Takotsubo syndrome: the Cinderella compared with common acute coronary syndromes

Takotsubo syndrome: the Cinderella compared with common acute coronary syndromes For the podcast associated with this article, please visit https://academic.oup.com/eurheartj/pages/Podcasts With the onset of the increasing use of emergency coronary angiography in patients with persistent angina pectoris and ECG changes in the 1980s, female patients with severe left ventricular dysfunction of unusual appearance and normal coronary arteries were documented (Figure 1). Figure 1 View largeDownload slide Typical appearance of the left ventricular angiogram in Takotsubo syndrome. Figure 1 View largeDownload slide Typical appearance of the left ventricular angiogram in Takotsubo syndrome. A few years later, Sato and colleagues from the Hiroshima City Hospital published five such cases and coined the term Takotsubo syndrome as the ventricle resembled the shape of a Japanese octopus trap.1 While it was first assumed that the syndrome would only affect individuals of Asian descent, shortly thereafter similar patients were published by French and American groups.2 Recently, a large international cohort put this under-recognized acute coronary syndrome on centre stage. It became clear that Takotsubo is much more common than anticipated, and potentially a lethal disease.3 Thus, it appeared timely to publish a Consensus Expert Statement on the subject. This Focus Issue presents both parts of the ‘International Expert Consensus Document on Takotsubo syndrome’ by Christian Templin and colleagues from the University Zurich in Switzerland.4,5 The document summarizes the current state of knowledge on the clinical presentation and characteristics of Takotsubo syndrome and tries to end controversies on its nomenclature. This statement also proposes new diagnostic criteria based on data from the International Takotsubo Registry, to improve diagnostic accuracy. Unlike Takotsubo which affects the microcirculation,6 classical forms of acute coronary syndromes are due to rupture or erosion of lipid-rich plaques in epicardial coronary arteries.7,8 Inflammation of atherosclerotic plaques is considered the prime mechanisms of plaque vulnerability, with interleukin-1 as the prototypical pro-inflammatory cytokine.9 Initially, interleukin-1 was implicated as a cardiodepressant in septic shock, but subsequently it has been recognized as a mediator of atherosclerosis, acute myocardial infarction, and heart failure. In their clinical review entitled ‘Interleukin-1 blockade in cardiovascular diseases: a clinical update’, Antonio Abbate and colleagues from the Virginia Commonwealth University in Richmond, Virginia in the USA10 note that interleukin-1 monoclonal antibodies prevent recurrent atherothrombotic cardiovascular events and, in ST-segment elevation myocardial infarction (STEMI), quench the inflammatory response and prevent heart failure. In heart failure, interleukin-1 appears to impair beta-adrenergic receptor signalling and intracellular calcium handling, and accordingly its inhibition improves exercise capacity. While interleukin-1 blockade is not immunosuppressive and not associated with opportunistic infections or increased risk of cancer, lethal outcomes may occur due to blunting of inflammation and in turn delayed presentation and diagnosis. The practical use of interleukin-1 blockade is currently experimental, but its potential is worth consideration. An acute occlusion of an epicardial coronary artery may be caused by plaque rupture or erosion. The latter is discussed in a Review article entitled ‘Plaque erosion: a new in vivo diagnosis and a potential major shift in the management of patients with acute coronary syndromes’ by Ik-Kyung Jang and colleagues from the Massachusetts General Hospital in Boston, Massachusetts in the USA.10 The advent of intravascular imaging techniques, particularly optical coherence tomography,11,12 has improved the understanding of plaque erosion. Appreciation of the distinct biological and clinical mechanisms of plaque erosion points to the possibility of tailored management strategies for patients presenting with acute coronary syndromes. This