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Effect of Arterial Size, Extent of Disease and Cardiovascular Medications on Nitrate-Induced Coronary Vasodilatation
S38
Heart, Lung and Circulation 2013;22:S1–S125
CSANZ 2013 Abstracts
ABSTRACTS
88 Does the 50% Delta Change Alter Clinical Outcomes in Chest Pain Presentations to the Emergency Department J. Sajeev ∗ , F. Gunawan, P. Wijesundera, S. Menon, L. Roberts, D. Tong, A. Baradi, D. Jackson, P. Naidu, G. New Box Hill Hospital, Australia Background: National Heart Foundation (NHF) ACS guidelines recommend the use of high sensitivity troponin assay (hsTrop). Two thousand and eleven addendum recommends a change in delta value () for hsTrop to 50%. Introduction of hsTrop assay at Box Hill Hospital, 30% was used as the cut off. However, this was changed to 50% six months later. Aim: To determine the clinical impact of 30–50% change for patients presenting with chest pain. Method: We retrospectively collected data from patients >18 years presenting with chest or abdominal pain and had hsTrop between January and March 2012. Results: We analysed 671 patients. 288 (43%) patients who had a STEMI or lacked serial hsTrop values, on dialysis or trauma-related were excluded. Remaining patients were followed up. Out of 383 patients, 148 (39%) with serial hsTrop had at least one abnormal troponin (>14 ng/ml). Thirteen (3.4%) fell within 30–50%. Ten had clinical indications suggestive of ACS and regardless of their hsTrop results went on to have cardiac investigations and management. Three patients with non-cardiac diagnosis had no further tests. At follow up (mean ± SD: 409 ± 13 days), these patients have not had any cardiac events. Conclusion: Our data supports the safety of NHF recommendation for change to 50%. This change affected only 3.4% of the patients and we did not miss any cardiac events. Our clinical decision to investigate 10 of the 13 patients who had <50% underscores the importance of not relying solely on hsTrop assay to diagnose ACS as emphasised in the NHF recommendations. http://dx.doi.org/10.1016/j.hlc.2013.05.089 89 Early Australian Experience With AbsorbTM Bioresorbable Scaffold Technology in “Real-World” Coronary Disease C. Arnott ∗ , M. Pitney, S. Ooi, N. Jepson Prince of Wales Hospital/Eastern and Southern Heart Clinic, Australia Introduction: Safety and efficacy of the AbsorbTM Bioresorbable Scaffold (ABRS) has been documented in “low-risk” lesions. “Real-world” data is limited and in this context we report the early experience with ABRS from two Australian centres. Methods: Between August 2010 and February 2013, 71 lesions in 44 patients (mean age 63 yrs, 59% male) were treated with ABRS (Clinical Trial 45%, Authorised Prescriber 55%). Diabetes was present in 24% and PCI
indication was ACS in 33% of patients. Outcomes were measured in-hospital, day 30, one and two years post-PCI. Procedural details: Lesion location – LAD 38%, RCA 51% and LCX 11%. Lesion complexity – 29% B2/C (AHA/ACC), moderate/severe calcification 14%, CTO 2.8% and long lesions 27%. In total, 68 scaffolds were implanted – average 1.5/pt (range 1–5). Average scaffold length/pt was 34 mm with planned overlap in 27% pts. Multi-vessel ABRS implantation was performed in 6.8% patients. Postdilatation was performed in all cases. Results: Procedural success was 100%. Device success was 99% – a scaffold could not be advanced in one patient (DES were successfully deployed). A “bailout” DES was needed in one case for a distal edge dissection. To date, 95% of patients have reached 30 days, 30% 12 months and 2% 24 months. There has been no myocardial infarction, cardiac death, scaffold thrombosis or target vessel revascularisation. There was one non-cardiac death at 21 months. Conclusions: This early local experience has demonstrated ABRS therapy to be highly safe and efficacious in complex and real-world disease (including long lesions, multi-vessel disease and CTOs). http://dx.doi.org/10.1016/j.hlc.2013.05.090 90 Effect of Arterial Size, Extent of Disease and Cardiovascular Medications on Nitrate-Induced Coronary Vasodilatation N. Kim 1,∗ , M. Pitney 2 , A. Lau 2 1 Faculty of Medicine, University of New South Wales, Australia 2 Department
