LC-MS-based serum fingerprinting reveals significant dysregulation of phospholipids in chronic heart failure.

Cardiac and extracardiac lipid metabolism is known to be significantly altered in the course of the heart failure with reduced ejection fraction (HF-REF), however the precise mechanisms are not fully elucidated. The aim of the study was to use of untargeted metabolomics to identify and validate changes in the blood metabolites profile, occurring as a result of HF-REF development. The analyses were performed first in the derivation set (36 chronic HF-REF patients and 19 controls without the disease) and repeated in validation cohort (31 chronic HF-REF patients and 20 controls). Independent analyses of both sets revealed statistically significant decline in intensities of phosphatidylcholine (PC): 34:4 and 36:5, lysophosphatidylcholine (lyso-PC): 14:0, 15:0, 18:0, 18:2, 20:3, lysophosphatidylethanolamine (lyso-PE): 18:1 and 18:2 in chronic HF-REF patients. More symptomatic patients and those with ischaemic etiology of HF-REF presented greater deficit in phospholipids (PLs) intensities. The decrease of identified PLs intensities (as compared to controls) correlated with decreased serum cholesterol level, impaired renal function, reduced exercise capacity, enhanced ventilatory response and metabolic parameters associated with altered fatty acids oxidation. In multiple regression analysis PLs deficit was significantly associated with age, carnitines serum intensity, renal function, uric acid, cholesterol level. In conclusion, HF-REF is associated with significant disturbances in phospholipids metabolism. Greater reduction in serum intensities of particular identified PLs is associated with older age, worse clinical condition, impaired oxidative muscle metabolism and enhanced catabolic status.

Takotsubo cardiomyopathy: serious early complications and two-year mortality - a 101 case study.

BACKGROUND: Takotsubo cardiomyopathy (TTC) is characterised by transient contractility disturbances of the apex of the left ventricle. METHODS: We enrolled 101 patients from the northern-eastern part of Poland in the years 2008-2012 who were hospitalised for TCC. The control group consisted of female patients diagnosed with anterior myocardial infarction with ST-segment elevation (anterior STEMI) (n = 101). RESULTS: 89 % of the study group were women. Patients with TTC had diabetes (12.6 % vs 29.7 %; p = 0.002) and hyperlipidaemia (36.8 % vs 64.4 %; p = 0.0001) significantly less frequently, and better kidney function assessed by estimated glomerular filtration rate versus patients with anterior STEMI (74.52 % vs 64.30 %; p = 0.004). In the TTC group there were more patients with chronic obstructive pulmonary disease (11.6 % vs 1.0 %; p = 0.002) and thyroid disturbances, especially hyperthyroidism (23.4 % vs 11.0 %; p = 0.021). In patients with TTC sudden cardiac arrest, pulmonary oedema and cardiogenic shock were observed less frequently than in the control group (14.7 % vs 30.7 %; p = 0.0078). Hospitalisations in TTC patients were less frequently complicated by pneumonia (20.0 % vs 35.6 %; p = 0.0148) and urinary infection (4.2 % vs 21.8 %; p = 0.0003). Cardiac rupture occurred in 3 patients with TTC and in 1 with anterior STEMI. In-hospital mortality was significantly lower in the group with TTC. Also, mortality at 30 days, 3 months, 1 year and 2.5 years was significantly lower in patients with TTC than in patients with MI (p = 0.035; p = 0.0226; p = 0.0075; p = 0.009). CONCLUSIONS: Previously considered to be a benign syndrome, TTC should be reconsidered as a clinical condition at risk for serious complications such as cardiac arrest, cardiogenic shock, pulmonary oedema and cardiac rupture leading to death and causing substantial early hazard. The prognosis in TTC is significantly better than in patients with anterior STEMI.

Metabolomics - A wide-open door to personalized treatment in chronic heart failure?

