Angiotensin receptor neprilysin inhibition compared with enalapril on the risk of clinical progression in surviving patients with heart failure.

BACKGROUND: Clinical trials in heart failure have focused on the improvement in symptoms or decreases in the risk of death and other cardiovascular events. Little is known about the effect of drugs on the risk of clinical deterioration in surviving patients. METHODS AND RESULTS: We compared the angiotensin-neprilysin inhibitor LCZ696 (400 mg daily) with the angiotensin-converting enzyme inhibitor enalapril (20 mg daily) in 8399 patients with heart failure and reduced ejection fraction in a double-blind trial. The analyses focused on prespecified measures of nonfatal clinical deterioration. In comparison with the enalapril group, fewer LCZ696-treated patients required intensification of medical treatment for heart failure (520 versus 604; hazard ratio, 0.84; 95% confidence interval, 0.74-0.94; P=0.003) or an emergency department visit for worsening heart failure (hazard ratio, 0.66; 95% confidence interval, 0.52-0.85; P=0.001). The patients in the LCZ696 group had 23% fewer hospitalizations for worsening heart failure (851 versus 1079; P<0.001) and were less likely to require intensive care (768 versus 879; 18% rate reduction, P=0.005), to receive intravenous positive inotropic agents (31% risk reduction, P<0.001), and to have implantation of a heart failure device or cardiac transplantation (22% risk reduction, P=0.07). The reduction in heart failure hospitalization with LCZ696 was evident within the first 30 days after randomization. Worsening of symptom scores in surviving patients was consistently more common in the enalapril group. LCZ696 led to an early and sustained reduction in biomarkers of myocardial wall stress and injury (N-terminal pro-B-type natriuretic peptide and troponin) versus enalapril. CONCLUSIONS: Angiotensin-neprilysin inhibition prevents the clinical progression of surviving patients with heart failure more effectively than angiotensin-converting enzyme inhibition. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT01035255.

Efficacy and safety of LCZ696 (sacubitril-valsartan) according to age: insights from PARADIGM-HF.

BACKGROUND: The age at which heart failure develops varies widely between countries and drug tolerance and outcomes also vary by age. We have examined the efficacy and safety of LCZ696 according to age in the Prospective comparison of angiotensin receptor neprilysin inhibitor with angiotensin converting enzyme inhibitor to Determine Impact on Global Mortality and Morbidity in Heart Failure trial (PARADIGM-HF). METHODS: In PARADIGM-HF, 8399 patients aged 18-96 years and in New York Heart Association functional class II-IV with an LVEF ≤40% were randomized to either enalapril or LCZ696. We examined the pre-specified efficacy and safety outcomes according to age category (years): <55 (n = 1624), 55-64 (n = 2655), 65-74 (n = 2557), and ≥75 (n = 1563). FINDINGS: The rate (per 100 patient-years) of the primary outcome of cardiovascular (CV) death or heart failure hospitalization (HFH) increased from 13.4 to 14.8 across the age categories. The LCZ696:enalapril hazard ratio (HR) was <1.0 in all categories (P for interaction between age category and treatment = 0.94) with an overall HR of 0.80 (0.73, 0.87), P < 0.001. The findings for HFH were similar for CV and all-cause mortality and the age category by treatment interactions were not significant. The pre-specified safety outcomes of hypotension, renal impairment and hyperkalaemia increased in both treatment groups with age, although the differences between treatment (more hypotension but less renal impairment and hyperkalaemia with LCZ696) were consistent across age categories. INTERPRETATION: LCZ696 was more beneficial than enalapril across the spectrum of age in PARADIGM-HF with a favourable benefit-risk profile in all age groups.

A putative placebo analysis of the effects of LCZ696 on clinical outcomes in heart failure.

