Accumulation of Deleterious Effects in Gastric Epithelial Cells and Vascular Endothelial Cells In Vitro in the Milieu of Helicobacter pylori Components, 7-Ketocholesterol and Acetylsalicylic Acid.

The Gastric pathogen Helicobacter pylori (HP) may influence the development of coronary heart disease (CHD). H. pylori induce reactive oxygen species (ROS), which transform cholesterol to 7-ketocholesterol (7-kCh), a CHD risk factor. Acetylsalicylic acid (ASA)-an Anti-aggregation drug used in CHD patients-may increase gastric bleeding and inflammation. We examined whether H. pylori driven ROS effects in the cell cultures of gastric epithelial cells (AGS) and vascular endothelial cells (HUVEC) progress in the milieu of 7-kCh and ASA. Cell cultures, exposed to 7-kCh or ASA alone or pulsed with the H. pylori antigenic complex-Glycine acid extract (GE), urease (UreA), cytotoxin associated gene A (CagA) protein or lipopolysaccharide (LPS), alone or with 7-kCh and ASA-were examined for ROS, apoptosis, cell integrity, interleukin (IL)-8, the activation of signal transducer, the activator of transcription 3 (STAT3), and wound healing. ASA and 7-kCh alone, and particularly in conjunction with H. pylori components, increased the ROS level and the rate of apoptosis, which was followed by cell disintegration, the activation of STAT3, and IL-8 elevation. AGS cells were unable to undergo wound healing. The cell ROS response to H. pylori components may be elevated by 7-kCh and ASA.

Helicobacter pylori Infection Acts Synergistically with a High-Fat Diet in the Development of a Proinflammatory and Potentially Proatherogenic Endothelial Cell Environment in an Experimental Model.

Classic atherosclerosis risk factors do not explain all cases of chronic heart disease. There is significant evidence that gut microbiota may influence the development of atherosclerosis. The widespread prevalence of chronic Helicobacter pylori (H. pylori, HP) infections suggests that HP can be the source of components that stimulate local and systemic inflammatory responses. Elevated production of reactive oxygen species during HP infection leads to cholesterol oxidation, which drives atherogenesis. The aim of this study is to explore the link between persistent HP infection and a high-fat diet in the development of proinflammatory conditions that are potentially proatherogenic. An in vivo model of Caviae porcellus infected with HP and exposed to an experimental diet was investigated for the occurrence of a proinflammatory and proatherogenic endothelial environment. Vascular endothelial primary cells exposed to HP components were tested in vitro for oxidative stress, cell activation and apoptosis. The infiltration of inflammatory cells into the vascular endothelium of animals infected with HP and exposed to a high-fat diet was observed in conjunction with an increased level of inflammatory markers systemically. The arteries of such animals were the least elastic, suggesting the role of HP in arterial stiffness. Soluble HP components induced transformation of macrophages to foam cells in vitro and influenced the endothelial life span, which was correlated with Collagen I upregulation. These preliminary results support the hypothesis that HP antigens act synergistically with a high-fat diet in the development of proatherogenic conditions.

Helicobacter pylori components increase the severity of metabolic syndrome and its hepatic manifestations induced by a high fat diet.

The metabolic syndrome, often accompanied by hepatic manifestations, is a high-risk factor for developing cardiovascular disease. Patients with metabolic dysfunction associated with steatohepatic disease (MASDL) are at significant risk of developing coronary artery disease. Atherosclerosis is a systemic inflammatory disorder in which several factors, including dietary or infectious factors, can cause an inflammatory response. Helicobacter pylori (HP) bacteria have been implicated in the progression of proatherogenic vascular endothelial lesions, moreover, our previous study in an experimental in vivo model of Cavia porcellus showed that HP components and high-fat substances acted synergistically in promoting vascular endothelial inflammation, leading to an early onset of a proatherogenic environment. In the present study, our goal was to determine the contribution of HP components to the development of hepatic manifestations of metabolic syndrome in an experimental model. Our results showed that HP infection in animals exposed to a high-fat diet increased oxidative stress and lipid peroxidation, followed by endothelial lipid deposition, impaired endothelial apoptosis, cell lysis, and increased vascular stiffness. Finally, histopathological analysis of liver tissue showed signs of MASLD development in HP-infected animals fed a high-fat diet.

Usefulness of extended holter ECG monitoring for serious arrhythmia detection in patients with heart failure and sleep apnea.

