In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser.
Two columns page  

Committee on Acute and Advanced Heart Failure

The HFA Committee on Acute and Advanced Heart Failure promotes, coordinates and overlooks study and research on the epidemiology, pathophysiology, diagnosis and management of Acute and Advanced Heart Failure in order to improve patients outcomes

Heart Failure (HF)

In order to achieve the above, the committee has recognized the importance

  • Consulting non-cardiologists involved in the management of acute heart failure (internists, intensive-care specialists, emergency medicine physicians, anesthesiologists, general physicians…).
  • Building a relationship between different health-care professionals; involved in the management of acute heart failure (nurses, pharmacists, hospital administrators …).

 

Article of the Month

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

Read article

Dr Rudiger wrote the Editorial

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.

References
  1. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 1992; 20:864–874
  2. van Diepen S, Vavalle JP, Newby LK, et al: The Systemic Inflammatory Response Syndrome in Patients With ST-Segment Elevation Myocardial Infarction. Crit Care Med 2013; 41:2080–2087
  3. Kohsaka S, Menon V, Lowe AM, et al; SHOCK Investigators: Systemic inflammatory response syndrome after acute myocardial infarction complicated by cardiogenic shock. Arch Intern Med 2005; 165:1643–1650
  4. Peschel T, Schönauer M, Thiele H, et al: Invasive assessment of bacterial endotoxin and inflammatory cytokines in patients with acute heart failure. Eur J Heart Fail 2003; 5:609–614
  5. Bianchi ME: DAMPs, PAMPs and alarmins: All we need to know about danger. J Leukoc Biol 2007; 81:1–5
  6. Lotze MT, Deisseroth A, Rubartelli A: Damage associated molecular pattern molecules. Clin Immunol 2007; 124:1–4
  7. Balligand JL, Ungureanu D, Kelly RA, et al: Abnormal contractile function due to induction of nitric oxide synthesis in rat cardiac myocytes follows exposure to activated macrophage-conditioned medium. J Clin Invest 1993; 91:2314–2319
  8. Kumar A, Brar R, Wang P, et al: Role of nitric oxide and cGMP in human septic serum-induced depression of cardiac myocyte contractility. Am J Physiol 1999; 276(1, Part 2):R265–R276
  9. Pathan N, Hemingway CA, Alizadeh AA, et al: Role of interleukin 6 in myocardial dysfunction of meningococcal septic shock. Lancet 2004; 363:203–209
  10. Mann DL: Inflammatory mediators and the failing heart: Past, present, and the foreseeable future. Circ Res 2002; 91:988–998
  11. Rudiger A, Singer M: Mechanisms of sepsis-induced cardiac dysfunction. Crit Care Med 2007; 35:1599–1608
  12. Rudiger A: Beta-block the septic heart. Crit Care Med 2010; 38(10 Suppl):S608–S612
  13. Heusch G, Schulz R, Rahimtoola SH: Myocardial hibernation: A delicate balance. Am J Physiol Heart Circ Physiol 2005; 288:H984–H999

Coordinator

Prof. V-P Harjola, FESC (Helsinki, FI) email

Committee

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)

Affiliates

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)

Workshop

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

Priorities

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 Surgeons
Write a practical recommendation on "organ dysfunction" in acute heart failure in conjunction with ESICM 


 

European Society
of Cardiology

Les Templiers
2035 Route des Colles
CS 80179 BIOT
06903 Sophia Antipolis
Cedex France

Phone: 33.4.92.94.76.00