Heart failure (HF) is a complex syndrome representing a final stage of various cardiovascular diseases. Despite significant improvement in the diagnosis and treatment (e.g. ACE-inhibitors, ß-blockers, aldosterone antagonists, cardiac resynchronization therapy) of the disease, prognosis of optimally treated patients remains very serious and HF mortality is still unacceptably high. Therefore there is a strong need for further exploration of novel analytical methods, predictive and prognostic biomarkers and more personalized treatment. The metabolism of the failing heart being significantly impaired from its baseline state may be a future target not only for biomarker discovery but also for the pharmacologic intervention. However, an assessment of a particular, isolated metabolite or protein cannot be fully informative and makes a correct interpretation difficult. On the other hand, metabolites profile analysis may greatly assist investigator in an interpretation of the altered pathway dynamics, especially when combined with other lines of evidence (e.g. metabolites from the same pathway, transcriptomics, proteomics). Despite many prior studies on metabolism, the knowledge of peripheral and cardiac pathophysiological mechanisms responsible for the metabolic imbalance and progression of the disease is still insufficient. Metabolomics enabling comprehensive characterization of low molecular weight metabolites (e.g. lipids, sugars, organic acids, amino acids) that reflects the complete metabolic phenotype seems to be the key for further potential improvement in HF treatment (diet-based or biochemical-based). Will this -omics technique one day open a door to easy patients identification before they have a heart failure onset or its decompensation?

The Role of Different Monocyte Subsets in the Pathogenesis of Atherosclerosis and Acute Coronary Syndromes.

The inflammation underlying both atherosclerosis and acute coronary syndromes is strongly related to monocyte-related actions. However, different monocyte subsets can play differential roles in the formation and destabilization of atherosclerotic plaque as well as healing of damaged myocardial tissue. Monocytes are currently being divided into three functionally distinct subsets with different levels of CD14 (cluster of differentiation 14) and CD16 expression. Thus, there are classical CD14++CD16-, intermediate CD14++CD16+ and non-classical CD14+CD16++ monocytes. Here, we summarize the current knowledge on complex activities of different monocyte subsets in atherosclerosis and acute coronary syndromes. Moreover, we discuss which monocyte subsets can serve either as predictive biomarkers of cardiovascular risk or as potential targets used in atherosclerosis and its complications.

MMP-9 in atrial remodeling in patients with atrial fibrillation.

INTRODUCTION: Atrial fibrillation (AF) is the most common arrhythmia and is associated with significant morbidity and mortality. The impact of matrix metalloproteinases (MMPs) on structural atrial remodeling and sustainment of AF in patients with persistent and permanent AF is unresolved. OBJECTIVES: The aim was to evaluate MMP-9 and its tissue inhibitor-1 (TIMP-1) as markers of atrial remodeling in patients with persistent AF (PAF) who underwent electrical cardioversion (ECV) and in patients with permanent AF (continuous AF, CAF). PATIENTS AND METHODS: Plasma levels of MMP-9 and TIMP-1, clinical findings, and echocardiographic parameters were evaluated in 39 patients with AF and in 14 controls with sinus rhythm. RESULTS: The concentrations of MMP-9 were significantly higher in patients with PAF and CAF compared to controls. There was a significant increase of MMP-9 after ECV in the persistent AF group. The values of TIMP-1 were not significantly different between the groups. In patients with AF, MMP-9 levels were positively related to posterior wall thickness of the LV (r=0.356, P=0.049) and body mass index (r=0.367, P=0.046). CONCLUSION: Elevated levels of MMP-9 were related to the occurrence and maintenance of AF. This suggests that MMP-9 can be a marker of atrial remodeling in patients with AF. Regulation of the extracellular collagen matrix might be a potential therapeutic target in AF.

Anti-inflammatory effects of atorvastatin treatment in chronic obstructive pulmonary disease. A controlled pilot study.