BACKGROUND: In patients with systolic heart failure (HF), coexisting sleep apnea may promote arrhythmia. Ambulatory Holter electrocardiogram (ECG) monitoring (AECG) is a method of arrhythmia and apnea evaluation. We hypothesized that 24-hour AECG in patients with HF who have a high risk of serious arrhythmia may be less accurate than AECG extended to 48 hours and that, moreover, arrhythmia may be related to apnea. METHODS: Eighty-four recordings of 48-hour AECG in 84 patients with ischemic HF (mean ejection fraction 34 ± 7%) were analyzed. Day 1, Day 2 were checked for ventricular tachycardia (VT) and supraventricular tachycardia (SVT). Estimated apnea-hypopnea index (est.AHI) was calculated using Holter, monitoring where est.AHI >15 indicates apnea. RESULTS: In 48-hour AECG, VT occurred in 34 patients (40.5%) whereas SVT in 17 patients (20.2%), and patients with est.AHI > 15 had higher VT occurrence. In two-sample one-sided test for proportions, 24-hour AECG from Day 1 showed a significantly lower percentage of patients with detected VT than 48-hour AECG-it was 23.8% (20 patients), meaning a significant underestimation with P = 0.0089. We assessed VT underestimation in the subgroups with regard to est.AHI, and found that it was present in Day 1 monitoring in the subgroups with est.AHI > 15. It was absent in the subgroups with est.AHI ≤ 15 and also in Day 2 monitoring. CONCLUSIONS: In patients with systolic HF, 24-hour AECG may have insufficient sensitivity regarding serious arrhythmia occurrence. If significant apnea was detected in the first day, extending the monitoring may be recommended.

Severe obesity impairs systolic and diastolic heart function - the significance of pulsed tissue Doppler, strain, and strain rate parameters.

BACKGROUND: We assessed the impact of morbid obesity on systolic and diastolic heart function in severely obese, but otherwise healthy subjects and age-matched controls. METHODS: Overall, 27 obese patients: 19 female (F) and 8 male (M) mean age 37 ± 9, mean body mass index (BMI) 46 ± 6 and 27 control subjects: mean age 36 ± 10, mean BMI 23 ± 3 were examined by transthoracic echocardiography, including tissue Doppler echocardiographic (TDE) assessment and speckle tracking echocardiography to measure left ventricular longitudinal, circumferential, and radial strain (S) and strain rate (SR) during systolic and early diastolic phase. RESULTS: Obese patients presented with enlargement of both ventricles and the left atrium, and thicker left ventricular wall. Although left ventricular ejection fraction (EF) as well as amplitude of tricuspid annulus plane systolic excursion (TAPSE) was similar, the amplitude of mitral annulus plane systolic excursion (MAPSE) and ventricular systolic and early diastolic velocities measured by TDE were significantly lower for both ventricles in the obese group. (RV S' 13 ± 3 cm/sec vs. 15 ± 2 cm/sec, P = 0.0057; LV S' lat 8.5 ± 1.6 cm/sec vs. 12.1 ± 2.8, P < 0.0001, E' lat: 12.4 ± 2.9 vs. 16.4 ± 3.5 cm/sec for left ventricular and E' 12 ± 3 cm/sec vs. 18 ± 4 for right ventricular velocities, P < 0.0001). Among the deformation parameters, systolic and diastolic circumferential and systolic radial strain and SR were decreased in the obese subjects, whereas longitudinal strain did not differ significantly. CONCLUSIONS: TDE parameters documented reduced systolic and diastolic function of both ventricles in obese patients. 2-dimensional speckle tracking analysis revealed that circumferential and radial but not longitudinal strain and SR were impaired in the obese group.

What Else Can AI See in a Digital ECG?

The electrocardiogram (ECG), considered by some diagnosticians of cardiovascular diseases to be a slightly anachronistic tool, has acquired a completely new face and importance thanks to its three modern features: the digital form of recording, its very frequent use, and the possibility of processing thousands of records by artificial intelligence (AI). In this review of the literature on this subject from the first 3 months of 2023, the use of many types of software for extracting new information from the ECG is described. These include, among others, natural language processing, backpropagation neural network and convolutional neural network. AI tools of this type allow physicians to achieve high accuracy not only in ECG-based predictions of the patient's age or sex but also of the abnormal structure of heart valves, abnormal electrical activity of the atria, distorted immune response after transplantation, good response to resynchronization therapy and an increased risk of sudden cardiac death. The attractiveness of the presented results lies in the simplicity of the examination by the staff, relatively low costs and even the possibility of performing the examination remotely. The twelve studies presented here are just a fraction of the novelties that the current year will bring.