AIMS: Although active-controlled trials with renin­angiotensin inhibitors are ethically mandated in heart failure with reduced ejection fraction, clinicians and regulators often want to know how the experimental therapy would perform compared with placebo. The angiotensin receptor-neprilysin inhibitor LCZ696 was compared with enalapril in PARADIGM-HF. We made indirect comparisons of the effects of LCZ696 with putative placebos. METHODS AND RESULTS: We used the treatment-arm of the Studies Of Left Ventricular Dysfunction (SOLVD-T) as the reference trial for comparison of an ACE inhibitor to placebo and the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity-Alternative trial (CHARM-Alternative) as the reference trial for comparison of an ARB to placebo. The hazard ratio of LCZ696 vs. a putative placebo was estimated through the product of the hazard ratio of LCZ696 vs. enalapril (active-control) and that of the historical active-control (enalapril or candesartan) vs. placebo. For the primary composite outcome of cardiovascular death or heart failure hospitalization in PARADIGM-HF, the relative risk reduction with LCZ696 vs. a putative placebo from SOLVD-T was 43% (95%CI 34­50%; P < 0.0001) with similarly large effects on cardiovascular death (34%, 21­44%; P < 0.0001) and heart failure hospitalization (49%, 39­58%; P < 0.0001). For all-cause mortality, the reduction compared with a putative placebo was 28% (95%CI 15­39%; P < 0.0001). Putative placebo analyses based on CHARM-Alternative gave relative risk reductions of 39% (95%CI 27­48%; P < 0.0001) for the composite outcome of cardiovascular death or heart failure hospitalization, 32% (95%CI 16­45%; P < 0.0001) for cardiovascular death, 46% (33­56%; P < 0.0001) for heart failure hospitalization, and 26% (95%CI 11­39%; P < 0.0001) for all-cause mortality. CONCLUSION: These indirect comparisons of LCZ696 with a putative placebo show that the strategy of combined angiotensin receptor blockade and neprilysin inhibition led to striking reductions in cardiovascular and all-cause mortality, as well as heart failure hospitalization. These benefits were obtained even though LCZ696 was added to comprehensive background beta-blocker and mineralocorticoid receptor antagonist therapy.

Biventricular response of the heart to endurance exercise training in previously untrained subjects.

BACKGROUND: Functional adaptation of the heart to regular strenuous exercise has not been fully elucidated yet, with different patterns of alterations being reported. We evaluated the effect of endurance exercise training (EET) on left (LV) and right ventricular (RV) mechanics in amateur individuals preparing for triathlon competitions. METHODS: Twenty-one subjects aged 33 ± 6 years underwent conventional and speckle tracking echocardiography at rest before and after a high-intensity (12.3 ± 1.0 h/week) 12-month EET. RESULTS: At follow-up, in addition to the improvement in LV diastolic parameters, a significant decrease in longitudinal (26.0 ± 3.3% vs. 24.3 ± 3.2%, P < 0.04), circumferential (24.3 ±4.3% vs. 20.1 ± 3.8%, P < 0.002), and radial strains (46.8 ± 18.3% vs. 37.8 ± 12.9%, P < 0.03), and rotation (9.7 ± 4.8% vs. 7.1 ± 4.0 deg, P < 0.04) was demonstrated at the apex, whereas the LV base was found to show an increase in rotation (-3.9 ± 2.8% vs. -5.9 ± 1.8 deg, P < 0.01). Overall hemodynamic effectiveness of the LV was preserved, as evidenced by the unchanged ejection fraction, cardiac output, twist, and torsion. RV systolic function as assessed by strain was significantly reduced with EET (28.1 ± 6.7% vs. 23.7 ± 8.6%, P < 0.03). CONCLUSIONS: EET modifies both LV and RV performance at rest in previously untrained subjects. The true nature of these changes (adaptive or maladaptive) is unclear, but the hypothesis of different responses of the LV apex and base, with the reduction in contractility of the former and increase in rotation of the latter, representing a protective mechanism that reduces myocardial stress might be considered.

Familial predisposition to vasovagal syncope.

