Marzenna Zielińska

Predictors of left ventricular thrombus formation in acute myocardial infarction treated with successful primary angioplasty with stenting.

Background:There are limited data referring to the incidence of left ventricle (LV) thrombus formation after successful primary percutaneous coronary intervention (PCI) with stenting, which is now the treatment of choice in patients with acute myocardial infarction (AMI). Previously reported results were often based on low or heterogeneous patient populations. Methods:To evaluate the prevalence of LV thrombus in the early period of AMI, 2,911 patients who had undergone successful primary stenting were retrospectively studied. Baseline demographic characteristics, angiographic findings, and antiplatelet treatment were analyzed to find predictors of thrombus formation. LV thrombus was diagnosed by 2-dimensional echocardiography within 3 to 5 days after PCI. Results:This complication was detected in 73 patients (2.5%). Patients with thrombus and patients without it were at the same age and had diabetes mellitus, prior myocardial infarction, and lipid disorders at the same frequency. The extent of coronary artery disease was similar in both groups. The incidence of LV thrombi was similar in patients treated with and without glycoprotein IIb/IIIa inhibitors (2.02% vs 2.9%, NS). According to results of multiple log-regression analysis, the presence of LV thrombus was strongly associated with anterior AMI, ejection fraction <40%, and previous hypertension. Conclusions:The incidence of left ventricular thrombus early after AMI is very low if primary PCI with stenting is successful, probably due to the salvage of myocardium at risk. Localization of AMI and the size of myocardium damage remain the most important independent predictors of LV thrombus formation irrespective of various treatments.

Levosimendan beyond inotropy and acute heart failure: Evidence of pleiotropic effects on the heart and other organs: An expert panel position paper

Levosimendan is a positive inotrope with vasodilating properties (inodilator) indicated for decompensated heart failure (HF) patients with low cardiac output. Accumulated evidence supports several pleiotropic effects of levosimendan beyond inotropy, the heart and decompensated HF. Those effects are not readily explained by cardiac function enhancement and seem to be related to additional properties of the drug such as anti-inflammatory, anti-oxidative and anti-apoptotic ones. Mechanistic and proof-of-concept studies are still required to clarify the underlying mechanisms involved, while properly designed clinical trials are warranted to translate preclinical or early-phase clinical data into more robust clinical evidence. The present position paper, derived by a panel of 35 experts in the field of cardiology, cardiac anesthesiology, intensive care medicine, cardiac physiology, and cardiovascular pharmacology from 22 European countries, compiles the existing evidence on the pleiotropic effects of levosimendan, identifies potential novel areas of clinical application and defines the corresponding gaps in evidence and the required research efforts to address those gaps.

The association between galectin-3 and clinical parameters in patients with fi rst acute myocardial infarction treated with primary percutaneous coronary angioplasty

BACKGROUND Galectin-3, a biomarker associated with fibrosis and inflammation, has been implicated in development and progression of heart failure (HF) and predicts increased mortality and morbidity in this condition. HF frequently develops after myocardial infarction (MI), contributing to worse outcome. The aim of this study is to assess the association between galectin-3 levels and various clinical parameters in acute phase of first MI treated with primary percutaneous coronary intervention (pPCI) in patients without prior HF. METHODS We included 145 consecutive patients with first acute MI treated with pPCI with stent implantation. Exclusion criteria were: prior HF, severe valvular diseases, coexisting cancers, connective tissue diseases and cirrhosis. Serum galectin-3 concentration was measured within 3-5 days after onset of acute MI. RESULTS Thirty-six patients with the highest galectin-3 levels (4th quartile, > 16 ng/mL) were compared to 109 subjects with a biomarker concentration ≤ 16 ng/mL. Elevated galectin-3 levels were more often observed in females, the elderly, subjects with coexisting diabetes, renaldysfunction and permanent atrial fi brillation (AF). Galectin-3 correlated with N-terminal pro-B-type natriuretic peptide (r = 0.27, p < 0.001) and high-sensitivity C-reactive protein (r = 0.20, p < 0.05). Multivariate analysis revealed that only new-onset AF and diuretics treatment during hospitalization were independently associated with galectin-3 levels > 16 ng/mL. CONCLUSIONS Elevated galectin-3 levels were associated with a higher rate of new-onset AF and diuretics treatment during hospitalization in patients with first MI treated with pPCI without prior HF.