Helicobacter pylori antigens as potential modulators of lymphocytes' cytotoxic activity.

Helicobacter pylori (H.p) colonizes human gastric mucosa and causes gastric and duodenal ulcer disease or gastric cancer. Various H.p compounds may modulate the host immune response in regards to tolerance of the infection or disease development. The aim of this study was to determine whether H.p lipopolysaccharide (LPS) and glycine acid extract antigens (GE) or E. coli LPS influence the cytotoxic activity of peripheral blood lymphocytes from H.p infected - H.p (+) or uninfected - H.p (-) individuals, in the presence or absence of exogenous interleukin (IL)12. Individual H.p status was defined by the urea breath test. Lymphocytes, stimulated or not with H.p, and control antigens, with or without IL-12, were used as effector cells and epithelial HeLa cells as targets. The cytotoxicity of lymphocytes was expressed as the percentage of dead target cells unable to reduce tetrazolium salt. The supernatants from HeLa/lymphocyte cultures were used for detection of the cellular cytotoxicity markers granzyme B and caspase 8. The natural cytotoxic activity of lymphocytes from H.p (+) was less than that of H.p (-) donors. This may have been due to fewer natural killer cells of CD3(-) CD56(+) Nkp46(+) phenotype in H.p (+) in comparison to H.p (-) subjects. H.p GE and standard E. coli LPS enhanced the cytotoxicity of lymphocytes towards target cells whereas H.p LPS downregulated this activity. The decrease in lymphocyte cytotoxicity in response to H.p LPS correlated with a lack of IL-2 and IL-12 production, inhibition of interferon-γ production, and low IL-10 secretion by mononuclear leukocytes. IL-12 significantly enhanced the natural as well as H.p LPS and H.p GE driven cytotoxic capacity of lymphocytes. In conclusion, H.p LPS may negatively modulate natural cytotoxic activity and cytokine secretion by immunocompetent cells and thus be involved in the maintenance of infection and development of gastric pathologies.

A systematic review of nonsynonymous single nucleotide polymorphisms in the renin-angiotensin-aldosterone system.

In this recent publication review the authors aimed to collect evidence of impact of nonsynonymous single nucleotide polymorphisms (nsSNP) in the renin-angiotensin-aldosterone system on patients' phenotype not only regarding arterial hypertension and its complications, but also the impact on other diseases of interest outside the field of cardiovascular medicine. PubMed database records published between 2017-2020 were searched and all positive case-control studies or positive studies with human DNA were selected. The search identified 104 articles, of which 22 were included on the basis of the inclusion criteria. This paper presents the impact of 44 nsSNPs in panels for genes of renin, angiotensinogen, angiotensin-converting enzyme, angiotensin receptor and aldosterone on the clinical picture of investigated cohorts or on the peptide-protein interactions as consequence of nsSNPs. Genetic variability in nsSNPs of the RAAS is involved in the pathogenesis of arterial hypertension and its complications, and surprisingly also in the pathogenesis of conditions not associated with elevated blood pressure, like neoplasms or inflammatory diseases.

Antibodies towards TVLLPVIFF Amino Acid Sequence of TNF Receptor Induced by Helicobacter pylori in Patients with Coronary Heart Disease.

BACKGROUND: Molecular mimicry between Helicobacter pylori (Hp) and the host components resulting in induction of cross-reacting antibodies has been suggested as accessory mechanism in the development of coronary heart disease (CHD). A potential target for antibodies induced during Hp infection by the components of these bacteria might be amino acid sequence TVLLPVIFF (P1) of tumor necrosis factor receptor (TNFR), which is exposed on vascular endothelium and immunocompetent cells, driving inflammation. AIM: To examine whether anti-P1 IgG are induced during Hp infection in CHD patients. METHODS: Sera from CHD patients infected with Hp (54) vs. sera of uninfected healthy donors (22) were tested by the ELISA for anti-H. pylori antibodies, anti-P1 IgG, and for antibodies towards control sequence IAKEGFEKIS (P2). Sera of Caviae porcellus infected experimentally with Hp (30) or uninfected (10) were included into this study. The same serum samples, which were positive for anti-P1 IgG, were adsorbed with Hp and then subjected to the ELISA. The biological activity of anti-P1 IgG was assessed in complement (C1q) binding assay. RESULTS: Sera of 43 CHD patients seropositive for anti-Hp IgG contained anti-P1 IgG binding C1q. Additionally, 10 serum samples of animals seropositive for anti-Hp IgG contained anti-P1 IgG. Anti-P1 IgG in tested sera were neutralized by their adsorption with Hp. CONCLUSION: In CHD patients infected with Hp, antibodies cross-reacting with TNFR common sequence are produced. Further studies are necessary to define immunogenic Hp determinants and to confirm possible cellular effects of cross-reacting antibodies.

