- Email: [email protected]
Intraoperative Transesophageal Echocardiography Diagnosis of Concomitant Hypertrophic Cardiomyopathy With Anomalous Insertion of a Papillary Muscle Band to the Interventricular Septum in a Patient for Aortic Valve Replacement
e56
LETTERS TO THE EDITOR
larger defects, loss of tidal volume could occur, and we wanted to alert practitioners to the possibility of defects of doublelumen tubes at this site. APPENDIX A. SUPPORTING INFORMATION
Supplementary material cited in this article is available online at doi:10.1053/j.jvca.2014.06.019.
Christian Seefelder, MD Department of Anesthesiology Perioperative and Pain Medicine Boston Children’s Hospital Boston, Massachusetts
Fig 1. Air bubbles entering the bronchial lumen containing the lavage fluid from the ventilated tracheal lumen of the double-lumen tube at the base of the double-lumen tube body.
Tube Left, at the time provided by Cardinal Health, Dublin, OH) was chosen at that time. At some point during whole-lung lavage of his left lung through the left-sided bronchial lumen of the double-lumen tube, continuous bubbling into the fluid-filled lumen was noted at the base of the tube (Video clip 1, Fig 1). It appeared more pronounced during positive-pressure inspiration but was continuous at other times. There was no obvious leakage of fluid into the ventilated lumen, although that lumen did appear to have a lot of condensation, but fluid was noted to intermittently drip off the outside of the tube (Fig 2). There was no obvious loss of tidal volume noted by the ventilator monitor. The lavage was completed uneventfully. Although there was no patient harm or procedural problem, this incident demonstrated the possibility of a defect of doublelumen tubes at the site of their connection. The leak in our case occurred at the site of connection between the body of the double-lumen tube and the insertion site of the 2 distinct external tubes connecting to the different lumens of the body of the tube. Because air was bubbling into the fluid, and seemingly more so with positive-pressure ventilation, it must have leaked from the tracheal lumen of the double-lumen tube to the bronchial lumen. This leak would not have been noticeable during normal use of the double-lumen tube, because bubbles would not have been seen. However, with
Fig 2. Drop of lavage fluid on the outside of the double-lumen tube at the base of the tube where the leak between the 2 lumens occurred.
http://dx.doi.org/10.1053/j.jvca.2014.06.019
Intraoperative Transesophageal Echocardiography Diagnosis of Concomitant Hypertrophic Cardiomyopathy With Anomalous Insertion of a Papillary Muscle Band to the Interventricular Septum in a Patient for Aortic Valve Replacement To the Editor: A 53-year-old man was admitted for surgery with a diagnosis of aortic valve stenosis, left ventricular outflow tract (LVOT) obstruction by systolic anterior motion of the mitral valve, and moderate-to-severe mitral regurgitation. Peak and mean LVOT gradients measured by transthoracic echocardiography were 91 mmHg and 51 mmHg, respectively. Intraoperative transesophageal echocardiography (TEE) showed calcific aortic stenosis with moderate aortic insufficiency and systolic anterior motion of the anterior leaflet of the mitral valve. The interventricular septum measured 2.86 cm in diastole, with anomalous insertion of a band from the anterolateral papillary muscle to the basal septum. Peak LVOT gradient was 208 mmHg in concurrence with moderate-tosevere mitral regurgitation (Fig 1, Video clip 1). The aortic valve was bicuspid and calcified. He underwent aortic valve replacement with a mechanical prosthesis, extended septal myectomy, and excision of an abnormal band to the ventricular septum. The anterolateral papillary muscle was bifid, with 1 head giving rise to the chordae and the other continued as a band to insert into the anterobasal septum. Postoperative TEE showed no LVOT obstruction, mild mitral regurgitation, and a mean gradient of 14 mmHg across the aortic valve prosthesis. Associated hypertrophic cardiomyopathy and LVOT narrowing by asymmetric hypertrophy are the 2 reasons for subvalvular obstruction in patients for aortic valve replacement.1 An asymmetric pattern of wall thickening occurs in 22% to 27% of aortic valve replacement patients, particularly in the
e57
LETTERS TO THE EDITOR
Fig 1. (A) Echocardiographic features of hypertrophic cardiomyopathy as seen in our patient reveals the anomalous band inserted on the ventricular septum and systolic anterior motion of mitral valve. The aortic valve was calcified and bicuspid. (B) The mid esophageal 5 chamber view shows flow acceleration in left ventricular outflow tract and mitral valve incompetence. (C) Zoom view showing insertion of anomalous band to ventricular septum.