UNLABELLED: Observational studies have suggested that statins may have beneficial effects on outcomes in chronic obstructive pulmonary disease (COPD) patients. These effects may be mediated through an anti-inflammatory effect of statins. The purpose of this pilot-study was to determine whether statins have an anti-inflammatory effect on the lungs of COPD patients. We conducted randomized, controlled, parallel group pilot-study to compare the effects of atorvastatin (n=12) or placebo (n=6) on lung inflammation in patients with mild to moderate COPD. The primary endpoint was change in CD45+ cells expression measured by immunohistochemistry and changes in expression of genes measured using microarrays in lung biopsy (TBB) samples before and after 12 weeks of treatment with atorvastatin 40 mg/day. All subjects had spirometry, lung volumes, diffusing capacity of the lungs for carbon monoxide (DLCO), St George's Respiratory Questionnaire (SGRQ), 6 minute walk distance (6 MWD), serum lipids, hs-CRP, induced sputum (IS), bronchoscopy and TBB carried out at baseline and after treatment. TBB specimens were processed for histology, immunohistochemistry and genome-wide association studies (GWAS) profiling. Seventeen subjects completed the study. There was a significant improvement in SGRQ with mean SGRQ decreased by 12 points after treatment with atorvastatin (P=0.012). Atorvastatin treatment produced a significant 34% reduction in sputum neutrophil count, and a 57% reduction in CD45+ cells in lung biopsies (expressed as integrated optical density -IOD; median IOD 62.51% before, 27.01% after atorvastatin treatment, P=0.008). In patients' lung tissue atorvastatin treatment produced downregulation of key genes involved in inflammatory processes, immune response, and leukocyte activation. These data demonstrate the pulmonary anti-inflammatory effects of atorvastatin in COPD patients with the potential for beneficial clinical effects. TRIAL REGISTRATION: ClinicalTrials.gov: NCT01748279.

Usefulness of automatic measurement of contrast flow intensity: an innovative tool in contrast-enhanced ultrasound imaging of atherosclerotic carotid plaque neovascularization. A pilot study.

AIM: Contrast-enhanced ultrasound imaging of the carotid arteries (CECU) permits direct, real-time visualization of neovascularization in atherosclerotic plaques and is a confirmed predictor of unstable atheromatous lesions. The aim of the study was the assessment of a new, automatically measured index of intensity in quantitative estimation of the contrast flow through the carotid plaque (till now assessed only visually). METHODS: Forty-four patients (mean age 70.4±11.4) with ultrasound diagnosed significant stenosis of internal carotid artery (ICA), after cerebrovascular or cardiovascular events, qualified for carotid artery stenting (CAS) were examined. The carotid ultrasound examinations with contrast agent Sonovue were performed. RESULTS: Visually in 22 patients (50%) contrast flow through the atherosclerotic plaques was found. In 17 patients (38.6%) massive, calcified atherosclerotic plaques were present. Patients with preserved contrast flow through the plaque more frequently had a history of cerebral stroke (P=0.04). Massive calcifications of atherosclerotic plaques correlated with a previous MI (P=0.03) and the degree of advancement of coronary artery disease (P=0.04), but not with a previous cerebral stroke. Contrast flow through the atherosclerotic plaque positively correlated with values of the index of intensity (r=0.69, P<0.00001). In patients with preserved contrast flow the mean value of the index of intensity was 22.24±3.55 dB as compared with 12.37±7.67 dB - a value present in patients without preserved contrast flow. No significant relation for the degree of calcifications and the value of the index of intensity was found. CONCLUSION: The assessment of the index of intensity is a novel, simple and automatic method to estimate the degree of contrast flow through the carotid plaque. The values of the index of intensity correlate with the contrast flow through the atherosclerotic plaque, but not with its calcification.

Myocardial perfusion and intima-media thickness in patients with subclinical hypothyroidism.