OBJECTIVE: A handful of studies suggest a familial predisposition to vasovagal syncope (WS) but the scope of information available to date is poor. The aim of our study was to evaluate the prevalence of vasovagal syncope and its familial occurrence in the young. METHODS AND RESULTS: The studied group consisted of 281 women and 111 men, aged 18-32 years. Forty-seven percent of the population had one brother or sister, and the mean number of individuals per family was 4.4 +/- 1.0. The questionnaire consisted of 30 questions regarding syncopal history. Syncope was reported in 32.1% of the patients studied (36.7% in women vs. 20.7% in men; P < 0.05), 29.1% of mothers, 16.8% of fathers, 30.9% of sisters and 14.2% of brothers. Logistic regression analysis revealed that positive history regarding the syncope in the whole group of students was related to the female gender (OR 2.17; CI: 1.28-3.7), the history of a syncope in mother (OR 1.74; CI: 1.09-2.78) and the history of a syncope in father (OR 2.22; CI: 1.28-3.86; P < 0.001). CONCLUSIONS: A positive history of syncope in male relatives increases the risk of syncope in men and women, whereas a positive history of syncope in female relatives increases the risk of syncope in women only. Female gender independently of the family history increases the risk of syncope. The genetics of the vasovagal syncope could be polygenic but the mechanisms of a transmission remain unclear to date.

Obstructive Sleep Apnea as a Predictor of Abnormal Heart Rate Turbulence.

Obstructive sleep apnea (OSA) causes dysfunction of the autonomic nervous system, but the exact mechanism has not been fully understood. The aim of this study was to analyse the relationship between the incidence and severity of OSA and heart rate turbulence (HRT). Seventy one patients with clinical suspicion of OSA were qualified to participate in the study. All participants took part in a survey and were subjected to laboratory tests, 24-hour electrocardiogram (ECG) Holter monitoring with HRT analysis and polysomnography. The group with OSA manifested significantly higher turbulence onset (TO) and lower turbulence slope (TS) as compared to the group without OSA. Older age, diabetes, hypertension and higher apnea/hypopnea index (AHI) were found to be independent risk factors for increased TO, whereas older age, higher body mass index (BMI), higher blood glucose levels, hypertension and higher AHI were independent risk factors for TS reduction. The AHI ≥65 criterion indicates abnormal HRT in patients with OSA with 94.9% sensitivity and 50.0% specificity, which gives a prediction accuracy of 85.7%. In summary, OSA should be considered as a predictor of abnormal HRT.

Obstructive sleep apnea as a predictor of reduced heart rate variability.

PURPOSE: This study aimed to analyze the relationship between the occurrence of obstructive sleep apnea (OSA) and heart rate variability (HRV) in a group of patients with clinical suggestion of OSA. METHODS: 104 patients with clinical suspicion of OSA were qualified to participate in the study (age: 53.15 ± 13.43 years). All participants took part in a survey and were subjected to laboratory tests, 24-hour ECG Holter monitoring, and polysomnography. The participants were divided into groups depending on the criterion of the presence of OSA. RESULTS: The analysis of time HRV demonstrated lower parameters of SDNN for the entire recording and a 15-minute fragment of daily activity, as well as a lower pNN50 for the entire recording in those patients with diagnosed OSA. A statistically significant difference was observed for the spectral analysis of the LF/HF which was higher in the participants with OSA during the 15-minute fragment of N3 sleep. A negative correlation was observed between AHI and the following parameters: SDSD from the entire Holter recording (r = -0.21, p < 0.05) and from the 15-minute fragment of daily activity (r = -0.19, p < 0.05), mRR from the fragment of N3 sleep (r = -0.19, p < 0.05) and VLF from the entire Holter recording (r = -0.26, p < 0.05). A statistically significant positive correlation between AHI and LF/HF in 15-minute fragments of N3 sleep was found (r = 0.26, p < 0.05). CONCLUSIONS: The study group of patients with OSA is characterized by reduced HRV. The higher AHI constitutes an independent predictor of reduced HRV, both in the sympathetic and parasympathetic components, and the sympathetic-parasympathetic balance.

Plasma YKL-40 levels correlate with the severity of coronary atherosclerosis assessed with the SYNTAX score.