Searching for serum biomarkers linking coronary heart disease and Helicobacter pylori infection using infrared spectroscopy and artificial neural networks.

Helicobacter pylori (Hp) Gram-negative bacteria cause gastritis or gastric ulcers. They may be involved in the development of systemic diseases i.e. coronary heart disease (CHD). Both Hp infection and CHD are related to inflammation accompanied by C-reactive protein (CRP), tumor necrosis factor alfa (TNF-α) and homocysteine. Low density lipoprotein (LDL) and triglicerides are a classic risk factors of CHD. Infrared spectroscopy has been introduced for monitoring chronic infections or endogenous disorders using specific absorption bands for biocomponents typed as diagnostic markers. In this study we selected specific motives of infrared radiation (IR) spectra for the sera from CHD patients infected with Hp. In total 141 sera were used: 90 from patients with CHD, all Hp positive, and 51 from healthy donors, 32 Hp negative and 21 Hp positive. Hp status was evaluated by anti-Hp IgG antibodies and/or 13C urea breath testing. IR spectra were measured using FT-IR/FT-NIR Spectrum 400 spectrometer (PerkinElmer) chemometrically analyzed using artificial neural networks and they showed differences in absorption bands corresponding to triglicerides, CRP, homocysteine, LDL and TNF-α, and selected component groups between CHD patients infected with Hp vs healthy uninfected donors (96.15% accuracy). Triglicerides and CRP were the best biomarkers linking Hp infection with CHD.

Flow-mediated skin fluorescence: A novel method for the estimation of sleep apnea risk in healthy persons and cardiac patients.

BACKGROUND: A pilot study revealed a relationship between the results of flow mediated skin fluorescence (FMSF) and of ECG-Holter-based estimated apnea/hypopnea index (eAHI) in asymptomatic individuals. The aim of this study was to test whether the results of FMSF show a relationship with the eAHI in patients with coronary artery disease or aortic stenosis. METHODS: Twenty-one patients (12 coronary disease, 9 aortic stenosis) and 37 healthy volunteers were included. FMSF was assessed before, during and after the pressure occlusion of the brachial artery, using a prototype device allowing the quantification of skin fluorescence. The values of FMSF expressed as baseline (BASE), maximum (MAX), and minimum (MIN) were analyzed. The percentages of ischemic response (IR) and hyperemic response (HR) were calculated. The eAHI was assessed from night ECG-Holter recordings. Differences between the groups and the relationships between the parameters were analyzed statistically. RESULTS: Mean ± standard deviation of BASE, MAX, MIN and IR were not significantly different in both groups (p > 0.05). HR was significantly lower in cardiac patients (14.7 ± 7.5 vs. 11.8 ± 5.1; p = 0.048), whose eAHI was significantly higher (11.0 ± 7.4 vs. 36.3 ± 16.5; p < 0.01). Negative correlation for MAX and eAHI was found in volunteers and patients: r = -0.38, p = 0.02 and r = -0.47, p = 0.03, respectively. In volunteers, HR had a negative correlation with eAHI: r = -0.34, p = 0.04. CONCLUSIONS: This pioneer study confirms that FMSF can be used to detect the negative correlation between MAX fluorescence and eAHI not only among healthy volunteers, but also among cardiac patients with coronary artery disease or aortic stenosis.

The prevalence and the prognostic value of microvolt T-wave alternans in patients with hypertrophic cardiomyopathy.

