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Abstract: Atrial fibrillation affects approximately three percent of the adults. Ablation strategies targeting the isolation of the pulmonary veins are the up-to-date cornerstones for atrial fibrillation ablations. However, a one-year success rate of repeated interventions is not more than 70%. Long-term efficacy of catheter ablation is presumably limited by electrical and structural remodeling of the atria, which results in a progressive increase in the duration of atrial fibrillation to become sustained. The potential pathophysiological importance of the epicardial adipose tissue, atrial fibrosis, autonomic nervous system and arrhythmogenic foci are documented by several studies. Increased volume, inflammation induced transformation to fibrosis and myocardial infiltration of atrial subepicardial fat in obese patients result in higher risk of atrial fibrillation development. Changes in atrial autonomic innervation under some conditions including regular physical exercise strongly promote arrhythmogenesis via the mechanism of enhanced triggered activity or abbreviated atrial refractoriness. Individualized management of possible trigger and substrate mechanisms are proposed to provide a novel basis for the effective treatment of atrial fibrillation. Pro-fibrotic signalling pathways can be inhibited by the suppression of renin-angiotensin-aldosterone system. Neuromodulation strategies include renal sympathetic denervation and ganglionic plexi ablation. Anticoagulation therapy has also been shown to reduce the burden of abnormal atrial remodeling. Possible novel catheter ablation techniques are used for right or left atrial linear lesions, scar homogenization and catheter ablation of complex fractionated atrial electrograms, rotors or ectopic foci. Beside these new management strategies, clinical consideration of factors of particular risks as obesity, hyperlipidaemia, hypertension, diabetes and obstructive sleep apnoe are also essential. Orv Hetil. 2018; 159(28): 1135–1145.

In patients with typical angina pectoris, inducible myocardial ischaemia and macroscopically normal coronaries (cardiac syndrome X (CSX)), a significantly elevated plasma level of terminal complement complex (TCC), the common end product of complement activation, has been observed without accompanying activation of the classical or the alternative pathways. Therefore, our aim was to clarify the role of the ficolin-lectin pathway in CSX. Eighteen patients with CSX, 37 stable angina patients with significant coronary stenosis (CHD) and 54 healthy volunteers (HC) were enrolled. Serum levels of ficolin-2 and ficolin-3, ficolin-3/MASP-2 complex and ficolin-3-mediated TCC deposition (FCN3-TCC) were determined. Plasma level of TCC was significantly higher in the CSX than in the HC or CHD group (5.45 versus 1.30 versus 2.04 AU/ml, P

Atrial fibrillation affects approximately three percent of the adults. Ablation strategies targeting the isolation of the pulmonary veins are the up-to-date cornerstones for atrial fibrillation ablations. However, a one-year success rate of repeated interventions is not more than 70%. Long-term efficacy of catheter ablation is presumably limited by electrical and structural remodeling of the atria, which results in a progressive increase in the duration of atrial fibrillation to become sustained. The potential pathophysiological importance of the epicardial adipose tissue, atrial fibrosis, autonomic nervous system and arrhythmogenic foci are documented by several studies. Increased volume, inflammation induced transformation to fibrosis and myocardial infiltration of atrial subepicardial fat in obese patients result in higher risk of atrial fibrillation development. Changes in atrial autonomic innervation under some conditions including regular physical exercise strongly promote arrhythmogenesis via the mechanism of enhanced triggered activity or abbreviated atrial refractoriness. Individualized management of possible trigger and substrate mechanisms are proposed to provide a novel basis for the effective treatment of atrial fibrillation. Pro-fibrotic signalling pathways can be inhibited by the suppression of renin-angiotensin-aldosterone system. Neuromodulation strategies include renal sympathetic denervation and ganglionic plexi ablation. Anticoagulation therapy has also been shown to reduce the burden of abnormal atrial remodeling. Possible novel catheter ablation techniques are used for right or left atrial linear lesions, scar homogenization and catheter ablation of complex fractionated atrial electrograms, rotors or ectopic foci. Beside these new management strategies, clinical consideration of factors of particular risks as obesity, hyperlipidaemia, hypertension, diabetes and obstructive sleep apnoe are also essential. Orv Hetil. 2018; 159(28): 1135-1145.Absztrakt: A pitvarfibrilláció prevalenciája a felnőttkorosztályban körülbelül három százalék. A ritmuskontroll céljából alkalmazott katéterablatiós terápia alapját jelenleg a pulmonalis vénák izolációja képezi, amelynek egyéves sikeraránya azonban többszöri beavatkozással sem emelhető 70% fölé. A beavatkozás hosszú távú eredményességét a pitvarokban bekövetkező elektromos és strukturális remodelláció korlátozza, amely az arrhythmia tartós fennmaradásához vezet. Az epicardialis zsírszöveti akkumuláció, a pitvari fibrosis, az autonóm idegrendszeri hatások, valamint a különféle arrhythmogen gócok lehetséges szerepét számos tanulmány elemezte. A pitvari epicardialis zsírszövet mennyisége, gyulladás indukálta fibroticus átalakulása és a myocardium zsíros infiltrációja, például obesitas esetén, pitvarfibrilláció fellépésére hajlamosít. Az autonóm szabályozás egyensúlyának megváltozása, például rendszeres sporttevékenység hatására, a triggerelt aktivitás fokozódása, valamint a pitvari refrakter periódus csökkenése révén indukálhat ritmuszavart. Hatékony terápia a lehetséges arrhythmogen trigger és szubsztrátmechanizmusok egyénre szabott komplex befolyásolása által valósulhat meg. A fibroticus folyamatok a renin-angiotenzin-aldoszteron rendszer gátlása révén lassíthatók. A neuromodulációs lehetőségek magukban foglalják a renalis denervációt, illetve a ganglionablatiót, és az antikoaguláns terápia pitvari remodellációt gátló hatásáról is ismertek adatok. A katéterablatiós beavatkozások lehetséges új irányait a jobb és bal pitvari lineáris laesiók alkalmazása, a heges területek homogenizálása mellett a komplex frakcionált pitvari elektrogramok, rotorok és az ectopiás fókuszok ablatiója képezik. Mindezek mellett kiemelt fontosságú a fennálló rizikófaktorok, úgymint obesitas, hyperlipidaemia, hypertonia, diabetes mellitus és obstruktív alvási apnoe hosszú távú, tervezett kezelése. Orv Hetil. 2018; 159(28): 1135–1145.

Objective: We examined the vascular system, from the microvasculature to the aorta, in diabetes mellitus, using non-invasive methods. Methods: We enrolled patients with type 1 diabetes: 17 patients without complications (DMW) and 19 patients with clinically manifest complications (DMC). Control group was represented by 34 healthy volunteers (C). We examined microvascular function with laser-Doppler flowmetry, using post-occlusive reactive hyperemia test and local heating. Arterial stiffness was studied by arteriograph, determining augmentation index and pulse wave velocity. We measured serum levels of sE-selectin and sICAM-1, markers of endothelial dysfunction. Results: Microvascular reactivity was significantly reduced in DMC-, and tendentiously in DMW groups. sE-selectin level was significantly higher in DMC group than in controls. Arterial stiffness was the highest in the DMC group and the lowest in the DMW group. Heart rate was significantly higher in both diabetic groups compared to controls. Time to maximum flow during PORH test tended to be the shortest in DMW group. Conclusions: Our results confirm impairment of the microvascular system in diabetic patients, even in early, uncomplicated stage of the disease, and might demonstrate diffuse hyperkinesis in the vascular system, resulting from the insulin effect or refering to the “vasodilation phase” of diabetes mellitus.

