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Sore Throat: A Harbinger of a Lethal Diagnosis
Abstracts
45 Sore Throat: A Harbinger of a Lethal Diagnosis K. Rajakariar 1,∗ , A. Koshy 1 , S. Tsui 1,2 , G. Proimos 1,3 1 Department
of Cardiology, Box Hill Hospital, Australia 2 Department of Radiology, Box Hill Hospital, Australia 3 Department of Cardiology, The Austin Hospital, Australia Background: Initial clinical diagnosis of aortic dissection can be challenging. Classical symptoms are often absent, and atypical presentations are associated with delayed diagnosis and increased mortality rates. We describe two cases of isolated throat discomfort as the only symptom of a Stanford type A aortic dissection. Case Presentation: In the first case, a previously healthy 77 year old man presented in significant distress with isolated throat discomfort. Electrocardiogram (ECG) showed transient high grade atrioventricular block with normal troponins. Transthoracic echocardiogram later demonstrated a 5.9 cm ascending aorta. A computed tomography (CT) aortogram confirmed type A aortic dissection extending into the great vessels. He suffered a cardiac arrest shortly after and died. The second case involved a 57 year old man who initially described chest pain, with an ECG demonstrating ST elevation in aVR with reciprocal infero-lateral ST depression and normal troponins. Coronary angiogram was unremarkable. Post-procedure, he complained of isolated throat discomfort raising suspicion of possible aortic dissection. Urgent CT aortogram was performed, and demonstrated a type A dissection extending into the great vessels. He subsequently underwent successful graft replacement. Conclusion: A sore throat may be the sole feature to prompt consideration of aortic dissection in a patient where symptoms are disproportionate to the overall clinical state. The throat discomfort is attributable to propagation of the dissection plane to the great vessels, as was the case in both patients. The contrasting case series illustrates the importance of considering this atypical symptom as an early manifestation of aortic dissection. http://dx.doi.org/10.1016/j.hlc.2016.06.046 46 The 3 Adrenergic Receptor Agonist, CL 216, 343, Promotes Angiogenesis
K. Bubb, O. Tang ∗ , T. Hansen, T. Huang, G. Figtree Kolling Institute, University of Sydney, Australia Background: 3 adrenergic receptor (3AR) agonists activate endothelial nitric oxide synthase (eNOS). We have demonstrated that this is at least partially due to decreased
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glutathionylation-mediated uncoupling of eNOS, restoring NO production, and decreasing superoxide generation. Given NO is a key regulator of angiogenesis, we have now examined the effect of 3AR on endothelial cell migration and tubule formation. Methods and Results: Angiogenesis was measured in vitro in human umbilical vein endothelial cells using migration and tubule formation assays; both recorded using timelapse video-microscopy. For migration assays, a scratch wound was produced in the cell monolayer. 12 hours post-scratch, wound closure was 57.8±4.6% in controls. Cells treated with the 3AR agonist, CL 216,343 (CL) exhibited a concentrationdependent increase in migration which was ∼20% greater at the higher concentrations (P<0.001, Two-way ANOVA). For tubule formation experiments, 1 x 104 cells were added to wells coated with matrigel and tubules formed over 4-12 hours. The formation of tubules was augmented by CL, with the maximal increase 70% higher than control (P<0.05, Student’s t-test). In both of these experiments, the NOS inhibitor, L-NAME (300 mol/L) abolished the CLdependent increase. Studies are ongoing to determine the effect of CL on in vivo angiogenesis and to elucidate the mechanisms. Conclusion: The 3 adrenergic agonist, CL 216, 343, increases angiogenesis in vitro by an NO-dependent mechanism. As 3AR agonists are clinically available for management of non-cardiac conditions, these findings may be imminently translatable as a new therapy for chronic myocardial or peripheral artery ischaemia. http://dx.doi.org/10.1016/j.hlc.2016.06.047 47 The Association of Obesity with Arterial Function and Structure - A Systematic Review and Meta-Analysis J. Ne 1,2,∗ , T. Cai 1,2 , D. Celermajer 1 , I. Caterson 2 , T. Gill 2 , C. Lee 2 , M. Skilton 2 1 The
University of Sydney, Sydney Medical School, Australia 2 Boden Institute of Obesity, Nutrition, Exercise and Eating Disorders, Australia Background: Obesity is an established risk factor for cardiovascular events. Although the mechanisms by which obesity affects cardiovascular risk have not been fully elucidated, atherosclerosis is likely to be involved. We undertook a comprehensive systematic review and meta-analysis to study how obesity (measured with BMI) is associated with brachial flow-mediated dilatation and carotid intima-media thickness, key non-invasive measures of arterial function and structure respectively. Methods: Electronic searches for “Obesity and flowmediated dilatation” and “Obesity and intima-media thickness” were performed using Ovid Medline and Embase databases. No language limits were applied. Meta-analysis was undertaken to obtain pooled estimates for the obese and healthy weight adults. Results: Of the 4822 articles retrieved, 19 studies on flowmediated dilatation and 19 studies on intima-media thickness