BACKGROUND: Nonsustained ventricular tachycardia (nVT) may have ominous implications for patients with hypertrophic cardiomyopathy (HCM). The microvolt T-wave alternans (TWA) has been proposed as a noninvasive tool-identifying patients at risk of sudden cardiac death and ventricular tachycardia/fibrillation (VT/VF). The aim of the study was to determine the significance of TWA in predicting nVT episodes and compare how other electrocardiographic parameters can predict the occurrence of nVT. METHODS: The study group consisted of 88 patients with HCM. TWA was assessed during exercise test using the CH2000 system. All patients underwent Holter monitoring (HM) within 2-4 weeks before TWA test (preexercise HM1) and immediately after (postexercise HM2). During HM, we analyzed: arrhythmias, QT intervals, the presence of late ventricular potentials (LP), heart rate variability, heart rate turbulence. RESULTS: Depending on TWA results, the patients were divided into two groups: TWA+; 46 patients (52.3%) with positive/indeterminate results, and TWA-; 42 patients (47.7%) with negative results. The nVT episodes were more frequent among TWA(+) both in HM1 and HM2. The presence of TWA increases the risk of postexercise nVT over twenty times (OR = 21.03). Moreover, in HM1, QTc and LP, and in HM2, again QTc and N-terminal precursor of brain natriuretic peptide proved to be significant predictors of nVT. The addition of TWA to the models did not improve the arrhythmia risk assessment. CONCLUSIONS: Repolarization abnormality plays an important role in generating nVT in patients with HCM, but TWA does not specifically predict the risk of arrhythmic end point.

Polymorphism of Interleukin-1 Gene Cluster in Polish Patients with Acute Coronary Syndrome.

BACKGROUND AND OBJECTIVES: Some experimental studies demonstrated adverse modulation of atherothrombosis by interleukin-1beta (IL-1b). To assess the relationship between the five most common variants of three polymorphisms of the IL1b gene cluster and the complexity of coronary atherosclerosis expressed in Gensini Score (GS), and the age of onset of the first acute coronary syndrome (ACS), we assessed the patients (pts) hospitalized due to ACS in this aspect. MATERIALS AND METHODS: 250 individuals were included. The single nucleotide polymorphisms of IL1b gene: transition T/C at -31 position, C/T at -511, and those of IL1 receptor antagonist gene (IL1RN)-variable number of tandem repeats allele 1, 2, 3, or 4-were determined by PCR. GS was calculated from the coronary angiogram performed at the index ACS. The impact of the presence of T or C and allele 1 to 4 at the investigated loci on the mean GS, GS greater than 40, mean age of onset of ACS, and the fraction of pts over 60 years of age at ACS were compared between the five most common genotype variants. RESULTS: The five most common variants were present in 203 pts (81.2%). Patients with pair 22 in ILRN had the lowest rate and those with pair 12 had the highest rate of ACS before 60 years of age (29.4 vs. 67.8%; p = 0.004). GS > 40 entailed an eight-fold increase of risk, as observed when pts with one T allele at locus -31 were compared with carriers of 2 or no T allele at this locus: OR 8.73 [CI95 4.26-70.99] p = 0.04. CONCLUSION: Interleukin-1 beta is subject to frequent genetic variability and our results show a potential relationship of this polymorphism with the extent of coronary atherosclerosis and age at the first ACS.

Repeatability of sleep apnea detection in 48-hour holter ECG monitoring.

BACKGROUND: There is a significant relationship between obstructive sleep apnea (OSA) and cardiovascular diseases. Reliability of new methods evaluating apnea in Holter ECG monitoring is still the matter of investigators' studies. METHODS: In 48-hour Holter ECG monitoring recordings of 63 patients, we assessed repeatability, comparing the results from both sleep periods. RESULTS: We found good repeatability in evaluation of apnea-hypopnea index value. There was moderate agreement in three categories, that is, normal or bordeline or apneic assignment. Assignment to "healthy" (normal and borderline) or apneic subgroup during consecutive sleep periods showed high repeatability. CONCLUSIONS: Holter ECG monitoring is a repetitive method of preliminary diagnosis in patients evaluated for sleep apnea syndrome.

Ivabradine as a heart rate-lowering agent in a patient with end-stage renal failure after heart transplantation.