Introduction YKL­40 is a protein released locally by inflammatory cells. Thus, it may constitute a biomarker of inflammatory conditions, such as atherosclerosis. Objectives The aim of the study was to determine YKL­40 levels in patients with ischemic heart disease and to analyze the correlation of this biomarker with the severity of coronary atherosclerosis. Patients and methods The study included 158 patients: 52 with stable ischemic heart disease and 67 with acute coronary syndrome: ST­segment elevation myocardial infarction (STEMI; n = 47) or non-ST­segment elevation myocardial infarction (NSTEMI; n = 20). The control group included 39 individuals without abnormalities in coronary vessels. We evaluated plasma YKL­40 levels and their correlation with the severity of coronary atherosclerosis assessed with the SYNTAX score. Results Patients with myocardial infarction had higher plasma YKL­40 levels than those with stable ischemic disease (median [range], 235.3 [161.6-366.1] ng/ml vs 61.2 [53.1-83.1] ng/ml; P <0.001) or controls (median [range], 235.3 [161.6-366.1] ng/ml vs 55.7 [51.2-75.2] ng/ml; P <0.001). No differences were found in YKL­40 concentrations between STEMI and NSTEMI patients (median [range], 263 [150.3-363.7] ng/ml and 214.9 [163.4-367.6] ng/ml, respectively; P = 0.7). The SYNTAX score in patients with ischemic heart disease correlated positively with YKL­40 concentrations (R = 0.34; P <0.001). Conclusions YKL­40 can be considered a potential biomarker of coronary atherosclerosis severity.

MMP-2, MMP-9, and TIMP-4 and Response to Aspirin in Diabetic and Nondiabetic Patients with Stable Coronary Artery Disease: A Pilot Study.

BACKGROUND: High on-aspirin treatment platelets reactivity (HPR) is a significant problem in long-term secondary prevention of cardiovascular events. We hypothesize that imbalance between platelets MMPs/TIMPs results in cardiovascular disorders. We also explored whether chronically elevated blood glucose affects MMP-2/TIMP-4 release from platelets. MATERIALS AND METHODS: Seventy patients with stable coronary artery disease, supplemented with aspirin, participated in this pilot study. The presence of HPR and/or diabetes mellitus was considered as the differentiating factor. Light aggregometry, impedance aggregometry, and ELISA tests for TXB2, MMP-2, MMP-9, and TIMP-4 were performed in serum, plasma, platelet-rich plasma, and platelets-poor plasma, as appropriate. RESULTS: Aspirin-HPR did not affect plasma MMP-2, MMP-9, and TIMP-4. Arachidonic acid-induced aggregation of platelets from aspirin-HPR patients did not lead to increased release of MMP-2, MMP-9, and TIMP-4. Studying patients at the lowest TXB2 serum concentration quartile revealed that high concentration of plasma TIMP-4 and TIMP-4 negatively correlated with TXB2 and platelet aggregation. Diabetics showed an increased plasma MMP-2 as well as an increased MMP-2 in supernatants after platelet aggregation. However, diabetes mellitus did not affect MMP-9 and TIMP-4. CONCLUSION: Aspirin-HPR did not affect the translocation and release of MMPs and TIMP-4 from platelets. TIMP-4 may serve as a marker of TXA2-mediated platelet aggregation. Chronically elevated plasma glucose increases plasma MMP-2, and HPR potentiates this phenomenon.

[Myocardial bridging of the left anterior descending coronary artery and dobutamine-induced left ventricular outflow tract gradient -- a case report]. / Mostek miesniowy w obrebie galezi przedniej zstepujacej lewej tetnicy wiencowej oraz podwyzszony w czasie dobutaminowej próby obciazeniowej gradient podzastawkowy w drodze odplywu z lewej komory serca -- opis przypadku.

We present a case of a 47-year-old patient with arterial hypertension and progressive ST segment changes with a T wave inversion during 2 years of observation. Coronary angiography showed myocardial bridging of LAD and no significant coronary artery stenosis. During subsequent two last years the patient was repeatedly hospitalised due to chest pain. During the last hospitalisation a dobutamine stress testing was performed which provoked an increased left ventricular outflow tract gradient. This finding may be attributed to an early phase of hypertrophic cardiomyopathy, or dobutamine specific phenomenon.