of Cardiology, Prince of Wales Hospital, Sydney,
Australia Background: Glyceryl trinitrate (GTN) given during coronary angiography (CA) can determine maximal vasodilatation of diseased and non-diseased arterial segments. Its use in invasive CA is very variable, and current guidelines do not specify if CA reporting should be done with or without GTN. Aim: We compared GTN response of normal and diseased, proximal and distal coronary arteries, and assessed the impact of vascular risk factors and cardiac medications. Method: In 74 consecutive CA cases in January to June 2012 during which GTN was administered, pre- and postGTN views in 467 coronary segments were compared by quantitative coronary angiography, assessing reference segment diameter, minimal luminal diameter (MLD), and % stenosis. Results: Pre-GTN
Post-GTN
Absolute
Percent
Reference
2.8 ± 0.8 mm
3.4 ± 1.1 mm*
0.6 ± 0.6 mm
24 ± 23%
MLD
1.8 ± 0.7 mm
2.3 ± 0.9 mm*
0.4 ± 0.5 mm
26 ± 27%
4.5 ± 12.1%
n/a
% Stenosis33 ± 16%
38 ± 17%*
Reference segments and MLD dilated post-GTN by about 25%, and overall % stenosis increased by 4.5%. Smaller arteries had greater % dilatation compared with
larger arteries. The MLD of stenoses <50% dilated significantly more than stenoses ≥50%. Long-acting nitrate therapy reduced GTN response by one-third, whilst lipidlowering therapy significantly increased GTN-induced vasodilatation in both diseased and non-diseased arteries. Diabetic GTN response was halved compared with non-diabetics. Gender, smoking, hypertension, and other vasodilator therapy had no effect. Conclusions: Coronary GTN response varies greatly between different sized arteries and arteries with differing level of disease. Individual patient factors such as diabetes and medications may have significant effect on this response. http://dx.doi.org/10.1016/j.hlc.2013.05.091 91 Effects of Obesity and the Metabolic Syndrome on Cardiac Structure, Function and Tolerance to Ischaemia E. Du Toit ∗ , D. Donner, I. Wensley, K. Salaveria, A. Bulmer Heart Foundation Research Center, School of Medical Science, Gold Coast Campus, Griffith University, Southport, Australia Background: Obesity increases risk of heart failure (HF) and together with its co-morbidities that constitute the metabolic syndrome (MetS), decreases myocardial tolerance to ischaemia. Whether obesity/MetS causes HF in the absence of hypertension and the mechanism for the obesity/MetS induced decrease in myocardial ischaemic tolerance is however unknown. We hypothesise that obesity/MetS induces adverse: (1) cardiac remodelling causing cardiac dysfunction and (2) Reperfiusion Injury Salvage Kinase (RISK) pathway function to reduce myocardial tolerance to ischaemia. Methods: Wistar rats were fed an obesogenic (OB) or a standard rat chow diet (CTRL) for 30 weeks and in vivo cardiac structure/function assessed (echocardiography). Isolated Langendorff perfused hearts were subjected to 40 min coronary artery ligation and reperfusion and functional recovery (Rate Pressure Product-RPP), infarct size, and RISK pathway function assessed (Western blot analysis). Results: Obesity/MetS had no effect on in vivo cardiac structure/function. Hearts from OB rats had poorer reperfusion RPPs (13,115 ± 562 for OB vs. 17,781 ± 1109 for CTRL, p < 0.05) and larger infarcts (36.3 ± 5.6% of AAR in OB vs. 14.1 ± 2.8% of AAR in CTRL rats, p < 0.01) than CTRLs. These changes were associated with reductions in RISK pathway function with a 30–50%, and a 40–60% reduction in Akt and GSK-3 expression and phosphorylation respectively in OB rats compared to CTRL. Expression of total eNOS was reduced by 25% in OB rats.