Background In coronary artery disease (CAD), body surface potential mapping (BSPM) may reveal minor electrical potential changes appearing in the depolarization phase even if pathological changes are absent on the conventional 12-lead ECG. We hypothesized that a simple BSPM parameter, Max/Min signifies successful percutaneous coronary intervention (PCI). Methods Ninety-two adult Caucasian patients with stable CAD and positive exercise test underwent coronary angiography. Seventy patients (age, 59 ± 8; 46 males) were revascularized by PCI (left anterior descending [LAD] in 38, right [RCA] in 17 and left circumflex [LCX] coronary artery in 15). Control groups contained 22 patients (age, 60 ± 8; 14 males) without intervention and 35 healthy subjects (age, 58 ± 2; 15 males). Left ventricular ejection fraction (LVEF, transthoracic echocardiography) and Max/Min BSPM parameter (63-lead Montreal system) were evaluated before and 4–40 days following coronary angiography. Max/Min was defined by the ratio of the highest maximum to the deepest minimum potential of all leads recorded by BSPM. Results Before PCI, Max/Min value of patients with LAD lesion (0.83 [0.74; 0.93]) was significantly lower while that with RCA lesion (1.63 [1.35; 1.99]) was significantly higher than that of healthy group (1.01 [0.970; 1.13]) (P < 0.05) and LVEF was significantly lower in LAD lesion (46.50% [43.00; 51.00]) than in the healthy group (55.00% [50.00; 58.75]) (P < 0.01). Max/Min value significantly increased from 0.83 [0.74; 0.93] to 0.92 [0.82; 0.99] (P < 0.01) following LAD PCI while significantly decreased from 1.63 [1.35; 1.98] to 1.35 [1.21; 1.43] (P < 0.01) post-RCA PCI. It did not vary significantly, however, either following LCX PCI or without intervention. LVEF significantly increased (from 46.50% [43.00; 51.00] to 49.00% [46.00; 51.00]) only after LAD PCI. Conclusion Max/Min parameter is suitable to follow patients after LAD and RCA PCI.

Summary Objective Multiple twin studies have demonstrated the heritability of anthropometric and metabolic traits. However, assessment of body composition parameters by bioimpedance analysis (BIA) has not been routinely performed in this setting. Design A cross-sectional study. Setting Study subjects were recruited and assessed at twin festivals or at major university hospitals in Italy, Hungary, and the United States to estimate the influence of genetic and environmental components on body composition parameters in a large, wide age range, international twin cohort by using bioelectrical impedance analysis. Subjects 380 adult twin pairs (230 monozygotic and 150 dizygotic pairs; male:female ratio, 68:32; age years 49.1±15.4; mean±standard deviation; age range 18–82) were included in the analysis. Results Heritability was calculated for weight (82%; 95% confidence interval [CI]: 78–85), waist and hip circumferences (74%; 95%CI: 68–79), body fat percentage (74%; 95%CI: 69–79), fat-free mass (74%; 95%CI: 69–79) and body mass index (79%; 95%CI: 74–83). The completely environmental model showed no impact of shared environmental effects on the variance, while unshared environmental effects were estimated as between 18% and 26%. Conclusions BIA findings provide additional evidence to the heritability of anthropometric attributes related to obesity and indicate the practical value of this simple method in supporting efforts to prevent obesity-related adverse health events.

The benefit of adjusted antiplatelet therapy in patients with myocardial infarction after primary percutaneous coronary intervention is not well elucidated. We aimed to identify patients with high on treatment platelet reactivity and to gradually adjust antiplatelet therapy. Materials and Methods We enrolled 133 acute myocardial infarction and 67 stable angina patients undergoing intracoronary stenting into our study. Maximal aggregation was determined with light transmission aggregometry. Aggregation > 50% induced by 5 μM ADP was indexed with high on-clopidogrel treatment platelet reactivity. In these cases 75 mg clopidogrel was doubled and control test was performed. Patients effectively inhibited with 150 mg clopidogrel were defined as clopidogrel pseudo non-responders. Patients with high platelet reactivity even on 150 mg clopidogrel were considered as clopidogrel real non-responders and were switched to ticlopidine. Results Aggregations (5ADP; p = 0.046) and the ratio of real non-responders (p = 0.013) were significantly higher in the myocardial infarction group. Most real non-responders were effectively treated with switch of therapy. The ratio of pseudo non-responders also tended to be higher in myocardial infarction. Platelet reactivity remained constant during follow-up; however, a new appearance of high platelet reactivity was observed at 6 and at 12 months. Conclusions Patients with acute myocardial infarction undergoing percutaneous coronary intervention may benefit from prospective platelet function testing, because of higher platelet reactivity and much higher ratio of clopidogrel real non-response. Switch of therapy may effectively overcome clopidogrel non-response. A new appearance of high platelet reactivity with unknown clinical significance is observed in both groups among the patients on clopidogrel.

Summary Background An association between reduced lung function and increased cardiovascular risk has been reported, but the underlying mechanisms are unknown. The aim of this study was to assess the heritability of lung function and to estimate its genetic association with arterial stiffness. Methods 150 monozygotic and 42 dizygotic healthy Hungarian and American Caucasian twin pairs (age 43 ± 17 years) underwent spirometry (forced vital capacity/FVC/, forced expiratory volume in 1 s/FEV 1 /; MIR Minispir, USA); and their brachial and central augmentation indices (AIx), and aortic pulse wave velocity (PWV) were measured by oscillometric Arteriograph (TensioMed Ltd, Budapest, Hungary). Phenotypic correlations and bivariate Cholesky decomposition models were applied. Results Age-, sex-, country- and smoking-adjusted heritability of FEV 1 , percent predicted FEV 1 , FVC and percent predicted FVC were 73% (95% confidence interval /CI/: 45–85%), 28% (95% CI: 0–67%), 68% (95% CI: 20–81%) and 45% (95% CI: 0–66%), respectively. Measured and percent predicted FVC and FEV 1 values showed no significant phenotypic correlations with AIx or aortic PWV, except for phenotypic twin correlations between measured FEV 1 , FVC with brachial or aortic augmentation indices which ranged between −0.12 and −0.17. No genetic covariance between lung function and arterial stiffness was found. Conclusions Lung function is heritable and the measured FVC and FEV are phenotypically, but not genetically, associated with augmentation index, a measure of wave reflection. This relationship may in turn reveal further associations leading to a better mechanistic understanding of vascular changes in various airway diseases.

Background Non-alcoholic fatty liver disease (NAFLD) has been linked to increased cardiovascular morbidity. However, genetic factors have an unclear role in this condition. Aims To analyse heritability of NAFLD and its association with abnormal vascular parameters in a large twin cohort. Methods Anthropometric and lipid metabolic parameters were obtained from 208 adult Hungarian twins (63 monozygotic and 41 dizygotic pairs; 58 men and 150 women; age 43.7 ± 16.7 years). B-mode ultrasonography was performed to detect steatosis and categorize severity. Brachial and aortic augmentation indices and aortic pulse wave velocity were assessed using oscillometry (TensioMed Arteriograph). Carotid intima media thickness (IMT) was measured using ultrasonography on the proximal common, distal common and internal carotid arteries. Results NAFLD was identified in 47 subjects (22.6%), of which 44 (93.6%) had mild and 3 (6.4%) had moderate steatosis. These subjects were older (age: 50.9 ± 14.3 vs. 41.5 ± 16.7 years, P

Background The body surface potential mapping (BSPM) method is sensitive in detecting minor electrical potential abnormalities, but its diagnostic value is unclear in detection and localization of significant coronary artery lesion (CAL) in patients after angina pectoris and without ischemic electrocardiogram abnormalities at the time of the BSPM record. Methods and Results Characteristic features and quantitative parameters of the isopotential maps during the depolarization were evaluated and compared with the result of coronary angiography in 228 patients (164 males; age, 61.6 ± 9.5 years). Twenty-three of them had their first angina, but the others had a history of earlier angina, unstable angina, non–ST-elevation infarction. Fifty-nine healthy subjects (32 males; age, 53.3 ± 12.2 years) served as control. The diagnostic power was high in detection of CAL among patients with previous ischemic events, but it was low in first angina. The accuracy of the CAL localization by multiple regression was different: at 90% specificity level, the sensitivity was near 80% for right/posterior descending CAL and slightly more than 60% for left anterior descending CAL but only 19% for first marginal/first diagonal CAL. Conclusions The BSPM changes during the depolarization could well indicate CAL only after previous ischemic events. Sensitivity and specificity of the CAL localization depended on the extension and location of the underlying myocardium damage.

