventricular volumes at the sixth month. CONCLUSIONS: ST-segment elevation on Q leads at rest is related to a poorer systolic function (more severe regional dysfunction, greater end-systolic volume, and less response to dobutamine). ST-segment elevation during exercise is independently related to a lesser contractile reserve. ST-segment elevation (at rest or during exercise) is not related to the evolution of volumes or regional dysfunction during the first 6 months after infarction.

Aged↗

PubMed1999

[The activation patterns during atrial fibrillation in an experimental model].

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.

Analysis of Variance↗

PubMed1999

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.

Animals↗

PubMed1998

[Acute changes in wavelength of the process of auricular activation induced by stretching. Experimental study].

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.

Animals↗

PubMed1998

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.

Animals↗

PubMed1998

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.

Animals↗

PubMed1997

Are double potentials markers of a specific zone of the atrioventricular junction in the isolated rabbit heart?

A study is made of the characteristics of the atrial potentials recorded in the Koch triangle and its proximity, their variations on modifying the site of cardiac pacing, and their usefulness as markers of a distinct zone of the AV junction. In 12 isolated and perfused rabbit heart preparations an analysis was made of the endocardial atrial electrograms recorded with a multiple electrode positioned in the AV junction. The electrograms were obtained during spontaneous rhythm and on pacing at the crista terminalis (CT), interatrial septum (IAS), left atrium, and right ventricle. Double potentials were frequently obtained. On pacing at the CT, high-low double potentials (DP [H-L]) were more frequent (P < 0.05) in the low CT (11% +/- 4% of the electrodes) and posterior zone of the Koch triangle (6% +/- 5%), than in the IAS (1% +/- 2%) and anterior zone of the Koch triangle (2% +/- 3%). A similar tendency was observed either on pacing at the left atrium or during spontaneous rhythm. During pacing at the IAS the percentages of low-high double potentials (DP (L-H]) were significantly higher (P < 0.05) in the low CT (7% +/- 6%). DP (H-L) were of low sensitivity in indicating a given zone; maximum sensitivity was 61% in the low CT when pacing at the CT. DP (L-H) proved even less sensitive in indicating a given zone, though their specificity was greater in the low CT (91%) during pacing at the IAS. The specific zones in which the highest percentages of DP (H-L) or DP (L-H) are obtained depend on the site of cardiac pacing. On pacing at the IAS, DP (L-H) are more specific of the low CT. During pacing at both the CT and at the IAS, DP (H-L) sensitivity in indicating a given zone is low.

Action Potentials↗

PubMed1997

Modification of atrioventricular nodal electrophysiology by selective radiofrequency delivery on the anterior or posterior approaches.

An analysis was made in 14 isolated and perfused rabbit hearts of the electrophysiological effects of selective radiofrequency (RF) delivery in the anterior (group I, n = 7) or posterior zone (group II, n = 7) of the Koch triangle, with the aim of modifying atrioventricular nodal (AVN) conduction without suppressing 1:1 transmission. After opening the right atrium, RF was delivered (0.5 W) with a 1-mm diameter unipolar electrode positioned in the selected zone until a prolongation of no less than 15% was obtained in the Wenckebach cycle length (WCL). Before and after (30 min) RF, anterograde and retrograde AVN refractoriness and conduction were evaluated, stimulating from the crista terminalis (CT), the interatrial septum (IAS), and from the RV epicardium. After RF, the following percentage increments were observed in group I: AH(CT) = 36% +/- 9%, AH(IAS) = 38% +/- 11%, WCL(CT) = 28% +/- 8%, WCL(IAS) = 22% +/- 6%, functional refractory period (FRP) of the AVN(CT) = 13% +/- 11%, FRP-AVN(IAS) = 13% +/- 8%, retrograde WCL = 20% +/- 19%, and retrograde FRPVA = 13% +/- 16%. The increments observed in group II and the significances of the differences with respect to group I were: AH(CT) = 11% +/- 14% (P < 0.01), AH(IAS) = 19% +/- 32% (NS), WCL(CT) = 42% +/- 14% (P < 0.05), WCL(IAS) = 42% +/- 16% (P < 0.01), FRP-AVN(CT) = 28% +/- 28% (NS), FRP-AVN(LAS) = 21% +/- 19% (NS), retrograde WCL = 35% +/- 24% (NS), and retrograde FRP = 16% +/- 13% (NS). In both groups, the AH interval variations were not correlated with those of the rest of the parameters analyzed. Truncated nodal function curves suggestive of a dual AV nodal pathway were obtained in three experiments, though in only one of them was this observed under basal conditions. In the other two experiments, with dual AV nodal physiology only after RF (one from each group), AV nodal reentrant tachycardias were triggered with atrial extrastimulus at coupling intervals equal to or shorter than at those that cause a sudden lengthening of the AH interval, RF delivered in the anterior and posterior zones of the Koch triangle produced effects of different magnitude on the AH interval and Wenckebach cycle length. In the anterior zone the AH interval was prolonged to a greater extent, while in the posterior zone the effects were greater on the Wenckebach cycle length. No correlation existed between the variations in AH interval and Wenckebach cycle length, regardless of where RF was delivered. The evaluation of anterograde AV nodal refractoriness was similar when stimulating from the crista terminalis or from the interatrial septum. By delivering RF, it was possible to induce dual AV nodal physiology and reentrant tachycardias.