CSANZ 2013 Abstracts
S39
Conclusions: Obesity/MetS had no effect on cardiac structure or function but decreased myocardial tolerance to ischaemia. This reduction in ischaemic tolerance was likely due to compromised RISK pathway function in Obesity/MetS. http://dx.doi.org/10.1016/j.hlc.2013.05.092 92 Elevation of High Sensitive Cardiac Troponin T in the Absence of Significant Obstructive Coronary Artery Disease J. Raval 1 , C. Gan 1,∗ , V. Nagaraja 2 , K. Rangasamy 1 , R. Talisayon 1 , D. Burgess 1 , A. Denniss 1 1 Department 2 Prince
of Cardiology, Blacktown Hospital, Australia of Wales Hospital, Australia
Introduction: The high-sensitivity TnT (HsTnT) assay is a very good screening test for myocardial injury, but the enhanced sensitivity comes at the cost of specificity which requires careful clinical consideration. Aim of the study was to find the different causes of troponin rise in the absence of significant coronary artery disease. Methods: The patients were selected from the Blacktown coronary angiography database from May 2011 to December 2012. The patients with HsTnT of more than 15 ng/L in the absence of significant coronary artery disease were included. Those with significant coronary artery disease and outpatients were excluded. Significant coronary artery disease was defined as >50% stenosis in one of the major epicardial arteries. From total of 1493 patients, 145 patients were selected. Results: Out of the 145 patients 76 were female, mean age 65.02 years, 43 had typical chest pain, 21 patients had ECG changes, 101 had hypertension and 36 were diabetic. The average TIMI score was 2.35, Framingham score was 22.45 and Grace Risk score was 13.44. In univariable analyses, HsTnT elevation was associated with diabetes mellitus (DM), and chronic kidney disease (CKD) (P < 0.001 for each). In multivariable logistic regression analysis DM and CKD were independently associated with HsTnT elevation. Conclusion: An elevated HsTnT level is a relatively common finding in hospitalised patients. Clinical history and ECG correlates the best rather than any risk score to identify troponin rise in the absence of obstructive coronary artery disease. http://dx.doi.org/10.1016/j.hlc.2013.05.093
ABSTRACTS
Heart, Lung and Circulation 2013;22:S1–S125
Heart, Lung and Circulation 2013;22:S1–S125
CSANZ 2013 Abstracts
ABSTRACTS
88 Does the 50% Delta Change Alter Clinical Outcomes in Chest Pain Presentations to the Emergency Department J. Sajeev ∗ , F. Gunawan, P. Wijesundera, S. Menon, L. Roberts, D. Tong, A. Baradi, D. Jackson, P. Naidu, G. New Box Hill Hospital, Australia Background: National Heart Foundation (NHF) ACS guidelines recommend the use of high sensitivity troponin assay (hsTrop). Two thousand and eleven addendum recommends a change in delta value () for hsTrop to 50%. Introduction of hsTrop assay at Box Hill Hospital, 30% was used as the cut off. However, this was changed to 50% six months later. Aim: To determine the clinical impact of 30–50% change for patients presenting with chest pain. Method: We retrospectively collected data from patients >18 years presenting with chest or abdominal pain and had hsTrop between January and March 2012. Results: We analysed 671 patients. 288 (43%) patients who had a STEMI or lacked serial hsTrop values, on dialysis or trauma-related were excluded. Remaining patients were followed up. Out of 383 patients, 148 (39%) with serial hsTrop had at least one abnormal troponin (>14 ng/ml). Thirteen (3.4%) fell within 30–50%. Ten had clinical indications suggestive of ACS and regardless of their hsTrop results went on to have cardiac investigations and management. Three patients with non-cardiac diagnosis had no further tests. At follow up (mean ± SD: 409 ± 13 days), these patients have not had any cardiac events. Conclusion: Our data supports the safety of NHF recommendation for change to 50%. This change affected only 3.4% of the patients and we did not miss any cardiac events. Our clinical decision to investigate 10 of the 13 patients who had <50% underscores the importance of not relying