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Kounis syndrome during coronary angiography at the Gold Coast Hospital
Abstract
S280
394 Intracoronary Abciximab to Improve Microvascular Function in Acute Coronary Syndrome Study (INTRACOR) S. Palmer 1,2 , J. Layland 1 , P. Williams 1 , C. Judkins 1,∗ , A. La Gerche 1 , A. Burns 1 , R. Whitbourn 1 , A. MacIsaac 1 , A. Wilson 1,2 1 St
Vincent’s Hospital, Melbourne, Victoria, Australia 2 Department of Medicine, St Vincent’s Hospital, Fitzroy, Victoria, Australia Background: The index of microcirculatory resistance (IMR), an invasive measure of coronary microvascular function, correlates with clinical outcomes in patients with stable angina and ST elevation myocardial infarction. The glycoprotein IIb/IIIa receptor inhibitor, abciximab, improves coronary microvascular function and reduces major cardiac adverse events in patients with acute coronary syndromes. We investigated whether an intracoronary bolus of abciximab in patients with non-ST elevation myocardial infarction (NSTEMI) would decrease IMR and improve microvascular function. Methods: We randomly assigned 36 patients presenting with NSTEMI to receive either a single bolus of intracoronary abciximab or placebo (saline) into the culprit vessel before percutaneous coronary intervention (PCI). The index of microvascular resistance was measured at baseline, 15 minutes after study drug administration and after PCI. Results: A single bolus of intracoronary abciximab resulted in a reduced IMR 15 minutes post drug administration (29 ± 11 at baseline vs. 25 ± 9 post drug administration, p = 0.048), whereas there was no significant change observed in the placebo group (18 ± 11 at baseline vs. 17 ± 9 post drug administration, p = 0.267). Following PCI, in contrast to those patients who received placebo, patients in the abciximab group showed a significantly improved IMR (29 ± 11 abciximab: vs. 18 ± 9, p = 0.002; placebo: 18 ± 11 vs. 17 ± 9, p = 0.811). Conclusion: This is the first study to demonstrate that a single bolus dose of intracoronary abciximab is able to improve coronary microvascular function in patients with NSTEMI undergoing PCI. http://dx.doi.org/10.1016/j.hlc.2015.06.395 395 Kounis syndrome during coronary angiography at the Gold Coast Hospital L. Guazzo 1,∗ , R. Markham 1,2 , K. Hyasat 1 , A. Rahman 1,3 1 Gold
Coast University Hospital, QLD, Australia 2 University of Queensland, QLD, Australia 3 Griffith University, Nathan, QLD, Australia A 52-year-old male with a background of hypertension was transferred from a regional hospital for a semi-elective coro-
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nary angiography following an electrically positive exercise stress test. He was found to have triple vessel disease, with a 90% stenosis of the left circumflex coronary artery (LCx). 20 minutes after the initial injection of contrast dye, he became tachypnoeic, tachycardic and hypotensive. Electrocardiogram revealed new ST-segment elevation in V1-V2 and repeat CA showed complete occlusion of the LCx without any evidence of dissection or perforation. Two drug eluting stents were deployed with good result, leading to a resolution of the patient’s chest pain and ST elevation. 10 minutes later, while in the recovery bay he experienced stridor, wheeze and developed severe angio-oedema. Intravenous adrenalin and hydrocortisone was administered. He was intubated, ventilated and transferred to the intensive care unit (ICU). Serum Tryptase was 62.7 ug/L (RR< 13.5 ug/L), in keeping with an anaphylactic reaction. He was extubated the following day and discharged three days later with full resolution of his symptoms. Kounis Syndrome (KS) is the occurrence of acute coronary syndrome (ACS) precipitated by an anaphylactic reaction. Type 1 is the occurrence of an ACS secondary to an allergic reaction in a patient with normal coronary arteries and is thought to occur from coronary vasospasm, secondary to an inflammatory cascade. Type 2 KS occurs in patients with documented coronary artery disease in which atheromatous plaque erosion and thrombus secondary to inflammatory cascade and vasospasm, is responsible for symptoms.