topic is further analysed in an article entitled ‘In vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction: a clinical, angiographic, and intravascular optical coherence tomography study’ by Bo Yu and colleagues from the 2nd affiliated hospital of Harbin Medical University in Heilongjiang, China.13 Using optical coherence tomography in 822 patients with STEMI, 25.4% were found to have plaque erosion and 68.6% had rupture. Plaque erosion was more frequent in younger females of less than 50 years, with a similar trend in males. Those with erosion were more often current smokers, but had fewer other coronary risk factors than those with rupture. There was a preponderance of erosions in the left anterior descending coronary artery or LAD and near a bifurcation (Figure 2). Thus, in STEMI, erosion is a predictable clinical entity distinct from rupture, and its recognition may change the therapeutic approach to these patients.14 These findings are put into context in an Editorial by Aloke Virmani Finn from CVPATH in Gaithersburg, Maryland in the USA.15 Figure 2 View largeDownload slide The spatial distribution of plaque erosion and plaque rupture in the coronary arteries. Bar graph (A): the spatial distribution of plaque erosion in three major epicardial arteries was similar to plaque rupture. Boxplots graph (B): in the LAD, most erosions (114/128, 89.1%) and ruptures (236/265, 89.1%) clustered within the first 40 mm from the coronary ostium. In the RCA, only half of erosions (33/64, 51.6%) and ruptures (128/244, 52.5%) were located within the first 40 mm and were more evenly distributed throughout the entire length of the coronary artery. LAD, left anterior descending artery; LCX, left circumflex artery; RCA, right coronary artery (from Dai J, Xing L, Jia H, Zhu Y, Zhang S, Hu S, Lin L, Ma L, Liu H, Xu M, Ren X, Yu H, Li L, Zou Y, Zhang S, Mintz GS, Hou J, Yu B. In vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction: a clinical, angiographical, and intravascular optical coherence tomography study. See pages 2077–2085). Figure 2 View largeDownload slide The spatial distribution of plaque erosion and plaque rupture in the coronary arteries. Bar graph (A): the spatial distribution of plaque erosion in three major epicardial arteries was similar to plaque rupture. Boxplots graph (B): in the LAD, most erosions (114/128, 89.1%) and ruptures (236/265, 89.1%) clustered within the first 40 mm from the coronary ostium. In the RCA, only half of erosions (33/64, 51.6%) and ruptures (128/244, 52.5%) were located within the first 40 mm and were more evenly distributed throughout the entire length of the coronary artery. LAD, left anterior descending artery; LCX, left circumflex artery; RCA, right coronary artery (from Dai J, Xing L, Jia H, Zhu Y, Zhang S, Hu S, Lin L, Ma L, Liu H, Xu M, Ren X, Yu H, Li L, Zou Y, Zhang S, Mintz GS, Hou J, Yu B. In vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction: a clinical, angiographical, and intravascular optical coherence tomography study. See pages 2077–2085). Cardiogenic shock is a feared complication of both Takotsubo and STEMI, and the last frontier in the management of acute coronary syndromes.16 In their article ‘Predicting the development of in-hospital cardiogenic shock in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: the ORBI risk score’, Vincent Auffret and colleagues aimed to derive and validate a readily useable risk score to identify patients at high risk of in-hospital cardiogenic shock in an initial and validation cohort.17 Eleven variables were independently associated with the development of in-hospital cardiogenic shock: age >70 years, prior stroke or transient ischaemic attack, cardiac arrest upon admission, anterior STEMI, delay of first medical contact to primary percutaneous coronary intervention (PCI) >90 min, Killip class, heart rate >90 bpm, a combination of systolic blood pressure <125 mmHg and pulse pressure <45 mmHg, glycaemia >10 mmol/L, culprit lesion of the left main coronary artery, and post-primary PCI TIMI flow grade <3 (Figure 3). The score derived from these variables allowed the classification of patients into four risk categories with cardiogenic