solely on hsTrop assay to diagnose ACS as emphasised in the NHF recommendations. http://dx.doi.org/10.1016/j.hlc.2013.05.089 89 Early Australian Experience With AbsorbTM Bioresorbable Scaffold Technology in “Real-World” Coronary Disease C. Arnott ∗ , M. Pitney, S. Ooi, N. Jepson Prince of Wales Hospital/Eastern and Southern Heart Clinic, Australia Introduction: Safety and efficacy of the AbsorbTM Bioresorbable Scaffold (ABRS) has been documented in “low-risk” lesions. “Real-world” data is limited and in this context we report the early experience with ABRS from two Australian centres. Methods: Between August 2010 and February 2013, 71 lesions in 44 patients (mean age 63 yrs, 59% male) were treated with ABRS (Clinical Trial 45%, Authorised Prescriber 55%). Diabetes was present in 24% and PCI
indication was ACS in 33% of patients. Outcomes were measured in-hospital, day 30, one and two years post-PCI. Procedural details: Lesion location – LAD 38%, RCA 51% and LCX 11%. Lesion complexity – 29% B2/C (AHA/ACC), moderate/severe calcification 14%, CTO 2.8% and long lesions 27%. In total, 68 scaffolds were implanted – average 1.5/pt (range 1–5). Average scaffold length/pt was 34 mm with planned overlap in 27% pts. Multi-vessel ABRS implantation was performed in 6.8% patients. Postdilatation was performed in all cases. Results: Procedural success was 100%. Device success was 99% – a scaffold could not be advanced in one patient (DES were successfully deployed). A “bailout” DES was needed in one case for a distal edge dissection. To date, 95% of patients have reached 30 days, 30% 12 months and 2% 24 months. There has been no myocardial infarction, cardiac death, scaffold thrombosis or target vessel revascularisation. There was one non-cardiac death at 21 months. Conclusions: This early local experience has demonstrated ABRS therapy to be highly safe and efficacious in complex and real-world disease (including long lesions, multi-vessel disease and CTOs). http://dx.doi.org/10.1016/j.hlc.2013.05.090 90 Effect of Arterial Size, Extent of Disease and Cardiovascular Medications on Nitrate-Induced Coronary Vasodilatation N. Kim 1,∗ , M. Pitney 2 , A. Lau 2 1 Faculty of Medicine, University of New South Wales, Australia 2 Department
of Cardiology, Prince of Wales Hospital, Sydney,
Australia Background: Glyceryl trinitrate (GTN) given during coronary angiography (CA) can determine maximal vasodilatation of diseased and non-diseased arterial segments. Its use in invasive CA is very variable, and current guidelines do not specify if CA reporting should be done with or without GTN. Aim: We compared GTN response of normal and diseased, proximal and distal coronary arteries, and assessed the impact of vascular risk factors and cardiac medications. Method: In 74 consecutive CA cases in January to June 2012 during which GTN was administered, pre- and postGTN views in 467 coronary segments were compared by quantitative coronary angiography, assessing reference segment diameter, minimal luminal diameter (MLD), and % stenosis. Results: Pre-GTN
Post-GTN
Absolute
Percent
Reference
2.8 ± 0.8 mm
3.4 ± 1.1 mm*
0.6 ± 0.6 mm
24 ± 23%
MLD
1.8 ± 0.7 mm
2.3 ± 0.9 mm*
0.4 ± 0.5 mm
26 ± 27%
4.5 ± 12.1%
n/a
% Stenosis33 ± 16%
38 ± 17%*
Reference segments and MLD dilated post-GTN by about 25%, and overall % stenosis increased by 4.5%. Smaller arteries had greater % dilatation compared with
larger arteries. The MLD of stenoses <50% dilated significantly more than stenoses ≥50%. Long-acting nitrate therapy reduced GTN response by one-third, whilst lipidlowering therapy significantly increased GTN-induced vasodilatation in both diseased and non-diseased arteries. Diabetic GTN response was halved compared with non-diabetics. Gender, smoking, hypertension, and other vasodilator therapy had no effect. Conclusions: Coronary GTN response varies greatly between different sized arteries and arteries with differing level of disease. Individual patient factors such as diabetes and medications may have significant effect on this response. http://dx.doi.org/10.1016/j.hlc.2013.05.091 