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Assessment of Myocardial Oxygenation, Strain and Diastology in MBYPC3 Hypertrophic Cardiomyopathy: A Cardiovascular Magnetic Resonance and Echocardiography Study
Abstracts
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incorporated in liposomes for functional analysis by patchclamp technique. Exposing the long NT isoform to 2 mM oxidised glutathione increased Po from 0.026±0.008 to 0.088± 0.014 without altering the magnitude of the current or the current–voltage relationship (n=6) while1 mM reduced glutathione decreased Po from 0.029±0.007 to 0.010±0.007 (n=5; p<0.05). However mutation of cysteines in the cytoplasmic loop I-II region attenuated the effect of glutathione on open probability (0.0135±0.003 vs 0.0143±0.003 n=10; p=NS) and altered protein folding assessed by thermal shift assay. Specifically we find that mutation of C543S is sufficient to confer sensitivity of Cav1.2 to glutathione and is responsible for modifying posttranslational folding. Our data provide evidence for direct regulation of Cav1.2 channel function by glutathione during oxidative stress. http://dx.doi.org/10.1016/j.hlc.2016.06.169 169 Acute Pericarditis: Predictors of the Presence of a Pericardial Effusion – The Experience in a Tertiary Centre U. Allahwala ∗ , J. Namkoong, B. Gray, S. Soo Hoo, C. Choong, R. Bhindi, G. Tofler Department of Cardiology, Royal North Shore Hospital, Sydney, Australia Background and aims: Acute pericarditis is a common diagnosis in patients presenting with chest pain. Whilst it generally has a benign course, significant pericardial effusion needs to be excluded. We sought to characterise the demographics of patients with pericarditis, as well as determine predictors of significant effusion. Methods: This was a single centre retrospective study of consecutive patients diagnosed with acute pericarditis from May 2013 – May 2015. Results: 254 patients were diagnosed with acute pericarditis, of whom 230 met ESC criteria. The mean age was 47.5, with 27% female. The majority of cases were idiopathic (61.7%), followed by viral (29.6%) and autoimmune (3%). 192 patients had a formal transthoracic echocardiogram, the majority of whom had either no or a trivial pericardial effusion (81.3%), with 11.5% having a small effusion, 4.7% moderate and 2.6% large. Patients with a significant effusion had a higher peak CRP (155.8 mg/L vs 44 mg/L, p<0.0001), lower albumin (37.6 g/L vs 41.7 g/L, p<0.05) and lower creatinine (74.4umol/L vs 84.7umol/L, p<0.05). Peak CRP also correlated with the size of effusion (R2 =0.29, p<0.0001). In those with a detectable troponin level, there was no difference in those with or without a significant pericardial effusion (2,733 ng/L vs 1,844 ng/L p = 0.71). The neutrophil to lymphocyte ratio was non-significantly higher in those with a significant effusion (10.5 vs 4.1, p=0.05). Conclusion: In patients presenting to hospital with acute pericarditis, peak CRP appears to be predictive of the presence and size of pericardial effusion, whilst troponin does not. These findings may have implications on which patients require admission for formal echocardiography. http://dx.doi.org/10.1016/j.hlc.2016.06.170
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170 Assessment of Myocardial Oxygenation, Strain and Diastology in MBYPC3 Hypertrophic Cardiomyopathy: A Cardiovascular Magnetic Resonance and Echocardiography Study S. Grover 1,2,∗ , R. Lloyd 1,2 , R. Perry 1,2 , P. Lou 1,2 , G. Srinivasan 1,2 , E. Haan 3 , L. Yeates 4 , R. Woodman 5 , J. Atherton 6 , C. Semsarian 4 , J. Selvanayagam 1,2 1 Flinders
Medical Centre, Adelaide, Australia Australian Health and Medical Research Institute, Adelaide, Australia 3 South Australian Clinical Genetics Service, Adelaide, Australia 4 Centenary Institute, University of Sydney, Sydney, Australia 5 Department of Statistics, Flinders University, Adelaide, Australia 6 Royal Brisbane Hospital, Brisbane, Australia 2 South
