The Effect of Intracoronary Infusion of Autologous Bone Marrow-Derived Lineage-Negative Stem/Progenitor Cells on Remodeling of Post-Infarcted Heart in Patient with Acute Myocardial Infarction.

Introduction: Regenerative capacity of the heart is limited, and the post-infarct left ventricle (LV) dysfunction is associated with poor prognosis. Administration of stem/progenitor cells (SPCs) is a promising approach for cardiac regeneration. Objectives: In the study, we assessed LV function and post-infarcted remodeling in patients with ST-elevated myocardial infarct (STEMI) who received autologous lineage-negative (LIN-) SPCs. Patients and methods: Patients with STEMI and one-vessel coronary artery disease treated with percutaneous revascularisation were divided into study group (LIN- group, 15 patients) that received standard therapy and autologous BM-derived LIN- SPCs and control group (standard therapy group, 19 patients). The cells were administered intracoronary 24 hours after STEMI. The follow-up was 12 months with subsequent non-invasive tests and laboratory parameter evaluation on days 1st, 3rd, and 7th as well as at 1st, 3rd, 6th and 12th month after STEMI. Results: All procedures related to SPCs administration were well tolerated by the patients. In 12-month follow-up, there were no major adverse cardiac events connected with LIN- SPCs administration. During 12-month follow-up, 9 patients from LIN- group (Responders) achieved an improvement in LV ejection fraction (>10% after 12 months) with no signs of unfavorable LV remodeling. Laboratory parameters analysis showed that Troponin T levels were significantly lower until day 7th in the Responders group, while brain natriuretic peptide (BNP) level remained significantly lower from day 3rd to 12th month respectively. Conclusions: Intracoronary infusion of autologous BM-derived LIN- stem/progenitor cells is feasible and safe for patient. Improvement in LV function and prevention of unfavorable remodeling in the 60% of study group seems relatively promising. Stem cell-based therapy for cardiac regeneration still needs more accurate and extensive investigations to estimate and improve their efficacy.

Novel Evidence of the Increase in Angiogenic Factor Plasma Levels after Lineage-Negative Stem/Progenitor Cell Intracoronary Infusion in Patients with Acute Myocardial Infarction.

Cell therapy raises hope to reduce the harmful effects of acute myocardial ischemia. Stem and progenitor cells (SPCs) may be a valuable source of trophic factors. In this study, we assessed the plasma levels of selected trophic factors in patients undergoing application of autologous bone marrow (BM)-derived, lineage-negative (Lin-) stem/progenitor cells into the coronary artery in the acute phase of myocardial infarction. The study group consisted of 15 patients with acute myocardial infarction (AMI) who underwent percutaneous revascularization and, afterwards, Lin- stem/progenitor cell administration into the infarct-related artery. The control group consisted of 19 patients. BM Lin- cells were isolated using immunomagnetic methods. Peripheral blood was collected on day 0, 2, 4, and 7 and after the first and third month to assess the concentration of selected trophic factors using multiplex fluorescent bead-based immunoassays. We found in the Lin- group that several angiogenic trophic factors (vascular endothelial growth factor, Angiopoietin-1, basic fibroblast growth factor, platelet-derived growth factor-aa) plasma level significantly increased to the 4th day after myocardial infarction. In parallel, we noticed a tendency where the plasma levels of the brain-derived neurotrophic factor were increased in the Lin- group. The obtained results suggest that the administered SPCs may be a valuable source of angiogenic trophic factors for damaged myocardium, although this observation requires further in-depth studies.

Variability of platelet response to clopidogrel is not related to adverse cardiovascular events in patients with stable coronary artery disease undergoing percutaneous coronary intervention.