shock rates of 1.3, 6.6, 11.7, and 31.8%. The score demonstrated high discrimination and adequate calibration in both cohorts. Thus, the ORBI risk score is a tool to identify high-risk STEMI patients developing cardiogenic shock and may be helpful with the availability of novel treatment options in these patients.18 The clinical usefulness of the score is further discussed in a thought-provoking Editorial by George Dangas from the Cardiovascular Research Foundation in New York.19 Figure 3 View largeDownload slide Multivariable predictors of in-hospital cardiogenic shock in the derivation cohort and their respective weights in the ORBI risk score. CI, confidence interval; OR, odds ratio; pPCI, primary percutaneous coronary intervention; TIA, transient ischaemic attack; SBP, systolic blood pressure (from Auffret V, Cottin Y, Leurent G, Gilard M, Beer J-C, Zabalawi A, Chagué F, Filippi E, Brunet D, Hacot J-P, Brunel P, Mejri M, Lorgis L, Rouault G, Druelles P, Cornily J-C, Didier R, Bot E, Boulanger B, Coudert I, Loirat A, Bedossa M, Boulmier D, Maza M, Le Guellec M, Puri R, Zeller M, Le Breton H; On behalf of the ORBI and RICOWorking Groups. Predicting the development of in-hospital cardiogenic shock in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: the ORBI risk score. See pages 2090–2102). Figure 3 View largeDownload slide Multivariable predictors of in-hospital cardiogenic shock in the derivation cohort and their respective weights in the ORBI risk score. CI, confidence interval; OR, odds ratio; pPCI, primary percutaneous coronary intervention; TIA, transient ischaemic attack; SBP, systolic blood pressure (from Auffret V, Cottin Y, Leurent G, Gilard M, Beer J-C, Zabalawi A, Chagué F, Filippi E, Brunet D, Hacot J-P, Brunel P, Mejri M, Lorgis L, Rouault G, Druelles P, Cornily J-C, Didier R, Bot E, Boulanger B, Coudert I, Loirat A, Bedossa M, Boulmier D, Maza M, Le Guellec M, Puri R, Zeller M, Le Breton H; On behalf of the ORBI and RICOWorking Groups. Predicting the development of in-hospital cardiogenic shock in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: the ORBI risk score. See pages 2090–2102). Myocardial infarction and gallstone disease are intrinsically linked via cholesterol metabolism. In their study entitled ‘Genetic variants in CYP7A1 and risk of myocardial infarction and symptomatic gallstone disease’, Anne Tybjaerg-Hansen and colleagues from the Rigshospitalet in Copenhagen, Denmark tested the hypothesis that genetic variants in the gene encoding cholesterol 7 alpha-hydroxylase (CYP7A1), the rate-limiting enzyme in the conversion of cholesterol to bile acids in the liver, are associated with risk of myocardial infarction and gallstone disease in the general population.20 During 7 years, myocardial infarction developed in 2326 individuals and gallstone disease in 2007. For rare mutations, CYP7A1 allele count was associated with an increase in LDL-cholesterol (LDL-C) of 12 for individuals with the highest vs. the lowest allele count. For common variants, CYP7A1 weighted allele scores in individuals with a score >0.04 vs. ≤0 were associated with stepwise increases in LDL-C of up to 2.4%, and with corresponding adjusted hazard ratios of 1.25 for myocardial infarction and 1.39 for gallstone disease. Thus, genetic variants in CYP7A1 which are associated with increased levels of LDL-C are associated with an increased risk of both myocardial infarction and gallstone disease. The editors hope that this issue of the European Heart Journal will be of interest to its readers. References 1 Sato H , Tateishi H , Uchida T. Takotsubo-type cardiomyopathy due to multivessel spasm. In: Kodama K , Haze K , Hon M , eds. Clinical Aspect of Myocardial Injury: From Ischemia to Heart Failure . Tokyo, Japan : Kagakuhyouronsha ; 1990 . p 56 – 64 . 2 Pavin D , Le Breton H , Daubert C. Human stress cardiomyopathy mimicking acute myocardial syndrome . Heart 1997 ; 78 : 509 – 511 . Google Scholar CrossRef Search ADS PubMed 3 Templin C , Ghadri JR , Diekmann J , Napp LC , Bataiosu DR , Jaguszewski M , Cammann VL , Sarcon A , Geyer V , Neumann CA. Clinical features and outcomes of Takotsubo (stress) cardiomyopathy . N Engl J Med 2015 ; 373 : 929 – 938 . Google Scholar CrossRef Search ADS PubMed 4 to be added at proof stage: International Expert Consensus Document on Takotsubo Syndrome – PART I: Characteristics and Clinical Presentation . Eur Heart J 2018 ; 39 : 2032 – 2046 . 