PURPOSE: The data concerning the relation between subclinical hypothyroidism (SH) and the risk of cardiovascular disease are divergent. We aimed to assess myocardial perfusion in contrast-enhanced echocardiography and intima-media thickness (IMT) in patients with SH. MATERIAL/METHODS: Forty females with SH without symptoms of coronary artery disease and 15 healthy female volunteers were examined. Echocardiographic evaluation of the left ventricle function as well as carotid and femoral IMT complex measurements were performed at baseline. Thereafter, dobutamine stress echocardiography with myocardial perfusion assessment at rest and on the peak of stress test was performed. SonoVue® intravenous bolus as a contrast medium was used. The myocardial perfusion was assessed by quantitative method using Q-LAB Philips software (ROI modality). The perfusion index was calculated (a number of left ventricle segments with improved perfusion/a number of all segments). RESULTS: A mean IMT value in the SH group was significantly higher than in the controls (0.7 mm vs. 0.38 mm, p=0.001). Myocardial perfusion at rest and at the peak of stress test was significantly lower in the SH patients as compared to the controls (at rest 120 Db in SH vs. 181 Db in controls, p=0.039 and at the peak of stress 115 Db and 188 Db, p=0.01, respectively). The perfusion index was not significantly worse in the SH group (p=0.6). IMT values negatively correlated with the myocardial perfusion index at the peak of stress (r=-0.54, p=0.014). CONCLUSIONS: In patients with SH contrast-enhanced echocardiographic examination revealed myocardial hypoperfusion and increased IMT. Our results may suggest that the patients with SH are at risk of the development of cardiovascular disease.

The importance of intima-media thickness (IMT) measurements in monitoring of atherosclerosis progress after myocardial infarction.

PURPOSE: Intima-media thickness (IMT) assessed in peripheral arteries correlates with presence and progression of atherosclerosis in coronary arteries. IMT measurements may help to select high risk patients and evaluate the efficacy of the therapy used. AIM: The aim of the study was to assess the usefulness of ultrasonographic measurement of IMT in atherosclerosis progress monitoring in patients after myocardial infarction (MI). PATIENTS AND METHODS: 70 men (mean age 52.8 ± 8.4) treated with PCI due to acute myocardial infarction, were enrolled in the study. All subjects underwent ultrasound examination of the IMT complex of: common carotid artery (CCA), carotid bulb and common femoral artery (CFA) during hospitalization and follow-up period (3.83 ± 1.29 years). RESULTS: During the follow-up 3 patients (4.3%) were not on any medications, 8 pts (11.4%) were on reduced doses of ß-blocker, statin or ACE-I (non-compliant pts.). The others (compliant) - 59 pts (84.3%) received standard pharmacological treatment after MI. Nevertheless, an increase of IMT complex value after follow-up compared to initial IMT values of all examined peripheral arteries was observed (respectively: IMT CCA - 0.91 ± 0.26 vs 1.10 ± 0.36, p=0.002, IMT of carotid bulb - 1.31 ± 0.55 vs 1.82 ± 0.69, p=0.012, IMT CFA - 1.38 ± 0.64 vs 1.97 ± 0.75, p=0.014). Non-compliant patients had statistically significant higher IMT values after follow-up when compared to compliant subjects (1.62 vs 1.20, p= 0.017). Patients with higher IMT values were reported to have cardiac events more frequently during the follow-up (p<0.05). CONCLUSIONS: Our results provide evidence that ultrasonographic IMT complex assessment of peripheral arteries in everyday clinical practice allows monitoring efficacy of pharmacological therapy in CAD patients after MI. They also suggest treatment intensification if necessary.

The rs1801133 polymorphism of methylenetetrahydrofolate reductase gene- the association with 5-year survival in patients with ST-elevation myocardial infarction.