BACKGROUND: Antiplatelet response to clopidogrel and its influence upon the risk of cardiovascular adverse events among patients with stable coronary artery disease undergoing percutaneous coronary intervention (PCI) has not been investigated fully. METHODS: Two hundred eleven patients treated with aspirin and clopidogrel were included in the study. Immediately before PCI, residual platelet reactivity testing with impedance aggregometry assay and a single-nucleotide polymorphism genotyping analysis targeting variants of CYP2C19, ABCB1, and PON1 genes was performed. After the index PCI, the patients were screened for cardiovascular events 6 months following bare-metal stent implantation or 12 months following drug-eluting stent implantation. RESULTS: High on-treatment platelet reactivity (HTPR) was observed in 19.43% individuals and low-TPR (LTPR) in 26.54%. In multivariate analysis, HTPR was significantly (p < 0.05) associated with a history of diabetes, higher systolic blood pressure, and platelet count comparing to that of other patients. LTPR was significantly associated with no history of hypertension, younger age, lower platelet count, absence of the CYP2C19*2 variant, and lower CRP plasma level. Overall, cardiac adverse events were noted in 14.23% patients. Survival analysis with the Cox proportional hazard model showed no influence of residual platelet reactivity during clopidogrel therapy upon both ischemic and hemorrhagic events. However, significant predictors for composite of major adverse cardiac events and hospitalization for cardiovascular causes were identified (the higher CCS class prior to coronary intervention and the higher creatinine serum concentration). CONCLUSIONS: The platelet response to clopidogrel has no impact upon post-procedural adverse events at mid-term follow-up in patients with stable CAD undergoing PCI. This finding suggests that routine platelet reactivity testing is not beneficial in this group of patients.

Cardiac safety of systemic therapy in breast cancer patients with high risk of atherosclerosis complications.

AIM: This study was designed to verify the efficacy of breast cancer treatment and its cardiac toxicity in population with significant cardiac comorbidities. MATERIALS & METHODS: Prospective observational study was conducted in 48 patients. RESULTS: The increase and dependence of echocardiographic parameter early/late were observed on hemoglobin level in all patients, and white blood cells and cholesterol in patients with diabetic were reported. Patients undergo left ventricle diameter change on treatment. CONCLUSION: Use of potentially cardiotoxic chemo regimens in breast cancer patients with cardiac comorbidities, with optimized cardiac therapy accordingly can save patients from development of early myocardial dysfunction induced by chemotherapy - limiting factor to minimize the risk is optimization of lipid level, red blood cell count and platelets count.

Inflammation markers are associated with metabolic syndrome and ventricular arrhythmia in patients with coronary artery disease.

BACKGROUND: Inflammation plays a major role in the development and progression of atherosclerosis and coronary artery disease (CAD). Inflammation markers, including white blood cell (WBC) count, C-reactive protein (CRP) and interleukin-6 (IL-6), are widely used for cardiovascular risk prediction. The aim of the study was to establish factors associated with WBC, CRP and IL-6 in patients with CAD. Two functional polymorphisms in genes encoding enzymes participating in adenosine metabolism were analyzed (C34T AMPD1, G22A ADA). METHODS: Plasma concentrations of IL-6 were measured using high-sensitivity ELISA kits, and the nephelometric method was used for high-sensitivity CRP (hs-CRP) measurement in 167 CAD patients. RESULTS: Presence of metabolic syndrome (MS) and its components, presence of heart failure, severity of CAD symptoms, severe past ventricular arrhythmia (sustained ventricular tachycardia [sVT] or ventricular fibrillation [VF]), lower left ventricle ejection fraction, higher left ventricle mass index, higher end-diastolic volume and higher number of smoking pack-years were significantly associated with higher WBC, CRP and IL-6. Strong associations with arrhythmia were observed for IL-6 (median 3.90 vs 1.89 pg/mL, p<0.00001) and CRP concentration (6.32 vs 1.47 mg/L, p=0.00009), while MS was associated most strongly with IL-6. CRP and IL-6 were independent markers discriminating patients with sVT or VF. There were no associations between AMPD1 or ADA genotypes and inflammation markers. CONCLUSIONS: WBC, CRP and IL-6 are strongly associated with components of the metabolic syndrome. Their strong association with life-threatening ventricular arrhythmia emphasizes the proarrhythmic role of inflammation in the increased cardiovascular risk of CAD patients.

[Coronary artery disease in women ­ how to prevent heart failure after myocardial infarction?].

