Acute coronary syndrome

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Classification according to ICD-10
I20.0 Unstable angina pectoris
I21 Acute myocardial infarction
ICD-10 online (WHO version 2019)

With the concept of acute coronary syndrome (English acute coronary syndrome , ACS) is used in medicine a spectrum of disease Heart circumscribed by the closure or severe narrowing of a coronary vessel caused. It ranges from unstable angina pectoris (UA) to the two main forms of myocardial infarction , non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI) (see ECG nomenclature ). The cause of the acute event is a critical reduction in blood flow, mostly due to the formation of a local thrombus on the floor of a plaque rupture or plaque erosion. While the blood clot usually completely closes the vessel in STEMI, the blood flow is maintained in unstable angina pectoris and in NSTEMI.

In emergency medicine, the term acute coronary syndrome is primarily used as the primary working diagnosis in the case of unclear, acute and long-lasting (> 20 minutes) cardiac symptoms. This work diagnosis is based on a life-threatening situation for the patient concerned. In almost a third of the approximately 2 million annual emergencies in Germany with a working diagnosis of acute coronary syndrome, the initial suspicion is confirmed: 15 percent are diagnosed with unstable angina pectoris, another 15 percent with NSTEMI or STEMI, and about 2% of the cases are stressful Cardiomyopathy .

Possible differential diagnoses for acute coronary syndrome can be of various kinds: They range from other cardiovascular diseases (e.g. cardiac arrhythmias , myocarditis ) to pulmonary diseases (e.g. pulmonary embolism ), skeletal diseases (e.g. rib fractures ), gastrointestinal diseases Tract (e.g. acute pancreatitis , perforated gastric ulcer ) to tumor diseases of the skeleton and the chest wall.

Classification

Acute coronary syndrome is divided into three clearly defined categories for risk stratification and targeted therapeutic treatment of the affected patients:

  • ST Elevation Myocardial Infarction (STEMI)
  • Non-ST Elevation Myocardial Infarction (NSTEMI)
  • unstable angina pectoris (UA)

An exact diagnosis is made by measuring biochemical markers (especially cardiac troponin T and I) and electrocardiography (EKG) . The guidelines of the German Society for Cardiology, which apply to Germany, rate STEMI and NSTEMI as definitive diagnoses. The joint guidelines of the American College of Cardiology (ACC) and the American Heart Association (AHA) , on the other hand, prefer the final diagnoses Q-wave myocardial infarction (Qw MI) or non-Q-wave myocardial infarction (NQMI). This distinction between transmural (affecting the entire thickness of the wall layer of the heart) and non-transmural myocardial infarction is also common in German-speaking countries. It is made on the basis of changes in the QRS complex in the ECG, which can usually be detected after 12 hours at the earliest.

ST elevation myocardial infarction

An ST elevation myocardial infarction can be assumed if one of the following ECG findings is present:

  • ST elevation at the J point in 2 related leads that exceed the following limits:
    • in V2 and V3 2.5 mm for men under 40 years of age,
    • in V2 and V3 2 mm for men over 40 years of age,
    • in V2 and V3 1.5 mm for women,
    • 1 mm in all other leads or
  • Left bundle branch block with typical infarct symptoms

As a rule, there is also an increase in cardiac markers with STEMI. In patients with a STEMI, the troponin level rises for the first time after about 3 hours and remains elevated for up to 2 weeks. If such an increase cannot be demonstrated, the diagnosis of STEMI must be questioned.

Non-ST elevation myocardial infarction and unstable angina pectoris

If the ECG does not show any ST elevation, a non-ST elevation myocardial infarction or unstable angina pectoris can be assumed. An exact diagnosis can be made via the troponin value after 3 hours at the earliest. While slightly increased values ​​can be detected for up to 72 hours in NSTEMI, the cardiac markers in unstable angina pectoris do not show any increased values.