5 to be added at proof stage: International Expert Consensus Document on Takotsubo Syndrome – PART II: Diagnostic Workup and Outcome . Eur Heart J 2018 ; 39 : 2047 – 2062 . 6 Lüscher TF , Templin C. Is takotsubo syndrome a microvascular acute coronary syndrome? Towards a new definition . Eur Heart J 2016 ; 37 : 2816 – 2820 . Google Scholar CrossRef Search ADS PubMed 7 Nilsson J. Atherosclerotic plaque vulnerability in the statin era . Eur Heart J 2017 ; 38 : 1638 – 1644 . Google Scholar CrossRef Search ADS PubMed 8 Partida RA , Libby P , Crea F , Jang IK. Plaque erosion: a new in vivo diagnosis and a potential major shift in the management of patients with acute coronary syndromes . Eur Heart J 2018 ; 39 : 2070 – 2076 . 9 Ridker PM , Luscher TF. Anti-inflammatory therapies for cardiovascular disease . Eur Heart J 2014 ; 35 : 1782 – 1791 . Google Scholar CrossRef Search ADS PubMed 10 Buckley LF , Abbate A. Interleukin-1 blockade in cardiovascular diseases: a clinical update . Eur Heart J 2018 ; 39 : 2063 – 2069 . 11 van der Sijde JN , Karanasos A , Villiger M , Bouma BE , Regar E. First-in-man assessment of plaque rupture by polarization-sensitive optical frequency domain imaging in vivo . Eur Heart J 2016 ; 37 : 1932 . Google Scholar CrossRef Search ADS PubMed 12 Toutouzas K , Benetos G , Karanasos A , Chatzizisis YS , Giannopoulos AA , Tousoulis D. Vulnerable plaque imaging: updates on new pathobiological mechanisms . Eur Heart J 2015 ; 36 : 3147 – 3154 . Google Scholar CrossRef Search ADS PubMed 13 Dai J , Xing L , Jia H , Zhu Y , Zhang S , Hu S , Lin L , Ma L , Liu H , Xu M , Ren X , Yu H , Li L , Zou Y , Zhang S , Mintz GS , Hou J , Yu B. In vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction: a clinical, angiographical, and intravascular optical coherence tomography study . Eur Heart J 2018 ; 39 : 2077 – 2085 . 14 Jia H , Dai J , Hou J , Xing L , Ma L , Liu H , Xu M , Yao Y , Hu S , Yamamoto E , Lee H , Zhang S , Yu B , Jang IK. Effective anti-thrombotic therapy without stenting: intravascular optical coherence tomography-based management in plaque erosion (the EROSION study) . Eur Heart J 2017 ; 38 : 792 – 800 . Google Scholar CrossRef Search ADS PubMed 15 Jinnouchi H , Virmani R , Finn AV. Are characteristics of plaque erosion defined by optical coherence tomography similar to true erosion in pathology? Eur Heart J 2018 ; 39 : 2086 – 2089 . 16 Luscher TF , Obeid S. From Eisenhower’s heart attack to modern management: a true success story! Eur Heart J 2017 ; 38 : 3066 – 3069 . Google Scholar CrossRef Search ADS PubMed 17 Auffret V , Cottin Y , Leurent G , Gilard M , Beer JC , Zabalawi A , Chague F , Filippi E , Brunet D , Hacot JP , Brunel P , Mejri M , Lorgis L , Rouault G , Druelles P , Cornily JC , Didier R , Bot E , Boulanger B , Coudert I , Loirat A , Bedossa M , Boulmier D , Maza M , Le Guellec M , Puri R , Zeller M , Le Breton H. Predicting the development of in-hospital cardiogenic shock in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: the ORBI risk score . Eur Heart J 2018 ; 39 : 2090 – 2102 . 18 Thiele H , Jobs A , Ouweneel DM , Henriques JPS , Seyfarth M , Desch S , Eitel I , Poss J , Fuernau G , de Waha S. Percutaneous short-term active mechanical support devices in cardiogenic shock: a systematic review and collaborative meta-analysis of randomized trials . Eur Heart J 2017 ; 38 : 3523 – 3531 . Google Scholar CrossRef Search ADS PubMed 19 Dangas G , Guedeney P. Prediction, staging, and outcomes of ischaemic cardiogenic shock after STEMI: a complex clinical interplay . Eur Heart J 2018 ; 39 : 2103 – 2105 . 20 Qayyum F , Lauridsen BK , Frikke-Schmidt R , Kofoed KF , Nordestgaard BG , Tybjaerg-Hansen A. Genetic variants in CYP7A1 and risk of myocardial infarction and symptomatic gallstone disease . Eur Heart J 2018 ; 39 : 2106 – 2116 . Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Heart Journal Oxford University Press