PURPOSE: Methylenetetrahydrofolate reductase (MTHFR) is an enzyme involved in endothelial nitric oxide synthase (eNOS) coupling and homocysteine metabolism. The rs1801133 polymorphism of the MTHFR gene affects risk of coronary artery disease. We assessed its influence on 5-year survival of patients with ST-elevation acute myocardial infarction (STEMI). MATERIAL/METHODS: The study group comprised consecutive patients with STEMI. Genotyping was performed with a TaqMan SNP Genotyping Assay using the ABI 7500 Real Time PCR System (Applied Biosystems). The analyzed end-point was all-cause 5-year survival. RESULTS: The study group comprised 637 patients (mean age 62.3 ± 11.9 years; 25.1% females, n=160; 5-year mortality 16.3%, n=104). The percentages of TT, CT and CC genotypes were: 10.8 (n=69), 39.7 (n=253) and 49.45 (n=315), respectively. No significant differences in clinical characteristics were identified between the genotypes (p>0.05 for all parameters). Eleven (15.9%) TT homozygotes, 40 (15.8%) heterozygotes and 53 (16.8%) CC homozygotes died during follow up (p=0.99 log-rank test). TT homozygotes presented only weak and insignificant tendency towards higher mortality rates in subgroups of patients ≤75 years old (15.6 vs. 11.54%, p=0.35) or with intermediate risk according to the GRACE risk score (13.3% vs. 8.76%, p=0.42). CONCLUSIONS: The rs1801133 polymorphism did not show significant association with 5-year survival.

Decreased free sphingoid base concentration in the plasma of patients with chronic systolic heart failure.

PURPOSE: In recent years, the role of sphingolipids in pathophysiology of the heart attracted much attention. Ceramide was found to be involved in the pathogenesis of cardiac dysfunction in animal models of ischemia/reperfusion injury, type 2 diabetes and lipotoxic cardiomyopathy. On the other hand, sphingosine-1-phosphate (S1P), has been shown to possess potent cardioprotective properties. The aim of the present study was to examine plasma concentrations of major sphingolipids in patients with chronic heart failure (HF). MATERIAL AND METHODS: The subjects were divided into two major groups: 1) with chronic systolic HF (n=47), and 2) healthy age-matched controls (n=15). Patients in the former group were further divided according to the underlying cause of HF (ischemic heart disease or idiopathic dilated cardiomyopathy, n=29 and 18, respectively). RESULTS: Plasma concentrations of S1P, sphinganine-1-phosphate and ceramide observed in both groups of HF patients were very close to these noted in the healthy controls, and no statistically significant differences were found. However, the level of free sphingosine and sphinganine in the plasma of patients with HF decreased by 25 and 27%, respectively, as compared to the control subjects. This effect was independent from the underlying cause of HF as the mean concentrations of these sphingoid bases in patients with ischemic and idiopathic HF were virtually the same. CONCLUSIONS: We conclude that chronic heart failure is associated with decreased concentration of free sphingoid bases in the plasma. However, despite lower availability of substrates required for synthesis of cardioprotective sphingoid base-1 phosphates, their plasma level remains stable.

Interleukin 6 is not necessary for STAT3 phosphorylation and myocardial hypertrophy following short term beta-adrenergic stimulation.

PURPOSE: In recent years several reports have suggested involvement of interleukin 6 (IL-6) in beta-adrenergic effects on myocardium, particularly in enhancement of STAT3 phosphorylation (downstream signal transducer of IL-6). Here we present a study of isoproterenol effects on hearts of IL-6 deficient mice. METHODS: Male 12 week old C57Bl6/J mice and age and sex matched mice from IL-6 knockout strain (C57Bl6/J(IL6-/-)) received a single intraperitoneal bolus of either isoproterenol (15 mg/kg) or placebo (0.9% NaCl) and were sacrificed after 1 or 24 hours (n=8 in each group). Another group of mice from both genotypes received a three-day isoproterenol treatment (20 mg/kg every 8h). Activation of STAT3 and MEK/ERK pathways were assessed after a single dose of isoproterenol by means of western blotting. RESULTS: After injection of placebo a significantly lower level of STAT3 phosphorylation was observed in IL-6 KO animals. This difference was abolished after isoproterenol both at 1 and 24-hour time points. Isoproterenol produced potent and rapid activation of both STAT3 and MEK/ERK pathways that returned to the levels of placebo treated controls after 24 hours. Lack of IL-6 did not affect phosphorylation of ERKs. Three-day treatment with isoproterenol caused significant increase of indices of RV and LV hypertrophy in both WT and IL-6 KO animals with no significant differences between genotypes. CONCLUSION: IL-6 is not necessary for isoproterenol induced STAT3 phosphorylation, but may affect activation of this pathway by mild non-specific stimuli. Lack of IL-6 does not affect activation of MEK/ERK pathway nor cardiac hypertrophy by beta-adrenergic agonists.