[Life saving angioplasty of left main coronary artery in a high risk patient]. / Ratujaca zycie angioplastyka pnia lewej tetnicy wiencowej u chorego wysokiego ryzyka.

A case a of a life-saving angioplasty of left main coronary artery (LMCA) is presented. A 75 year old patient with a history of diabetes, previous CABG and carotid surgery was admitted to our hospital with symptoms of early post-infarct angina. Coronary angiography revealed significant stenosis of LMCA, in addition to previously known multi-vessel diffuse CAD. Taking into consideration a very high risk of repeat CABG surgery a decision was made to perform an angioplasty. The intervention was carried out with good angiographic effect and the patient was discharged home few days later, free from angina. In 9 month follow-up angiography there was no restenosis in LMCA. In patients to whom cardiac surgery presents very high risk, an angioplasty of LMCA can be life-saving, with good long term effects.

[Successful percutaneous angioplasty of renal artery in a patient with severe arterial hypertension and symptoms of hyperaldosteronism: a case report]. / Skuteczny zabieg przezskórnej angioplastyki tetnicy nerkowej u chorego z ciezkim nadcisnieniem tetniczym i objawami hiperaldosteronizmu.

Arterial hypertension may result from renal artery stenosis. In this type of hypertension renin-angiotensin-aldosterone system is activated and patients often produce signs of hyperaldosteronism. It must be distinguished from primary hyperaldosteronism in order to chose a proper therapy. In this paper we describe a case of a 65-years-old man with severe arterial hypertension, which was difficult to control pharmacologically. The patient revealed symptoms which suggested primary hyperaldosteronism (except normal plasma renin activity). Only imaging techniques allowed diagnose of renal artery stenosis and carry out successful percutaneous angioplasty of renal artery.

[The influence of deterioration of clinical condition on the change of revascularisation method in coronary artery disease]. / Wplyw zaostrzenia stanu klinicznego na zmiane metody rewaskularyzacji w chorobie wiencowej. Omówienie metod postepowania na podstawie opisywanego przypadku.

A case of a 52-year old woman with diabetes mellitus and symptomatic, multivessel coronary disease is presented. The patient underwent coronary angiography. Taking in consideration the intensity of atherosclerotic lesions and vessels diameter, she was initially selected for cardiovascular surgery. However, because of sudden deterioration of clinical condition caused by myocardial infarction the strategy of cardiac revascularisation was changed. The patient underwent multivessel percutaneous coronary intervention with good result in short- and 6-month observation.

[Estimation of the P wave and PQ interval dispersion in patients after the myocardial infarction]. / Ocena dyspersji zalamka P i odstepu PQ u chorych po przebytym zawale miesnia serca.

AIM: Because in patients with the recent myocardial infarction the noticeable differences in the P wave and PQ interval dispersion were observed in comparison to the control group, consisted of the healthy persons, it was an intresting problem to define the period of persistence of these visible changes on the electrocardiograms made in patients after the myocardial infarction. The aim of the study was to estimate the P wave and PQ interval dispersion in patients after the myocardial infarction in dependence on its location and applied fibrynolytical treatment. MATERIAL AND METHOD: The investigations were conducted on 36 male and female patients in age 40 to 84 years (mean 56 +/- 10,8 years), divided into groups of patients suffering from the inferior myocardial infarction and anterior myocardial infarction. The estimation of P wave and PQ interval dispersion was made by two independent researches on the 12 offtake electrocardiogram, by using scanner and computer program Photo-Finish. There were analysed electrocardiograms made in 10th day, 6 weeks of recovery and successively in 3rd, 6th, and 12th month after the recovery. During the each investigation the echocardiography was made to state the dimension of the left atrium and the blood samples was taken for the measurement of the atrial natriuretic peptide concentration (ANP). CONCLUSIONS: In all the investigated patients the P wave dispersion was significantly higher till 3 months after the myocardial infarction in comparison to the healthy control group, and the minimal and maximal lasting periods of both the P wave and PQ interval as well as the PQ interval dispersion hadn't significant difference comparing to the control group. In all the patients the P wave dispersion was significantly lower in the following examinations made in 3rd, 6th and 12th month of recovery comparing to the initial examination. ALL the examinations proved, that the maximal and minimal lasting period of PQ interval was significantly higher in the 6th week and 3rd, 6th and 12th month of recovery comparing to the examination made in the 10th day after the myocardial infarction. There were no differences between the P wave and the PQ interval dispersion in males and females, in the patients with the inferior myocardial infarction in comparison to the patients with the anterior myocardial infarction as well as in the patients treated fibrinolytically compared to these treated otherwise. It was no correlation between the left atrium dimensions and the P wave and PQ interval dispersion and the ANP concentration was positively correlated to the minimal lasting period of the P wave and the PQ interval in time 12 months after the myocardial infarction.