Cardiovascular disease has been the most common cause of death and disability in women. The prevelence of cardiovascular diseases in women increases dramatically with age as the population ages and women's life expectancy inareases. Compared with men, women with coronary artery diseases are older and more likely to have hyprtension, diabetes and congestive heart failure. Principles of diagnostic and therapeutic management of women are similar to those in men. Clinical trials focusing on treatment alternatives in women have demonstrated improvements in outcomes with advances in technologies and contemporary therapies. All efforts should be focused on the proper screening, prevention and referral for treatment of women with coronary artery disease in order to impact the increasing mortality from heart failure.

[The role of biochemical markers with special regard to troponin, CK-MB, NT-proBNP as early biomarkers of cardiotoxicity among women after chemotherapy due to breast cancer].

Introduction: Cardiotoxicity of drugs in oncology is a growing problem which cardiologists and oncologists have to struggle with. So far, researchers have been looking for biochemical markers which could help to extract a group more prone to developing complications after chemotherapy. Authors' reports are inconsistent in this topic. Aim: This study assesses the role of troponin I, CK-MB and NT-proBNP as early predictive markers for later cardiotoxicity among patients with breast cancer treated with chemotherapy. Methods: One hundred five patients with breast cancer, without either heart failure or more than moderate severity of valvular heart diseases were qualified to the study. Results: NT-proBNP concentration significantly increased just after the first cycle of chemotherapy, either in a subgroup which developed cardiotoxicity or without this end point (p<0.001, p=0.004). CK-MB did not change significantly during observation. Troponin I did not change in any of the patients. During observation HDL-cholesterol concentration significantly decreased. A transient increase of the concentration of LDL-cholesterol had been noted, but later it decreased below baseline level. Conclusion: Troponin I has too low sensitivity to be used as a prognostic marker for further cardiotoxicity after chemotherapy. No prognostic values have been noted of NT-proBNP and CK-MB due to the lack of differences in both a subgroup with and without cardiotoxicity.

[Pregnant woman with pulmonary hypertension]. / Nadcisnienie plucne w ciazy.

Pulmonary hypertension is a disease with diverse etiology. According to the New ESC guidelines, pregnancy is contraindicated for a patent with pulmonary hypertension and qualify such patent to class IV NYHA, regardless of the reason of hypertension. Pregnancy is revived for a patient with pulmonary hypertension despite of the fact that recent treatment methods including specific therapy with the endothelin receptor antagonistst (bosentan), phosphodiesterase inhibitors (sildenafil) and prostacyclin analogs (iloprost) were introduced. In the case of coincidence of pregnancy and pulmonary hypertension, patients should be managed in a center with expertise in pulmonary hypertension with all therapeutic options available.

Coronary artery disease. A study of three polymorphic sites of adenosine deaminase gene.

OBJECTIVES: The role of adenosine as a cardioprotective agent is well known and recent experimental studies suggest that impairment of adenosine-related signal transduction contributes to the pathophysiology of chronic heart failure. The recent observation of an association between ADA, genetic polymorphism and coronary artery disease (CAD) prompted us to study the possible relevance of three intragenic polymorphic sites of the ADA gene (ADA1, ADA2 and ADA6). METHODS AND RESULTS: 136 non-diabetic patients with coronary artery disease and 246 healthy blood donors from the white Italian population of Central Italy and 129 non-diabetic patients with CAD and 204 newborns from the white Polish population were studied. ADA1, ADA2 and ADA6 genotypes were determined by DNA analysis. In males, the proportion of ADA1 *2 (P = 0.0001) and ADA2 *2 (P = 0.005) alleles is lower in CAD than in controls. In males, the haplotype distribution of the pairs ADA1-ADA2, ADA1-ADA6 and ADA2-ADA6 shows statistically significant differences between coronary artery disease and controls. CONCLUSIONS: The present study suggests a complex association between ADA gene and coronary artery diseases. Besides the control of adenosine concentration due to deamination of adenosine, also other functions of the ADA gene could have a role in the susceptibility and/ or clinical course of coronary artery disease.