Adiponectin--an independent marker of coronary artery disease occurrence rather than a degree of its advancement in comparison to the IMT values in peripheral arteries.

OBJECTIVE: The aim of the study was to establish whether adiponectin may act as an independent risk factor of coronary artery disease (CAD) and if adiponectin has potential relations with a new marker of cardiovascular risk -intima-media thickness (IMT). METHODS: 165 patients, who had undergone coronary angiography due to symptoms of CAD were enrolled. Selected clinical and biochemical risk factors were assessed, adiponectin concentrations and IMT were measured. RESULTS: A significantly lower adiponectin concentrations in the CAD group, as compared to the controls, were found. Adiponectin concentration did not correlate with a degree of coronary vessels changes advancement. No correlation between adiponectin concentrations and IMT values in the studied peripheral arteries were found. The value of 9.8 ug/ml has been assigned as a cut-off value. Adiponectin concentrations <9.8 µg/ml had the highest positive predictive value (PPV=95.7%) and specificity (90.9), but low sensitivity (30.8). In the multilogistic regression analysis significant variables influencing the appearance of CAD were found: HDL-C (p=0.011, OR=0.88, 95%CI 0.80-0.97), IMT in CCA (p=0.0048, OR=5.25, 95%CI 1.65-16.75), IMT in CFA (p=0.015, OR=1.65, 95%CI 1.10-2.48 ), and adiponectin concentration <9.8 µg/ml (p=0.032, OR=28.95, 95%CI 1.31-641.48). CONCLUSIONS: Adiponectin is an independent risk factor of coronary artery disease occurrence, but not its advancement. No correlation between adiponectin concentration and IMT values in peripheral arteries was shown.

Real-time myocardial contrast echocardiography as a useful tool to select candidates for coronary revascularization among patients with end-stage renal disease - a 3-year follow-up study.

PURPOSE: To evaluate a real-time myocardial contrast echocardiography (MCE) as a tool to select candidates for coronary revascularization among patients with ESRD and to assess the rate of revascularization and mortality. MATERIAL/METHODS: 58 ESRD patients were screened for CAD using MCE. We analyzed the rate of coronary revascularization during 3-year follow-up. Patients with and without perfusion disturbances on MCE were compared. RESULTS: CAD was found in 46.2% patients out of 39 who underwent coronary angiography. 11 (39.3%) patients out of 28 from the group with perfusion defects on MCE underwent revascularization procedure (21.4% - PCI, 17.9% - CABG). No one from the group without perfusion defects had revascularization procedure. Perfusion defect (OR 1.37 CI 1.37-1.86, p=0.022) was related to revascularization in multivariant analysis (OR 12.87, CI 1.86-89.21, p=0.025). There was no difference in mortality between the group which underwent invasive procedures and treated conservatively (p=0.6643). In ROC analysis defects on MCE and CAD on angiography were equally good in anticipating combined end-point (AUC 0.716, CI 95% 0.544-0.851 and AUC 0.747, CI 95% 0.577-0.875, p=0.701) and death (AUC 0.752, CI 95% 0.582-0.878 and AUC 0.729, CI 95% 0.558-0.861, p=0.805). CONCLUSIONS: Our results indicate that MCE is a safe and uncomplicated method which may help along with other methods to select candidates for coronary revascularization among ESRD patients. In our study coronary revascularization procedures were successful but they did not improve patients' survival on 3-year follow-up.

Iatrogenic femoral pseudoaneurysms - a simple solution of inconvenient problem?