elderly, and women with hypertension.2 Asymmetric wall thickening occurs most commonly in the septum at the basal and midcavity levels and can cause subvalvular obstruction in severely hypertrophied ventricles with small intracavity volume and may resemble the morphology of hypertrophic cardiomyopathy. In patients with asymmetric hypertrophy, the mechanical narrowing and squeezing of the LVOT leads to abnormal flow velocities across the LVOT, which may persist after aortic valve replacement, and adversely affects the prognosis. However systolic anterior motion of the mitral valve usually is absent, although it may appear in hyperdynamic ventricles once the afterload of aortic stenosis is relieved. Septal myectomy3 during aortic valve replacement is indicated in patients with either a demonstrable dynamic subaortic gradient or marked septal hypertrophy (septal-free wall ratio 4 1.3). The clinical diagnosis of hypertrophic cardiomyopathy is based on the demonstration of left ventricular hypertrophy in the absence of another disease process that reasonably can account for the magnitude of hypertrophy present. The left ventricular hypertrophy rarely exceeds more than 20 mm in systemic hypertension or aortic stenosis; and, in patients with these conditions, coexistent hypertrophic cardiomyopathy should be suspected when the left ventricular wall thickness is more than 25 mm and associated with LVOT obstruction because of systolic anterior motion, papillary muscle anomalies, and abnormally elongated anterior mitral leaflet.4 The intraoperative increase in LVOT gradient also points to the dynamic nature of LVOT obstruction in hypertrophic cardiomyopathy due to change in loading conditions induced by anesthesia. In patients for aortic valve replacement, LVOT should be interrogated by pulse-wave and/or color-flow Doppler to document subvalvular obstruction. If systolic anterior motion of the mitral valve is detected, then further anomalies in the
spectrum of hypertrophic cardiomyopathy should be identified. Preoperative 2-D transthoracic echocardiography may not be reliable to diagnose anomalies of papillary muscles as the delineation often requires multiple off-axis images. Cardiac magnetic resonance imaging or TEE can diagnose these variations and can guide the surgical approach. Residual LVOT gradient after surgery leads to persistence of symptoms and adversely affects the long-term prognosis. The contribution of an anomalous papillary band in creating LVOT obstruction is not clear, and systolic anterior motion of the mitral valve was probably the dominant mechanism of LVOT obstruction. APPENDIX A. SUPPLEMENTARY MATERIAL
Supplementary material cited in this article is available online at doi:10.1053/j.jvca.2014.06.023.
Praveen Kerala Varma, Mch* Suneel Puthuvassery Raman, MD† Koniparambil Pappu Unnikrishnan, MD† Simran Kundan, Mch* Shrinivas Vitthal Gadhinglajkar, MD† *Division of Cardiac Surgery †Division of Anesthesiology Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, India
REFERENCES 1. Bach DS: Subvalvular left ventricular outflow obstruction for patients undergoing aortic valve replacement for aortic stenosis: Echocardiographic recognition and identification of patients at risk. J Am Soc Echocardiogr 18:1155-1162, 2005
e58
LETTERS TO THE EDITOR
2. Dweck MR, Joshi S, Murigu T, et al: Left ventricular remodeling and hypertrophy in patients with aortic stenosis: insights from cardiovascular magnetic resonance. J Cardiovasc Magn Reson 14:50, 2012 3. Kayalar N, Schaff HV, Daly RC, et al: Concomitant septal myectomy at the time of aortic valve replacement for severe aortic stenosis. Ann Thorac Surg 89:459-464, 2010 4. Gersh BJ, Maron BJ, Bonow RO, et al: ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Developed in collaboration with the American Association for Thoracic Surgery, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, and Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol 58:e212-e260, 2011 http://dx.doi.org/10.1053/j.jvca.2014.06.023
Association Between Adenosine Diphosphate-Induced Platelet Aggregation and Bleeding Outcome in Coronary Artery Surgery To the Editor: We read with great interest the recently published retrospective study by Dalen et al.1 To investigate the association between adenosine diphosphate (ADP)-induced platelet aggregation and postoperative blood loss as well as transfusion requirements, 88 adult patients with an acute coronary syndrome (ACS) undergoing primary isolated coronary artery surgery (CAS) were enrolled in a prospective observational study.1 The authors did not find a significant association between ADP-induced platelet aggregation and postoperative blood loss, while there was a significant association between ADP-induced