Background: Myocardial oxygenation is impaired in patients with hypertrophic cardiomyopathy (G+LVH+) and gene positive patients without hypertrophy (G+LVH-). Whether this is the initiating step prior to development of hypertrophy or abnormalities in left ventricle relaxation is unknown, and the relationship between abnormalities of echocardiographic speckle tracking strain and myocardial oxygenation has not been examined. Method: A total of 43 patients (12 G+LVH+, 13 G+LVH -, 11 gene negative (G-) and 7 normal volunteers (NV)), underwent 2D transthoracic echocardiography for assessment of diastolic function and speckle tracking strain, and Cardiovascular Magnetic Resonance (CMR) imaging for assessment of ventricular volumes, mass and blood oxygen level dependent (BOLD) imaging with vasodilator stress. Results: Reduced myocardial oxygenation was seen in patients with LVH (-4±10%) when compared to G+LVH-, p=0.05; G-, p=0.001, NV, p=0.002). A blunted BOLD response to stress was seen in patients expressing the G+LVH- patients (4±8%), when compared to gene negative controls (14±13%, p=0.02). G+LVH+ patients exhibited abnormal diastolic function including lower E prime (E’), higher E to E’ ratio (E:E’) and greater left atrial area in contrast to the G+LVH- group who all had normal values for these indices. However, there were no differences in diastolic function between the G+LVHand G- group (p=0.2). Reduced global longitudinal strain (GLS) and regional strain was detected in the G+LVH+ group compared with all other groups (G+LVH-, p=0.05; G-, p=0.01; NV p=0.03). There were no differences in GLS and regional strain between the G+LVH- group and the G- (p=0.7) and control groups (p=0.9). Conclusion: A blunted myocardial oxygenation response to vasodilator stress precedes changes in LV strain, wall thickness or diastolic function. Changes in BOLD signal intensity may be a surrogate marker for preclinical hypertrophic cardiomyopathy and lead to development of preventative strategies. http://dx.doi.org/10.1016/j.hlc.2016.06.171
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incorporated in liposomes for functional analysis by patchclamp technique. Exposing the long NT isoform to 2 mM oxidised glutathione increased Po from 0.026±0.008 to 0.088± 0.014 without altering the magnitude of the current or the current–voltage relationship (n=6) while1 mM reduced glutathione decreased Po from 0.029±0.007 to 0.010±0.007 (n=5; p<0.05). However mutation of cysteines in the cytoplasmic loop I-II region attenuated the effect of glutathione on open probability (0.0135±0.003 vs 0.0143±0.003 n=10; p=NS) and altered protein folding assessed by thermal shift assay. Specifically we find that mutation of C543S is sufficient to confer sensitivity of Cav1.2 to glutathione and is responsible for modifying posttranslational folding. Our data provide evidence for direct regulation of Cav1.2 channel function by glutathione during oxidative stress. http://dx.doi.org/10.1016/j.hlc.2016.06.169 169 Acute Pericarditis: Predictors of the Presence of a Pericardial Effusion – The Experience in a Tertiary Centre U. Allahwala ∗ , J. Namkoong, B. Gray, S. Soo Hoo, C. Choong, R. Bhindi, G. Tofler Department of Cardiology, Royal North Shore Hospital, Sydney, Australia Background and aims: Acute pericarditis is a common diagnosis in patients presenting with chest pain. Whilst it generally has a benign course, significant pericardial effusion needs to be excluded. We sought to characterise the demographics of patients with pericarditis, as well as determine predictors of significant effusion. Methods: This was a single centre retrospective study of consecutive patients diagnosed with acute pericarditis from May 2013 – May 2015. Results: 254 patients were diagnosed with acute pericarditis, of whom 230 met ESC criteria. The mean age was 47.5, with 27% female. The majority of cases were idiopathic (61.7%), followed by viral (29.6%) and autoimmune (3%). 192 patients had a formal transthoracic echocardiogram, the majority of whom had either no or a trivial pericardial effusion (81.3%), with 11.5% having a small effusion, 4.7% moderate and 2.6% large. Patients with a significant effusion had a higher peak CRP (155.8 mg/L vs 44 mg/L, p<0.0001), lower albumin (37.6 g/L vs 41.7 g/L, p<0.05) and lower creatinine (74.4umol/L vs 84.7umol/L, p<0.05). Peak CRP also correlated with the size of effusion (R2 =0.29, p<0.0001). In those with a detectable troponin level, there was no difference in those with or without a significant pericardial effusion (2,733 ng/L vs 1,844 ng/L p = 0.71). The neutrophil to lymphocyte ratio was non-significantly higher in those with a significant effusion (10.5 vs 4.1, p=0.05). Conclusion: In patients presenting to hospital with acute pericarditis, peak CRP appears to be predictive of the presence and size of pericardial effusion, whilst troponin does not. These findings may have implications on which patients require admission for formal echocardiography. http://dx.doi.org/10.1016/j.hlc.2016.06.170
.. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .
170 Assessment of Myocardial Oxygenation, Strain and Diastology in MBYPC3 Hypertrophic Cardiomyopathy: A Cardiovascular Magnetic Resonance and Echocardiography Study S. Grover 1,2,∗ , R. Lloyd 1,2 , R. Perry 1,2 , P. Lou 1,2 , G. Srinivasan 1,2 , E. Haan 3 , L. Yeates 4 , R. Woodman 5 , J. Atherton 6 , C. Semsarian 4 , J. Selvanayagam 1,2 1 Flinders
Medical Centre, Adelaide, Australia Australian Health and Medical Research Institute, Adelaide, Australia 3 South Australian Clinical Genetics Service, Adelaide, Australia 4 Centenary Institute, University of Sydney, Sydney, Australia 5 Department of Statistics, Flinders University, Adelaide, Australia 6 Royal Brisbane Hospital, Brisbane, Australia 2 South
Background: Myocardial oxygenation is impaired in patients with hypertrophic cardiomyopathy (G+LVH+) and gene positive patients without hypertrophy (G+LVH-). Whether this is the initiating step prior to development of hypertrophy or abnormalities in left ventricle relaxation is unknown, and the relationship between abnormalities of echocardiographic speckle tracking strain and myocardial oxygenation has not been examined. Method: A total of 43 patients (12 G+LVH+, 13 G+LVH -, 11 gene negative (G-) and 7 normal volunteers (NV)), underwent 2D transthoracic echocardiography for assessment of diastolic function and speckle tracking strain, and Cardiovascular Magnetic Resonance (CMR) imaging for assessment of ventricular volumes, mass and blood oxygen level dependent (BOLD) imaging with vasodilator stress. Results: Reduced myocardial oxygenation was seen in patients with LVH (-4±10%) when compared to G+LVH-, p=0.05; G-, p=0.001, NV, p=0.002). A blunted BOLD response to stress was seen in patients expressing the G+LVH- patients (4±8%), when compared to gene negative controls (14±13%, p=0.02). G+LVH+ patients exhibited abnormal diastolic function including lower E prime (E’), higher E to E’ ratio (E:E’) and greater left atrial area in contrast to the G+LVH- group who all had normal values for these indices. However, there were no differences in diastolic function between the G+LVHand G- group (p=0.2). Reduced global longitudinal strain (GLS) and regional strain was detected in the G+LVH+ group compared with all other groups (G+LVH-, p=0.05; G-, p=0.01; NV p=0.03). There were no differences in GLS and regional strain between the G+LVH- group and the G- (p=0.7) and control groups (p=0.9). Conclusion: A blunted myocardial oxygenation response to vasodilator stress precedes changes in LV strain, wall thickness or diastolic function. Changes in BOLD signal intensity may be a surrogate marker for preclinical hypertrophic cardiomyopathy and lead to development of preventative strategies. http://dx.doi.org/10.1016/j.hlc.2016.06.171