Diagnostic accuracy of 64-slice CT angiography in the evaluation of in-stent restenosis is improved compared to previous CT methods. The image quality and exact diagnostic performance is, however, limited by several method, stent and patient-related factors. In this retrospective multicenter study the first results with dual source 64-slice scanner are presented in a Hungarian post PCI patient population (n=99). Radiation dose was 11.3±5.2 mSv (average±STD) using a helical scan. In 5.6% of all (n=142) examined stents clinicians were not able to give a final diagnosis using CT scan. This limitation showed correlation with the stent diameter. Nondiagnostic stents were smaller compared to the diagnostic stents (diameter 2.4±0.2 mm versus 3.2±0.5 mm, average±STD, respectively,P

Background Drug-eluting coronary stent implantation emerged as a safe and effective therapeutic approach by preventing coronary restenosis and reducing the need for further revascularization. However, in contrast to bare metal stents, recent data suggest a unique underlying pathology, namely late coronary stent thrombosis and delayed endothelial healing. Objective To report a case of very late coronary stent thrombosis (834 days after implantation) requiring repeat urgent target-vessel revascularization. Importantly, six days before the acute coronary event, combined nonsteroidal anti-inflammatory drug therapy was initiated. Results Although a dual antiplatelet regimen was continuously maintained, aggregation measurements indicated only partial antiplatelet effect, which returned to the expected range when nonsteroidal antiinflammatory drugs were omitted. Conclusions The observation indicates that, even 834 days after drug-eluting stent implantation, effective combined antiplatelet therapy might be crucial in certain individuals and the possible impact of drug interactions should not be underestimated. Further efforts should focus on the challenging task of identifying patients or medical situations with prolonged, increased risk of stent thrombosis.

Combined intracoronary and intramyocardial administration might improve outcomes for bone-marrow-derived stem cell therapy for acute myocardial infarction. In this paper patients with left ventricular ejection fraction less than 45% after acute myocardial infarction were randomly assigned stem cell delivery via intramyocardial injection and intracoronary infusion 3–6 weeks or 3–4 months after AMI. Their data shows that combined cardiac stem cell delivery induces a moderate but significant improvement in myocardial infarct size and left ventricular function. Background Combined intracoronary and intramyocardial administration might improve outcomes for bone-marrow-derived stem cell therapy for acute myocardial infarction (AMI). We compared the safety and feasibility of early and late delivery of stem cells with combined therapy approaches. Methods Patients with left ventricular ejection fraction less than 45% after AMI were randomly assigned stem cell delivery via intramyocardial injection and intracoronary infusion 3–6 weeks or 3–4 months after AMI. Primary end points were changes in infarct size and left ventricular ejection fraction 3 months after therapy. Results A total of 60 patients were treated. The mean changes in infarct size at 3 months were −3.5 ± 5.1% (95% CI −5.5% to −1.5%, P = 0.001) in the early group and −3.9 ± 5.6% (95% CI −6.1% to −1.6%, P = 0.002) in the late group, and changes in ejection fraction were 3.5 ± 5.6% (95% CI 1.3–5.6%, P = 0.003) and 3.4 ± 7.0% (95% CI 0.7–6.1%, P = 0.017), respectively. At 9–12 months after AMI, ejection fraction remained significantly higher than at baseline in both groups. In the early and late groups, a mean of 200.3 ± 68.7 × 106 and 194.8 ± 60.4 × 106 stem cells, respectively, were delivered to the myocardium, and 1.30 ± 0.68 × 109 and 1.29 ± 0.41 × 109 cells, respectively, were delivered into the artery. A high number of cells was required for significant improvements in the primary end points. Conclusions Combined cardiac stem cell delivery induces a moderate but significant improvement in myocardial infarct size and left ventricular function.

SummaryCombined antiplatelet therapy reduces recurrent atherothrombotic events in stable coronary disease patients; however, high residual platelet reactivity measured ex vivo still raises concerns as a condition related to treatment failure. Alpha-2 adrenoceptor enhances platelet reactivity and might contribute to this phenomenon. For the present study, 121 stable angina patients on standard dual antiplatelet therapy (75 mg clopidogrel and 100 mg acetylsalicylic acid) were recruited. Born aggregometry was performed with adenosine diphosphate (ADP),collagen and epnephrine. To verify platelet adrenergic activity, potentiation by low-dose epinephrine and inhibition by selective alpha-2 receptor blocker atipamezole were determined. To assess the P2Y12-specific residual activity, cangrelor was used. Plasma norepinephrine, soluble CD40-ligand, high-sensitivity-C-reactive protein (hsCRP) - and in 24 subjects platelet P-selectin positivity were measured. Epinephrine - at very low concentration (10-9g/ml) - significantly potentiates (1.25 µM ADP: 26.5% vs. 43%; 5 µM ADP: 53% vs. 64.5%; collagen: 17% vs 42%, p

Systemic factors and blood flow velocity related to atherosclerosis have been examined mainly separately or by in vitro studies. The aim of our study was to investigate the association between local coronary blood flow (corrected TIMI frame count, CTFC) and systemic atherosclerosis-related inflammatory parameters such as soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (Il-6), high sensitivity C-reactive protein (hsCRP) and von Willebrand factor (vWF) in humans. We enrolled the following groups of ischemic heart disease (IHD) patients: patients with coronary stenosis and stable (CAD, n = 96) or unstable angina (ACS, n = 27), patients with documented myocardial ischemia and normal coronary angiogram (NEG, n = 68). Patient groups showed only marginal differences in CTFC or sICAM-1 levels. In contrast, when IHD patients were studied individually, general positive correlation was found between CTFC and sICAM-1 level (r = 0.33; in NEG r = 0.25; in CAD r = 0.37; in ACS r = 0.61), being the strongest in ACS. The relation was independent from age, gender, BMI, smoking, hypertension, diabetes, previous myocardial infarction, family history of IHD, medication, hsCRP, IL-6 and vWF levels. (odds ratio, OR = 6.4; CI 95%: 2.43-16.84; p < 0.05). Nevertheless, correlation between CTFC and IL-6, hsCRP, vWF levels was not found. These results indicate inverse correlation between coronary blood flow and adhesion molecule production independently from conventional cardiovascular risk factors and inflammatory markers.