platelet aggregation and number of platelet concentrates transfused.1 In this type of study, some methodologic issues should be addressed. Patient selection is very important. In the present study,1 patients receiving prasugrel and ticagrelor were excluded.1 Certain proportions of patients on clopidogrel therapy have a high degree of residual platelet “on-treatment” reactivity. Together with platelet function recovery following drug cessation, we may assume that a certain proportion of patients in the present study have had ADP-receptor activity within almost a normal range.1 Ability to predict bleeding using platelet function testing is of limited value if observed values of ADP-receptor activity are close to normal range. Therefore, in further studies, we would recommend to also include patients preoperatively exposed to prasugrel or ticagrelor. In this way, the study cohort would consist of 3 subgroups with respect to preoperative exposure to (1) clopidogrel, (2) prasugrel and (3) ticagrelor. We assume that predictability of bleeding would be more accurate in patients having more pronounced ADP platelet-receptor inhibition. Dalen et al1 reported that platelet aggregation was not associated with postoperative blood loss, but was associated
significantly with number of platelet concentrates administered.1 It remains unclear whether consultant anesthesiologists/ intensivists were aware of platelet function test findings. Even if they were blinded to results of platelet function testing, there are some drawbacks in defining endpoints such as bleeding amount and transfusion requirements that should be discussed. Rosengart2 et al recently evaluated the ability of platelet function testing to identify patients at increased risk for bleeding and transfusion requirements.2 The authors described a very interesting way to define bleeding outcomes.2 Variables such as chest tube output and transfusion requirements were expressed dichotomously and a composite outcome indicative of surgery-related bleeding was defined.2 For further research, we suggest choosing such a composite endpoint because it incorporates 2 outcomes whose incidence is inversely related.2 Using this composite endpoint it is possible to control for the confounding effect of procoagulant blood components transfusion that are administered routinely by the attending anesthesiologist if deemed necessary, regardless of being unaware of platelet function testing. Administered procoagulant blood components certainly reduce the amount of chest tube output and hamper the association between platelet function test results and bleeding amount by reducing sensitivity of platelet function tests in predicting blood loss. Moreover, the International Initiative for Hemostasis Management in Cardiac Surgery recently proposed a universal definition of perioperative bleeding in adult cardiac surgery.3 This definition inevitably should be evaluated in further investigations as this multistage definition may help to obtain more precise and reliable results. Prediction of excessive bleeding and transfusion requirements is a challenging issue and requires an individual approach using platelet function testing. However, some aforementioned methodologic considerations might help to provide more accurate and reliable results in this important field. The concept of bleeding risk prediction using platelet function tests should be revisited in the context of an evergrowing proportion of patients being exposed preoperatively to more potent antiplatelet drugs; and in such a subgroup of patients, potential benefits could be the greatest. We congratulate the authors on their elegant and timely research. Mate Petricevic, MD* Bojan Biocina, MD, PhD* Martina Zrno Mihaljevic, MD* Kresimir Kolic, MD† *School of Medicine University of Zagreb, University Hospital Center Zagreb, Cardiac Surgery Department, Zagreb, Croatia †School of Medicine University of Split University Hospital Center Split, Department of Clinical Diagnostics, Split, Croatia
REFERENCES 1. Dalen M, van der Linden J, Holm M, et al: Adenosine Diphosphate-Induced Single-Platelet Count Aggregation and Bleeding in Clopidogrel-Treated Patients Undergoing Coronary Artery Bypass Grafting. J Cardiothorac Vasc Anesth. http://dx.doi.org/10.1053/j. jcva.2013.10.007, 2014 2. Rosengart TK, Romeiser JL, White LJ, et al: Platelet activity measured by a rapid turnaround assay identifies coronary artery bypass
LETTERS TO THE EDITOR
larger defects, loss of tidal volume could occur, and we wanted to alert practitioners to the possibility of defects of doublelumen tubes at this site. APPENDIX A. SUPPORTING INFORMATION
Supplementary material cited in this article is available online at doi:10.1053/j.jvca.2014.06.019.