91 Effects of Obesity and the Metabolic Syndrome on Cardiac Structure, Function and Tolerance to Ischaemia E. Du Toit ∗ , D. Donner, I. Wensley, K. Salaveria, A. Bulmer Heart Foundation Research Center, School of Medical Science, Gold Coast Campus, Griffith University, Southport, Australia Background: Obesity increases risk of heart failure (HF) and together with its co-morbidities that constitute the metabolic syndrome (MetS), decreases myocardial tolerance to ischaemia. Whether obesity/MetS causes HF in the absence of hypertension and the mechanism for the obesity/MetS induced decrease in myocardial ischaemic tolerance is however unknown. We hypothesise that obesity/MetS induces adverse: (1) cardiac remodelling causing cardiac dysfunction and (2) Reperfiusion Injury Salvage Kinase (RISK) pathway function to reduce myocardial tolerance to ischaemia. Methods: Wistar rats were fed an obesogenic (OB) or a standard rat chow diet (CTRL) for 30 weeks and in vivo cardiac structure/function assessed (echocardiography). Isolated Langendorff perfused hearts were subjected to 40 min coronary artery ligation and reperfusion and functional recovery (Rate Pressure Product-RPP), infarct size, and RISK pathway function assessed (Western blot analysis). Results: Obesity/MetS had no effect on in vivo cardiac structure/function. Hearts from OB rats had poorer reperfusion RPPs (13,115 ± 562 for OB vs. 17,781 ± 1109 for CTRL, p < 0.05) and larger infarcts (36.3 ± 5.6% of AAR in OB vs. 14.1 ± 2.8% of AAR in CTRL rats, p < 0.01) than CTRLs. These changes were associated with reductions in RISK pathway function with a 30–50%, and a 40–60% reduction in Akt and GSK-3 expression and phosphorylation respectively in OB rats compared to CTRL. Expression of total eNOS was reduced by 25% in OB rats.
CSANZ 2013 Abstracts
S39
Conclusions: Obesity/MetS had no effect on cardiac structure or function but decreased myocardial tolerance to ischaemia. This reduction in ischaemic tolerance was likely due to compromised RISK pathway function in Obesity/MetS. http://dx.doi.org/10.1016/j.hlc.2013.05.092 92 Elevation of High Sensitive Cardiac Troponin T in the Absence of Significant Obstructive Coronary Artery Disease J. Raval 1 , C. Gan 1,∗ , V. Nagaraja 2 , K. Rangasamy 1 , R. Talisayon 1 , D. Burgess 1 , A. Denniss 1 1 Department 2 Prince
of Cardiology, Blacktown Hospital, Australia of Wales Hospital, Australia
Introduction: The high-sensitivity TnT (HsTnT) assay is a very good screening test for myocardial injury, but the enhanced sensitivity comes at the cost of specificity which requires careful clinical consideration. Aim of the study was to find the different causes of troponin rise in the absence of significant coronary artery disease. Methods: The patients were selected from the Blacktown coronary angiography database from May 2011 to December 2012. The patients with HsTnT of more than 15 ng/L in the absence of significant coronary artery disease were included. Those with significant coronary artery disease and outpatients were excluded. Significant coronary artery disease was defined as >50% stenosis in one of the major epicardial arteries. From total of 1493 patients, 145 patients were selected. Results: Out of the 145 patients 76 were female, mean age 65.02 years, 43 had typical chest pain, 21 patients had ECG changes, 101 had hypertension and 36 were diabetic. The average TIMI score was 2.35, Framingham score was 22.45 and Grace Risk score was 13.44. In univariable analyses, HsTnT elevation was associated with diabetes mellitus (DM), and chronic kidney disease (CKD) (P < 0.001 for each). In multivariable logistic regression analysis DM and CKD were independently associated with HsTnT elevation. Conclusion: An elevated HsTnT level is a relatively common finding in hospitalised patients. Clinical history and ECG correlates the best rather than any risk score to identify troponin rise in the absence of obstructive coronary artery disease. http://dx.doi.org/10.1016/j.hlc.2013.05.093
ABSTRACTS
Heart, Lung and Circulation 2013;22:S1–S125