A 56 year-old woman with a transplanted heart, with arterial hypertension and chronic pulmonary obstructive disease, was hospitalised because of palpitations, dyspnea, chest pain and oedema. After cyclosporine treatment she was diagnosed with renal failure, which was treated by hemodialysis. Heart rate (HR) at admission was 100, mean HR in 24-hour Holter monitoring was 106 bpm. Ivabradine was added to the treatment. The dose of 2.5 mg bid was doubled after three days. Mean HR in control Holter monitoring was 81. Ivabradine was well tolerated in this patient. The clinical benefits were observed soon after application and maintained during the follow-up.

Ankyrins in human health and disease - an update of recent experimental findings.

Ankyrins are adaptor molecules that in eukaryotic cells form complexes with ion channel proteins, cell adhesion and signalling molecules and components of the cytoskeleton. They play a pivotal role as scaffolding proteins, in the structural anchoring to the muscle membrane, in muscle development, neurogenesis and synapse formation. Dysfunction of ankyrins is implicated in numerous diseases such as hereditary spherocytosis, neurodegeneration of Purkinje cells, cardiac arrhythmia, Brugada syndrome, bipolar disorders and schizophrenia, congenital myopathies and congenital heart disease as well as cancers. Detecting either down- or over-expression of ankyrins and ergo their use as biomarkers can provide a new paradigm in the diagnosis of these diseases. This paper provides an outline of knowledge about the structure of ankyrins, and by making use of recent experimental research studies critically discusses their role in several health disorders. Moreover, therapeutic options utilizing engineered ankyrins, designed ankyrin repeat proteins (DARPins), are discussed.

Interleukin-1b and interleukin-1 receptor inhibitor gene cluster polymorphisms in patients with coronary artery disease after percutaneous angioplasty or coronary artery bypass grafting.

BACKGROUND: Pro-inflammatory cytokine interleukin-1b (IL-1b) plays a role in atherosclerosis. The results of several studies on the association between polymorphism of the IL-1b gene cluster and the course of coronary atherosclerosis have been inconclusive. AIM: To investigate retrospectively whether the patients with the most common variants of polymorphism of the IL-1b gene cluster differ with respect to localisation and extent of coronary atherosclerosis to a degree which may influence the treatment strategy. METHODS: Ninety-two consecutive out-patients (age 39-83, male sex 74%) with coronary artery disease confirmed by angiography were included. In this group, 23 patients underwent coronary artery bypass grafting (CABG) and 69 percutaneous coronary interventions (PCI) of whom in 16 repeated treatment was performed. The polymorphisms of the IL-1b gene - transition C/T at -511 and -31 position - as well as of the IL-1 receptor antagonist gene (IL-1RN) - an 86-base pair variable-number tandem repeat in intron 2 - were determined by PCR. Out of the 54 theoretically possible combinations of polymorphisms, 17 were found in the studied group. The three most common combinations of polymorphisms were selected. The fraction of patients treated by means of primary or elective percutaneous coronary intervention (pPCI, ePCI) and by means of CABG were compared between the subgroups with one of the 3 most common combinations of polymorphisms. RESULTS: The most frequent combinations of polymorphisms were - Variant A: -31 C/T, -511C/T, RN 1/1 - 32.6%; Variant B: -31T/T, -511C/C, RN 1/1 - 27.1%; Variant C: -31C/T, -11C/T, RN 1/2 - 10.8%. The remaining patients (29.5%) represented 14 variants present in very small subgroups consisting only of 1, 2 or 3 persons. Statistical analysis showed that patients with the second most common variant of studied polymorphisms (variant B) were significantly more frequently treated with CABG in comparison to the two other variants. Also, repeated PCI was most frequent in this subgroup. CONCLUSION: The data presented here suggest that carriers of the two relatively frequent variants of the IL-1b gene at -31 and -511 position, i.e. -31TT and -511CC, are at a higher risk of developing coronary artery disease requiring surgical treatment or two-stage percutaneous angioplasty.

The effects of intracoronary autologous mononuclear bone marrow cell transplantation on cardiac arrhythmia and heart rate variability.