Ischaemic preconditioning – Current knowledge and potential future applications after 30 years of experience

Ischaemic preconditioning (IPC) phenomenon has been known for thirty years. During that time several studies showed that IPC provided by brief ischaemic and reperfusion episodes prior to longer ischaemia can bestow a protective effect to both preconditioned and also remote organs. IPC affecting remote organs is called remote ischaemic preconditioning. Initially, most IPC studies were focused on enhancing myocardial resistance to subsequent ischaemia and reperfusion injury. However, preconditioning was found to be a universal phenomenon and was observed in various organs and tissues including the heart, liver, brain, retina, kidney, skeletal muscles and intestine. Currently, there are a lot of simultaneous studies are underway aiming at finding out whether IPC can be helpful in protecting these organs. The mechanism of local and remote IPC is complex and not well known. Several triggers, intracellular pathways and effectors, humoral, neural and induced by genetic changes may be considered potential pathways in the protective activity of local and remote IPC. Local and remote IPC mechanism may potentially serve as heart protection during cardiac surgery and may limit the infarct size of the myocardium, can be a strategy for preventing the development of acute kidney injury development and liver damage during transplantation, may protect the brain against ischaemic injury. In addition, the method is safe, non-invasive, cheap and easily applicable. The main purpose of this review article is to present new advances which would help to understand the potential mechanism of IPC. It also discusses both its potential applications and utility in clinical settings.

Vitamin D level and extent of coronary stenotic lesions in patients with first acute myocardial infarction

BACKGROUND The study aimed to examine the relationship between vitamin D levels and the extent of coronary stenotic lesions in patients with ST-segment elevation myocardial infarction (STEMI). Experimental evidence points to the involvement of multiple factors in coronary plaque formation, including vitamin D. Little is known, however, about the association of vitamin D level with the intensity of atherosclerosis. METHODS Serum concentrations of 25-hydroxyvitamin D [25(OH)D] were measured in 130 consecutive patients with the first acute STEMI treated with primary percutaneous coronary intervention. STEMI was the first symptom of coronary artery disease (CAD). The study population was divided into patients with single and multi-vessel CAD. The angiographic severityof CAD was also determined based on the Gensini score. RESULTS The median 25(OH)D concentration was 11.12 ng/mL (25th and 75th percentile: 6.05; 17.12). Insufficient (20-30 ng/mL), deficient (10-20 ng/mL) and severely deficient(< 10 ng/mL) 25(OH)D levels were present in 18%, 35% and 45% of the individuals, respectively. Only 2 (2%) of patients had proper 25(OH)D levels (> 30 ng/mL). The 25(OH)D concentrations between patients with single- and multi-vessel CAD did not differ significantly (10.2 vs. 11.4 ng/mL, p = 0.62). There was no significant correlation between 25(OH)D levels and Gensini score (r = -0.0221, p = 0.81). CONCLUSIONS The study demonstrated that vitamin D level is not associated with the severity of coronary lesions in patients with the first STEMI. A high prevalence of vitamin D deficiency in these patients was confirmed.

Platelet reactivity and mean platelet volume as risk markers of thrombogenesis in atrial fibrillation

Atrial fibrillation (AF) is associated with increased risk of thromboembolic complications. One of the markers of the increased risk of hypercoagulable state is platelet hyperreactivity. The aim of the study was to assess impact of arrhythmia on platelet reactivity. METHODS The study included 36 (mean age 48,3; range 21-60) male patients with lone atrial fibrillation, with exclusion of concomitant diseases known to trigger hypercoagulable state. The AF patients underwent cardioversion to restore sinus rhythm and were subsequently under observation for 1month. Echocardiography, ECG and blood collection was performed before cardioversion (T0) and 4weeks after successful cardioversion (T1). During the study period patients have been contacted and examined every week and 24h ECG monitoring was performed. Platelet reactivity was assessed based on changes of CD62 and CD42b expression on platelet surface after stimulation with thrombin. Also changes in MPV were assessed. RESULTS In all patients sinus rhythm was maintained at the end of the study period, however in 14 patients recurrences of AF were observed, confirmed by 24h ECG monitoring (atrial fibrillation recurrence group - AFR) and 22 patients maintained sinus rhythm throughout the whole study period (SR group). Mean fluorescence intensity (MFI) of CD62 on thrombin stimulated platelets decreased significantly 4weeks after electrical cardioversion as compared to T0 (48.04±22.42 vs 41.47±16.03; p<0.01). Also MFI of CD42b on thrombin stimulated platelets decreased significantly 4weeks after electrical cardioversion as compared to T0 (22.16±10.82 vs 12.06±5.99; p<0.0001). Platelets reactivity estimated by CD 62 expression in SR group decreased significantly after 4weeks observation (58.01±15.26 vs 46.57±13.44; p<0.001) opposite to AFR group 35.66±21.87 vs 34.54±16.4; p-ns). Moreover there were significant differences between basal reactivity during AF between SR and AFR groups (58.01±15.26 vs 35.66±21.87; p-0.01). MFI of CD42b on thrombin stimulated platelets decreased significantly both in AFR and SR groups (22.05±11.36 vs 13.8±6.03; p<0.001 and 21.87±14.18 vs 10.04±5.09; p<0005). MPV decreased significantly 4weeks after electrical cardioversion as compared to T0 (8.81±0.19 vs 8.42±0.14; p<0.0001). CONCLUSION The changes of platelet reactivity to thrombin observed after restoration of sinus rhythm in patients prove that arrhythmia intrinsically leads to increased reactivity of platelets.