Animals↗

PubMed1996

Modifications in the evolution of the dominant frequency in ventricular fibrillation induced by amiodarone, diltiazem, and flecainide. An experimental study.

In 22 anesthetized mongrel dogs, spectral methods were used to analyze the surface electrocardiogram (ECG) for the time course of the dominant frequency in ventricular fibrillation and its modifications under the influence of amiodarone, diltiazem, and flecainide. The ECG was recorded over 5 minutes after triggering ventricular fibrillation. Following A/D conversion and by applying the Fourier fast transform, the frequency spectrum of the signals was obtained. In group 1 (5 dogs), the ECGs were obtained without prior drug administration; group 2 (5 dogs) first received amiodarone, 5 mg/kg; group 3 (7 dogs) received diltiazem, 0.2 mg/kg; and group 4 (5 dogs) received flecainide, 2 mg/kg. All drugs were administered intravenously. An initial increase in the dominant frequency of ventricular fibrillation was found in the control group and also in the groups that received amiodarone, diltiazem, or flecainide. Diltiazem significantly increased the dominant frequency and diminished the arrhythmia-slowing process. Amiodarone and flecainide tended to diminish the dominant frequency.

Amiodarone↗

PubMed1995

Continuous heart rate variability monitoring through complex demodulation implemented with the fast Fourier transform and its inverse.

UNLABELLED: A new method for the analysis of 24-hour heart rate variability (HRV) using complex demodulation (CDM) implemented with the fast Fourier transform (FFT) and its inverse is described. In a control group with palpitations and dizzy spells (n = 30, 47.2 +/- 16.7 years) the relationship between HRV parameters and subject age was investigated. CDM was used to obtain the amplitude and frequency of the low frequency (LF) and high frequency (HF) oscillations for 8 diurnal hours and 4 nocturnal hours. Differences between the two periods were seen in the LF/HF ratio (2.2 +/- 0.6 vs 1.5 +/- 0.6; P < 0.0001), HF amplitudes (12 +/- 6 vs 17 +/- 7 normalized units, P < 0.05), and in the mean frequency of the LF oscillations (0.078 +/- 0.008 vs 0.073 +/- 0.007 Hz, P < 0.01). During the daytime, age was inversely correlated to HF amplitude (r = -0.60), directly correlated to HF mean central frequency (r = 0.40), inversely correlated to LF amplitude (r = -0.55), and likewise inversely correlated to LF mean central frequency (r = -0.74, P < 0.001). At night, age was only inversely correlated to HF amplitude and to LF mean central frequency. CONCLUSIONS: Continuous HRV monitoring through CDM implemented with the FFT and its inverse differentiates the periods of diurnal activity and nocturnal rest as an expression of two different activity states of the autonomic nervous system. It allows nonstationary analysis, and separately provides mean and instantaneous oscillation amplitude and frequency. Subject age is not equally related to mean amplitude and frequency of a given oscillation.

Adolescent↗

PubMed1994

The influence of different electrode configurations on the inhibitory effect of subthreshold high-frequency stimuli.