Takotsubo syndrome: the Cinderella compared with common acute coronary syndromes

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Abstract

For the podcast associated with this article, please visit https://academic.oup.com/eurheartj/pages/Podcasts With the onset of the increasing use of emergency coronary angiography in patients with persistent angina pectoris and ECG changes in the 1980s, female patients with severe left ventricular dysfunction of unusual appearance and normal coronary arteries were documented (Figure 1). Figure 1 View largeDownload slide Typical appearance of the left ventricular angiogram in Takotsubo syndrome. Figure 1 View largeDownload slide Typical appearance of the left ventricular angiogram in Takotsubo syndrome. A few years later, Sato and colleagues from the Hiroshima City Hospital published five such cases and coined the term Takotsubo syndrome as the ventricle resembled the shape of a Japanese octopus trap.1 While it was first assumed that the syndrome would only affect individuals of Asian descent, shortly thereafter similar patients were published by French and American groups.2 Recently, a large international cohort put this under-recognized acute coronary syndrome on centre stage. It became clear that Takotsubo is much more common than anticipated, and potentially a lethal disease.3 Thus, it appeared timely to publish a Consensus Expert Statement on the subject. This Focus Issue presents both parts of the ‘International Expert Consensus Document on Takotsubo syndrome’ by Christian Templin and colleagues from the University Zurich in Switzerland.4,5 The document summarizes the current state of knowledge on the clinical presentation and characteristics of Takotsubo syndrome and tries to end controversies on its nomenclature. This statement also proposes new diagnostic criteria based on data from the International Takotsubo Registry, to improve diagnostic accuracy. Unlike Takotsubo which affects the microcirculation,6 classical forms of acute coronary syndromes are due to rupture or erosion of lipid-rich plaques in epicardial coronary arteries.7,8 Inflammation of atherosclerotic plaques is considered the prime mechanisms of plaque vulnerability, with interleukin-1 as the prototypical pro-inflammatory cytokine.9 Initially, interleukin-1 was implicated as a cardiodepressant in septic shock, but subsequently it has been recognized as a mediator of atherosclerosis, acute myocardial infarction, and heart failure. In their clinical review entitled ‘Interleukin-1 blockade in cardiovascular diseases: a clinical update’, Antonio Abbate and colleagues from the Virginia Commonwealth University in Richmond, Virginia in the USA10 note that interleukin-1 monoclonal antibodies prevent recurrent atherothrombotic cardiovascular events and, in ST-segment elevation myocardial infarction (STEMI), quench the inflammatory response and prevent heart failure. In heart failure, interleukin-1 appears to impair beta-adrenergic receptor signalling and intracellular calcium handling, and accordingly its inhibition improves exercise capacity. While interleukin-1 blockade is not immunosuppressive and not associated with opportunistic infections or increased risk of cancer, lethal outcomes may occur due to blunting of inflammation and in turn delayed presentation and diagnosis. The practical use of interleukin-1 blockade is currently experimental, but its potential is worth consideration. An acute occlusion of an epicardial coronary artery may be caused by plaque rupture or erosion. The latter is discussed in a Review article entitled ‘Plaque erosion: a new in vivo diagnosis and a potential major shift in the management of patients with acute coronary syndromes’ by Ik-Kyung Jang and colleagues from the Massachusetts General Hospital in Boston, Massachusetts in the USA.10 The advent of intravascular imaging techniques, particularly optical coherence tomography,11,12 has improved the understanding of plaque erosion. Appreciation of the distinct biological and clinical mechanisms of plaque erosion points to the possibility of tailored management strategies for patients presenting with acute coronary syndromes. This topic is further analysed in an article entitled ‘In vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction: a clinical, angiographic, and intravascular optical coherence tomography study’ by Bo Yu and colleagues from the 2nd affiliated hospital of Harbin Medical University in Heilongjiang, China.13 Using optical coherence tomography in 822 patients with STEMI, 25.4% were found to have plaque erosion and 68.6% had rupture. Plaque erosion was more frequent in younger females of less than 50 years, with a similar trend in males. Those with erosion were more often current smokers, but had fewer other coronary risk factors than those with rupture. There was a preponderance of erosions in the left anterior descending coronary artery or LAD and near a bifurcation (Figure 2). Thus, in STEMI, erosion is a predictable clinical entity distinct from rupture, and its recognition may change the therapeutic approach to these patients.14 These findings are put into context in an Editorial by Aloke Virmani Finn from CVPATH in Gaithersburg, Maryland in the USA.15 Figure 2 View largeDownload slide The spatial distribution of plaque erosion and plaque rupture in the coronary arteries. Bar graph (A): the spatial distribution of plaque erosion in three major epicardial arteries was similar to plaque rupture. Boxplots graph (B): in the LAD, most erosions (114/128, 89.1%) and ruptures (236/265, 89.1%) clustered within the first 40 mm from the coronary ostium. In the RCA, only half of erosions (33/64, 51.6%) and ruptures (128/244, 52.5%) were located within the first 40 mm and were more evenly distributed throughout the entire length of the coronary artery. LAD, left anterior descending artery; LCX, left circumflex artery; RCA, right coronary artery (from Dai J, Xing L, Jia H, Zhu Y, Zhang S, Hu S, Lin L, Ma L, Liu H, Xu M, Ren X, Yu H, Li L, Zou Y, Zhang S, Mintz GS, Hou J, Yu B. In vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction: a clinical, angiographical, and intravascular optical coherence tomography study. See pages 2077–2085). Figure 2 View largeDownload slide The spatial distribution of plaque erosion and plaque rupture in the coronary arteries. Bar graph (A): the spatial distribution of plaque erosion in three major epicardial arteries was similar to plaque rupture. Boxplots graph (B): in the LAD, most erosions (114/128, 89.1%) and ruptures (236/265, 89.1%) clustered within the first 40 mm from the coronary ostium. In the RCA, only half of erosions (33/64, 51.6%) and ruptures (128/244, 52.5%) were located within the first 40 mm and were more evenly distributed throughout the entire length of the coronary artery. LAD, left anterior descending artery; LCX, left circumflex artery; RCA, right coronary artery (from Dai J, Xing L, Jia H, Zhu Y, Zhang S, Hu S, Lin L, Ma L, Liu H, Xu M, Ren X, Yu H, Li L, Zou Y, Zhang S, Mintz GS, Hou J, Yu B. In vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction: a clinical, angiographical, and intravascular optical coherence tomography study. See pages 2077–2085). Cardiogenic shock is a feared complication of both Takotsubo and STEMI, and the last frontier in the management of acute coronary syndromes.16 In their article ‘Predicting the development of in-hospital cardiogenic shock in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: the ORBI risk score’, Vincent Auffret and colleagues aimed to derive and validate a readily useable risk score to identify patients at high risk of in-hospital cardiogenic shock in an initial and validation cohort.17 Eleven variables were independently associated with the development of in-hospital cardiogenic shock: age >70 years, prior stroke or transient ischaemic attack, cardiac arrest upon admission, anterior STEMI, delay of first medical contact to primary percutaneous coronary intervention (PCI) >90 min, Killip class, heart rate >90 bpm, a combination of systolic blood pressure <125 mmHg and pulse pressure <45 mmHg, glycaemia >10 mmol/L, culprit lesion of the left main coronary artery, and post-primary PCI TIMI flow grade <3 (Figure 3). The score derived from these variables allowed the classification of patients into four risk categories with cardiogenic shock rates of 1.3, 6.6, 11.7, and 31.8%. The score