[Sick sinus syndrome and conduction disorders in women--frequency, treatment]. / Choroba wezla zatokowego, zaburzenia przewodzenia przedsionkowo-komorowego u kobiet-czestosc wystepowania, postepowanie.

Conduction disorders in women are often presented as sick sinus syndrome in comparison to men who have more often disturbances of AV conduction diseases and sinus carotid diseases. Nearly every heart disease with prevalence of ischeamic heart disease and idiopathic degenerative fibrotic process, which leads to reduction number of trigger cells, can result in conduction disorders. As a gold standard in treatment is pacemaker implantation with appropriate pacing mode, after exclusion a reversable reason of the disease.

[Maternal arrhythmias during pregnancy. Practical review]. / Zaburzenia rytmu serca u kobiet w ciazy. Przeglad praktyczny.

Pregnancy is accompanied by a variety of cardiovascular changes in normal women, and these changes can increased incidence of maternal cardiac arrhythmias. Supraventricular and ventricular arrhythmias reguiring treatment are rarely seen during pregnancy in healthy women. Structural cardiac defects or residual defects after repair may contribute to the occurrence of clinically relevant arrhythmias. Arrhythmias during pregnancy include a wide spectrum. The most common are simple ventricular and atrial ectopy, sinusal tachycardia and supraventricular tachycardia. The foetus may suffer both haemodynamic alternations and adverse effects of the treatment (teratogenic risk, foetal growth and development). The management of arrhythmias in pregnant women is similar to that taken in patients who are not pregnant.

Defibrillator implantation early after myocardial infarction.

BACKGROUND: The rate of death, including sudden cardiac death, is highest early after a myocardial infarction. Yet current guidelines do not recommend the use of an implantable cardioverter-defibrillator (ICD) within 40 days after a myocardial infarction for the prevention of sudden cardiac death. We tested the hypothesis that patients at increased risk who are treated early with an ICD will live longer than those who receive optimal medical therapy alone. METHODS: This randomized, prospective, open-label, investigator-initiated, multicenter trial registered 62,944 unselected patients with myocardial infarction. Of this total, 898 patients were enrolled 5 to 31 days after the event if they met certain clinical criteria: a reduced left ventricular ejection fraction (< or = 40%) and a heart rate of 90 or more beats per minute on the first available electrocardiogram (ECG) (criterion 1: 602 patients), nonsustained ventricular tachycardia (> or = 150 beats per minute) during Holter monitoring (criterion 2: 208 patients), or both criteria (88 patients). Of the 898 patients, 445 were randomly assigned to treatment with an ICD and 453 to medical therapy alone. RESULTS: During a mean follow-up of 37 months, 233 patients died: 116 patients in the ICD group and 117 patients in the control group. Overall mortality was not reduced in the ICD group (hazard ratio, 1.04; 95% confidence interval [CI], 0.81 to 1.35; P=0.78). There were fewer sudden cardiac deaths in the ICD group than in the control group (27 vs. 60; hazard ratio, 0.55; 95% CI, 0.31 to 1.00; P=0.049), but the number of nonsudden cardiac deaths was higher (68 vs. 39; hazard ratio, 1.92; 95% CI, 1.29 to 2.84; P=0.001). Hazard ratios were similar among the three groups of patients categorized according to the enrollment criteria they met (criterion 1, criterion 2, or both). CONCLUSIONS: Prophylactic ICD therapy did not reduce overall mortality among patients with acute myocardial infarction and clinical features that placed them at increased risk. (ClinicalTrials.gov number, NCT00157768.)

Autosomal dominant polycystic kidney disease and hypertension are associated with left ventricular mass in a gender-dependent manner.