Fever in myocardial infarction: Is it still common, is it still predictive?

BACKGROUND Before introduction of reperfusion therapy, fever was frequently observed in patients with acute myocardial infarction (AMI). Little is known about this symptom during the widespread use of primary percutaneous coronary intervention (pPCI). The aim of this study was to assess, whether body temperature is a predictor of impaired left ventricular systolic function in patients with AMI. METHODS Our cohort included 171 patients (48 women) aged 57 (51-67) years, admitted due to the first AMI with ST elevation treated with successful pPCI. Standard body temperature measurements were performed twice a day. Left ventricular function was assessed by echocardiography using the wall motion score index (WMSI) and ejection fraction (EF). The following inflammatory response markers were determined on admission: C-reactive protein, fibrinogen and white blood cell count. RESULTS Within 48 h of observation the median (1(st); 3(rd) quartiles) peak body temperature was 37.0°C (36.7-37.2°C). A temperature above 37.5°C was observed only in 17 (10%) patients. There was no significant correlation between peak body temperature and any of the determined inflammatory response markers. WMSI was assessed at 1.3 (1.1-1.6), whereas EF at 56% (49-62%). There was no significant correlation between the left ventricular function and peak body temperature or determined markers of inflammation. CONCLUSIONS In the era of pPCI and aggressive antiplatelet treatment, fever is not a common symptom associated with uncomplicated AMI and thus not correlated with left ventricular function and markers of inflammation.

Prognostic value of myeloperoxidase concentration in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention ☆

Inflammation plays an important role on every stage of atherosclerosis. Myeloperoxidase (MPO), a leukocyte-derived enzyme that participates in the innate immunity, probably is involved in many stages of atherothrombosis. According to the recent studies, MPO is related with unfavorable outcome in patients with chest pain and acute coronary syndromes. Its role in prediction of outcomes after ST-segment elevation myocardial infarction (STEMI) remains unclear. The aim of the study was to assess if elevated MPO level is a predictor of long-term adverse cardiac events in patients with STEMI treated with primary percutaneous coronary intervention (pPCI). MATERIAL AND METHODS We evaluated data of 127 patients with STEMI. Plasma levels of MPO collected on admission and the 3rd-4th day of hospitalization were measured by ELISA method. C-reactive protein (CRP) and N-terminal prohormone of B-type natriuretic peptide (NT-proBNP) were also determined. All patients were followed-up prospectively for the occurrence of major adverse cardiovascular events (MACE) defined as unscheduled coronary revascularization procedure, stroke, reinfarction or all-cause death. RESULTS After 14months of follow-up 20% of patients developed MACE. Elevated MPO levels collected on the 3rd-4th day of STEMI were the predictor of death, reinfarction, the need for coronary revascularization and all adverse events taken together. In multivariate analysis, MPO and CRP levels assessed on the 3rd-4th day of hospitalization revealed to be significant predictors of MACE. MPO demonstrated to be significantly better predictor of MACE than NT-proBNP level. CONCLUSIONS Myeloperoxidase is a prognostic marker in patients with STEMI treated with pPCI.

Platelets miRNA as a Prediction Marker of Thrombotic Episodes

The blood platelets are crucial for the coagulation physiology to maintain haemostatic balance and are involved in various pathologies such as atherosclerosis and thrombosis. The studies of recent years have shown that anucleated platelets are able to succeed protein synthesis. Additionally, mRNA translation in blood platelets is regulated by miRNA molecules. Recent works postulate the possibility of using miRNAs as biomarkers of atherosclerosis and ischemic episodes. This review article describes clinical studies that presented blood platelets miRNAs expression profile changes in different thrombotic states, which suggest use of these molecules as predictive biomarkers.

Optimization of atrio-ventricular delay in patients with dual-chamber pacemaker

Development and advances in heart pacing over the last nearly half a century allowed to save numerous lives by providing pacing support in bradycardia and complete heart block. Nevertheless, long-term follow up of patients with implanted pacemaker showed unfavorable remodeling of the heart, both from hemodynamic as well as electrical standpoint. The optimal programmed pacemaker setting, apart from the optimal place for ventricular stimulation, is essential to obtain the best hemodynamic and the clinical after-effects of the stimulation of the heart and to minimize potential unfavorable effects. In patients with dual-chamber pacemaker (DDD) the correct function of the left ventricle of the heart depends mainly on the electric delays between the stimulated chambers. Atrio-ventricular delay (AVD) during dual-chamber pacing influences left ventricle contraction function through preload modulation. Improperly programmed AVD in the DDD pacemaker can have unfavorable hemodynamic results. Various methods have been developed during last few decades (right heart catheterization, ventriculography, peak endocardial acceleration, echocardiography, and impedance cardiography), however only echocardiography and reocardiography are currently in general use. There should be noticed too, that also the application of special algorithms present in modern pacemakers allowing for dynamic changes of the time of the delay represents certain alternative to individual AVD optimization.