Biomedical subjects

L Mainar

Publications and source records attributed to L Mainar.

6 recordsLinked to original sources

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

[The assessment of cardiac involvement in a case of a thoracic injury from a firearm].

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.

Adult↗

PubMed1996

[Cardiac angiosarcoma].

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.

Adult↗