Christian Seefelder, MD Department of Anesthesiology Perioperative and Pain Medicine Boston Children’s Hospital Boston, Massachusetts
Fig 1. Air bubbles entering the bronchial lumen containing the lavage fluid from the ventilated tracheal lumen of the double-lumen tube at the base of the double-lumen tube body.
Tube Left, at the time provided by Cardinal Health, Dublin, OH) was chosen at that time. At some point during whole-lung lavage of his left lung through the left-sided bronchial lumen of the double-lumen tube, continuous bubbling into the fluid-filled lumen was noted at the base of the tube (Video clip 1, Fig 1). It appeared more pronounced during positive-pressure inspiration but was continuous at other times. There was no obvious leakage of fluid into the ventilated lumen, although that lumen did appear to have a lot of condensation, but fluid was noted to intermittently drip off the outside of the tube (Fig 2). There was no obvious loss of tidal volume noted by the ventilator monitor. The lavage was completed uneventfully. Although there was no patient harm or procedural problem, this incident demonstrated the possibility of a defect of doublelumen tubes at the site of their connection. The leak in our case occurred at the site of connection between the body of the double-lumen tube and the insertion site of the 2 distinct external tubes connecting to the different lumens of the body of the tube. Because air was bubbling into the fluid, and seemingly more so with positive-pressure ventilation, it must have leaked from the tracheal lumen of the double-lumen tube to the bronchial lumen. This leak would not have been noticeable during normal use of the double-lumen tube, because bubbles would not have been seen. However, with
Fig 2. Drop of lavage fluid on the outside of the double-lumen tube at the base of the tube where the leak between the 2 lumens occurred.
http://dx.doi.org/10.1053/j.jvca.2014.06.019
Intraoperative Transesophageal Echocardiography Diagnosis of Concomitant Hypertrophic Cardiomyopathy With Anomalous Insertion of a Papillary Muscle Band to the Interventricular Septum in a Patient for Aortic Valve Replacement To the Editor: A 53-year-old man was admitted for surgery with a diagnosis of aortic valve stenosis, left ventricular outflow tract (LVOT) obstruction by systolic anterior motion of the mitral valve, and moderate-to-severe mitral regurgitation. Peak and mean LVOT gradients measured by transthoracic echocardiography were 91 mmHg and 51 mmHg, respectively. Intraoperative transesophageal echocardiography (TEE) showed calcific aortic stenosis with moderate aortic insufficiency and systolic anterior motion of the anterior leaflet of the mitral valve. The interventricular septum measured 2.86 cm in diastole, with anomalous insertion of a band from the anterolateral papillary muscle to the basal septum. Peak LVOT gradient was 208 mmHg in concurrence with moderate-tosevere mitral regurgitation (Fig 1, Video clip 1). The aortic valve was bicuspid and calcified. He underwent aortic valve replacement with a mechanical prosthesis, extended septal myectomy, and excision of an abnormal band to the ventricular septum. The anterolateral papillary muscle was bifid, with 1 head giving rise to the chordae and the other continued as a band to insert into the anterobasal septum. Postoperative TEE showed no LVOT obstruction, mild mitral regurgitation, and a mean gradient of 14 mmHg across the aortic valve prosthesis. Associated hypertrophic cardiomyopathy and LVOT narrowing by asymmetric hypertrophy are the 2 reasons for subvalvular obstruction in patients for aortic valve replacement.1 An asymmetric pattern of wall thickening occurs in 22% to 27% of aortic valve replacement patients, particularly in the
e57
LETTERS TO THE EDITOR
Fig 1. (A) Echocardiographic features of hypertrophic cardiomyopathy as seen in our patient reveals the anomalous band inserted on the ventricular septum and systolic anterior motion of mitral valve. The aortic valve was calcified and bicuspid. (B) The mid esophageal 5 chamber view shows flow acceleration in left ventricular outflow tract and mitral valve incompetence. (C) Zoom view showing insertion of anomalous band to ventricular septum.