[The role of TNF-alpha in the etiopathogenesis of heart failure]. / Udzial TNF-alpha w etiopatogenezie niewydolnosci serca.

Clinical evidence demonstrates participation of several cytokines in cardiac heart failure pathogenesis, in particular tumor necrosis factor-alpha (TNF-alpha), which induces left ventricular dysfunction, acute pulmonary edema and congestive cardiomyopathy. Increased levels of TNF-alpha in patients with heart failure were proved and may have prognostic significance. Absent in normal myocardium, produced in the myocardium in response to volume overload, TNF-alpha can depress cardiac function directly and indirectly by induction of nitric oxide synthase produced by macrophages, cardiac myocytes and other cells. The most of TNF-alpha effects are performed by two receptors termed as TNF-RI and TNF-RII identified on the surface of many cells. The extracellular domain fragments of both receptors shed from cell surface can be detected as soluble forms sTNF-RI and sTNF-RII in the urine and blood, and their blood levels in patients with severe heart failure are elevated. There are various pharmacological agents that block the biological effects of TNF-alpha, however only two of them have been used in patients with heart failure: pentoxifylline and etanercept. Encouraging effects of this studies must be regarded as provisional because of relatively small numbers of treated patients. Preliminary results of other randomized, multicenter and in large patients populations trials, planned till 2002 year indicate the possibility of novel anti-TNF strategies in heart failure; treatment is well tolerated and can be effective. It is thought, that recombinantly produced TNF-alpha soluble receptor being now evaluated clinically can determine the progress in heart failure treatment.

[The influence of physical exercise on heart rate variability]. / Wplyw wysilku fizycznego na parametry zmiennosci rytmu serca.

Heart rate variability is controlled by the influence of autonomic nervous system, whereas one part of the system modulates the activity of the other. There is evidence of increased sympathetic activity in patients (pts) with essential hypertension. The aim of the study was to assess the persisting influence of increased sympathetic activity 30 min after moderate physical exercise on heart rate variability in patients with arterial hypertension. The study was performed in 19 patients (10 women, mean age 52.7 +/- 9.5 years and 9 men, mean age 37.7 +/- 8.8 years) with stage I (6 pts) and stage II (13 pts) arterial hypertension. All studied pts had sinus rhythm, were free of diabetes, coronary heart disease and congestive heart failure. 24-hour Holter monitoring was performed and for 30 min before the exercise test the pts stayed in supine rest. The exercise tests were performed between 10 and 11 a.m. Immediately after the exercise all pts stayed in supine position for 30 min. The heart rate variability parameters were studied using Holter monitoring system Medilog Optima Jet and were then analysed statistically. The mean energy expenditure during the exercise was 5.8 +/- 1.1 METs and the maximal heart rate was 148.1 +/- 20.3 bpm. All studied HRV parameters were significantly different in the assessed time period compared to the baseline values (p < 0.001). Significant correlation was found between the age of the studied patients and the mean RR interval, what can be considered as a hyperkinetic (hyperadrenergic) circulatory status and shorter RR interval in younger pts. Significant negative correlation between the age and SDNN parameter (r = -0.65, p < 0.001), 30 min after the exercise mirrors the prolonged adrenergic influence in older pts. The present study shows that the influence of moderate physical exercise on heart rate variability in pts with essential hypertension is extended over 30 min period after exercise and is more pronounced in older pts. The studies on HRV should be performed at longer time intervals after exercise.

