The year in cardiology 2018: acute coronary syndromes
█ Current opinion
Petr Widimsky, MD, DrSc, FESC1, Filippo Crea, MD, PhD FESC2, Ronald K. Binder, MD, FESC3 and Thomas F. Lüscher, MD, FRCP, FESC4,5
1Cardiocenter, Third Faculty of Medicine, Charles University, Hospital Kralovske Vinohrady, Prague, CzechRepublic;
2Istituto di Cardiologia, Universita Catolica del Santo Cuore, I- 00168 Roma, Italy;
3Cardiology and Intensive Care, University Teaching Hospital Klinikum Wels Grieskirchen A-4600 Wels, Austria and
4Royal Brompton and Harefield Hospitals and Imperial College, London, United Kingddom and
5Center for Molecular Cardiology, University Zurich, Switzerland
CThe management of acute coronary syndromes (ACS) is a true success story. Indeed, in 1955 when the then President of the United States Dwight D. Eisenhower had an infarction, the President’s personal physician, Dr. Howard Snyder, interpreted his symptoms as a gastrointestinal illness (1). It took 10 hours to transfer him to a local hospital where an electrocardiograph had to be brought in from another hospital – a situation that today would be malpractice (2). The ECG showed an anterolateral acute myocardial infarction with ST-segment elevations or a STEMI as we would call it today based on the recent definition of myocardial infarction (3). Based on the Fourth Universal Definition of Myocardial Infarction Eisenhower experienced a clear cut type 1 infarction (Table 1). Today, we distinguish not only 5 types of infarction, but also myocardial injury, defined by an elevated cardiac troponin (cTn) value, which is also is associated with an adverse prognosis. To differentiate myocardial injury from myocardial infarction, criteria in addition to abnormal biomarkers are required such as ECG changes and evidence of ischemia.
In the 50ies not many diagnostic tools or even any effective treatment was available (4). Not only was an ECG not commonly available, cardiac enzymes were still to be introduced and unavailable at that time. The management of acute myocardial infarction was mainly “tender loving care”, i.e. nitroglycerin and morphine for pain relief. Defibrillation had still to be introduced by Paul M. Zoll a year later (5). Aspirin was labelled as remedy for fever and pain and considered contraindicated for heart patients (6) until Sir John Vane discovered that it inhibits platelet aggregation (7), Betablockers had still to be developed by Sir James Black, Nobel Prize Laureate in 1988 (8) Finally, Akiro Endo’s seminal discovery of statins only occurred in the 70ties and shown to reduce mortality as late as 1992. Lastly, it took another couple years until inhibitors of the P2Y12 receptor became common: practice (11, 12). The most important step, proved to be rapid and effective reperfusion and revascularization. Although streptokinase and later tissue plasminogen activators were somewhat successful, it required a bold colleague such as Andreas R. Grüntzig to develop percutaneous coronary intervention (13, 14). Later, stents (and especially drug eluting stents) improved the results of primary percutaneous coronary angioplasty and made it the first line therapy in patients with acute coronary syndromes ACS (15, 16). As a result of all these impressive developments, mortality of acute myocardial infarction declined stepwise, but eventually dramatically over the past decade (17) (Figure 1). Again this year further steps have been taken to improve the management of patients with ACS as outlined in this review.
The studies included in this review deal initially with pathophysiologic mechanisms, early diagnosis, risk stratification and outcomes in specific subpopulations, the mid portion reports new data on pharmacotherapy while the last part provides latest data on interventional treatment of acute coronary syndromes.