elderly, and women with hypertension.2 Asymmetric wall thickening occurs most commonly in the septum at the basal and midcavity levels and can cause subvalvular obstruction in severely hypertrophied ventricles with small intracavity volume and may resemble the morphology of hypertrophic cardiomyopathy. In patients with asymmetric hypertrophy, the mechanical narrowing and squeezing of the LVOT leads to abnormal flow velocities across the LVOT, which may persist after aortic valve replacement, and adversely affects the prognosis. However systolic anterior motion of the mitral valve usually is absent, although it may appear in hyperdynamic ventricles once the afterload of aortic stenosis is relieved. Septal myectomy3 during aortic valve replacement is indicated in patients with either a demonstrable dynamic subaortic gradient or marked septal hypertrophy (septal-free wall ratio 4 1.3). The clinical diagnosis of hypertrophic cardiomyopathy is based on the demonstration of left ventricular hypertrophy in the absence of another disease process that reasonably can account for the magnitude of hypertrophy present. The left ventricular hypertrophy rarely exceeds more than 20 mm in systemic hypertension or aortic stenosis; and, in patients with these conditions, coexistent hypertrophic cardiomyopathy should be suspected when the left ventricular wall thickness is more than 25 mm and associated with LVOT obstruction because of systolic anterior motion, papillary muscle anomalies, and abnormally elongated anterior mitral leaflet.4 The intraoperative increase in LVOT gradient also points to the dynamic nature of LVOT obstruction in hypertrophic cardiomyopathy due to change in loading conditions induced by anesthesia. In patients for aortic valve replacement, LVOT should be interrogated by pulse-wave and/or color-flow Doppler to document subvalvular obstruction. If systolic anterior motion of the mitral valve is detected, then further anomalies in the
spectrum of hypertrophic cardiomyopathy should be identified. Preoperative 2-D transthoracic echocardiography may not be reliable to diagnose anomalies of papillary muscles as the delineation often requires multiple off-axis images. Cardiac magnetic resonance imaging or TEE can diagnose these variations and can guide the surgical approach. Residual LVOT gradient after surgery leads to persistence of symptoms and adversely affects the long-term prognosis. The contribution of an anomalous papillary band in creating LVOT obstruction is not clear, and systolic anterior motion of the mitral valve was probably the dominant mechanism of LVOT obstruction. APPENDIX A. SUPPLEMENTARY MATERIAL
Supplementary material cited in this article is available online at doi:10.1053/j.jvca.2014.06.023.
Praveen Kerala Varma, Mch* Suneel Puthuvassery Raman, MD† Koniparambil Pappu Unnikrishnan, MD† Simran Kundan, Mch* Shrinivas Vitthal Gadhinglajkar, MD† *Division of Cardiac Surgery †Division of Anesthesiology Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, India
REFERENCES 1. Bach DS: Subvalvular left ventricular outflow obstruction for patients undergoing aortic valve replacement for aortic stenosis: Echocardiographic recognition and identification of patients at risk. J Am Soc Echocardiogr 18:1155-1162, 2005
e58
LETTERS TO THE EDITOR
2. Dweck MR, Joshi S, Murigu T, et al: Left ventricular remodeling and hypertrophy in patients with aortic stenosis: insights from cardiovascular magnetic resonance. J Cardiovasc Magn Reson 14:50, 2012 3. Kayalar N, Schaff HV, Daly RC, et al: Concomitant septal myectomy at the time of aortic valve replacement for severe aortic stenosis. Ann Thorac Surg 89:459-464, 2010 4. Gersh BJ, Maron BJ, Bonow RO, et al: ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Developed in collaboration with the American Association for Thoracic Surgery, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, and Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol 58:e212-e260, 2011 http://dx.doi.org/10.1053/j.jvca.2014.06.023