[One-year observation of QT and corrected QT interval dispersion in patients with myocardial infarction]. / Roczna obserwacja dyspersji odstepu QT calkowitej i skorygowanej u chorych z przebytym zawalem miesnia serca.

The aim of the study was to evaluate, if the QT and corrected QT interval dispersion (QTd and QTcd) is a predictor of ventricular arrhythmia during one-year observation in patients with myocardial infarction (MI). Investigations were performed in 36 patients with MI, including 22 men and 14 women, aged 40-84 years. Considered criteria was: sex, MI location, applied/non applied thrombolytic treatment, after which patients were classified into 6 groups. I group--14 women aged 45-84. II group--22 men aged 40-71. III group--22 patients aged 43-68 with inferior wall MI (IMI). IV group--14 patients aged 40-84 with anterior wall MI (AMI). V group--29 patients aged 40-72 with MI treated thrombolytically. VI group--7 patients aged 43-84 with MI, not treated thrombolytically. Control group consisted of 15 healthy persons, aged 27-64. Standard 12-outputs ECG was performed on the 10nd day after admission to the hospital. For further observation ECG is provided within the 6th week, 3rd month, 6th month and 12th month after admission to the hospital were used. Holter monitoring was also performed on the 10nd day and 12th month after admission to the hospital. In patients with MI, independently of its sex, location and treatment, QTd and QTcd was initially increased. In patients treated thrombolytically QTcd was significantly decreasing during following months of observation, what hasn't been observed in patients not treated thrombolytically. There was no correlation between QTd, QTcd and non-sustained ventricular tachycardia in patients with MI.

Left main aneurysm and what's next?

The purpose of the case report is to present a case of a 65-year-old male, referred for coronary angiography because of a typical chest pain. The coronary angiography showed an aneurysm of the left main coronary artery. Despite the absence of obvious ischemic symptoms and because of the potential complications of the aneurysm with a width of 15 mm, the patient underwent surgery.

Soluble Cell Adhesion Molecules - Does Estimating sVCAM-1 and sICAM-1 Concentration Provide Additional Information About Cardiovascular Risk in Patients with Coronary Artery Disease?

OBJECTIVES: Cell adhesion molecules (CAM) are thought to have a great impact on endothelium functioning. Interaction between CAM and a receptor may lead to macrophage activation and the release of multiple enzymes such as elastases and colagenases. These enzymes can, in turn, play a role in atherosclerotic plaque destabilization and initiation of acute coronary syndrome (ACS). The main aim of this study was to assess the role of sVCAM-1 and sICAM-1 in the risk stratification of ACS. MATERIAL AND METHODS: 63 patients - mean age 62.7 ± 9.5 years (26 women, 37 men) - were included in the study. Patients were divided into two groups: I - patients with acute coronary syndrome (ACS) diagnosed by coronary angiography (n = 45: 15 women; 30 men); and II - patients without apparent CAD in coronary angiography (n = 18: 11 women, 7 men). In both groups, samples required for sVCAM-1 and sICAM-1 level measurements were collected before the angiography. RESULTS: Mean age, prevalence of arterial hypertension, diabetes mellitus and chronic kidney disease did not differ between the groups. Levels of sVCAM-1 and sICAM-1 were significantly higher in group I (group I vs. group II: 850.3 ± 337.9 vs. 675.9 ± 178.8; p = 0.02 and 737.2 ± 353.5 vs. 428.5 ± 157.3; p = 0.001 respectively). ROC analysis revealed that there is significantly higher risk of ACS above the level of 700.15 ng/mL for sVCAM-1 and 407.8 ng/mL for sICAM-1. The level of sVCAM-1 was also found to be an independent risk factor of NSTEMI, OR 1.003 (95% CI: 1.0007-1.004); p = 0.007, but not of STEMI (p > 0.05). CONCLUSIONS: Levels of sVCAM-1 and sICAM-1 were found to be negative predictors of acute coronary syndrome. Further studies should assess the relationship between sVCAM-1 and sICAM-1 levels and the survival of patients suffering from CAD.