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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: 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.

Primary amyloidosis is a rare disease, cardiac involvement occurs in up to 40% of patients. Diffuse amyloid deposits cause an impairment of myocardial systolic and diastolic function. In this paper we are presenting a case of a 54-year-old woman. The woman was admitted because of progressive fatigue, dyspnoea, chest pain, later she experienced hypotension, dyspepsia, and enterorrhagia. ECG showed decrease in QRS amplitude. We have found an echocardiographic evidence of wall hypertrophy. Right cardiac catheterization showed a restrictive situation. Immunobinding of serum and urine revealed monoclonal kappa light chains. The diagnosis was determined by rectal biopsy. Unfortunately, amyloid deposits caused progressive heart failure, hemorrhage, and death just before the diagnosis of primary amyloidosis could be determined on the basis of results of the immunofixations of serum and urine proteins (detection of the monoclonal light chains kappa) and from biopsy specimens taken from rectum (amyloid deposits).