Association Between Adenosine Diphosphate-Induced Platelet Aggregation and Bleeding Outcome in Coronary Artery Surgery To the Editor: We read with great interest the recently published retrospective study by Dalen et al.1 To investigate the association between adenosine diphosphate (ADP)-induced platelet aggregation and postoperative blood loss as well as transfusion requirements, 88 adult patients with an acute coronary syndrome (ACS) undergoing primary isolated coronary artery surgery (CAS) were enrolled in a prospective observational study.1 The authors did not find a significant association between ADP-induced platelet aggregation and postoperative blood loss, while there was a significant association between ADP-induced platelet aggregation and number of platelet concentrates transfused.1 In this type of study, some methodologic issues should be addressed. Patient selection is very important. In the present study,1 patients receiving prasugrel and ticagrelor were excluded.1 Certain proportions of patients on clopidogrel therapy have a high degree of residual platelet “on-treatment” reactivity. Together with platelet function recovery following drug cessation, we may assume that a certain proportion of patients in the present study have had ADP-receptor activity within almost a normal range.1 Ability to predict bleeding using platelet function testing is of limited value if observed values of ADP-receptor activity are close to normal range. Therefore, in further studies, we would recommend to also include patients preoperatively exposed to prasugrel or ticagrelor. In this way, the study cohort would consist of 3 subgroups with respect to preoperative exposure to (1) clopidogrel, (2) prasugrel and (3) ticagrelor. We assume that predictability of bleeding would be more accurate in patients having more pronounced ADP platelet-receptor inhibition. Dalen et al1 reported that platelet aggregation was not associated with postoperative blood loss, but was associated
significantly with number of platelet concentrates administered.1 It remains unclear whether consultant anesthesiologists/ intensivists were aware of platelet function test findings. Even if they were blinded to results of platelet function testing, there are some drawbacks in defining endpoints such as bleeding amount and transfusion requirements that should be discussed. Rosengart2 et al recently evaluated the ability of platelet function testing to identify patients at increased risk for bleeding and transfusion requirements.2 The authors described a very interesting way to define bleeding outcomes.2 Variables such as chest tube output and transfusion requirements were expressed dichotomously and a composite outcome indicative of surgery-related bleeding was defined.2 For further research, we suggest choosing such a composite endpoint because it incorporates 2 outcomes whose incidence is inversely related.2 Using this composite endpoint it is possible to control for the confounding effect of procoagulant blood components transfusion that are administered routinely by the attending anesthesiologist if deemed necessary, regardless of being unaware of platelet function testing. Administered procoagulant blood components certainly reduce the amount of chest tube output and hamper the association between platelet function test results and bleeding amount by reducing sensitivity of platelet function tests in predicting blood loss. Moreover, the International Initiative for Hemostasis Management in Cardiac Surgery recently proposed a universal definition of perioperative bleeding in adult cardiac surgery.3 This definition inevitably should be evaluated in further investigations as this multistage definition may help to obtain more precise and reliable results. Prediction of excessive bleeding and transfusion requirements is a challenging issue and requires an individual approach using platelet function testing. However, some aforementioned methodologic considerations might help to provide more accurate and reliable results in this important field. The concept of bleeding risk prediction using platelet function tests should be revisited in the context of an evergrowing proportion of patients being exposed preoperatively to more potent antiplatelet drugs; and in such a subgroup of patients, potential benefits could be the greatest. We congratulate the authors on their elegant and timely research. Mate Petricevic, MD* Bojan Biocina, MD, PhD* Martina Zrno Mihaljevic, MD* Kresimir Kolic, MD† *School of Medicine University of Zagreb, University Hospital Center Zagreb, Cardiac Surgery Department, Zagreb, Croatia †School of Medicine University of Split University Hospital Center Split, Department of Clinical Diagnostics, Split, Croatia
REFERENCES 1. Dalen M, van der Linden J, Holm M, et al: Adenosine Diphosphate-Induced Single-Platelet Count Aggregation and Bleeding in Clopidogrel-Treated Patients Undergoing Coronary Artery Bypass Grafting. J Cardiothorac Vasc Anesth. http://dx.doi.org/10.1053/j. jcva.2013.10.007, 2014 2. Rosengart TK, Romeiser JL, White LJ, et al: Platelet activity measured by a rapid turnaround assay identifies coronary artery bypass