[Novel mechanisms in the initiation and maintenance of atrial fibrillation: tailored individual treatment]. / Új felismerések a pitvarfibrilláció genezisében és fenntartásában: az egyénre szabott kezelés lehetoségei.

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.

A Simple Numerical Body Surface Mapping Parameter Signifies Successful Percutaneous Coronary Artery Intervention.

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.

Heritability of venous biomechanics.

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%). CONCLUSIONS: 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.

[Results of randomized studies on cardiac resynchronization therapy and the reevaluation of cardiac ventricular activation in left bundle branch block]. / A randomizált szívreszinkronizációs vizsgálatok eredményei és a bal-Tawara-szár-blokkos kamrai aktiváció újraértelmezése.

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.

Evidence for a strong genetic influence on carotid plaque characteristics: an international twin study.

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 mm2 in longitudinal plane; 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.

Heritability of non-alcoholic fatty liver disease and association with abnormal vascular parameters: a twin study.

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 < 0.001) and had a higher body mass index (BMI; 30.1 ± 5.2 vs. 24.6 ± 4.1 km/m(2) , P < 0.001) than non-NAFLD twins. Based on 91 same-sex twin pairs, heritability analysis indicated no discernible role for genetic components in the presence of NAFLD (95% confidence interval, 0.0-36.0%), while shared and unshared environmental effects accounted for 74.2% and 25.8% of variations adjusted for age and BMI. Augmentation indices and carotid IMT in twins with NAFLD were increased at most examined locations (P < 0.05-P < 0.001). CONCLUSION: These findings do not support heritability of NAFLD, although it coexists with vascular parameters linked to increased cardiovascular risk, underscoring the importance and value of prevention in this very common disorder.

Assessment of coronary artery calcification using dual-source computed tomography in adult asymptomatic patients with type 1 diabetes mellitus.

BACKGROUND: Experience with dual-source computed tomography (DSCT) for detecting coronary artery calcification (CAC) in patients with type 1 diabetes is limited. MATERIAL/METHODS: A non-contrast DSCT scan was acquired in 46 type 1 diabetic patients. All scans were suitable for evaluating CAC expressed in Agatston-scores (effective radiation dose 0.66 [0.59-0.81] mSv; median [interquartile range]). RESULTS: In 21 patients Agatston scores were > or =1 (range 1-2353), while 25 patients had no detectable calcium deposits in the coronary arteries. Patients with vs. without CAC had higher age (52 [44-59] vs. 41 [38-48] yrs; p=0.0045), longer duration of diabetes (25.3 [23.4-36.3] vs. 23.3 [15.7-30.4] yrs; p=0.0238), greater waist circumference (88 [77-98] vs. 79 [75-87] cm; p=0.0147) and BMI (26.7 [24.5-28.4] vs. 22.6 [21.7-25.6] kg/m(2); p=0.0109). Moreover, patients with vs. without detectable CAC had higher serum LDL-cholesterol (3.35 [3.15-3.53] vs. 2.92 [2.62-3.33] mmol/l; p=0.0069) and serum uric acid values (236 [191-266] vs. 200 [170-219] micromol/l; p=0.0437). Hypertension was more frequent (p=0.0144) in patients with than without CAC. The 2 subgroups did not differ in long-term average HbA1c values (7.97 [7.30-8.56] vs. 8.06 [7.24-9.05]%; p=0.7491); however, estimated insulin sensitivity (estimated glucose disposal rate) was lower in patients with vs. without detectable CAC (7.43 [5.73-8.58] vs. 9.24 [8.22-10.72] mg/kg/min; p=0.0017). CONCLUSIONS: Non-invasive detection of CAC is feasible with a low dose DSCT scan. CAC in type 1 diabetic patients is associated with cardiovascular risk factors rather than with long-term glycemic control.

Beat-to-beat interplay of heart rate, ventricular depolarization, and repolarization.

To improve malignant arrhythmia risk stratification, the causal and random components of spatiotemporal dynamics of heart rate (RR distances), ventricular depolarization sequence, and repolarization disparity were studied based on body surface potential map records taken for 5 minutes, in resting, supine position on 14 healthy subjects (age range, 20-65 years) and on 6 arrhythmia patients (age range, 59-70 years). Beat-to-beat QRS and QRST integral maps, Karhunen-Loève (KL) coefficients, RR, and nondipolarity index time series were computed. Tight relationship was found between RR and QRS integrals in healthy subjects with less association in arrhythmia patients. Tight KL-domain multiple linear association (r(2) > 0.72) was found between the QRS and QRST integral dynamics (ie, depolarization sequence and repolarization disparity). Beat-to-beat probability of the generation of significant nondipolarity index spikes was proportional to the QRST KL-component standard deviations (SD(i)) and inversely proportional with the mean dipolar KL components (M(i)) of the average QRST integral map.