Risk factors

The first manifestation of acute coronary syndrome is usually preceded by many years of development. The atherosclerosis is the underlying disease that almost all cardiovascular events. Various risk factors promote the development and progression of atherosclerosis:

Non-influenceable risk factors:

Influencable risk factors:

Prognosis and consequential risk

While hospital mortality in acute coronary syndrome has been reduced in recent years, the pre-hospital mortality rate remains extremely high: 37 percent of patients with a myocardial infarction die before they even reach hospital.

During the initial hospitalization, around 3 percent of patients die as a result of acute coronary syndrome. At 6 percent, the mortality with ST elevation myocardial infarction is considerably higher than with non-ST elevation myocardial infarction (3 percent) and unstable angina pectoris (1 percent).

In addition to the acute event, there is a significant risk of suffering another cardiovascular event after an acute coronary syndrome (residual risk). Analyzes of the 5-year mortality of patients with an acute coronary syndrome show that a large proportion of ACS deaths only occur in an outpatient setting, i.e. after initial hospitalization (STEMI: 68 percent; NSTEMI: 86 percent; UA: 97 Percent). Overall, the 5-year mortality in acute coronary syndrome is around 20 percent. The long-term mortality risk is largely independent of the type of first manifestation of the acute coronary syndrome: The 5-year mortality in STEMI (19 percent), NSTEMI (22 percent) and unstable angina pectoris (17 percent) differ only slightly. In addition, a Swedish registry with 108,000 patients showed that after a first myocardial infarction there is an 18.3% risk of another cardiovascular event (repeated myocardial infarction, stroke or CV death) within the first year.

Secondary prevention

The primary goal of secondary prevention after an acute coronary syndrome is to inhibit the progression of atherosclerosis and to reduce the high residual risk, i.e. to prevent a new cardiovascular event. With the help of lifestyle changes, e.g. B. quitting smoking, regular physical activity and a change in diet, the risk of a secondary event can be reduced. Overall, however, the effect of lifestyle changes is limited, so drug therapies are usually used as well.

Anti-aggregation therapy

So-called platelet inhibitors (e.g. acetylsalicylic acid, prasugrel , ticagrelor , clopidogrel ) are used to prevent the formation of new thrombi.

Cholesterol lowering therapy

Treatment with lipid-lowering drugs , primarily statins (e.g. simvastatin ), is standard in secondary prevention after acute coronary syndrome. Statin therapy is primarily aimed at lowering LDL cholesterol to the recommended target values ​​of below 80 mg / dl (European Society of Cardiology) or 70 mg / dl (German Society for Cardiology). The influence of high LDL cholesterol levels on cardiovascular risk has been clearly documented. Various studies also show that the use of statins reduces the frequency of cardiovascular events by up to 38 percent. The remaining extremely high residual risk of over 60 percent can be explained, among other things, by the fact that the majority of patients do not achieve the recommended target values ​​for various parameters such as blood pressure or blood lipids: Despite statin therapy, only a quarter of patients have LDL cholesterol and HDL cholesterol in the target range.

The drug-based increase in HDL cholesterol ("good cholesterol") is considered a possible therapeutic approach to further reduce the residual risk of cardiovascular events. Epidemiological data show that high HDL-C levels correlate with a low risk of cardiovascular events. Nicotinic acid derivatives and fibrates , for example, have an influence on HDL cholesterol . However, both preparations have multiple effects on lipid metabolism . More specifically, the HDL cholesterol can be increased by inhibiting the cholesterol ester transfer protein (CETP) . With the CETP inhibitor anacetrapib, one (of a total of three so far) substances that cause an increase in HDL cholesterol via complete or selective CETP inhibition is currently still in clinical trials. The phase III study of dalcetrapib with 15,000 subjects was terminated by Roche in early May 2012 due to a lack of clinical efficacy.

