Acute heart failure and early development of left ventricular dysfunction in patients with ST segment elevation acute myocardial infarction managed with primary percutaneous coronary intervention
Authors:
J. Pařenica 1; P. Kala 1; J. Jarkovský 2; M. Poloczek 1; O. Toman 1; M. Pávková Goldbergová 3; J. Maňoušek 1; K. Prymusová 4; L. Kubková 1; M. Tesák 1; L. Elbl 1; Z. Čermáková 5; J. Špinar 1
Authors‘ workplace:
Interní kardiologická klinika Lékařské fakulty MU a FN Brno, pracoviště Bohunice, přednosta prof. MU Dr. Jindřich Špinar, CSc., FESC
1; Institut biostatistiky a analýz Lékařské a Přírodovědecké fakulty MU Brno, ředitel doc. RNDr. Ladislav Dušek, Ph. D.
2; Ústav patologické fyziologie Lékařské fakulty MU Brno, přednostka prof. MU Dr. Anna Vašků, CSc.
3; Kardiologické oddělení Nemocnice Podlesí a. s., přednosta prim. MU Dr. Marian Branny
4; Oddělení klinické biochemie a hematologie FN Brno, pracoviště Bohunice, přednosta doc. MU Dr. Milan Dastych, CSc.
5
Published in:
Vnitř Lék 2011; 57(1): 43-51
Category:
Original Contributions
Overview
Background:
Acute heart failure during ST elevation myocardial infarction (STEMI) makes worse prognosis. The aim of the work was to find independent factors with relationship to acute heart failure (AHF) and the early development of left ventricular dysfunction within the prospective followed patients with STEMI.
Methods:
A total of 593 patients with STEMI treated by primary PCI (164 patients with AHF) were the study population. The activity of BNP and NT‑ ProBNP were measured at hospital admission and 24 h after MI onset. Left ventricular angiography was done before PCI; echocardiography was undertaken between the third and fifth day after MI.
Results:
The patients with AHF had higher level of glycaemia, creatinine, uric acid, HDL‑cholesterol, leukocytosis and natriuretic peptid. The total hospital mortality was 3.7%. 0.2% within the patients without AHF, 3.2%, 14.3%, resp. 63.6% within the patients with mild AHF, with pulmonary oedema, resp. with cardiogenic shock. The patients with AHF had lower ejection fraction (45.4 ± 11.9% vs 53.0 ± 10.3%). According to the multiple logistic regression we found higher glycaemia, age, heart rate, anterior wall MI, lower aortic pulse pressure and collaterals of infarct related artery as factors with independent relationship to AHF. Higher glycaemia, age, heart rate, anterior wall MI and lower aortic pulse pressure were found as independent factors with relationship to left ventricular dysfunction. According to ROC analysis possible cut off corresponding with AHF we suggested 29.5 mm Hg for LVEDP, 28.5 for dP/ dt/ P, 9.5 mmol/ l for glycaemia, 50 mm Hg for aortic pulse pressure.
Conclusions:
Our results found the development of AHF in one third of patients with STEMI. AHF increases the risk of in‑hospital mortality and the risk depends upon severity of failure. As the independent factors with relationship to development of AHF or left ventricular dysfunction we detected higher glycaemia, heart rate, anterior wall MI, age. Lower risk had patients with higher aortic pulse pressure.
Key words:
STEMI – primary PCI – acute heart failure – left ventricular dysfunction
Sources
1. Widimský P, Želízko M, Janský P et al. Jak léčíme akutní koronární syndromy v České republice? Výsledky registru CZECH. Cor Vasa 2007; 49: K237– K239.
2. Gibson CM. NRMI and current treatment patterns for ST‑elevation myocardial infarction. American Heart Journal 2004; 148 (Suppl 1): S29– S33.
3. Mandelzweig L, Battler A, Boyko V et al. The second Euro Heart Survey on acute coronary syndromes: characteristics, treatment, and outcome of patients with ACS in Europe and the Mediterranean Basin in 2004. Eur Heart J 2006; 27: 2285– 2293.