BACKGROUND: The results of stem cell therapy after myocardial infarction (MI) have been conflicting. The effects of this therapy on ventricular arrhythmias and autonomic control of heart rate have not yet been established. AIM: To assess the effects of bone marrow cell (BMC) transplantation on the occurrence of arrhythmias and heart rate variability (HRV) parameters in short-term observation after ST-elevation myocardial infarction (STEMI). METHODS: Sixty patients with STEMI who underwent primary PCI, were randomly assigned to two groups: Group 1 - 36 patients selected for active treatment (autologous BMC, intracoronary injection mean 7 days after STEMI), and Group 2 - 24 control patients not treated with BMC transplantation. In all patients the infarct-related artery was the left anterior descending, and the left ventricular ejection fraction was < 40%. Two Holter sessions were performed: at baseline (HM1), on average 6 days after MI, and another one (HM2), 1 month after BMC implantation. From these recordings the frequency of non-sustained ventricular tachycardia (nsVT) episodes and the parameters of HRV were calculated. RESULTS: Both groups were comparable with regard to demographic data, the presence of risk factors and electrocardiographic parameters. In HM2 examination the frequency of nsVT tended to be higher in Group 1 (25 vs. 12.5%, NS). The HRV analysis showed lower HF and significant SDNN increase in the BMC group. In controls all the HRV parameters increased. The increase in HF was significantly lower in the BMC group than in controls (22.4 vs. 89.2 ms(2), p $lt 0.011). CONCLUSIONS: 1. During the first month after the intracoronary injection of BMC, non-significant increase of nsVT was observed. 2. The lack of significant increase in HF power after BMC infusion may be a sign of depressed parasympathetic tone.

Autoantibodies to a specific peptide epitope of human Hsp60 (ATVLA) with homology to Helicobacter pylori HspB in H. pylori-infected patients.

Helicobacter pylori (Hp) may initiate autoimmunity as a result of molecular mimicry. The aim of this study was to compare the level of IgG antibodies to a specific epitope (P1 peptide) of human heat shock protein (Hsp)60 homologous to Hp Hsp60 (HspB) in the sera of healthy donors (HD), patients with Hp-related gastritis or coronary heart disease (CHD), uninfected or with Hp infection confirmed by rapid urease test, histological examination (dyspeptic patients) the 13 C urea breath test (13 C UBT), and anti-Hp antibodies (healthy donors, CHD patients). The Anti-P1 IgG induction by Hp was verified by adsorption of sera with these bacteria and by experimental immunization of Caviae porcellus with Hp. Cytokine secretion by THP-1Blue™ monocytes in response to P1 was also assessed. Anti-P1 antibodies were detected in patients with gastritis or CHD infected with Hp and they were not found in uninfected individuals or asymptomatic carriers. No antibodies were raised against P2 in any group. Reduced cross-reactivity to P1 was exhibited by sera adsorbed with Hp. Caviae porcellus infected with Hp produced anti-P1 autoantibodies. THP-1XBlue™ monocytes responded to P1 by production of proinflammatory cytokines. Autoantibodies against P1 in Hp-positive patients with gastritis or CHD and upregulation of proinflammatory cytokines by P1 may contribute to the pathogenesis of Hp infection.

Quantitative assessment of the rotation and twist of the left ventricle during dobutamine stress echocardiography: a comparison of patients with and without significant coronary artery disease.

BACKGROUND: The rotation and twist of the left ventricle (LV) have been comprehensively evaluated at rest. However, little is known about rotational mechanics during dobutamine stress echocardiography (DSE). AIMS: We aimed to quantify and compare the basal and apical rotation and twist of the LV at rest as well as at the peak and recovery stages of DSE in patients with and without coronary artery disease (CAD). METHODS: We enrolled 91 patients, including 48 patients with CAD and 43 patients without CAD (mean [SD] age, 62 [9] years and 61 [10] years, respectively). Coronary artery disease was defined as the presence of stenoses of 50% or more in the left main coronary artery and/or stenoses of 70% or more in other epicardial arteries. Rotation was measured by 2­dimensional speckle­tracking echocardiography, and twist was calculated as the difference between the basal and apical rotation. RESULTS: Neither rotation nor twist differed between patients with and without CAD at rest, although apical rotation was significantly greater in the CAD group at peak DSE (mean [SD], 5.43° [3.45°] vs 3.71° [3.52°], P = 0.01) and at recovery (mean [SD], 5.05° [3.65°] vs 2.87° [2.73°], P <0.01). On the contrary, the absolute value for basal rotation at recovery was higher in patients without CAD (mean [SD], 3.87° [3.37°] vs 2.63° [2.43°], P = 0.03). In both groups, the rotation and twist did not change significantly during the dobutamine challenge. CONCLUSIONS: During DSE, we observed differences in LV rotation between patients with and without CAD, revealing the effect of ischemia on deformation parameters.