Drainage of pleural effusions in the course of unrecognised constrictive pericarditis: a cause of severe haemodynamic deterioration.

Constrictive pericarditis (CP) is a rare disease which can be easily overlooked in the absence of typical pericardial calcification. One of its most frequent manifestations is pleural effusion. We present a case report of a patient with unrecognised CP in whom plerocentesis led to haemodynamic collapse, and we speculate about the potential pathomechanism. No obvious criterion of CP or severe systolic dysfunction was found in baseline echocardiography. We consider that patients with advanced CP are remarkably prone to haemodynamic decompensation secondary to pleural drain.

Admission B-type natriuretic peptide level predicts long-term survival in low risk ST-elevation myocardial infarction patients.

BACKGROUND: In patients with acute myocardial infarction (AMI), B-type natriuretic peptide (BNP) is a predictor of short- and medium-term mortality. AIM: To evaluate the long-term prognostic value of a single measurement of plasma BNP in low risk patients with first ST-elevation myocardial infarction (STEMI). METHODS: Plasma BNP concentrations were analysed on admission in 211 patients, median age 68 (56.0-75.0) years, admitted with first STEMI and treated with primary percutaneous coronary intervention (PPCI). Left ventricular ejection fraction (LVEF) was assessed by echocardiography during the first 24 h. Patients were followed for a median 48.2 (42.3-72.6) months. RESULTS: The median BNP level was 92.5 (36.3-199.2) pg/mL. During the follow-up period, 79.6% of patients survived. Logistic regression analysis indicated that among the assessed clinical, biochemical, angiographic and echocardiographic parameters, the best predictors of mortality were age, LVEF, maximal creatinine concentration and BNP measurements, (p < 0.05). In multivariate Cox regression analysis for the prediction of death, only age remained significant (p = 0.00007). Admission BNP level > 400 pg/mL indicated patients with the highest risk of death (47.1% vs 22% and 18.4% in patients with BNP level < 100 pg/mL and 100-400 pg/mL, respectively; p < 0.05). CONCLUSIONS: A single measurement of BNP on admission can improve long-term risk stratification in low risk first STEMI patients treated with PPCI.

GRACE, TIMI, Zwolle and CADILLAC risk scores--do they predict 5-year outcomes after ST-elevation myocardial infarction treated invasively?

BACKGROUND: GRACE, TIMI, Zwolle, and CADILLAC are risk scores designed for predicting short-term outcome after acute coronary syndromes. The aim of our study was to test their utility for a prognosis of 5-year survival in a "real-life" population of patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary interventions (pPCI). METHODS: Our registry consisted of consecutive patients with STEMI treated with pPCI. Five-year follow-up was performed with all-cause mortality as the end-point. RESULTS: Out of 505 patients (mean age 58.6±11.3 years) 32 died during the first 30 days (6.3%) and an additional 74 within 5 years (15.6%). PCI was successful in 95.2% (n=481). Prognostic values (c statistics) for predicting 5-year mortality equaled: 0.742 (CI 0.69-0.79) for the GRACE risk score, 0.727 (CI 0.67-0.78) for TIMI, 0.72 (CI 0.67-0.77) for Zwolle, and 0.687 (CI 0.63-0.74) for CADILLAC. In a univariate analysis all the scores were associated with the 5-year outcome. CONCLUSIONS: GRACE, TIMI, and Zwolle risk scores predicted well 5-year all-cause mortality in patients with STEMI treated with pPCI. Our data show that the usefulness of initial bedside risk assessment can be further extended for long-term follow-up.

[Metastatic malignant cardiac tumour--a case report]. / Wtórny nowotwór zlosliwy serca.

We present a case of a 58 year-old patient with metastatic malignant cardiac tumour in whom the first manifestation of heart involvement was cardiac tamponade.

Hypotensive effect of atorvastatin is not related to changes in inflammation and oxidative stress.