Reactive free radical and oxidant production leads to DNA damage during myocardial ischemia/reperfusion. Consequent overactivation of poly(ADP-ribose) polymerase (PARP) promotes cellular energy deficit and necrosis. We hypothesized that PARP is activated in circulating leukocytes in patients with myocardial infarction and reperfusion during primary percutaneous coronary intervention (PCI). In 15 patients with ST segment elevation acute myocardial infarction, before and after primary PCI and 24 and 96 h later, we determined serum hydrogen peroxide concentrations, plasma levels of the oxidative DNA adduct 8-hydroxy-2'-deoxyguanosine (8OHdG), tyrosine nitration, PARP activation, and translocation of apoptosis-inducing factor (AIF) in circulating leukocytes. Plasma 8OHdG levels and leukocyte tyrosine nitration were rapidly increased by PCI. Similarly, poly(ADP-ribose) content of the leukocytes increased in cells isolated just after PCI, indicating immediate PARP activation triggered by reperfusion of the myocardium. In contrast, serum hydrogen peroxide concentrations and the translocation of AIF gradually increased over time and were most pronounced at 96 h. Reperfusion-related oxidative/nitrosative stress triggers DNA damage, which leads to PARP activation in circulating leukocytes. Translocation of AIF and lipid peroxidation occurs at a later stage. These results represent the first direct demonstration of PARP activation in human myocardial infarction. Future work is required to test whether pharmacological inhibition of PARP may offer myocardial protection during primary PCI.

Introduction In situ biomechanical properties of peripheral large veins were compared between asymptomatic young patients who had previously unilateral femoro-popliteal deep venous thrombosis (DVT) and age-matched, healthy controls; the aim of this study was to assess local or generalized alterations of venous wall biomechanics in postthrombotic patients. Patients and methods Inner diameters of both common femoral veins, right axillary vein, and right internal jugular veins were measured in two directions by ultrasonography. Venous pressure was altered by posture changes (standing and lying) and by application of graded and controlled Valsalva. Ten postthrombotic young patients without any symptoms and 11 age-matched control subjects were included. Results In postthrombotic patients, both the affected and unaffected common femoral vein diameters and capacities were larger at low transmural pressures than those for the control group, but they demonstrated significantly less distensibility when higher pressures were applied. Similarly, in the internal jugular vein, capacity without Valsalva was significantly higher in postthrombotic patients and distensibility was reduced (statistically significant in the erect position). Pressure-induced changes in axillary vein diameter were negligible. Conclusions In situ diameter and capacity changes, and in situ distensibility of the femoral veins on both sides (i.e., the side of previous thrombosis as well as the disease-free side) and of the jugular veins are reduced in the young DVT patients compared to veins of the age-matched, healthy controls. The pathophysiological mechanism of generalized venous wall changes in these young DVT patients remains unknown.

The European Society of Cardiology (ESC) has published guidelines for the investigation of patients with suspected heart failure and, if the diagnosis is proven, their subsequent management. Hospitalisation provides a key point of care at which time diagnosis and treatment may be refined to improve outcome for a group of patients with a high morbidity and mortality. However, little international data exists to describe the features and management of such patients. Accordingly, the EuroHeart Failure survey was conducted to ascertain if appropriate tests were being performed with which to confirm or refute a diagnosis of heart failure and how this influenced subsequent management. Methods The survey screened consecutive deaths and discharges during 2000-2001 predominantly from medical wards over a 6-week period in 115 hospitals from 24 countries belonging to the ESC, to identify patients with known or suspected heart failure. Results A total of 46,788 deaths and discharges were screened from which 11,327 (24%) patients were enrolled with suspected or confirmed heart failure. Forty-seven percent of those enrolled were women. Fifty-one percent of women and 30% of men were aged >75 years. Eighty-three percent of patients had a diagnosis of heart failure made on or prior to the index admission. Heart failure was the principal reason for admission in 40%. The great majority of patients (>90%) had had an ECG, chest X-ray, haemoglobin and electrolytes measured as recommended in ESC guidelines, but only 66% had ever had an echocardiogram. Left ventricular ejection fraction had been measured in 57% of men and 41% of women, usually by echocardiography (84%) and was

BACKGROUND: In coronary artery disease (CAD), body surface potential mapping (BSPM) may reveal minor electrical potential changes appearing in the depolarization phase even if pathological changes are absent on the conventional 12‐lead ECG. We hypothesized that a simple BSPM parameter, Max/Min signifies successful percutaneous coronary intervention (PCI). METHODS: Ninety‐two adult Caucasian patients with stable CAD and positive exercise test underwent coronary angiography. Seventy patients (age, 59 ± 8; 46 males) were revascularized by PCI (left anterior descending [LAD] in 38, right [RCA] in 17 and left circumflex [LCX] coronary artery in 15). Control groups contained 22 patients (age, 60 ± 8; 14 males) without intervention and 35 healthy subjects (age, 58 ± 2; 15 males). Left ventricular ejection fraction (LVEF, transthoracic echocardiography) and Max/Min BSPM parameter (63‐lead Montreal system) were evaluated before and 4–40 days following coronary angiography. Max/Min was defined by the ratio of the highest maximum to the deepest minimum potential of all leads recorded by BSPM. RESULTS: Before PCI, Max/Min value of patients with LAD lesion (0.83 [0.74; 0.93]) was significantly lower while that with RCA lesion (1.63 [1.35; 1.99]) was significantly higher than that of healthy group (1.01 [0.970; 1.13]) (P < 0.05) and LVEF was significantly lower in LAD lesion (46.50% [43.00; 51.00]) than in the healthy group (55.00% [50.00; 58.75]) (P < 0.01). Max/Min value significantly increased from 0.83 [0.74; 0.93] to 0.92 [0.82; 0.99] (P < 0.01) following LAD PCI while significantly decreased from 1.63 [1.35; 1.98] to 1.35 [1.21; 1.43] (P < 0.01) post‐RCA PCI. It did not vary significantly, however, either following LCX PCI or without intervention. LVEF significantly increased (from 46.50% [43.00; 51.00] to 49.00% [46.00; 51.00]) only after LAD PCI. CONCLUSION: Max/Min parameter is suitable to follow patients after LAD and RCA PCI.

Background: The EUROHEART programme is a rolling programme of cardiovascular surveys among the member nations of the European Society of Cardiology (ESC). These surveys will provide information on the nature of cardiovascular disease and its management. This manuscript describes a survey into the nature and management of heart failure. Aims: The EuroHeart Failure survey aims to describe the quality of hospital care, diagnostic and therapeutic, for patients with suspected or confirmed heart failure in ESC member countries. Patients will be interviewed subsequent to hospital discharge to assess their understanding of their condition, side effects from and their compliance with therapy and their satisfaction with the management for heart failure. The quality of management will be judged against the recommendations contained in the ESC guidelines on diagnosis and treatment of heart failure. Outcome will be further assessed by repeat interviews in 6-12 months time. A further survey of heart failure in 2001/2002 is also planned. Methods: A prospective survey of all deaths and discharges from medical (cardiology, internal medicine and geriatric medicine) and cardiac surgical wards to identify patients with heart failure, suspected or confirmed. Approximately 70 hospital clusters, comprising two to six hospitals in each cluster, in 24 member countries of the ESC are conducting the study. At the time of writing, approximately 30000 deaths and discharges have been screened and approximately 4000 patients have been enrolled. Conclusions: The EuroHeart Survey will allow actual practice to be compared to ESC guidelines on the diagnosis and treatment of heart failure. The surveys and guidelines should prove mutually informative. The main EuroHeart Failure project will be completed by late 2000. However, new centres volunteering to participate in the study (contact corresponding author) may he accepted providing they have the necessary research personnel and provided funding can hi: agreed fur statistical support anti administration. (C) 2000 European Society of Cardiology. All rights reserved.