demonstrated high discrimination and adequate calibration in both cohorts. Thus, the ORBI risk score is a tool to identify high-risk STEMI patients developing cardiogenic shock and may be helpful with the availability of novel treatment options in these patients.18 The clinical usefulness of the score is further discussed in a thought-provoking Editorial by George Dangas from the Cardiovascular Research Foundation in New York.19 Figure 3 View largeDownload slide Multivariable predictors of in-hospital cardiogenic shock in the derivation cohort and their respective weights in the ORBI risk score. CI, confidence interval; OR, odds ratio; pPCI, primary percutaneous coronary intervention; TIA, transient ischaemic attack; SBP, systolic blood pressure (from Auffret V, Cottin Y, Leurent G, Gilard M, Beer J-C, Zabalawi A, Chagué F, Filippi E, Brunet D, Hacot J-P, Brunel P, Mejri M, Lorgis L, Rouault G, Druelles P, Cornily J-C, Didier R, Bot E, Boulanger B, Coudert I, Loirat A, Bedossa M, Boulmier D, Maza M, Le Guellec M, Puri R, Zeller M, Le Breton H; On behalf of the ORBI and RICOWorking Groups. Predicting the development of in-hospital cardiogenic shock in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: the ORBI risk score. See pages 2090–2102). Figure 3 View largeDownload slide Multivariable predictors of in-hospital cardiogenic shock in the derivation cohort and their respective weights in the ORBI risk score. CI, confidence interval; OR, odds ratio; pPCI, primary percutaneous coronary intervention; TIA, transient ischaemic attack; SBP, systolic blood pressure (from Auffret V, Cottin Y, Leurent G, Gilard M, Beer J-C, Zabalawi A, Chagué F, Filippi E, Brunet D, Hacot J-P, Brunel P, Mejri M, Lorgis L, Rouault G, Druelles P, Cornily J-C, Didier R, Bot E, Boulanger B, Coudert I, Loirat A, Bedossa M, Boulmier D, Maza M, Le Guellec M, Puri R, Zeller M, Le Breton H; On behalf of the ORBI and RICOWorking Groups. Predicting the development of in-hospital cardiogenic shock in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: the ORBI risk score. See pages 2090–2102). Myocardial infarction and gallstone disease are intrinsically linked via cholesterol metabolism. In their study entitled ‘Genetic variants in CYP7A1 and risk of myocardial infarction and symptomatic gallstone disease’, Anne Tybjaerg-Hansen and colleagues from the Rigshospitalet in Copenhagen, Denmark tested the hypothesis that genetic variants in the gene encoding cholesterol 7 alpha-hydroxylase (CYP7A1), the rate-limiting enzyme in the conversion of cholesterol to bile acids in the liver, are associated with risk of myocardial infarction and gallstone disease in the general population.20 During 7 years, myocardial infarction developed in 2326 individuals and gallstone disease in 2007. For rare mutations, CYP7A1 allele count was associated with an increase in LDL-cholesterol (LDL-C) of 12 for individuals with the highest vs. the lowest allele count. For common variants, CYP7A1 weighted allele scores in individuals with a score >0.04 vs. ≤0 were associated with stepwise increases in LDL-C of up to 2.4%, and with corresponding adjusted hazard ratios of 1.25 for myocardial infarction and 1.39 for gallstone disease. Thus, genetic variants in CYP7A1 which are associated with increased levels of LDL-C are associated with an increased risk of both myocardial infarction and gallstone disease. The editors hope that this issue of the European Heart Journal will be of interest to its readers. References 1 Sato H , Tateishi H , Uchida T. Takotsubo-type cardiomyopathy due to multivessel spasm. In: Kodama K , Haze K , Hon M , eds. Clinical Aspect of Myocardial Injury: From Ischemia to Heart Failure . Tokyo, Japan : Kagakuhyouronsha ; 1990 . p 56 – 64 . 2 Pavin D , Le Breton H , Daubert C. Human stress cardiomyopathy mimicking acute myocardial syndrome . Heart 1997 ; 78 : 509 – 511 . Google Scholar CrossRef Search ADS PubMed 3 Templin C , Ghadri JR , Diekmann J , Napp LC , Bataiosu DR , Jaguszewski M , Cammann VL , Sarcon A , Geyer V , Neumann CA. Clinical features and outcomes of Takotsubo (stress) cardiomyopathy . N Engl J Med 2015 ; 373 : 929 – 938 . Google Scholar CrossRef Search ADS PubMed 4 to be added at proof stage: International Expert Consensus Document on Takotsubo Syndrome – PART I: Characteristics and Clinical Presentation . Eur Heart J 2018 ; 39 : 2032 – 2046 . 