We sought to determine if atorvastatin lowers blood pressure in patients with previously diagnosed and well-controlled essential arterial hypertension and if this effect could be related to anti-inflammatory and anti-oxidative effects. Among 92 patients with essential arterial hypertension, we studied 56 non-smoking and normolipemic: 39 were randomized to receive 80 mg atorvastatin daily for 3 months (statin-treated patients, ST), and the rest continued a previous hypotensive therapy (statin-free patients, SF). Blood pressure was measured using a 24-h ambulatory blood pressure measurement device. Serum levels of high-sensitivity C-reactive protein (hs-CRP), total antioxidant status (TAS) and plasma peroxides (assessed by Oxystat) were measured in both groups. The mean change in systolic BP (SBP) for atorvastatin was -5.7 mmHg (95% confidence interval CI, -4.1 to -7.2 mmHg), and the mean change in diastolic BP (DBP) was -3.9 mmHg (95% CI, -2.7 to -5.0 mmHg). No change in BP in SF patients was observed. In the ST group, hs-CRP and peroxides did not significantly decrease. In the SF group, concentrations of hs-CRP proceeded to decrease while peroxides increased. In the ST group, changes in hs-CRP correlated with changes in total cholesterol and low-density lipoprotein cholesterol (r = 0.41, p = 0.013 and r = 0.35, p = 0.04, respectively) but did not correlate with changes in BP. The hypotensive statin effect was independent of the hypolipemic effect. During three months of observation, TAS concentrations in both groups remained stable. In this randomized study, additionally administered atorvastatin to non-smoking and normolipemic patients with well-controlled essential arterial hypertension resulted in reduction of BP. This effect was not followed by significant changes in hs-CRP, TAS or Oxystat concentrations. The hypotensive effect of atorvastatin did not depend on anti-inflammatory, anti-oxidative or hypolipemic actions.

Circadian variations of interleukin 6 in coronary circulations of patients with myocardial infarction.

UNLABELLED: We hypothesize that higher morbidity of patients with ST-segment elevation myocardial infarction (STEMI) in the out-of-office hours differences in outcome after myocardial infarction may depend on the concentrations of inflammatory cytokines. The aim of the study was to determine the relation between the time of percutaneous coronary intervention (PCI) and local concentration of interleukin 6 (IL-6) and its soluble receptors (sIL-6R and sgp130) in patients with STEMI. METHODS AND RESULTS: The study included 32 patients with invasively treated left anterior descending artery occlusion and no significant co-morbidities. Blood samples were drawn from coronary sinus and aorta before and after intervention. Patients admitted in the afternoon (13-20) presented significantly higher mean IL-6 levels in all samples than patients admitted in the morning. There was a positive correlation between time of intervention and concentrations of IL-6 in all samplings, but also with transcardiac IL-6 gradient at the end of procedure and IL-6 increase during PCI. We did not find any significant association between time of PCI and concentrations of sIL-6R and sgp130, time from pain to balloon, angiographic parameters or medical history. CONCLUSIONS: Coronary concentration of IL-6 in patients with STEMI is significantly higher in the afternoon than in the morning. This might be involved in increased morbidity of those patients.

Influence of atorvastatin on blood pressure control in treated hypertensive, normolipemic patients - An open, pilot study.

AIMS: The aim of the study was to determine whether a high dose of atorvastatin lowers blood pressure (BP) in normolipemic patients with well controlled primary arterial hypertension and if this effect is associated with alteration of biomarkers of endothelial function and oxidative stress. In this open-label study, normolipemic patients (n=56) were randomized in the proportion of 2:1 to receive atorvastatin 80 mg daily for 3 months (statin-treated, ST n=39), or to previous therapy (statin-free, SF). BP was measured using a 24-h ambulatory BP measurement device. Plasma levels of 6-keto-PGF(1alpha) (prostacyclin metabolite), serum nitric oxide (NO) and levels of autoantibodies immunoglobulin G against oxidatively modified low-density lipoprotein (ox-LDL) were measured. MAJOR FINDINGS: The mean change in systolic BP and diastolic BP for ST was - 5.7 mmHg (95% CI -4.1 to -7.2 mmHg) and -3.9 mmHg (95% CI -2.7 to -5.0 mmHg), respectively. Hypotensive statin effect was independent of lipid lowering. No change of BP in SF patients was observed. In ST, prostacyclin metabolites and NO concentrations were not significantly increased and autoantibodies against ox-LDL concentrations did not change. In ST, the decrease in BP correlated with increase in NO and decrease in autoantibodies against ox-LDL. PRINCIPAL CONCLUSION: High-dose atorvastatin resulted in reduction of BP independently of lipid-lowering effect, changes in endothelial function and oxidative stress, but it was related to the increase in NO and decrease in autoantibodies against ox-LDL. However, because of the open design of the study, these results should be carefully debated.

Percutaneous coronary interventions affect concentrations of interleukin 6 and its soluble receptors in coronary sinus blood in patients with stable angina.

Coronary stenting may create local inflammatory reaction. Interleukin 6 effects depend on the presence of soluble receptors (sIL-6R and sgp130) that facilitate or impede interleukin 6 signal transduction. Concentrations of interleukin 6 and its soluble receptors were assessed in aorta and coronary sinus after stenting in optimally treated stable angina patients scheduled for elective stenting. Baseline levels of interleukin 6 and its soluble receptors in patients did not differ from healthy controls. Initial levels of sIL-6R in aorta were significantly higher than in coronary sinus but this difference disappeared after intervention. Stenting caused interleukin 6 concentration increase to a similar extent both in coronary sinus and in aorta. Moreover, there was significantly higher sgp130 concentration in coronary sinus than in aorta. Coronary intervention increases concentration of interleukin 6 in patients with stable angina. It affects the cardiac level of interleukin 6 soluble receptors what may influence the local inflammatory reaction.