BACKGROUND: The aim of this study was to compare echocardiographic parameters in patients with autosomal dominant polycystic kidney disease (ADPKD) and in controls with normal kidney function taking into account gender and the presence of hypertension. METHODS: 47 patients with ADPKD (age 36.3 ± 11.0 years) and 49 healthy controls (36.8 ± 9.2 years) were enrolled. M-mode echocardiography was performed in all subjects. Left ventricular hypertrophy (LVH) was diagnosed when the left ventricular mass index (LVMI) was greater than or equal to 125 g/m2 in males and 110 g/m2 in females. RESULTS: The prevalence of LVH was greater in ADPKD patients than in controls (13% vs. 2%; p=0.05). Among females, ADPKD patients demonstrated greater LVMI (87.9 ± 18.5 vs. 68.8 ± 15 g/m2, p=0.00009) than controls. There was a positive correlation between LVMI and blood pressure in ADPKD females (Rs=0.54, p=0.027 for systole blood pressure-SBP and Rs=0.50, p=0.0053 for diastole blood pressure-DBP) but not in males. CONCLUSION: Left ventricular mass is increased in ADPKD females with normal renal function. A positive correlation between SBP and DBP and LVMI was found in ADPKD females but not in ADPKD males.

Association of C34T AMPD1 gene polymorphism with features of metabolic syndrome in patients with coronary artery disease or heart failure.

OBJECTIVE: The common C34T polymorphism in the AMP deaminase-1 (AMPD1) gene results in an inactive enzyme in homozygotes for the mutated T allele. Some studies have shown an association of T allele with longer survival in heart failure (HF) and/or coronary artery disease (CAD). The aim of this study was to assess genotype-phenotype correlations in such patients, with emphasis on components of the metabolic syndrome. METHODS: Ninety-seven patients with CAD without HF (CAD+ HF-) and 104 with HF (HF+) were genotyped by PCR-RFLP. The genetic control group comprised 200 newborns. RESULTS: No significant differences were found in the frequency of AMPD1 genotypes between the groups. In the CAD+ HF- group, the carriers of T allele compared to CC homozygotes had significantly lower values of waist circumference (89.5+/-8.5 versus 97.7+/-11.2 cm; p = 0.00029), waist/hip ratio (p = 0.0059) and BMI (p = 0.045). There was no diabetes or fasting glycaemia > or =126 mg/dL in T carriers, while these features were present in 25% of CC homozygotes (p = 0.0024). In the HF+ group, a tendency towards a lower prevalence of diabetes (20 % versus 41%; p = 0.068) and significantly lower systolic blood pressure (p = 0.048) were observed in T allele carriers. CONCLUSIONS: C34T AMPD1 polymorphism may be associated with reduced frequency of obesity in CAD patients and of hyperglycaemia and diabetes in both CAD and HF patients. Morphometric parameters associated with adipose tissue distribution and parameters of glucose metabolism should be analysed as potential confounders in further studies on the role of polymorphisms of AMPD1 and other genes associated with AMP and adenosine metabolism in cardiovascular disease.

Middle cerebral artery flow after angioplasty and stenting of symptomatic internal carotid artery stenosis.

BACKGROUND AND PURPOSE: Improved haemodynamics in the middle cerebral arteries (MCAs) after carotid artery endaterectomy (CEA) has been demonstrated in a number of studies, whereas similar analyses on carotid angioplasty and stenting (CAS) remain insignificant. The purpose of the study was to test whether CAS affects haemodynamic parameters of MCA ipsilaterally and contralaterally to the side of the procedure in patients with symptomatic internal carotid artery (ICA) stenosis, assessed by transcranial Doppler (TCD) examination. MATERIAL AND METHODS: Carotid angioplasty and stenting was performed in 51 patients (39 men and 12 women) aged 45-86 (mean age: men 65.5 years, women 69 years) after first ever ischaemic stroke. Patients were divided into three groups: with CAS of the left stenotic ICA - group I, with CAS of the right stenotic ICA - group II and group III with CAS of the left stenotic ICA and right ICA occlusion. RESULTS: Increase of MCAs flow after CAS was recorded both in ipsilateral MCAs and contralateral MCAs. Although an increase of MCAs flow was observed, it was not significant in either MCAs of group I and II patients, or in ipsilateral MCAs of individuals in group III. An evident increase of blood flow after CAS occurred in cMCAs of group III individuals. Similar results were received with reference to Gosling's pulsatility index. CONCLUSIONS: Carotid angioplasty and stenting improves blood flow in both the ipsilateral and contralateral middle cerebral artery in patients with symptomatic carotid artery stenosis. Carotid angioplasty and stenting seems to be more effective in patients with symptomatic carotid artery stenosis combined with contralateral carotid artery occlusion than in individuals with symptomatic carotid artery stenosis alone.