4. Steg PG, Dabbous OH, Feldman LJ et al. Determinants and Prognostic Impact of Heart Failure Complicating Acute Coronary Syndromes: Observations From the Global Registry of Acute Coronary Events (GRACE). Circulation 2004; 109: 494– 499.
5. Wu AH, Parsons L, Every NR et al. Hospital outcomes in patients presenting with congestive heart failure complicating acute myocardial infarction: A report from the Second National Registry of Myocardial Infarction (NRMI‑ 2). J Am Coll Cardiol 2002; 40: 1389– 1394.
6. Santoro GM, Carrabb N, Migliorini A et al. Acute heart failure in patients with acute myocardial infarction treated with primary percutaneus coronary intervention. Eur J Heart Fail 2008; 10: 780– 785.
7. Spencer FA, Meyer TE, Gore JM et al. Heterogeneity in the Management and Outcomes of Patients With Acute Myocardial Infarction Complicated by Heart Failure: The National Registry of Myocardial Infarction. Circulation 2002; 105: 2605– 2610.
8. Widimsky P, Hlinomaz O, Kala P et al. Diagnostika a léčba akutního infarktu s elevacemi ST. Doporučení České kardiologické spole. Cor Vasa 2010; 51: 724– 740.
9. Tomasz R, Zbigniew S, Artur D et al. Early abciximab administration before transfer for primary percutaneous coronary interventions for ST‑elevation myocardial infarction reduces 1‑year mortality in patients with high‑risk profile. Results from EUROTRANSFER Registry. Am Heart J 2009; 158: 569– 575.
10. Christopher MO, Wendy AG, Barry FU et al. Continuous intravenous dobutamine is associated with an increased risk of death in patients with advanced heart failure: Insights from the Flolan International Randomized Survival Trial (FIRST). Am Heart J 1999; 138: 78– 86.
11. Moiseyev VS, Pöder P, Drejevs N et al. Safety and efficacy of a novel calcium sensitizer, levosimendan, in patients with left ventricular failure due to an acute myocardial infarction. A randomized, placebo‑ controlled, double‑blind study (RUSSLAN). Eur Heart J 2002; 23: 1422– 1432.
12. Rokyta jr. R, Pechman V. The effects of Levosimendan on global haemodynamics in patients with cardiogenic shock. Neuro Endocrinol Lett 2006; 27: 121– 127.
13. Mebazaa A, Nieminen MS, Packer M et al. Levosimendan vs Dobutamine for Patients With Acute Decompensated Heart Failure: The SURVIVE Randomized Trial. JAMA 2007; 297: 1883– 1891.
14. Wallentin L, Becker RC, Budaj A et al. Ticagrelor versus Clopidogrel in Patients with Acute Coronary Syndromes. N Engl J Med 2009; 361: 1045– 1057
15. Špinar J, Janský P, Kettner J et al. Doporučení pro diagnostiku a léčbu akutního srdečního selhání. Cor Vasa 2006; 48: K3– K31.
16. Souček M, Nevrlka J, Říháček I et al. Zvýšená aktivita sympatiku a možnosti terapeutického ovlivnění. Vnitř Lék 2007; 53: 554– 559.
17. Zuanetti G, Mantini L, Hernandez‑ Bernal F. Relevance of heart rate as a prognostic factor in patients with acute myocardial infarction: insight from the GISSI‑ 2 study. Eur Heart J 1998 (Suppl F): 19– 26.
18. Remppis A, Ehlermann P, Giannitsis E et al. Cardiac Troponin T Levels at 96 Hours Reflect Myocardial Infarct Size: A Pathoanatomical Study. Cardiology 2000; 93: 249– 253.
19. Velazquez EJ, Francis GS, Armstrong PW et al. An international perspective on heart failure and left ventricular systolic dysfunction complicating myocardial infarction: the VALIANT registry. Eur Heart J 2004; 25: 1911– 1919.
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