Coronary sinus concentrations of interleukin 6 and its soluble receptors are affected by reperfusion and may portend complications in patients with myocardial infarction.

UNLABELLED: Interleukin 6 (IL-6) is a pleiotropic cytokine involved in both inflammatory reaction and myocardial response to stress. Its effects largely depend on the concentration of the soluble receptors (sIL-6R and sgp130). We investigated the production of IL-6, sIL-6R and sgp130 by the heart during ischemia and reperfusion. METHODS: The levels of IL-6 were determined in blood of 34 patients with first myocardial infarction (STEMI), left anterior descending (LAD) artery occlusion, otherwise normal coronaries, without significant co-morbidities and 16 comparable subjects with stable ischemic heart disease and lesion in LAD. Blood samples from coronary sinus (CS) and aorta (Ao) were drawn before percutaneous intervention (PCI), immediately after and at the end of the procedure. Venous blood from 30 healthy volunteers served as control. RESULTS: STEMI patients presented high IL-6 concentrations that increased further after reperfusion when its levels in CS became significantly higher than in Ao. In both groups prior to the PCI there were significantly higher concentrations of sIL-6R in Ao than in CS. This difference disappeared immediately after reperfusion. STEMI patients who experienced cardiovascular complications had higher IL-6 concentration and higher transcardiac sIL-6R gradient than patients with event-free hospitalisation. This association was confirmed in multivariate logistic regression analysis. Myocardial infarction increases concentration of IL-6 that is further elevated by reperfusion. A transcardiac gradient of sIL-6R during ischemia may indicate that large amounts of soluble IL-6 receptors are bound to the infarcted heart and thus affect signal transduction. IL-6 and initial sIL-6R gradient may portend complications in STEMI patients.

Lack of ST-segment depression normalization after PCI is a predictor of 5-year mortality in patients with ST-elevation myocardial infarction.

BACKGROUND: The significance of dynamic changes in a depressed ST-segment in the reciprocal changes after percutaneous coronary intervention (PCI) of patients with ST-elevation myocardial infarction (STEMI) is unknown, so the aim of this study was to evaluate the significance of reciprocal ST-segment depression normalization (STN) on long-term mortality in patients with STEMI treated with primary PCI. METHODS AND RESULTS: Data for 247 consecutive patients with STEMI were analyzed; 84 patients were excluded because of exclusion or incomplete inclusion criteria, so finally, 163 patients successfully treated with primary PCI were included. The study group was divided into 3 subgroups according to percentage of STN: poor STN (<30%), partial STN (30-70%), complete STN (>70%). Complete STN occurred in 63%, partial in 24% and poor in 13% of patients. STN correlated with late mortality (15% vs 28% vs 38% respectively, p=0.012). Patients who died during the follow-up period had a lower mean percentage reduction of initial ST-segment depression after PCI (50% vs 75%, p=0.001). Percentage reduction of initial ST-segment depression after PCI was a significant and independent risk factor of long-term mortality (odds ratio 1.01; 95% confidence interval: 1.00-1.02; p=0.02). CONCLUSIONS: These data revealed the use of reciprocal changes normalization as a novel tool for assessment of long-term risk of death in patients after successful primary PCI for STEMI.

TIMI Risk Score accurately predicts risk of death in 30-day and one-year follow-up in STEMI patients treated with primary percutaneous coronary interventions.