Survival improvement by beta-blocker treatment in patients with chronic heart failure appears to be related to the intermediate-term changes in left ventricular function. The therapeutic potential of beta blockade might be increased by early identification of patients in whom left ventricular function would deteriorate. We aimed at predicting the intermediate-term effect of bisoprolol on left ventricular systolic and diastolic function in patients with dilated cardiomyopathy. Twenty-five patients with symptomatic chronic heart failure treated with bisoprolol were investigated. As a background, tailored therapy with digitalis, diuretics and vasodilators was given. Prediction of the 6-month (intermediate-term) effect of bisoprolol was investigated, using baseline values and short-term (1-month) changes of simple, noninvasive parameters obtained at rest and during maximal exercise. Multivariate analysis resulted in reliable predictions, there was close correlation between the observed and predicted changes of left atrial filling pressure (R = 0.87) and left ventricular ejection fraction (R = 0.74). The baseline value of left ventricular ejection fraction, short-term changes of the pulse amplitude and the double product proved independent predictors of intermediate-term changes of left ventricular ejection fraction. The baseline value of mean pulmonary capillary wedge pressure, heart rate, and increase in heart rate during maximal exercise were predictors of the intermediate-term changes in mean pulmonary capillary wedge pressure. In dilated cardiomyopathy, the intermediate-term effects of bisoprolol on left ventricular ejection fraction and mean pulmonary capillary wedge pressure can be predicted reliably by simple noninvasive variables in the early treatment phase.

Atrial pacing (AP), despite its beneficial hemodynamic and antiarrhythmic effect, is still an underused mode of stimulation. The main purpose of this study was to evaluate the long-term results of AP. Sixty four patients (pts) with sinus node disease (28 male and 36 female: mean age 54.2; range: 44-88 years), 3.2% of the total implantation at our clinic were treated with AP between 1982-96. Criteria for atrial pacing were: no AV block in the history, no AV-block during carotid sinus massage, Wenckebach point130/min, left atrium50 mm, left ventricular EF40%. The indication for pacing was predominant sinus bradycardia (SB) in 34 pts and tachycardia-bradycardia syndrome (TBS) in 30 pts. Pts with TBS were on antiarrhythmic treatment, while most pts with SB received no antiarrhythmic drugs. All the pts were checked up at every 3-6 month. Sixty-two pts were followed for 3-154 (mean: 67) months, two pts were lost for follow-up. Repeated lead dislodgment occurred in two pts, which made a pacing mode change necessary. Four pts died during the follow-up period for non-cardiac reasons. At the end of the follow-up period the data of 60 pts were available for evaluation (33 pts with SB, 27 pts with TBS). All the pts with SB were in sinus rhythm, and no patient developed AV block by the end of the follow-up period. Seven out of 27 pts with TBS developed chronic atrial fibrillation, 3 out of them suffered a cerebral embolism; the remaining 20 pts were in sinus rhythm, and the number of paroxysmal attacks decreased significantly, which improved their quality of life significantly. Three pts in this group developed a temporary complete AV block, which regressed with decreasing the dosage of antiarrhythmic drugs. Atrial pacing is proved to be a safe and reliable treatment for sick sinus syndrome. Proper patient selection is crucial in preventing the development of AV conduction disturbance. Atrial stimulation had a satisfactory long-term antiarrhythmic effect in pts with sick sinus syndrome (SSS).

Nitric oxide has an important role in the development of the structure and function of the airways and vessel walls. Fractional exhaled nitric oxide (FE(NO)) is inversely related to the markers and risk factors of atherosclerosis. We aimed to estimate the relative contribution of genes and shared and non-shared environmental influences to variations and covariation of FE(NO) levels and the marker of elasticity function of arteries. Adult Caucasian twin pairs (n = 117) were recruited in Hungary, Italy and in the United States (83 monozygotic and 34 dizygotic pairs; age: 48 ± 16 SD years). FE(NO) was measured by an electrochemical sensor-based device. Pulse wave reflection (aortic augmentation index, Aix(ao)) was determined by an oscillometric method (Arteriograph). A bivariate Cholesky decomposition model was applied to investigate whether the heritabilities of FE(NO) and Aix(ao) were linked. Genetic effects accounted for 58% (95% confidence interval (CI): 42%, 71%) of the variation in FE(NO) with the remaining 42% (95%CI: 29%, 58%) due to non-shared environmental influences. A modest negative correlation was observed between FE(NO) and Aix(ao) (r = -0.17; 95%CI:-0.32,-0.02). FE(NO) showed a significant negative genetic correlation with Aix(ao) (r(g) = -0.25; 95%CI:-0.46,-0.02). Thus in humans, variations in FE(NO) are explained both by genetic and non-shared environmental effects. Covariance between FE(NO) and Aix(ao) is explained entirely by shared genetic factors. This is consistent with an overlap among the sets of genes involved in the expression of these phenotypes and provides a basis for further genetic studies on cardiovascular and respiratory diseases.

If New York Heart Association Class II-IV heart failure is present, and ejection fraction ≤35%, electrocardiographic QRS width ≥ 120 ms in the presence of left bundle branch block, cardiac resynchronization therapy is indicated. Reevaluation of the data of cardiac resynchronization trials and electrophysiologic findings in left bundle branch block provided evidence that "true" left bundle branch block requires a QRS width of ≥130 ms (in woman) and ≥140 ms (in man). In "true" left bundle branch block, after the 40th ms of the QRS notched/slurred R waves are characteristic in minimum two of I, aVL, V1, V2, V5 and V6 leads, in addition to a ≥40 ms increase of the QRS complex, as compared to the original QRS complex. In contrast, slowly and continuously widened "left bundle branch block like" QRS patterns are mostly occur in left ventricular hypertrophy or in a metabolic/infiltrative disease.A jelenleg érvényes irányelvek szerint szisztolés szívelégtelenség New York Heart Association II–IV. osztályaiban, ha a bal kamra ejekciós frakciója ≤35%, a QRS-komplexus ≥120 ms és az EKG bal-Tawara-szár-blokkot mutat, biventricularis pacemakerkezelés indikált. A szív reszinkronizációs kezelése és korábbi humán elektrofiziológiai és patológiai adatok újraértelmezése azt mutatja, hogy ha a bal-Tawara-szár-blokkban mért QRS szélessége ≤130 ms (nőkben), illetve ≤140 ms (férfiakban), nem beszélhetünk valódi bal-Tawara-szár-blokkról. Ez utóbbiban az aszinkrón balkamra-aktiváció jellemzője nőkben ≥130 ms, férfiakban ≥140 ms QRS-idő, a depolarizáció kezdetét40 ms-mal követő csomós, kettős megtöretést mutató R-hullám az I, aVL és V1, V2, V5 és V6 EKG-elvezetés közül legalább kettőben, a korábban dokumentált nem szárblokkos ingerületvezetéshez képest ≥40 ms késés, ami hirtelen jön létre. Lassan, folyamatosan szélesedő bal-Tawara-szár-blokk-„szerű” QRS-komplexus bal mellső hemiblokk és hypertrophia együttesére vagy metabolikus/infiltratív kóreredetre utal. Orv. Hetil., 2013, 154, 688–693.