Joint position statement of the Polish Cardiologic Society, the Polish Gynaecological Society and the Polish Menopause and Andropause Society on the effect of postmenopausal hormone replacement therapy on the cardiovascular system.

The group of experts representing the Polish Cardiologic Society, the Polish Gynecological Society and the Polish Menopause and Andropause Society has issued this Joint Position Statement based on the review of available literature on the effect of postmenopausal hormone replacement therapy on the cardiovascular system. The results of older clinical and epidemiological studies are confronted with the most recently published data. The importance of type, doses and delivery route of hormones is discussed with respect to the cardiovascular safety of HRT.

Diagnostic and prognostic value of rapid pacing stress echocardiography for the detection of coronary artery disease: influence of pacing mode and concomitant antiischemic therapy (final results of multicenter study Pol-RAPSE).

AIM: Assessment of safety, diagnostic, and prognostic value of a stress echocardiography protocol based on rapid pacing in patients with implanted permanent pacemakers according to the pacing mode (AAI/DDD or VVI) and concomitant antiischemic therapy. MATERIAL AND METHODS: 149 rapid pacing stress echo tests were performed in 100 patients (33 females, 67 males, aged 47-79, mean 65 +/- 8 years), utilizing previously implanted permanent pacemakers. Left ventricular segmental contractility was assessed at rest, during pacing at the rate of 100/minutes and then at 85% of maximal age-predicted heart rate. Each pacing stage lasted for 3 minutes. The test was performed using only VVI pacing mode in 27 patients in whom atrial pacing was not possible. In the remaining 73 patients AAI/DDD pacing mode was initially used in all 73 patients and followed by VVI pacing in 49 patients. Angiographic coronary stenosis of at least 50% was considered significant. RESULTS: No severe adverse effects were observed. Mean duration of the test was 7 +/- 2 minutes for VVI pacing and 10 +/- 2 minutes for both AAI/DDD and VVI pacing. Among 149 tests performed, AAI/DDD mode was used in 73 (49%), while in VVI mode was used in 76 (51%) tests. Significant increase in heart rate comparing to baseline was achieved[[68/minutes vs. 129/minutes (P < 00001)]], also in patients treated with beta-blockers[[69/minutes vs. 129/minutes (P < 00001)]], whereas, blood pressure remained unchanged between rest and rapid pacing stage. Wall motion score index increased significantly (from 1.32 vs. 1.49 in AAI/DDD to 1.36 vs. 1.65 in VVI mode). Among all 149 tests, 89 (60%) were considered positive, 57 (38%) negative, and 3 (2%) - nondiagnostic. Sensitivity, specificity, accuracy, positive, and negative predictive values for significant coronary stenosis were respectively: 91%, 75%, 83%, 81%, and 88%. For AAI/DDD mode the above values were: 91%, 81%, 86%, 82%, 91%, while for VVI mode they were: 91%, 68%, 80%, 80%, 84% (ns). In patients treated with beta-blockers test accuracy was - 79%., with ACE inhibitors - 84%, and with nitrates - 93%. During 1-year follow-up 5 (5%) cardiac deaths and 9 (9,1%) myocardial infarctions occurred. The risk of myocardial infarction or cardiac death was significantly higher in patients with positive comparing to negative result of RAPSE test. Complications hazard ratio associated with positive result of RAPSE was 13.5 (95% confidence interval, 1.7-106.0, P + 0.0133) for AAI/DDD mode and 7.9 (95% confidence interval, 1.0-60.9, P + 0.00472) for VVI mode. CONCLUSIONS: Rapid pacing stress echo test using permanent pacemaker is a rapid and safe diagnostic technique. The accuracy is good for both pacing modes, including tests performed in patients treated with beta-blockers. The test can be utilized as a technique of choice in noninvasive diagnostics of coronary disease and prognostic assessment in patients with permanent pacemakers.