PURPOSE: A femoral artery pseudoaneurysm - is the most common complication associated with invasive coronary interventions. The aim of the study was to analyze the effectiveness of various methods used for femoral pseudoaneurysm treatment and to assess how routine use of radial approach leads to reduction of these site complications. METHODS: The study comprised 1854 consecutive patients who were hospitalized in years 2005-2008 and underwent coronary angiography (with or without angioplasty) via femoral artery access. Since 2009 routine radial approach has been introduced for both coronary angiography and angioplasty. In patients with symptoms suggesting entry site complications Doppler ultrasound was performed. RESULTS: Femoral access site complications requiring additional procedures were observed in 63 patients (3.4%): in 56 femoral pseudoaneurysms (88.8%) and in 7 arteriovenous fistulas (11.1%) were diagnosed (all appeared after coronary angioplasty). The patients were treated in following ways: standard compression with an elastic bandage prolonged to 12 hours - in 14 cases (25%), ultrasound guided compression - in 13 patients (23.2%), finger compression followed by standard compression with an elastic bandage prolonged to 12 hours or ice compress - in 10 patients (17.8%), surgical treatment - in 3 patients (5.3%). Only 2 patients required thrombin injection (3.6%). Since the time routine radial approach was introduced extreme reduction in the rate of local complications was registered. CONCLUSION: Although iatrogenic femoral pseudoaneurysms following invasive percutaneous coronary interventions are still important complications, most of them can be treated conservatively. It seems that radial access completely eliminates the risk of this complication.

Early and long-term prognosis of patients with coronary artery disease treated with percutaneous coronary interventions in 2005. Experience of single large-volume PCI center.

PURPOSE: The progress which has been made in interventional cardiology contributes to the gradual improvement of the results of CHD (coronary heart disease) therapy. The aim of the study was the assessment of early and long-term prognosis in all the patients with CHD treated invasively in one large-volume PCI center in 2005. MATERIAL AND METHODS: 1390 consecutive patients with CHD treated with PCI in 2005 were included in the analysis. Patients with ST-elevation myocardial infarction (STEMI) accounted for 50% of cases, patients with stable angina (SA) amounted to 25%, and patients with non-ST elevation acute coronary syndromes (NSTE-ACS) constituted 25%. Mean follow-up was 738 (±237) days. RESULTS: The highest mortality during the hospitalization was noted within the STEMI group(SA vs. NSTE-ACS vs. STEMI; 0% vs. 0.3% vs. 4.1%, respectively; p<0.001). The highest mortality during a 2-year follow-up was also observed in the STEMI group (SA vs. NSTE-ACS vs. STEMI, 6.3% vs. 8.5% vs. 13.8%, respectively; p<0.001). Multiple regression model showed that independent risk factors for death during the follow-up were: age, glycaemia at admission, heart rate, blood pressure, ejection fraction, STEMI, ineffective PCI (R=0.3613; F(10.131)=19.672; p<0.0001 for the model). CONCLUSIONS: The highest relative increase of mortality after the discharge of patients with CHD undergoing PCI referred to the patients with NSTE-ACS. However, in the real life PCI practice STEMI patients have the worst hospital and long-term prognosis. Well recognized risk factors for death in patients with CHD are still of great importance in negative prognosis of patients undergoing PCI.

Blood pressure in relation to neurogenic, inflammatory and endothelial dysfunction biomarkers in patients with treated essential arterial hypertension.

