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EDITORIAL

Acute heart failure, no reflow, cardiogenic shock, and beyond

Pages 59-60 | Published online: 10 Jul 2009

Dear Readers of Acute Cardiac Care,

This issue brings to the stage complex problems of management of acute heart failure, acute interventions, and hemodynamic compromise. Several of the publications represent reports from the 2008 European Society of Cardiology Working Group on Acute Cardiac Care Meeting held in Versailles in October 2008. Hospitalizations for acute heart failure are associated with high post-discharge morbidity and mortality. Harinstein et al. Citation[1] review the potential role of vasopressin antagonists in these patients. Later on in the journal, Harinstein et al. Citation[2] present the epidemiologic factors, risk stratification, and prognostic factors associated with this syndrome. The strongest prognostic factors include blood pressure, body weight, renal function, QRS duration, and the presence of coronary artery disease. Gheorghiade et al. Citation[3] review all the available data supporting the use of Digoxin in acute heart failure. Being a classical ‘old drug’ with a strong historical belief in its effectiveness, it looks like we have been using this drug for many years without well-established evidence. While it may be an ideal drug for the treatment of acute heart failure syndromes, it warrants further investigation in large clinical trials.

Primary angioplasty for acute myocardial infarction (MI) has become the major method of acute revascularization, making one of the largest clinical impact in the acute cardiac care setup. Arnoud et al. Citation[4] discuss the issues raised around various aspects of acute revascularization for myocardial infarction at the Versailles meeting. Clearly, the extent of myocardial reperfusion is a strong predictor of outcome and using myocardial blush and ST segment resolution are readily available parameters reflecting myocardial no reflow. The importance of strategies which reduce time to treatment and limit the thrombotic burden before or during percutaneous interventions (PCI) are discussed below.

Vrints Citation[5] discusses in detail the pathophysiology of no reflow. Lethal reperfusion injury to both the endothelial cells and the cardiomyocytes related to the effects of oxidative stress, paradoxical vasoconstriction caused by endothelial dysfunction, plugging of the capillaries by endothelial blebs, and mechanical compression by myocardial edema are all related to the reperfusion injury. New therapeutic approach of the no-reflow phenomenon emerge from our understanding the complex physiology of no reflow.

The role of genetic factors on prognostic outcomes is now a field of intense research in many disciplines. Whether genetic factors are playing a role in modifying interventions is presented by Moses et al. Citation[6]. The authors have studied the relationship between the PLA2 polymorphism of the platelet glycoprotein IIbIIIa (GPIIIa) receptor and major adverse cardiac events after percutaneous coronary intervention. While polymorphism was relatively frequent, the homozygous variant was infrequent (0.5%) and practically, the presence of PLA2 had no influence on clinical outcomes in this study. This is an important study and while not yielding positive association, is an attempt to identifying genetic markers that will guide us in future interventions.

A fascinating paper by Zahn et al. Citation[7] shows the statistics of daily practice in a large interventional center. ST elevation (STEMI) and non-ST elevation (NSTEMI) myocardial infarction seem to occur with similar frequencies, where invasive strategies are applied in a high percentage in both groups. Despite the similarity in the clinical approach in both clinical categories, in-hospital mortality is twice as high in STEMI compared to NSTEMI patients. Severe pump failure that results from an acute coronary event is a major challenge for the acute care interventionalists as well as for the acute care intensivists. Acute intervention, mechanical and pharmacological support should be promptly administered. Tsagalou et al. Citation[8] report on the optimization of hemodynamic support for the patients using levosimendan on top of catecholamine therapy in patients with carcinogenic shock. The prognosis of the patients is strongly affected by creatinine clearance as discussed by Vis et al. Citation[9] in this issue.

Finally, a report on databases for cardiology Citation[10] is of a high importance in creating a wide-based knowledge of common practice and outcome in Europe. The acute cardiac care journey ends with two educational images, mitral annular calcifications Citation[11] and a rare case of aortic dissection with left atrial compression Citation[12], that conclude this issue.

References

  • Harinstein ME, Filippatos GS, Gheorghiade M. Acute heart failure syndromes: the role of vasopressin antagonists. Acute Cardiac Care. 2009; 11: 60–4
  • Harinstein ME, Filippatos GS, Gheorghiade M. Acute heart failure syndromes: epidemiology, risk stratification and prognostic factors. Acute Cardiac Care. 2009; 11: 76–81
  • Gheorghiade M, Harinstein ME, Filippatos GS. Digoxin for the treatment of chronic and acute heart failure syndromes. Acute Cardiac Care. 2009; 11: 82–6
  • Arnoud WJ, Van 't Hof J, Zijlstra F. The success of primary angioplasty: beyond TIMI flow. Summary of a presentation held at acute cardiac care meeting in Paris, October 2008. Acute Cardiac Care 2009; 11: 65–67
  • Vrints CJM. Pathophysiology of the no-reflow phenomenon. Acute Cardiac Care. 2009; 11: 68–75
  • Moses JW, Leon M, Dangas G, Syros G, Mehran R, Weisz G, et al. Role of PLA2 polymorphism on clinical events after percutaneous coronary intervention. Acute Cardiac Care. 2009; 11: 87–90
  • Zahn R, Schweppe F, Zeymer U, Schiele R, Gitt AK, Mark B, et al. Reperfusion therapy for acute ST-elevation and non ST-elevation myocardial infarction: What can be achieved in daily clinical practice in unselected patients at an interventional center?. Acute Cardiac Care. 2009; 11: 91–7
  • Tsagalou EP, Kanakakis J, Anastasiou-Nana MI, Drakos SG, Ntalianis AS, Malliaras K. Hemodynamic effects of levosimendan in acute myocardial infarction complicated by cardiogenic shock and high systemic vascular resistance. Acute Cardiac Care. 2009; 11: 98–105
  • Vis MM, Schaaf RJ, Sjauw KD, Tijssen JG, Baan J, Koch KT, et al. Creatinine clearance is independently associated with one year mortality in a primary PCI cohort with cardiogenic shock. Acute Cardiac Care. 2009; 11: 106–111
  • Danchin N, Lablanche JM, Komajda M, Tubaro M, Maseri A, Pristipino C. On behalf of G8 Cardio-Associazione Nazionale Medici Cardiologi Ospedalieri (ANMCO). Societe′ Francaise De Cardiologie (SFC) Database. The development of an international, common, prospective, cardiology database. Acute Cardiac Care. 2008; 11: 112–119
  • Zeina AR, Makhoul N, Nachtigal A. Mitral annulus caseous calcification imaged with 64-slice MDCT. Acute Cardiac Care. 2009; 11: 120–1
  • Chue CD, Routledge HC, Epstein ACR. Aortic dissection with left atrial compression: an unusual cause of breathlessness. Acute Cardiac Care. 2009; 11: 122–3

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