Our mission is to become a worldwide reference for education in the field for all professionals involved in the process to disseminate knowledge & skills of Acute Cardiovascular Care.
Our mission is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe.
Our mission is to promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our mission is to reduce the burden of cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Our mission is to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death.
Our mission is to improve quality of life and longevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
The ESC Working Groups' goal is to stimulate and disseminate scientific knowledge in different fields of cardiology.
The ESC Councils' goal is to share knowledge among medical professionals practising in specific cardiology domains.
OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
In order to achieve the above, the committee has recognized the importance
The Committee's article has been chosen by Dr Alain Rudiger, , from the University Hospital Zurich, Switzerland.
The Systemic Inflammatory Response Syndrome in Patients With ST-Segment Elevation Myocardial Infarction
Critical Care Medicine: September 2013 - Volume 41 - Issue 9 - p 2080–2087
van Diepen, Sean MD, MSc; Vavalle, John P. MD, MHS; Newby, L. Kristin MD, MHS; Clare, Robert MS; Pieper, Karen S. MS; Ezekowitz, Justin A. MBBCh, MSc; Hochman, Judith S. MD; Mahaffey, Kenneth W. MD; Armstrong, Paul W. MD; Granger, Christopher B. MD
Systemic Inflammation After Myocardial Infarction*
SIRS, the systemic inflammatory response syndrome, is defined by the presence of two or more of the following criteria: heart rate > 90 beats/min, respiration rate > 20 breaths/min, body temperature > 38°C or < 36°C, or leukocyte count > 12 or < 4 x 109/L (1). In this issue of Critical Care Medicine, van Diepen et al (2) analyzed the charts of 1,843 patients with ST-elevation myocardial infarction (STEMI). They found that SIRS was present at admission in 25.0% of the patients. In comparison to patients without SIRS, their risk for death, cardiogenic shock, heart failure, or stroke during the following 90 days was substantially higher (21.6% vs 11.9%, p < 0.001). Each additional SIRS criterion was statistically associated with an increased risk for adverse outcome, with heart rate being the strongest prognosticator of all four SIRS criteria. At 24 hours, 8.1% of STEMI patients fulfilled two or more SIRS criteria, and the frequency of adverse events was 21.7% compared to 10.1% (p < 0.001) in patients without SIRS. Mortality was higher among patients with SIRS at either time-point. Thanks to this study, the SIRS criteria can now be used as easily available risk assessment tools in the clinical management of patients with myocardial infarction.
Clearly, SIRS variables can develop in STEMI patients as a result of hemodynamic deterioration. A large myocardial infarction will impair cardiac output and cause cardiogenic shock. Heart and respiration rates will increase in order to compensate for low stroke volume and metabolic acidosis, respectively. These physiological alterations are triggered by the sympathetic autonomous nervous system, which is stimulated by hemodynamic compromise, chest pain, and anxiety. Adrenergic hormones also facilitate the detachment of leukocytes from the endothelium, increasing the numbers of circulating neutrophils during acute stress.
Another cause for SIRS in STEMI patients is, of course, a concomitant infection. A retrospective analysis of the SHOCK trial revealed that 13% of patients with myocardial infarction complicated by cardiogenic shock were suffering from a culture-positive infection (3). The predominant pathogens were Staphylococcus aureus, Klebsiella pneumonia, and Pseudomonas aeruginosa. Patients with infections had a lower systemic vascular resistance, suggesting that sepsis-induced vasodilation contributes to the shock state. Patients with infections also required longer durations of mechanical ventilation and hospital stay. Invasive interventions, such as insertion of central venous catheters, increased the risk of concomitant infections. Others have postulated bacterial translocation of the gut as a source for inflammation in patients with heart failure (4).
However, it is important to note that inflammation can be initiated without any underlying infection. Inflammation in STEMI patients can be triggered by the release of damage-associated molecular patterns (DAMPs) from the necrotic myocardium. DAMPs are intracellular structures and include, among others, high-mobility group box 1 proteins, mitochondrial components, and heat shock proteins (5). Such danger signaling molecules are probably also discharged from underperfused tissues during cardiogenic shock. Subsequently, DAMPs are recognized by cells of the innate immune system, which in turn activate an intracellular cascade and finally switch on genes encoding for cytokines, such as interleukins (ILs) and tumor necrosis factor (TNF)-α (6). These inflammatory mediators are released into the circulation, promoting local and, at sufficient concentrations, systemic inflammation. Although the goal of local inflammation is the repair of damaged cardiac and noncardiac tissues, systemic inflammation alerts the jeopardized organism and deploys adaptive mechanisms.
Last but not least, clinicians should realize that inflammatory mediators, such as TNF-α, IL-6, and nitric oxide, reversibly depress myocardial contractility (7–9), potentially leading to heart failure (10, 11), However, myocardial depression reduces cellular oxygen expenditure in a condition, in which myocardial oxygen supply is impaired, creating a new balance between cellular energy generation and consumption (12). Consequently, the cells at risk might survive in a viable, but noncontracting, state (hibernating myocardium) (13). Hence, inflammation-induced myocardial depression can be viewed as an adaptive mechanism in patients with coronary artery disease and impaired myocardial perfusion. When coronary flow is reestablished, the viable cells have the potential for full functional recovery.
Prof. V-P Harjola, FESC (Helsinki, FI) email
J Parissis FESC (Basel, CH) H Skouri FHFA FESC (Beirut, LB)M B Yilmaz FESC (Sivas, TR)H-P Brunner L Rocca FESC (Maastricht, NL)J Bauersachs FESC (Hannover, DE)A Ristic FESC (Belgrade, RS)S Collins SAEM (Nashville, US)W Mullens (Genk, BE)O Chioncel (Bucharest, RO)A Rudiger (Zurich, CH)
A Mebazaa FESC (Paris, FR)M Banaszewski FESC (Warsaw, PL)J-L Lambert Rodriguez FHFA FESC (Oviedo, ES)J Masip FESC (Barcelona, ES)J Spinar FESC (Brno, CZ)G Filippatos FESC (Athens, GR) (ex-officio)
Mechanical Circulatory Support devices in heart failure - Programme- 27-28 April 2012 Wroclaw, Poland
International consensus on pre-hospital & initial management of acute heart failure - Common standpoints for emergency physicians and cardiologists - 15-16 March 2013 Munich, Germany
Finalise the position paper on AHF "call for action" of the European Federation of Internal Medicine, the European Society of Emergency Medicine, the European Society of Intensive care Medicine, the primary care physicians WONCA and the Council of Cardiology Practice of the ESC.
Publish the paper on "Recommendations for admission in CCU and ICU" involving same societies.
Conduct a survey on the impact of devices in the outcome in acute heart failure patients in conjunction with ESICM and European Society of Cardiac SurgeonsWrite a practical recommendation on "organ dysfunction" in acute heart failure in conjunction with ESICM
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