[Acute thrombosis during carotid artery stenting treated with percutaneous embolectomy in a patient resistant to heparin]. / Przezskórna angioplastyka tetnicy szyjnej wewnetrznej powiklana ostra zakrzepica leczona przezskóna embolektomia u chorego z opornoscia na heparyne.

A case of a 61-year-old man with previous stroke, treated with stent implantation due to carotid artery stenosis, is presented. During the elective procedure we observed acute thrombosis in the carotid artery due to heparin resistance unknown before. Embolectomy with open filter of the distal neuroprotection system was successfully performed. The second procedure, after a few months with a direct thrombin inhibitor, was fully successful.

Angiographic severity of coronary artery disease and cardiovascular risk in acute coronary syndrome in patients with metabolic syndrome.

BACKGROUND: The extent of angiographic lesions, size of infarct, and in-hospital and long-term prognosis in patients with metabolic syndrome (MS) have not been clearly determined. AIM: The aim of the study was to investigate the effect of MS on the severity of coronary artery disease (CAD) and cardio-vascular risk evaluated using the GRACE 2.0 risk score and left ventricular ejection fraction (LVEF) in patients with first acute coronary syndrome (ACS) treated with coronary angioplasty. METHODS: The study was conducted in a group of 160 consecutive patients hospitalised for their first ACS. Coronary angiogra-phy was assessed and an echocardiographic evaluation of LVEF was performed. MS was diagnosed according to the National Cholesterol Education Programme-Adult Treatment Panel III criteria. Cardiovascular risk was evaluated using the GRACE 2.0 score. Statistical analysis was performed using the STATISTICA software version 12.0. RESULTS: Diagnostic criteria for MS were met by 53.5% of the patients. Patients with and without MS did not differ in angio-graphic severity of CAD and cardiovascular risk as evaluated with the GRACE 2.0 score. LVEF was significantly elevated in patients with MS. In the examined group the angiographic severity of CAD correlated positively with age, body mass index (BMI) and the homeostatic model assessment for insulin resistance (HOMA-IR) index. The cardiovascular risk correlated positively with age, BMI, fasting insulin levels, and HOMA-IR, and inversely with blood pressure and triglyceride levels. The multivariable regression model for predicting the LVEF value indicated that the strongest prognostic factor was the type of ACS. CONCLUSIONS: The associations between the angiographic severity of CAD and age, BMI, and insulin resistance (IR) confirm the involvement of these parameters in coronary atherosclerosis. The correlations between the estimated cardiovascular risk and IR indicate the prognostic value of metabolic parameters in patients after first ACS. The type of ACS is the strongest predictor of LVEF at discharge in this population.

ADA*2 allele of the adenosine deaminase gene may protect against coronary artery disease.

BACKGROUND/AIMS: The common G22A polymorphism in the adenosine deaminase (ADA) gene leads to substitution Asp8Asn. The lower activity of the enzyme encoded by A22 (ADA*2) allele may increase tissue concentrations of adenosine, a potent cardioprotective agent. In a case-control study, we investigated the association between ADA polymorphism and coronary artery disease (CAD). METHODS: A hundred and seventy-one CAD patients from the north-western part of Poland and 200 consecutive newborns from the same population were genotyped by PCR-RFLP. RESULTS: Twenty-five ADA*1/*2 heterozygotes (12.5%) and 2 ADA*2/*2 homozygotes (1%) were found in the control group, while only 10 *1/*2 heterozygotes (5.9%) and no *2/*2 homozygotes were found in the CAD group. Frequencies of ADA*2 carriers (5.9% vs. 13.5%, p = 0.015) and ADA*2 allele (2.9% vs. 7.3%, p = 0.0083) were lower in CAD patients than in controls. Among CAD patients, a significantly lower proportion of *2 allele carriers was treated with diuretics and ACE inhibitors when compared to *1/*1 wild-type homozygotes. CONCLUSION: ADA*2 allele may decrease genetic susceptibility to CAD. ADA should be added to the list of candidate genes modifying the risk of cardiovascular diseases.