45 Sore Throat: A Harbinger of a Lethal Diagnosis K. Rajakariar 1,∗ , A. Koshy 1 , S. Tsui 1,2 , G. Proimos 1,3 1 Department
of Cardiology, Box Hill Hospital, Australia 2 Department of Radiology, Box Hill Hospital, Australia 3 Department of Cardiology, The Austin Hospital, Australia Background: Initial clinical diagnosis of aortic dissection can be challenging. Classical symptoms are often absent, and atypical presentations are associated with delayed diagnosis and increased mortality rates. We describe two cases of isolated throat discomfort as the only symptom of a Stanford type A aortic dissection. Case Presentation: In the first case, a previously healthy 77 year old man presented in significant distress with isolated throat discomfort. Electrocardiogram (ECG) showed transient high grade atrioventricular block with normal troponins. Transthoracic echocardiogram later demonstrated a 5.9 cm ascending aorta. A computed tomography (CT) aortogram confirmed type A aortic dissection extending into the great vessels. He suffered a cardiac arrest shortly after and died. The second case involved a 57 year old man who initially described chest pain, with an ECG demonstrating ST elevation in aVR with reciprocal infero-lateral ST depression and normal troponins. Coronary angiogram was unremarkable. Post-procedure, he complained of isolated throat discomfort raising suspicion of possible aortic dissection. Urgent CT aortogram was performed, and demonstrated a type A dissection extending into the great vessels. He subsequently underwent successful graft replacement. Conclusion: A sore throat may be the sole feature to prompt consideration of aortic dissection in a patient where symptoms are disproportionate to the overall clinical state. The throat discomfort is attributable to propagation of the dissection plane to the great vessels, as was the case in both patients. The contrasting case series illustrates the importance of considering this atypical symptom as an early manifestation of aortic dissection. http://dx.doi.org/10.1016/j.hlc.2016.06.046 46 The 3 Adrenergic Receptor Agonist, CL 216, 343, Promotes Angiogenesis
K. Bubb, O. Tang ∗ , T. Hansen, T. Huang, G. Figtree Kolling Institute, University of Sydney, Australia Background: 3 adrenergic receptor (3AR) agonists activate endothelial nitric oxide synthase (eNOS). We have demonstrated that this is at least partially due to decreased
S21
.. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. ..
glutathionylation-mediated uncoupling of eNOS, restoring NO production, and decreasing superoxide generation. Given NO is a key regulator of angiogenesis, we have now examined the effect of 3AR on endothelial cell migration and tubule formation. Methods and Results: Angiogenesis was measured in vitro in human umbilical vein endothelial cells using migration and tubule formation assays; both recorded using timelapse video-microscopy. For migration assays, a scratch wound was produced in the cell monolayer. 12 hours post-scratch, wound closure was 57.8±4.6% in controls. Cells treated with the 3AR agonist, CL 216,343 (CL) exhibited a concentrationdependent increase in migration which was ∼20% greater at the higher concentrations (P<0.001, Two-way ANOVA). For tubule formation experiments, 1 x 104 cells were added to wells coated with matrigel and tubules formed over 4-12 hours. The formation of tubules was augmented by CL, with the maximal increase 70% higher than control (P<0.05, Student’s t-test). In both of these experiments, the NOS inhibitor, L-NAME (300 mol/L) abolished the CLdependent increase. Studies are ongoing to determine the effect of CL on in vivo angiogenesis and to elucidate the mechanisms. Conclusion: The 3 adrenergic agonist, CL 216, 343, increases angiogenesis in vitro by an NO-dependent mechanism. As 3AR agonists are clinically available for management of non-cardiac conditions, these findings may be imminently translatable as a new therapy for chronic myocardial or peripheral artery ischaemia. http://dx.doi.org/10.1016/j.hlc.2016.06.047 47 The Association of Obesity with Arterial Function and Structure - A Systematic Review and Meta-Analysis J. Ne 1,2,∗ , T. Cai 1,2 , D. Celermajer 1 , I. Caterson 2 , T. Gill 2 , C. Lee 2 , M. Skilton 2 1 The
University of Sydney, Sydney Medical School, Australia 2 Boden Institute of Obesity, Nutrition, Exercise and Eating Disorders, Australia Background: Obesity is an established risk factor for cardiovascular events. Although the mechanisms by which obesity affects cardiovascular risk have not been fully elucidated, atherosclerosis is likely to be involved. We undertook a comprehensive systematic review and meta-analysis to study how obesity (measured with BMI) is associated with brachial flow-mediated dilatation and carotid intima-media thickness, key non-invasive measures of arterial function and structure respectively. Methods: Electronic searches for “Obesity and flowmediated dilatation” and “Obesity and intima-media thickness” were performed using Ovid Medline and Embase databases. No language limits were applied. Meta-analysis was undertaken to obtain pooled estimates for the obese and healthy weight adults. Results: Of the 4822 articles retrieved, 19 studies on flowmediated dilatation and 19 studies on intima-media thickness