Obesity, blood pressure and arterial stiffness are heritable traits interconnected to each other but their possible common genetic and environmental etiologies are unknown.We studied 228 monozygotic and 150 dizygotic twin pairs aged 18-82 years from Italy, Hungary and the United States, of which 45 monozygotic and 38 dizygotic pairs were discordant for body mass index (BMI; intrapair difference (Δ) in BMI ≥ 3 kg/m(2)). Blood pressure components and arterial stiffness were measured by TensioMed Arteriograph.Hypertension was more prevalent among obese than non-obese individuals (55% vs. 29%, p0.001). Age-, sex- and country-adjusted heritability estimates were high for hemodynamic measures (45%-58%) and BMI (78%). According to bivariate Cholesky decomposition, phenotypic correlations between BMI and blood pressure components (r = -0.15 to 0.24, p0.05) were largely explained by additive genetic factors (65%-77%) with the remaining explained by the unique environment. When controlling for genetic factors within all monozygotic pairs, ΔBMI was significantly correlated with Δbrachial systolic blood pressure (SBP) and diastolic blood pressure (DBP), Δmean arterial pressure, and Δaortic SBP (r = 0.15-0.17, p0.05). For the same measures, heavier co-twins of BMI-discordant monozygotic pairs had significantly higher values than their leaner counterparts (p0.05).Blood pressure components are moderately correlated with BMI, largely because of shared genetic factors. However, for the association of BMI with brachial SBP and DBP, aortic SBP and mean arterial pressure, acquired, modifiable factors were also found to be important.

Objective— Altered venous biomechanics may contribute to the pathogenesis of venous diseases, and their heritability is less known. Methods and Results— Seventy-eight monozygotic twin pairs (aged 42.4±16.8 years) and 24 same-sex dizygotic twin pairs (aged 50.5±16.1 years) were examined. Anteroposterior and mediolateral diameters of the common femoral vein were measured by ultrasonography. Measurements were made both in supine and in standing body positions, with or without controlled forced expiration (Valsalva test). High correlation of diameter, capacity, and distensibility values was found between twin pairs. The univariate heritability (A), shared (C), and unshared (E) environmental effects model has shown 39.3% genetic component of the variance of low pressure, 37.9% of high-pressure venous capacity, and 36.4% of maximal capacity changes, even after elimination of sex, age, and body weight effects. Bivariate Cholesky analysis revealed substantial covariance of inherited body weight and venous capacity components (57.0%–81.4%). Conclusion— Femoral vein capacity and elasticity depend ≈30% to 40% on genetic factors, and this value in the standing body position can reach 50%. A relatively high genetic covariance was found between weight and femoral vein capacity and elasticity. Our work might yield some new insights into the inheritance of venous diseases that are associated with altered venous biomechanics and help elucidate the involved genes.

Background and Purpose— Few family studies reported moderate genetic impact on the presence and scores of carotid plaques. However, the heritability of carotid plaque characteristics remains still unclear. Twin studies more reliably estimate the relative contribution of genes to these traits in contrast to family study design. Methods— One hundred ninety-two monozygotic and 83 dizygotic adult twin pairs (age 49±15 years) from Italy, Hungary, and the United States underwent B-mode and color Doppler ultrasound of bilateral common, internal, and external carotid arteries. Results— Age-, sex-, and country-adjusted heritability was 78% for the presence of carotid plaque (95% CI, 55%–90%), 74% for plaque echogenicity (hypoechoic, hyperechoic, or mixed; 95% CI, 38%–87%), 69% for plaque size (area in mm 2 in longitudinal plane; < or >50 percentile; 95% CI, 16%–86%), 74% for plaque sidedness (unilateral or bilateral; 95% CI, 25%–90%), 74% for plaque numerosity (95% CI, 26%–86%), 68% (95% CI, 40%–84%), and 66% (95% CI, 32%–90%) for the presence of plaque in carotid bulbs and proximal internal carotid arteries. No role of shared environmental factors was found. Unique environmental factors were responsible for the remaining variance (22%–34%). Controlling for relevant covariates did not change the results significantly. Conclusions— The heritability of ultrasound characteristics of carotid plaque is high. Unshared environmental effects account for a modest portion of the variance. Our findings should stimulate the search for genes responsible for these traits.

Central blood pressure and aortic stiffness have been consistently reported as strong cardiovascular risk factors. Twin studies by comparing identical with nonidentical twins produce information on the relative contribution of genes and environment.One hundred and fifty-four monozygotic (MZ) and 42 dizygotic (DZ) twin pairs (age 43 ± 17 years) from Hungary and the United States underwent brachial and central augmentation index (AIx), brachial and central pressure, and aortic pulse wave velocity (PWV) measurements with the invasively validated Arteriograph device. Bivariate Cholesky decomposition models were applied.Age-adjusted, sex-adjusted and country-adjusted heritability was 60.0% for central SBP [95% confidence interval (CI), 44.8-69.6%], 50.1% for aortic PWV (95%CI, 26.0-66.8%), 48.7% for aortic AIx (95%CI, 1.7-74.0%), 46.8% for brachial AIx (95%CI, 1.1-73.8%), 46.7% for central pulse pressure (PP) (95%CI, 12.4-61.4%), and 30.0% for brachial PP (95%CI, 0.0-53.4%). Central SBP and PP had strong bivariate correlations with brachial (r = 0.461 and 0.425) and central AIx (r = 0.457 and 0.419), as well as with aortic PWV (r = 0.341 and 0.292, all P0.001). Brachial PP had a weak correlation with brachial AIx (r = -0.118, P0.05), central AIx (r = -0.122, P0.05), and none with aortic PWV (r = 0.08, P = n.s.). Genetic factors explained a moderate phenotypic correlation between central PP, SBP, brachial SBP and aortic PWV.Central systolic and PPs, brachial PP, AIx, aortic PWV are moderately heritable. A moderate genetic covariance among aortic PWV and central PP, central SBP and brachial SBP was found.

Body surface QRS potentials were recorded with 63 chest leads in 20 patients with proximal single-vessel disease located on either the left anterior descending coronary artery (n = 10), the right coronary artery (n = 6), or the left circumflex coronary artery (n = 4) before, during, and after percutaneous transluminal coronary angioplasty. In each case, three consecutive inflations of relatively short duration (37 +/- 14 seconds) were carried out. Electrical activity was displayed as unipolar electrograms and body surface potential maps. The total QRS complex duration decreased in 14 of the 20 patients. Focal conduction disturbances were observed in six cases; all six had left anterior descending coronary artery occlusion and two were also accompanied by a clear shortening of the right epicardial breakthrough time. In these two cases, an initial activation loss seemed to be characteristic, whereas in the other four cases, a rather diffuse slowing of intraventricular conduction, especially during the terminal portion of the QRS, could be observed. Individual and group mean isointegral difference body surface potential maps (during-minus-before dilation) were considered valuable for the interpretation of localized changes in intraventricular conduction during percutaneous transluminal coronary angioplasty, and their individual variations could, at least partly, be explained by the presence or absence of collateral circulation. Two different hypotheses are suggested to account for the QRS complex shortening observed during short-term myocardial ischemic injury: (1) coronary artery occlusion delayed activation of the portion of the septal region that is normally activated early during the QRS, and/or (2) coronary artery occlusion increased the speed of propagation within the ventricles. Both of these hypotheses are discussed in light of earlier clinical and experimental results.

According to the literature, electrocardiographic signs of right ventricular hypertrophy have low sensitivity. The cause of this low sensitivity may be attributed to the original studies that were performed mostly in children with hypoplastic left ventricles or congenital heart abnormalities. In adulthood cases of normal or hypertrophic left ventricles, electrocardiographic right ventricular hypertrophy can only be detected during the late phase of ventricular depolarization. Two hundred four adult cardiac patients with complete noninvasive and invasive records were systematically studied by conventional and vectocardiographic methods. The terminal QRS (S wave) of the standard lead I has proved to be informative for detecting electrocardiographic signs in the presence of elevated right ventricular pressure. In cases of chronic right ventricular pressure overload (right ventricular hypertrophy) the terminal depolarization QRS vectors pointed posteriorly and to the right; therefore, a characteristic terminal S wave was represented in the standard lead I. If right and left ventricular hypertrophy were simultaneously present, the same resultant vectors pointed posteriorly and slightly to the left. In these cases, notching of the declining phase of the R wave was frequent, and a flatness of the terminal R wave portion was characteristic. The latter electrocardiographic sign has been called "simultaneous overloading of both ventricles" by the authors. The clinical utility of the new signs have also been proved by statistical methods.