5 to be added at proof stage: International Expert Consensus Document on Takotsubo Syndrome – PART II: Diagnostic Workup and Outcome . Eur Heart J 2018 ; 39 : 2047 – 2062 . 6 Lüscher TF , Templin C. Is takotsubo syndrome a microvascular acute coronary syndrome? Towards a new definition . Eur Heart J 2016 ; 37 : 2816 – 2820 . Google Scholar CrossRef Search ADS PubMed 7 Nilsson J. Atherosclerotic plaque vulnerability in the statin era . Eur Heart J 2017 ; 38 : 1638 – 1644 . Google Scholar CrossRef Search ADS PubMed 8 Partida RA , Libby P , Crea F , Jang IK. Plaque erosion: a new in vivo diagnosis and a potential major shift in the management of patients with acute coronary syndromes . Eur Heart J 2018 ; 39 : 2070 – 2076 . 9 Ridker PM , Luscher TF. Anti-inflammatory therapies for cardiovascular disease . Eur Heart J 2014 ; 35 : 1782 – 1791 . Google Scholar CrossRef Search ADS PubMed 10 Buckley LF , Abbate A. Interleukin-1 blockade in cardiovascular diseases: a clinical update . Eur Heart J 2018 ; 39 : 2063 – 2069 . 11 van der Sijde JN , Karanasos A , Villiger M , Bouma BE , Regar E. First-in-man assessment of plaque rupture by polarization-sensitive optical frequency domain imaging in vivo . Eur Heart J 2016 ; 37 : 1932 . Google Scholar CrossRef Search ADS PubMed 12 Toutouzas K , Benetos G , Karanasos A , Chatzizisis YS , Giannopoulos AA , Tousoulis D. Vulnerable plaque imaging: updates on new pathobiological mechanisms . Eur Heart J 2015 ; 36 : 3147 – 3154 . Google Scholar CrossRef Search ADS PubMed 13 Dai J , Xing L , Jia H , Zhu Y , Zhang S , Hu S , Lin L , Ma L , Liu H , Xu M , Ren X , Yu H , Li L , Zou Y , Zhang S , Mintz GS , Hou J , Yu B. In vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction: a clinical, angiographical, and intravascular optical coherence tomography study . Eur Heart J 2018 ; 39 : 2077 – 2085 . 14 Jia H , Dai J , Hou J , Xing L , Ma L , Liu H , Xu M , Yao Y , Hu S , Yamamoto E , Lee H , Zhang S , Yu B , Jang IK. Effective anti-thrombotic therapy without stenting: intravascular optical coherence tomography-based management in plaque erosion (the EROSION study) . Eur Heart J 2017 ; 38 : 792 – 800 . Google Scholar CrossRef Search ADS PubMed 15 Jinnouchi H , Virmani R , Finn AV. Are characteristics of plaque erosion defined by optical coherence tomography similar to true erosion in pathology? Eur Heart J 2018 ; 39 : 2086 – 2089 . 16 Luscher TF , Obeid S. From Eisenhower’s heart attack to modern management: a true success story! Eur Heart J 2017 ; 38 : 3066 – 3069 . Google Scholar CrossRef Search ADS PubMed 17 Auffret V , Cottin Y , Leurent G , Gilard M , Beer JC , Zabalawi A , Chague F , Filippi E , Brunet D , Hacot JP , Brunel P , Mejri M , Lorgis L , Rouault G , Druelles P , Cornily JC , Didier R , Bot E , Boulanger B , Coudert I , Loirat A , Bedossa M , Boulmier D , Maza M , Le Guellec M , Puri R , Zeller M , Le Breton H. Predicting the development of in-hospital cardiogenic shock in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: the ORBI risk score . Eur Heart J 2018 ; 39 : 2090 – 2102 . 18 Thiele H , Jobs A , Ouweneel DM , Henriques JPS , Seyfarth M , Desch S , Eitel I , Poss J , Fuernau G , de Waha S. Percutaneous short-term active mechanical support devices in cardiogenic shock: a systematic review and collaborative meta-analysis of randomized trials . Eur Heart J 2017 ; 38 : 3523 – 3531 . Google Scholar CrossRef Search ADS PubMed 19 Dangas G , Guedeney P. Prediction, staging, and outcomes of ischaemic cardiogenic shock after STEMI: a complex clinical interplay . Eur Heart J 2018 ; 39 : 2103 – 2105 . 20 Qayyum F , Lauridsen BK , Frikke-Schmidt R , Kofoed KF , Nordestgaard BG , Tybjaerg-Hansen A. Genetic variants in CYP7A1 and risk of myocardial infarction and symptomatic gallstone disease . Eur Heart J 2018 ; 39 : 2106 – 2116 . Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

Journal

European Heart JournalOxford University Press

Published: Jun 7, 2018

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