Subthreshold stimuli trains may inhibit the response to a subsequent suprathreshold stimulus; the inhibitory effect decreases or even disappears when the subthreshold stimuli are delivered apart from the suprathreshold stimulus. The purpose of this study is to analyse, in atrial epicardium, the influence of different electrode configurations upon the inhibitory effect of subthreshold stimuli trains delivered at a short distance from the explored zone. In 18 anaesthetized dogs, the basal atrial effective refractory period was determined using an epicardial unipolar cathodal electrode. A second determination was performed when a subthreshold stimuli train (1 ms cathodal pulses, 800 Hz, and intensity 10% less than the diastolic threshold of the train) was delivered prior to the extrastimulus through: (a) 8 electrodes equidistant (4.5 mm) from the central test electrode (Group 1, n = 5); (b) a 1 mm wide ring electrode, 2.5 mm from the central test electrode (Group 2, n = 7); and (c) a 3.5 mm wide ring electrode, 2.5 mm from the central test electrode (Group 3, n = 6). A third determination was performed in all experiments delivering both the subthreshold stimuli train and the extrastimulus through the same central test electrode. Atrial effective refractory period did not vary significantly with respect to the basal values in Group 1 (141 +/- 22 vs 142 +/- 25 ms; ns) though it increased in Group 2 (168 +/- 27 vs 142 +/- 18 ms; P < 0.01) and in Group 3 (160 +/- 20 vs 133 +/- 25 ms; P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

[The spectral analysis of heart rate variability. The methodological aspects].

OBJECTIVES: A study is made of the influence of methodology on the analysis of cardiac cycle variability in terms of frequency and time domains. METHODS: Twenty-five individuals were divided into three groups: 1) non-smokers (n = 10); 2) smokers (n = 8); and 3) non-smokers without guided respiratory frequency (n = 7). An analysis was made of RR variability during 5 min intervals in time domain (standard deviation, variation coefficient, and difference between maximum and minimum RR), and frequency domain (spectral analysis, Fast Fourier Transform algorithm using 5 types of data windows). RESULTS: On comparing the results obtained in the 25 individuals with the 5 data windows, significant differences were observed (ANOVA; p < 0.001) in maximum and total amplitudes of the spectrum (in absolute terms) in the low frequency band (0.04-0.15 Hz). No significant differences were found between the normalized values or between the low/high (0.15-0.40 Hz) frequency ratio: W1 = 1.63 +/- 0.30; W2 = 1.62 +/- 0.29; W3 = 1.65 +/- 0.31; W4 = 1.52 +/- 0.26, and W5 = 1.55 +/- 0.27 (X +/- SE). On averaging the RR intervals each 5 cycles, significant differences were encountered for great part of the parameters studied. No significant differences were encountered for great part of the parameters studied. No significant differences were noted between the non-smokers as regards the use or non-use of a metronome (low/high frequency ratio in group 1 = 1.85 +/- 0.39 vs group 3 = 1.78 +/- 0.43; NS). The linear regressions between the variability parameters in terms of time and frequency domains (absolute values), and age (group 1) were significant, with greater regression coefficients on using the linear transformation of an exponential model. On comparing groups 1 and 2, a non statistically significant trend towards smaller maximum and total amplitudes (absolute values) was noted in group 2 for both frequency bands. CONCLUSIONS: 1) The type of data window (Fourier analysis) introduces significant modifications of some parameters expressed in absolute values, but not between normalized values; 2) signal averaging greatly modifies the information obtained; 3) the decrease in variability parameters observed with age fits better to an exponential model; 4) no differences were detected on guiding or not respiratory frequency, and 5) smoking appears to induce a tendency towards reducing cardiac cycle variability.

Adult↗

PubMed1993

Radiofrequency versus pharmacologic modification of the atrioventricular node.

Although transcatheter radiofrequency modification of the atrioventricular (AV) node has been proposed as curative treatment in AV nodal reentry tachycardias, its role for the control of the ventricular rate in atrial tachyarrhythmias remains unclear. The aim of this study was to analyze the acute effect of radiofrequency current on AV nodal conduction and refractoriness, and to compare it with the effects of two antiarrhythmic drugs such as amiodarone (class III) and flecainide (class I). Twenty-one dogs were studied: (1) radiofrequency group (5 W for less than 45 seconds; 2 to 12 discharges; seven dogs); (2) amiodarone group (5 mg/kg intravenously; seven dogs); and (3) flecainide group (2 mg/kg intravenously; seven dogs). The following parameters were measured under basal conditions and after each procedure: AH interval, AV nodal functional refractory period, Wenckebach cycle length, minimum R-R interval during atrial fibrillation, and fitting of AV nodal function curve to a hyperbolic equation using its linear transformation. The AV nodal effective refractory period could not be calculated in any dog in the basal study because it was shorter than the atrial functional refractory period.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone↗