This study describes the simulation of the more common types of conduction blocks with a computer model of the heart incorporating anisotropic propagation. The rationale was to test the model as to its ability to simulate these blocks by physiologically justifiable adjustments of the conduction system alone. The complete blocks were generated by simply blocking conduction totally at selected sites in the proximal conduction system, and the incomplete blocks by slowing down the conduction velocity in the proximal system. Also simulated were the left fascicular blocks and the bilateral blocks. All simulated electrocardiograms, vectorcardiograms, body surface potential maps, and epicardial isochrones for these blocks were similar to clinically observed data, with the exception of the left posterior hemiblock, which was slightly atypical. This could be because such blocks are usually accompanied by other cardiac pathologies not included in our simulations. The model also supports van Dam's observation that during left bundle branch block the passage of activation from right to left occurs via slow myocardial activation with no evidence of a local delay due to a septal barrier. Finally, the model suggests that a left bundle branch block with a normal frontal plane QRS axis may simply represent a case of an incomplete left bundle block, whereas one that exhibits a left axis QRS deviation in the frontal plane represents a more severe complete left bundle branch block.

The electrocardiographic diagnosis of significant coronary artery stenosis (CAD) is often based on the investigation of the left ventricular repolarization changes during exercise ECG stress test (EST). Our aim was to prove that the electric activity of the left atrium can indicate the ischemic damage of the left ventricle, and furthermore, it is able to indicate CAD without exercise.Patients with chest complaints but without evidence of acute coronary syndrome were investigated by EST and body surface potential mapping (BSPM, 63 leads). CAD was proven in 45 cases (32 men, years 40-76) and excluded in 50 cases (35 men, years 38-72) with coronary angiography. Left atrial electric potentials (EP-LA) before and after 0.08 mg sublingual nitroglycerine administration differed significantly (p0.001) in the two groups. According to Fischer linear discriminant analysis, this difference in % (EP-LA(d%)) was the best separating parameter: below limit of -14.17% (CAD prevalence was considered) this parameter predicted CAD with 93% sensitivity, 100% specificity,10 positive and 0.05 negative likelihood ratio (weighted for prevalence). The EST predicted CAD with 71% sensitivity, 78% specificity, 2.43 positive and 0.28 negative likelihood ratios.The electrical activity changes of the left atrium seemed to be suitable to predict CAD as an EST-alternative resting method.

Combined antiplatelet therapy reduces recurrent atherothrombotic events in stable coronary disease patients; however, high residual platelet reactivity measured ex vivo still raises concerns as a condition related to treatment failure. Alpha-2 adrenoceptor enhances platelet reactivity and might contribute to this phenomenon. For the present study, 121 stable angina patients on standard dual antiplatelet therapy (75 mg clopidogrel and 100 mg acetylsalicylic acid) were recruited. Born aggregometry was performed with adenosine diphosphate (ADP), collagen and epinephrine. To verify platelet adrenergic activity, potentiation by low-dose epinephrine and inhibition by selective alpha-2 receptor blocker atipamezole were determined. To assess the P2Y(12)-specific residual activity, cangrelor was used. Plasma norepinephrine, soluble CD40-ligand, high-sensitivity-C-reactive protein (hsCRP) - and in 24 subjects platelet P-selectin positivity were measured. Epinephrine - at very low concentration (10(-9)g/ml) - significantly potentiates (1.25 microM ADP: 26.5% vs. 43%; 5 microM ADP: 53% vs. 64.5%; collagen: 17% vs 42%, p0.001) while atipamezole inhibits ADP- and collagen-induced platelet aggregations (1.25 microM ADP: 26.5% vs. 23%; 5 microM ADP: 53% vs. 47%; collagen: 17% vs. 11%, p0.001). Patients with high adrenergic activity have significantly increased baseline ADP- and collagen-induced platelet aggregation. Based on cangrelor's efficacy, these patients have significantly more residual P2Y(12) activity as well. HsCRP and soluble CD40-ligand levels were similar. In conclusion, stable coronary heart disease patients with prominent adrenoceptor activity in vitro have significantly increased platelet aggregability and more functional P2Y(12) receptor, indicating poor inhibitory response to thienopyridines. Therefore, platelet adrenergic receptor represents a considerable, dynamic factor of high residual platelet reactivity and might contribute to cardiovascular events indicating failure of antiplatelet therapy.

Patients with moderate or severe heart failure often have some form of intraventricular conduction abnormality and increased QRS duration on the routine electrocardiogram. The most common pattern is the left bundle branch block, when the electrical activation of both ventricles is disturbed and the lateral wall of the left ventricle is significantly delayed. The use of cardiac pacing to coordinate the impaired electrical activation and myocardial contraction is called cardiac resynchronization therapy (CRT). Randomized trials of cardiac resynchronization were demonstrated to improve left ventricular systolic function, exercise tolerance, quality of life, and reduction in rehospitalization frequency of the patients. Resynchronization also prolongs survival in patients with NYHA Class III or IV heart failure and left ventricular ejection fraction =or35%. Recent developments using electro-anatomic mapping, contact and noncontact endocardial mapping have demonstrated that the correct positioning of the pacing electrodes provides better resynchronization and better response to CRT. Body surface potential mapping and noninvasive electrocardiographic imaging provide also a deeper insight into the mechanism of cardiac electrical depolarization and contributing to develop the selection method of best pacing sites for patients referred for CRT.

Background Percutaneous coronary intervention (PCI) is an important therapeutic strategy in patients with ischaemic heart disease. Our aim was to clarify the extent of endothelial injury induced by PCI in stable angina (SA) or in acute ST-elevation myocardial infarction (STEMI). Methods Circulating endothelial cell (CEC) count, von Willebrand factor (vWF) and soluble intercellular adhesion molecule-1 (sICAM-1) levels were determined pre-, post-, 24 and 96h after PCI in patients with SA ( n =23) and with STEMI ( n =28). To provide control data regarding the effect of angiography itself stable angina patients with coronarography only ( n =23) were enrolled. Results PCI and coronarography in stable angina patients caused measurable, but only non-significant elevation of CEC count and plasma vWF ( p =NS). In STEMI, significantly higher baseline CEC count ( p =0.019) and vWF plasma levels ( p =0.046) were found compared to SA with PCI/or coronarography. After PCI, explicit increase in CEC count was observed (significant peak at 24h) ( p =0.036). Positive correlation was found between baseline CKMB and CEC count at 24h ( r =0.51, p Conclusion Both coronary angiography and elective PCI cause only mild endothelial injury. However, in patients with STEMI, not only the procedure itself but myocardial ischemia and the ongoing atherothrombotic process might be responsible for the prolonged and more pronounced endothelial damage.

The authors present the case of a patient with symptomatic sinus bradycardia. Implantation of a rate responsive atrial pacemaker improved the exercise capacity of the patient, but exercise intolerance was still intermittently present. Only Holter monitoring could reveal the development of AAI, R pacemaker syndrome that led to the symptoms. Reprogramming of the pacemaker eliminated the phenomenon.