PURPOSE: Clinical relevance of relations among blood pressure (BP), inflammation, endothelial dysfunction and sympathetic activation is unknown. Study aimed, whether in patients with diagnosed and treated essential arterial hypertension (HTN) biomarkers of inflammation (hs-C-reactive protein, hs-CRP), endothelial dysfunction (endothelin-1, ET-1), and sympathetic nervous system modulation (epinephrine, E and norepinephrine, NE) could be related to BP values. MATERIAL AND METHODS: In 62 patients with diagnosed and treated HTN (mean time of disease 5±3.2 years), serum hs-CRP and ET-1 as well as plasma E and NE concentrations were measured. 24-hour ambulatory blood pressure measurement device (ABPM) was used to estimate efficacy of treatment. RESULTS: A positive correlation between epinephrine and norepinephrine concentrations was found (r=0.246, p=0.05), however such a statistically significant correlation neither to hs-CRP, nor ET-1 were found. Patients with the highest hs-CRP and NE concentrations had the highest systolic (SBP) and diastolic (DBP) blood pressure values. Similar relation was found in subgroup of patients with suboptimal blood pressure values (SPB l 130mmHg, DBP l 80mmHg). In a group of optimal treated patients, elevated levels of ET-1 and NE related to increased blood pressure values. ROC analysis identified ET-1 as statistically significant to diagnose elevated blood pressure: 0.665 (95% Confidence interval 0.512 to 0.796). CONCLUSIONS: In patients with diagnosed and treated arterial hypertension, there are relations among measurements of hs-CRP, ET-1, NE and blood pressure values in spite of treatment, which may improve understanding of mechanisms involving inflammation, endothelial dysfunction and sympathetic nerve activation and may identify patients with refractory hypertension.

Silent pulmonary embolism in a patient with acute myocardial infarction and type B acute aortic dissection - a case report.

A 69-year-old man while being treated for type B aortic dissection was also found to have acute myocardial infarction. The patient initially was treated conservatively. Prophylactic anticoagulant treatment of potential thrombosis was not given because of aortic dissection. Stent-graft implantation to the thoracic aorta was considered at the time. Unexpectedly, elective computer tomography (CT), revealed 2 large thrombi at the bifurcation of the pulmonary trunk. The patient did not show any symptoms of pulmonary embolism. Heparin therapy was initiated immediately. The patient responded well to the therapy and on transesophageal echocardiography and subsequent CT no embolic material was found. Since that time, the patient is receiving oral anticoagulation. The case we present raises the question of anticoagulation prophylaxis in the presence of aortic dissection in bedridden patients. Failure to use such therapy in our patient could have resulted in an unfavorable clinical outcome.

High-sensitivity C-reactive protein and total antioxidant status in patients with essential arterial hypertension and dyslipidemia.

PURPOSE: To assess low-grade, systemic inflammation and antioxidant status as additional factors contributing to pathophysiology of essential arterial hypertension (HTN) and compare them with traditional risk factors, like abnormal lipids profile, considering their potential diagnostic usefulness. MATERIAL AND METHODS: Serum high-sensitivity C-reactive protein (hs-CRP) concentrations and total antioxidant status (TAS) were measured in 143 subjects - 71 patients with diagnosed HTN and in 72 healthy controls. RESULTS: In hypertensive patients, as compared to healthy control group, the median hs-CRP concentration was higher (2.0 mg/L, 25%; 75% quartile range: 0.1; 27.1 vs 0.4 mg/L, 25%; 75% quartile range: 0.0; 4.6, respectively, p<0.001) and TAS concentration lower (1.4 mmol/L, 25%; 75% quartile range: 1.0; 2.1 vs 1.5 mmol/L, 25%; 75% quartile range: 0.5; 1.8, respectively, p=0.048). Hypertensives had higher low-density lipoprotein cholesterol concentration (LDL-C) as well as triglycerides concentration (TG) and lower high-density lipoprotein cholesterol concentration (HDL-C). Higher diagnostic sensitivity was found for hs-CRP (87%) and for TAS (89%). According to the global linear regression analysis, age, gender, hs-CRP, TAS and HDL-C were the only parameters influencing the occurrence of HTN. ROC analysis identified hs-CRP, HDL-C and TG as statistically significant to diagnose HTN (0.839; 0.816 and 0.855, respectively). Moreover, in ROC analysis there were no differences in hs-CRP and TAS in females and males. CONCLUSIONS: These results indicate that low-grade, systemic inflammation measured by hs-CRP as well as antioxidant status assessed by TAS, in the presence of traditional risk factors, are significant factors contributing to pathophysiology and diagnosis of essential arterial hypertension.