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Abstract Background We evaluated the associations among angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism, ACE activity and post-myocardial infarction (MI) left ventricular dysfunction and acute heart failure (AHF) early after presentation with MI with ST-segment elevation (STEMI). Methods A total of 556 patients with STEMI treated by primary PCI (421 patients without AHF and 135 patients with AHF) were the study population. The activity of BNP, NT-ProBNP and ACE 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 In comparison with the II genotypes group, the DD/ID group had a higher level of ACE activity upon hospital admission (p < 0.001). We found a significantly higher level of ACE activity in patients with moderate LV dysfunction (EF 40-54%) in comparison both with patients with preserved LV function (EF ≥55%) and with patients with severe LV dysfunction (p = 0.028). A non-significant trend towards a higher incidence of mild AHF (22.1% vs. 16.02%, p = 0,093), a significantly higher value of end-systolic volume (ESV/BSA) (30.0 ± 12.3 vs. 28.5 ± 13.0; p < 0.05) and lower EF (50.2 ± 11.1 vs. 52.7 ± 11.7; p < 0.05) in the DD/ID genotypes group was noted. Even after multiple adjustments according to multivariate models, the EF for the DD/ID group remained significantly lower (p = 0,033). The DD/ID genotypes were associated with a significantly higher risk of EF Conclusions These results suggest that the I/D polymorphism of ACE is associated with the development of LV dysfunction in the acute phase after STEMI. We demonstrated for the first time an association of the low ACE activity with the severe LV dysfunction, although patients with moderate LV dysfunction had higher level ACE activity than patients with preserved LV function.

Background: We compared the prognostic capacity of conventional and novel invasive parameters derived from the slope of the preload recruitable stroke work relationship (PRSW) in STEMI patients and assessed their contribution to the TIMI risk score., Methods: Left ventricular end-diastolic pressure (EDP), ejection fraction (EF), pressure adjusted maximum rate of pressure change in the left ventricle (dP/dt/P), aortic systolic pressure to EDP ratio (SBP/EDP) and end-diastolic volume adjusted stroke work (EW), derived from the slope of the PRSW relationship, were obtained during the emergency cardiac catheterization in 523 STEMI patients. The predictive power of the analyzed parameters for 30-day and 1-year mortality was evaluated using C-statistics and reclassification analysis was adopted to assess the improvement in TIMI score., Results: The highest area under the curve (AUC) values for 30-day mortality were observed for EW (0.872(95% confidence interval 0.801-0.943)), SBP/EDP (0.843(0.758-0.928)) and EF (0.833(0.735-0.931)); p<0.001 for all values. For 1-year mortality the best predictive value was found for EW (0.806(0.724-0.887) and EF (0.793(0.703-0.883)); p<0.001 for both. The addition of EDP, SBP/EDP ratio and EW to TIMI score significantly increased the AUC according to De Long's test. For 30-day mortality, increased discriminative power following addition to the TIMI score was observed for EW and SBP/EDP (Integrated Discrimination Improvement was 0.086(0.033-0.140), p=0.002 and 0.078(0.028-0.128), p=0.002, respectively)., Conclusions: EW and SBP/EDP are prognostic markers with high predictive value for 30-day and 1-year mortality. Both parameters, easily obtained during emergency catheterization, improve the discriminatory capacity of the TIMI score for 30-day mortality., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Introduction: Cardiogenic shock (CS) is the leading cause of mortality in patients with acute myocardial infarction (AMI). Inflammatory response seems to be common response in patients with AMI, especially those with CS. We have therefore conducted a study to determine diagnostic and prognostic utility of interleukin 6 (IL6) levels in the cohort of patients with cardiogenic and septic shock (SS) and in a control group of patients with uncomplicated AMI., Methods: In this prospective study 71 patients fulfilled the inclusion criteria: 30 patients with cardiogenic shock, 21 patients with septic shock and 20 patients with ST elevation myocardial infarction (STEMI). Plasma levels of IL6 were measured at 8 time points. The main endpoint was 3 month mortality., Results: We have shown that the highest IL6 levels during the first week were recorded in patients with septic shock with peak value at admission. The maximum level of IL6 was detected between 12 to 24 hours after the onset of MI among patients with cardiogenic shock. According to Receiver operating characteristic (ROC) statistics levels of IL6 > 357 pg/ml at admission (AUC 0.730, p = 0.031) were typical for patients with CS in comparison with control group of STEMI patients. Values of IL6 > 1 237 pg/ml at admission and > 1 071 pg/ml at 24 hours (after admission?) were typical for thouse in septic shock in comparison with CS patients. We found only a non-significant trend of IL6 for the prediction of mortality in the cohort of CS patients for levels 1 854 pg/ml (AUC 0.769, p = 0.066) sampled 12 hours after admission. There was no association of plasma levels of IL6 with mortality in septic shock patients., Conclusions: Patients with cardiogenic shock demonstrated more pronounced cytokine response as evidenced by increased levels of IL6 compared to patients with uncomplicated STEMI. Levels of IL6 peaked in SS patients at admission, in CS patients 12-24 hours after admission. In daily clinical practice routine measurement of IL6 levels for prediction of prognosis both in cardiogenic and septic shock are of little value mainly due to significant interindividual variability of IL6 values.

Inflammation plays an important role in the pathophysiology of acute coronary syndrome as well as in the process of atherosclerosis in general. At the moment of myocardial ischaemia, local and systemic inflammatory reaction is amplified; in ischaemic myocardium there is increased expression of proinflammatory cytokines, particularly interleukin-6, which mediates C reactive protein (CRP) production by hepatocytes. CRP activates the complement cascade and thereby contributes to the lysis and removal of damaged cardiomyocytes. Whereas in a healthy population CRP levels range from 1.2 to 2.0 mg / l, in patients with ACS the levels of CRP significantly increase with the peak of 2nd to 4th day from the onset of myocardial infarction. Peak CRP levels ranged from 20 to 250 mg / l in patients with STEMI treated conservatively, the median of peak of CRP levels was 79 mg/ l in patients with anterior wall STEMI treated with primary PCI. There is a recommendation of CRP evaluation within the early risk stratification of patients with ACS according to the current ESC guidelines. In patients with NSTEMI, CRP levels > 10 mg/ l are associated with increased longterm mortality. In patients with STEMI treated with primary PCI, CRP levels > 79 mg/ l could predict negative left ventricle remodelation. The predictive value of GRACE risk score was improved using CRP, levels > 22 mg/ l predicted worse prognosis in patients with either STEMI or NSTEMI treated invasively. However, if also cardiac troponin and natriuretic peptides in addition to GRACE risk score were used, CRP levels were useless in further risk stratification improvement. In clinical practice, in terms of coinciding infection, problems with CRP levels interpretation can occur as well. Several patients either in cardiogenic shock or after cardiopulmonary resuscitation have signs of systemic inflammatory response, and sometimes it is very difficult to decide whether there is a necessity to iniciate the antibio-tic therapy because of infectious cause. In patients after cardiopulmonary resuscitation, CRP levels > 180 mg/ l indicate highly probable infection, but with the poor sensitivity. For patients in cardiogenic shock, procalcitonin appears to be more useful for the detection of infection; in this group of patients, procalcitonin levels > 2 ng/ ml are common, and levels > 10 ng/ ml indicate infection undoubtedly.

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.