BACKGROUND: TIMI Risk Score for ST-elevation myocardial infarction (STEMI) was developed in a cohort of patients treated with fibrinolysis. It was though to predict in-hospital and short-term prognosis. Later studies validated this approach in large cohorts of patients, regardless of the applied treatment and presented its good power to predict 30-day mortality. AIM: We applied the TIMI Risk Score to our registry of STEMI patients treated with primary percutaneous intervention (pPCI) to validate the possibility to predict one-year survival. METHODS: Our registry comprised 494 consecutive patients (mean age 58.5+/-11.3 years) with STEMI treated with pPCI who were followed for approximately one year. STEMI was diagnosed based on typical criteria: chest pain, ECG changes and rise in myocardial necrosis markers. In all patients TIMI Risk Score for STEMI was calculated and they were divided into three groups: low risk (0-5 points), medium risk (6-7) and high risk (>7 points). Multivariate logistic regression analysis, Kaplan-Meier survival analysis with Cox and log-rank tests as well as c statistics from receiver-operator curves (ROC) were used for statistical analysis. RESULTS: TIMI 3 flow was obtained in 95.5% of patients. Median TIMI risk score was 4 (ranging from 0 to 10). During follow-up there were 47 deaths (9.5%). There was a statistically significant difference in survival between all risk groups both in 30-day and one-year follow-up (p <0.001 log-rank test). TIMI Risk Score had good power to predict 30-day (c statistic 0.834, 95% CI 0.757-0.91, p <0.0001) as well as one-year mortality (c statistic 0.809, 95% CI 0.739-0.878, p <0.0001). Interestingly, when we excluded from the analysis all patients who died during the first 30 days, TIMI Risk score maintained its very good prognostic value. All analysed risk groups significantly differed between each other with respect to mortality (p <0.05, log-rank test) and the c statistic was 0.745 (95% CI 0.612-0.879, p <0.0002). In multivariate logistic regression analysis TIMI Risk Score was one of the independent risk factors of death during one-year follow-up (OR 1.59, p <0.001). CONCLUSIONS: TIMI Risk Score accurately defines the population of STEMI patients who are at high risk of death not only during the first 30 days, but also during a long-term follow-up. This simple score should be included in the discharge letters because it contains very useful information for further care.

The effect of glycoprotein IIIa A1/A2 gene polymorphism on one-year outcome in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention.

INTRODUCTION: Glycoprotein IIb/IIIa (GP IIb/IIIa) is a platelet receptor composed of two subunits coded by individual genes. GP IIIa gene has two alleles: A1 and A2. The A2 allele determines higher platelet activity and was investigated many times as a potential risk factor of ACS. The influence of A1/A2 polymorphism on the prognosis in patients with ST-segment elevation myocardial infarction (STEMI) has not been analysed so far. AIM: Evaluation of the relationship between GP IIb/IIIa A1/A2 gene polymorphism and one-year prognosis in patients with STEMI treated with primary percutaneous coronary intervention (pPCI). METHODS: 171 patients (23.9%--women, 39.7%--anterior MI) with STEMI treated successfully with pPCI as well as 121 healthy subjects from a reference group were enrolled in the study. Genotyping was performed using restriction fragment length polymorphism analysis (RFLP). In one-year follow-up the primary end point included deaths and infarctions. The following methods were used in statistical analysis: chi(2) as well as Mann-Whitney test, Kaplan-Meier survival analysis, Cox regression model and multivariate analysis. RESULTS: The percentage of A2 allele carriers was similar in STEMI patients and in subjects from the reference group (27.4% vs. 21.5%, p=0.24). No statistically significant difference in the incidence of primary end point between the A1A1 homozygotes and A2 allele carriers (A1A2/A2A2 genotype) was observed among STEMI patients. In Cox regression analysis, the variables associated with death or MI were: ejection fraction (RR 0.912, p=0.01) and systolic blood pressure on admission (RR 0.97, p=0.049). The variables categorised as unfavourable predictors included: Killip class >2 and heart ratio on admission >100/min (p <0.05, log-rank test). CONCLUSION: No relationship between GP IIb/IIIa A1/A2 gene polymorphism and STEMI incidence as well as one-year prognosis in patients with STEMI treated with pPCI was documented.

[Development of heart failure in the course of coronary artery disease--the role of genetic factors]. / Rozwój niewydolnosci serca w przebiegu choroby wiencowej--rola czynników genetycznych.

The number of patients suffering from heart failure is constantly increasing. One of its main causes is coronary artery disease, especially myocardial infarction. Progression of heart failure depends both on the extent of ischaemic injury and the course of subsequent adaptive processes. Genetic methods may help to find individuals at high risk of developing heart failure. There are multiple genes influencing circulatory system, some of their alleles may potentially affect progression of the disease. Among the most promising targets are genes of the renin-angiotensin-aldosterone system: insertion/deletion (L/D) polymorphism of angiotensin converting enzyme gene, polymorphisms of angiotensinogen, angiotensin receptors (AT1 and AT2) and aldosterone syntase genes. Other genetic factors, which may affect are different gene variants of adrenergic receptors (beta1, beta2, alpha2C), AMP deaminase-1, endothelin-1, endothelial nitric oxide syntase, precursors of natriuretic peptides and inflammatory factors (TNF-alpha, IL-6, MCP-1, TGF, MMP-2). Furthermore, the response to drugs may depend on genetic background, that is why pharmacogenetics creates new possibilities to tailor the best therapy for each patients with heart failure. Therefore research in the field of genetic factors affecting the development of heart failure has not only scientific, but also practical value.