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Apneustic Center

The Experts below are selected from a list of 3 Experts worldwide ranked by ideXlab platform

Dimitris Siablis – 1st expert on this subject based on the ideXlab platform

  • Re: Bradyarrhythmias during Use of the AngioJet System
    Journal of Vascular and Interventional Radiology, 2007
    Co-Authors: Dimitris Karnabatidis, Konstantinos Katsanos, George C. Kagadis, Dimitris Siablis

    Abstract:

    Editor: We read with great interest the article by Dwarka et al (1) in the October issue of JVIR regarding the occurrence of bradyarrhythmias during central venous application of the AngioJet thrombectomy catheter (Possis Medical, Minneapolis, Minn). We have also recently published our experience on the matter, describing similar phenomena during intrapulmonary activation of the device (2). However, we would like to express our skepticism with respect to the mechanistic explanation provided for the bradyarrythmias by the authors and our disagreement with the proposed rationale for pre-treatment with gadolinium or streptomycin. Indeed, the AngioJet device uses lateral saline jets, which are combined with periods of negative pressure vacuums due to the Bernoulli effect, so as to simultaneously macerate and aspirate thrombi. Nevertheless, mechanical pressure wave fronts propagate radially and in a cross-sectional level perpendicular to the distal catheter tip. Should one contemplate carefully the anatomy of the large vessels and heart, it is rather improbable that pressure waves originating from an AngioJet catheter that is activated in pulmonary branches, especially those of the right lung lobe, will have an influence on left ventricular electrophysiology. To our utmost surprise, the authors proposed that pretreatment with gadolinium or streptomycin may prevent stretch-induced activation of endothelial receptors by the hydrodynamic jets. After careful review of the cited literature (1), however, it is well understood that mechanical stimulation of stretch-activated receptors of ventricular myocytes may lead to shorter refractory intervals and decreased re-polarization periods. As a result, extrasystoles and pro-arrhythmogenic re-entry cycles may occur, which are actually tachyarrhythmias. All that notwithstanding, the AngioJet invokes bradycardia and type III heart block, which has been documented electrocardiographically (3). Moreover, activation of the AngioJet catheter in the pulmonary vessels causes not only bradyarrhythmia but also disruption of normal breathing. Both Siablis et al (2) and Zeni et al (4) have reported episodes of shortness of breath and apnea, which is even more difficult to explain. In addition, it was stated that aura symptoms with associated cutaneous erythema were also experienced (2). Hence, the generation of rapidly degrading local humoral byproducts during rheolytic maceration of thrombus is a more plausible explanation. Liberated adenosine may be incriminated for the short-lasting bradyarrythmias, whereas serotonin has been proposed as an explanation for the erythema and the aura symptoms (2). Conversely, we have proposed that mechanical irritation of the afferent vagal pulmonary c-fibers that underline the wall of pulmonary vessels and stimulate the Apneustic Center in the central nervous system could account for the apnea phenomena (2). In our experience, pre-treatment with aminophylline and short-lasting activation of the AngioJet device has produced satisfactory results in limiting the aforementioned complications. Nevertheless, because neither the above suggestions nor the ones proposed by Dwarka et al (1) bear any credible scientific evidence or at least experimental proof of concept, we think that the necessary cautiousness during central venous operation of the AngioJet device cannot be overstressed.

Dimitris Karnabatidis – 2nd expert on this subject based on the ideXlab platform

  • Re: Bradyarrhythmias during Use of the AngioJet System
    Journal of Vascular and Interventional Radiology, 2007
    Co-Authors: Dimitris Karnabatidis, Konstantinos Katsanos, George C. Kagadis, Dimitris Siablis

    Abstract:

    Editor: We read with great interest the article by Dwarka et al (1) in the October issue of JVIR regarding the occurrence of bradyarrhythmias during central venous application of the AngioJet thrombectomy catheter (Possis Medical, Minneapolis, Minn). We have also recently published our experience on the matter, describing similar phenomena during intrapulmonary activation of the device (2). However, we would like to express our skepticism with respect to the mechanistic explanation provided for the bradyarrythmias by the authors and our disagreement with the proposed rationale for pre-treatment with gadolinium or streptomycin. Indeed, the AngioJet device uses lateral saline jets, which are combined with periods of negative pressure vacuums due to the Bernoulli effect, so as to simultaneously macerate and aspirate thrombi. Nevertheless, mechanical pressure wave fronts propagate radially and in a cross-sectional level perpendicular to the distal catheter tip. Should one contemplate carefully the anatomy of the large vessels and heart, it is rather improbable that pressure waves originating from an AngioJet catheter that is activated in pulmonary branches, especially those of the right lung lobe, will have an influence on left ventricular electrophysiology. To our utmost surprise, the authors proposed that pretreatment with gadolinium or streptomycin may prevent stretch-induced activation of endothelial receptors by the hydrodynamic jets. After careful review of the cited literature (1), however, it is well understood that mechanical stimulation of stretch-activated receptors of ventricular myocytes may lead to shorter refractory intervals and decreased re-polarization periods. As a result, extrasystoles and pro-arrhythmogenic re-entry cycles may occur, which are actually tachyarrhythmias. All that notwithstanding, the AngioJet invokes bradycardia and type III heart block, which has been documented electrocardiographically (3). Moreover, activation of the AngioJet catheter in the pulmonary vessels causes not only bradyarrhythmia but also disruption of normal breathing. Both Siablis et al (2) and Zeni et al (4) have reported episodes of shortness of breath and apnea, which is even more difficult to explain. In addition, it was stated that aura symptoms with associated cutaneous erythema were also experienced (2). Hence, the generation of rapidly degrading local humoral byproducts during rheolytic maceration of thrombus is a more plausible explanation. Liberated adenosine may be incriminated for the short-lasting bradyarrythmias, whereas serotonin has been proposed as an explanation for the erythema and the aura symptoms (2). Conversely, we have proposed that mechanical irritation of the afferent vagal pulmonary c-fibers that underline the wall of pulmonary vessels and stimulate the Apneustic Center in the central nervous system could account for the apnea phenomena (2). In our experience, pre-treatment with aminophylline and short-lasting activation of the AngioJet device has produced satisfactory results in limiting the aforementioned complications. Nevertheless, because neither the above suggestions nor the ones proposed by Dwarka et al (1) bear any credible scientific evidence or at least experimental proof of concept, we think that the necessary cautiousness during central venous operation of the AngioJet device cannot be overstressed.

George C. Kagadis – 3rd expert on this subject based on the ideXlab platform

  • Re: Bradyarrhythmias during Use of the AngioJet System
    Journal of Vascular and Interventional Radiology, 2007
    Co-Authors: Dimitris Karnabatidis, Konstantinos Katsanos, George C. Kagadis, Dimitris Siablis

    Abstract:

    Editor: We read with great interest the article by Dwarka et al (1) in the October issue of JVIR regarding the occurrence of bradyarrhythmias during central venous application of the AngioJet thrombectomy catheter (Possis Medical, Minneapolis, Minn). We have also recently published our experience on the matter, describing similar phenomena during intrapulmonary activation of the device (2). However, we would like to express our skepticism with respect to the mechanistic explanation provided for the bradyarrythmias by the authors and our disagreement with the proposed rationale for pre-treatment with gadolinium or streptomycin. Indeed, the AngioJet device uses lateral saline jets, which are combined with periods of negative pressure vacuums due to the Bernoulli effect, so as to simultaneously macerate and aspirate thrombi. Nevertheless, mechanical pressure wave fronts propagate radially and in a cross-sectional level perpendicular to the distal catheter tip. Should one contemplate carefully the anatomy of the large vessels and heart, it is rather improbable that pressure waves originating from an AngioJet catheter that is activated in pulmonary branches, especially those of the right lung lobe, will have an influence on left ventricular electrophysiology. To our utmost surprise, the authors proposed that pretreatment with gadolinium or streptomycin may prevent stretch-induced activation of endothelial receptors by the hydrodynamic jets. After careful review of the cited literature (1), however, it is well understood that mechanical stimulation of stretch-activated receptors of ventricular myocytes may lead to shorter refractory intervals and decreased re-polarization periods. As a result, extrasystoles and pro-arrhythmogenic re-entry cycles may occur, which are actually tachyarrhythmias. All that notwithstanding, the AngioJet invokes bradycardia and type III heart block, which has been documented electrocardiographically (3). Moreover, activation of the AngioJet catheter in the pulmonary vessels causes not only bradyarrhythmia but also disruption of normal breathing. Both Siablis et al (2) and Zeni et al (4) have reported episodes of shortness of breath and apnea, which is even more difficult to explain. In addition, it was stated that aura symptoms with associated cutaneous erythema were also experienced (2). Hence, the generation of rapidly degrading local humoral byproducts during rheolytic maceration of thrombus is a more plausible explanation. Liberated adenosine may be incriminated for the short-lasting bradyarrythmias, whereas serotonin has been proposed as an explanation for the erythema and the aura symptoms (2). Conversely, we have proposed that mechanical irritation of the afferent vagal pulmonary c-fibers that underline the wall of pulmonary vessels and stimulate the Apneustic Center in the central nervous system could account for the apnea phenomena (2). In our experience, pre-treatment with aminophylline and short-lasting activation of the AngioJet device has produced satisfactory results in limiting the aforementioned complications. Nevertheless, because neither the above suggestions nor the ones proposed by Dwarka et al (1) bear any credible scientific evidence or at least experimental proof of concept, we think that the necessary cautiousness during central venous operation of the AngioJet device cannot be overstressed.