http://dx.doi.org/10.1016/j.hlc.2015.06.396
S280
394 Intracoronary Abciximab to Improve Microvascular Function in Acute Coronary Syndrome Study (INTRACOR) S. Palmer 1,2 , J. Layland 1 , P. Williams 1 , C. Judkins 1,∗ , A. La Gerche 1 , A. Burns 1 , R. Whitbourn 1 , A. MacIsaac 1 , A. Wilson 1,2 1 St
Vincent’s Hospital, Melbourne, Victoria, Australia 2 Department of Medicine, St Vincent’s Hospital, Fitzroy, Victoria, Australia Background: The index of microcirculatory resistance (IMR), an invasive measure of coronary microvascular function, correlates with clinical outcomes in patients with stable angina and ST elevation myocardial infarction. The glycoprotein IIb/IIIa receptor inhibitor, abciximab, improves coronary microvascular function and reduces major cardiac adverse events in patients with acute coronary syndromes. We investigated whether an intracoronary bolus of abciximab in patients with non-ST elevation myocardial infarction (NSTEMI) would decrease IMR and improve microvascular function. Methods: We randomly assigned 36 patients presenting with NSTEMI to receive either a single bolus of intracoronary abciximab or placebo (saline) into the culprit vessel before percutaneous coronary intervention (PCI). The index of microvascular resistance was measured at baseline, 15 minutes after study drug administration and after PCI. Results: A single bolus of intracoronary abciximab resulted in a reduced IMR 15 minutes post drug administration (29 ± 11 at baseline vs. 25 ± 9 post drug administration, p = 0.048), whereas there was no significant change observed in the placebo group (18 ± 11 at baseline vs. 17 ± 9 post drug administration, p = 0.267). Following PCI, in contrast to those patients who received placebo, patients in the abciximab group showed a significantly improved IMR (29 ± 11 abciximab: vs. 18 ± 9, p = 0.002; placebo: 18 ± 11 vs. 17 ± 9, p = 0.811). Conclusion: This is the first study to demonstrate that a single bolus dose of intracoronary abciximab is able to improve coronary microvascular function in patients with NSTEMI undergoing PCI. http://dx.doi.org/10.1016/j.hlc.2015.06.395 395 Kounis syndrome during coronary angiography at the Gold Coast Hospital L. Guazzo 1,∗ , R. Markham 1,2 , K. Hyasat 1 , A. Rahman 1,3 1 Gold
Coast University Hospital, QLD, Australia 2 University of Queensland, QLD, Australia 3 Griffith University, Nathan, QLD, Australia A 52-year-old male with a background of hypertension was transferred from a regional hospital for a semi-elective coro-
.. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .
nary angiography following an electrically positive exercise stress test. He was found to have triple vessel disease, with a 90% stenosis of the left circumflex coronary artery (LCx). 20 minutes after the initial injection of contrast dye, he became tachypnoeic, tachycardic and hypotensive. Electrocardiogram revealed new ST-segment elevation in V1-V2 and repeat CA showed complete occlusion of the LCx without any evidence of dissection or perforation. Two drug eluting stents were deployed with good result, leading to a resolution of the patient’s chest pain and ST elevation. 10 minutes later, while in the recovery bay he experienced stridor, wheeze and developed severe angio-oedema. Intravenous adrenalin and hydrocortisone was administered. He was intubated, ventilated and transferred to the intensive care unit (ICU). Serum Tryptase was 62.7 ug/L (RR< 13.5 ug/L), in keeping with an anaphylactic reaction. He was extubated the following day and discharged three days later with full resolution of his symptoms. Kounis Syndrome (KS) is the occurrence of acute coronary syndrome (ACS) precipitated by an anaphylactic reaction. Type 1 is the occurrence of an ACS secondary to an allergic reaction in a patient with normal coronary arteries and is thought to occur from coronary vasospasm, secondary to an inflammatory cascade. Type 2 KS occurs in patients with documented coronary artery disease in which atheromatous plaque erosion and thrombus secondary to inflammatory cascade and vasospasm, is responsible for symptoms.
http://dx.doi.org/10.1016/j.hlc.2015.06.396