Background Previous data suggest that bone marrow–derived stem cells (BM-SCs) decrease the infarct size and beneficially affect the postinfarction remodeling. Methods The Myocardial Stem Cell Administration After Acute Myocardial Infarction Study is a multicenter, prospective, randomized, single-blind clinical trial designed to compare the early and late intracoronary or combined (percutaneous intramyocardial and intracoronary) administration of BM-SCs to patients after acute myocardial infarction (AMI) with reopened infarct-related artery. The primary end points are the changes in resting myocardial perfusion defect size and left ventricular ejection fraction (gated single photon emission computed tomography [SPECT] scintigraphy) 3 months after BM-SCs therapy. The secondary end points relate to evaluation of (1) the safety and feasibility of the application modes, (2) the changes in left ventricular wall motion score index (transthoracic echocardiography), (3) myocardial voltage and segmental wall motion (NOGA mapping), (4) left ventricular end-diastolic and end-systolic volumes (contrast ventriculography), and (5) the clinical symptoms (Canadian Cardiovascular Society [CCS] anina score and New York Heart Association [NYHA] functional class) at follow-up. Three hundred sixty patients are randomly assigned into 1 of 4 groups: group A, early treatment (21-42 days after AMI) with intracoronary injection; group B, early treatment with combined application; group C, late treatment (3 months after AMI) with intracoronary delivery; and group D, late treatment with combined administration of BM-SCs. Besides the BM-SCs therapy, the standardized treatment of AMI is applied in all patients. Conclusions The Myocardial Stem Cell Administration After Acute Myocardial Infarction Trial is the first randomized trial to investigate the effects of the combined (intramyocardial and intracoronary) and the intracoronary mode of delivery of BM-SCs therapy in the early and late periods after AMI.

The original hypothesis of the development of human atherosclerosis and ischemic heart disease called "response-to-injury" suggested the loss of integrity of the endothelium as the first step of the process. The recent version of this hypothesis emphasizes the term of endothelial dysfunction, that can be triggered by any of the well known cardiovascular risk factors. The atherosclerotic process, starting with endothelial dysfunction is a slow grade inflammatory process, promoting the oxidation of the low density lipoprotein molecules, activation of cell adhesion molecules as well as various ligands and cytokines, and activating immunological processes resulting in the development of unstable atherosclerotic plaque, followed by plaque rupture and formation of atherothrombotic lesions. Among the laboratory methods used for the detection of endothelial dysfunction, the flow mediated vasodilation (FMD) is increasingly known. A novel method is the laser Doppler flowmetry, still adapted to routine clinical tests. Clinical experiments are currently running with the coronarographic evaluation of intravascular flow velocity (slow coronary flow phenomenon), and also with the isolation and clinical evaluation of the circulating endothelial cells in patients with ischemic heart disease.

Body surface potential mapping has been shown to be a useful tool in the diagnosis and localization of remote non-Q wave and Q wave myocardial infarction, but human expertise is required to interpret the maps.To identify quantitative body surface potential mapping parameters that could enable a computer-based diagnosis.Body surface isopotential maps (63 unipolar leads) were recorded in 86 patients with remote Q wave and 71 patients with remote non-Q wave myocardial infarction. Twenty-four healthy adults served as control subjects. Myocardial infarctions were classified using standard electrocardiogram leads in the acute and chronic phases, and were validated by coronary angiography, ventriculography and thallium scintigraphy.Two simple quantitative parameters with high diagnostic power were identified: the time interval between the peak minimum and the peak maximum potentials (time-shift), and the ratio of these potentials (maximum to minimum ratio [max/min]). Both parameters showed significant differences between infarction patients and normal control subjects, and optimum cut-off values were determined using receiver operating characteristic curves (anterior infarction: time-shift of -4 ms or less, max/min of 0.6 or less; posterior infarction: time-shift of 8 ms or greater, max/min of 1.25 or greater). The sensitivities of the two parameters were 100% and 97%, and the specificities were 99% and 100%, respectively, in the anterior Q wave infarction group, compared with sensitivities of 88% and 100%, and specificities of 94% and 95%, respectively, in the posterior Q wave infarction group. In the anterior non-Q wave infarction group, sensitivity was 35% for both parameters, specificity was 100% for both parameters, and only infarctions associated with a low ejection fraction were detected, indicating that infarction size may influence the power of the tests.Time-shift and max/min are two new, simple, powerful parameters for infarction diagnosis and may also be suitable for automated, computer-based processing.

BACKGROUND: National surveys suggest that treatment of heart failure in daily practice differs from guidelines and is characterized by underuse of recommended medications. Accordingly, the Euro Heart Failure Survey was conducted to ascertain how patients hospitalized for heart failure are managed in Europe and if national variations occur in the treatment of this condition. METHODS: The survey screened discharge summaries of 11304 patients over a 6-week period in 115 hospitals from 24 countries belonging to the ESC to study their medical treatment. RESULTS: Diuretics (mainly loop diuretics) were prescribed in 86.9% followed by ACE inhibitors (61.8%), beta-blockers (36.9%), cardiac glycosides (35.7%), nitrates (32.1%), calcium channel blockers (21.2%) and spironolactone (20.5%). 44.6% of the population used four or more different drugs. Only 17.2% were under the combination of diuretic, ACE inhibitors and beta-blockers. Important local variations were found in the rate of prescription of ACE inhibitors and particularly beta-blockers. Daily dosage of ACE inhibitors and particularly of beta-blockers was on average below the recommended target dose. Modelling-analysis of the prescription of treatments indicated that the aetiology of heart failure, age, co-morbid factors and type of hospital ward influenced the rate of prescription. Age 70 years, in patients with respiratory disease and increased in cardiology wards, in ischaemic heart failure and in male subjects. Prescription of cardiac glycosides was significantly increased in patients with supraventricular tachycardia/atrial fibrillation. Finally, the rate of prescription of antithrombotic agents was increased in the presence of supraventricular arrhythmia, ischaemic heart disease, male subjects but was decreased in patients over 70. CONCLUSION: Our results suggest that the prescription of recommended medications including ACE inhibitors and beta-blockers remains limited and that the daily dosage remains low, particularly for beta-blockers. The survey also identifies several important factors including age, gender, type of hospital ward, co morbid factors which influence the prescription of heart failure medication at discharge.

Summary Background Heart failure is a prevalent condition that is generally treated in primary care. The aim of this study was to assess how primary-care physicians think that heart failure should be managed, how they implement their knowledge, and whether differences exist in practice between countries. Methods The survey was undertaken in 15 countries that had membership of the European Society of Cardiology (ESC) between Sept 1, 1999, and May 31, 2000. Primary-care physicians' knowledge and perceptions about the management of heart failure were assessed with a perception survey and how a representative sample of patients was managed with an actual practice survey. Findings 1363 physicians provided data for 11 062 patients, of whom 54% were older than 70 years and 45% were women. 82% of patients had had an echocardiogram but only 51% of these showed left ventricular systolic dysfunction. Ischaemic heart disease, hypertension, diabetes mellitus, atrial fibrillation, and major valve disease were all common. Physicians gave roughly equal priority to improvement of symptoms and prognosis. Most were aware of the benefits of ACE inhibitors and β blockers. 60% of patients were prescribed ACE inhibitors, 34% β blockers but only 20% received these drugs in combination. Doses given were about 50% of targets suggested in the ESC guidelines. If systolic dysfunction was documented, ACE inhibitors were more likely and β blockers less likely to be prescribed than when there was no evidence of systolic dysfunction. Interpretation Results from this survey suggest that most patients with heart failure are appropriately investigated, although this finding might be as a result of high rates of hospital admissions. However, treatment seems to be less than optimum, and there are substantial variations in practice between countries. The inconsistencies between physicians' knowledge and the treatment that they deliver suggests that improved organisation of care for heart failure is required.