See also

Individual evidence

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  2. ↑ a b c d C. W. Hamm: Guidelines: Acute Coronary Syndrome (ACS) . Part 1: ACS without persistent ST elevation. In: Zeitschrift für Kardiologie , 2004, 93, pp. 72–90. doi: 10.1107 / s00392-004-1064-2
  3. ↑ a b c d e f Pocket guidelines: Acute coronary syndrome without ST elevation (NSTE-ACS) - Update 2009 . German Society for Cardiology - Heart and Circulatory Research e. V.
  4. ^ F. Post, T. Münzel: The acute coronary syndrome. A diagnosis that is poorly handled in practice. In: The internist. 2010; 8, pp. 953-962.
  5. ^ Medical Association of North Rhine: Further information and differential diagnostics for the certified case report "patient with acute heart problems"
  6. ^ CW Hamm: Guidelines: Acute Coronary Syndrome (ACS) . Part 2: Acute coronary syndrome with ST elevation. In: Z Kardiol. 2004; 93, pp. 324-341. doi: 10.1007 / s00392-004-0109-x
  7. ↑ EM Antmann et al .: ACC / AHA Guidelines for the Management With ST-Elevation Myocardial Infarction. In: J Am Coll Cardiol . 2004; 44, pp. §1-E211.
  8. ↑ Kristian Thygesen et al .: "Fourth Universal Definition of Myocardial Infarction (2018)" Journal of the American College of Cardiology Volume 72, Issue 18, October 2018
  9. ^ A b Peter Libby : Current Concepts of the Pathogenesis of the Acute Coronary Syndromes . In: Circulation . tape 104 , no. 3 , July 17, 2001, p. 365-372 ( circ.ahajournals.org [accessed May 17, 2011]).
  10. ^ Federal health reports . Robert Koch Institute , 2006, No. 33
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  12. ↑ a b K. AA Fox et al .: Underestimated and under-recognized: the late consequences of acute coronary syndrome (GRACE UK-Belgian Study). In: Eur Heart J . 2010, doi: 10.1093 / eurherartj / ehq326
  13. ↑ Jernberg T et al .: "Cardiovascular risk in post-myocardial infarction patients: nationwide real world data demonstrate the importance of a long-term perspective." In: Eur Heart J. 2015: 36 (19), pp. 1163-70. doi: 10.1093 / eurheartj / ehu505
  14. ↑ L. Wallentin: Ticagrelor versus clopidogrel in patients with acute coronary syndromes. In: N Engl J Med. 2009 Sep 10; 361 (11), pp. 1045-1057. doi: 10.1056 / NEJMoa0904327 .
  15. ↑ Graham et al .: European guidelines on cardiovascular disease prevention in clinical practice: executive summary. In: Eur Heart J. 2007; 28, pp. 2375-2414. doi: 10.1093 / euroheartj / ehm316
  16. ↑ Ference BA et al .: “Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. " In: Eur Heart J. 2017: 38 (32), pp. 2459-72. doi: 10.1093 / eurheartj / ehx144
  17. ^ P. Libby et al .: The Forgotten Majority. Unfinished Business in Cardiovascular Risk Reduction. In: J Am Cardiol. 2005; 46, pp. 1225-1228. doi: 10.1016 / j.jacc.2005.07.006
  18. ^ AK Gitt et al .: Prevalence and overlap of different lipid abnormalities in statin-treated patients at high cardiovascular risk in clinical practice in Germany. In: Clinical Research in Cardiology 2010; 99, pp. 723-733. doi: 10.1107 / s00392-010-0177-z
  19. ↑ P. Barter et al .: HDL cholesterol, very low levels of LDL cholesterol, and cardiovascular events. In: N Engl J Med . 2007; 357, pp. 1301-1310.
  20. ↑ CP Cannon et al .: Safety of Anacetrapib in Patients with or at High Risk for Coronary Heart Disease In: N Engl J Med. 2010; 363, pp. 2406-2415.
  21. ↑ J. Niesor et al .: Dalcetrapib binds to and changes the conformation of CETP in a Unique Manner. In: Circulation , 2009, 120, p. 445: Abstract 1092.
  22. ↑ Roche reports on the phase III study with dalcetrapib . (PDF; 81 kB) Roche GmbH, May 7, 2012, press release.