Diagnostic value of body surface potential mapping in assessment of the coronary artery lesion after angina pectoris and without repolarization changes on the electrocardiogram.

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.

Analysis of platelet alpha2-adrenergic receptor activity in stable coronary artery disease patients on dual antiplatelet therapy.

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%, p < 0.001) 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%, p < 0.001). 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.

[New results in the research of the biomechanics of the venous system]. / Ujabb eredmények a vénás rendszer biomechanikájának kutatásában.

The upright posture of man had been a major evolutional challenge. The mechanisms responsible for orthostatic tolerance mostly affect the venous system. In this paper, we discuss new results regarding the biomechanics of the venous system highlighting a rather neglected field, the biomechanical properties of the vein wall. These properties change according to localization of veins, age, gender and body mass. The anti-gravitational adaptation of veins is a complex process involving all three layers of the venous wall. Local myogenic and humoral mechanisms as well as systemic hormonal and nervous influences control the adaptive processes in the veins. Long term adaptation involves structural and functional remodeling of the venous wall. Disorders of the veins mostly cause pathological remodeling. Hemodynamic factors (pressure and flow) together with inflammatory processes may lead to pathological alterations, changing the biomechanical properties of the vein wall, which further contribute to the reservation and progression of venous dysfunction. Appropriate testing of venous function can reveal biomechanical disorders even in clinically asymptomatic patients. Thus, biomechanical investigation of veins not only helps to understand the underlying pathomechanism but it also can contribute to early diagnosis and follow-up of venous disorders. When recognized in time, pathological remodeling can be prevented or treated. In this way, the incidence of venous disorder could be cut back reducing both human suffering and material loss.

Design and rationale for the Myocardial Stem Cell Administration After Acute Myocardial Infarction (MYSTAR) Study: a multicenter, prospective, randomized, single-blind trial comparing early and late intracoronary or combined (percutaneous intramyocardial and intracoronary) administration of nonselected autologous bone marrow cells to patients after acute myocardial infarction.

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.

Survival in cardiac resynchronization therapy. What do we know?

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 =or<35%. 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.

Inverse correlation between coronary blood flow velocity and sICAM-1 level observed in ischemic heart disease patients.

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.

Generalized changes in venous distensibility in postthrombotic patients.

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.

Alternative complement pathway activation during invasive coronary procedures in acute myocardial infarction and stable angina pectoris.

The effect of invasive percutaneous coronary procedures on complement activation has not been elucidated. We enrolled stable angina patients with elective percutaneous coronary intervention (SA-PCI, n=24), diagnostic coronary angiography (CA, n=52) and 23 patients with ST segment elevation myocardial infarction and primary PCI (STEMI-PCI). Complement activation products (C1rC1sC1inh, C3bBbP and SC5b-9) were measured on admission, 6 and 24h after coronary procedures. The alternative pathway product, C3bBbP significantly and reversibly increased 6h after elective PCI (baseline: 7.81AU/ml, 6h: 16.09AU/ml, 24h: 4.27AU/ml, p<0.01, n=23) and diagnostic angiography (baseline: 6.13AU/ml, 6h: 12.08AU/ml, 24h: 5.4AU/ml, p<0.01, n=52). Six hour C3bBbP values correlated with post-procedural CK, creatinine level and the applied contrast material volume (r=0.41, r=0.4, r=0.3, p<0.05, respectively). In STEMI-PCI, baseline C3bBbP level was higher, compared to SA-PCI or CA patients (11.33AU/ml vs. 7.81AU/ml or 6.13AU/ml, p<0.001). Similarly, the terminal complex (SC5b-9) level was already elevated at baseline compared to SA-PCI group (3.49AU/ml vs. 1.87AU/ml, p=0.011). Complement pathway products did not increase further after primary PCI. Elective coronary procedures induced transient alternative complement pathway activation, influenced by the applied contrast volume. In STEMI, the alternative complement pathway is promptly activated during the atherothrombotic event and PCI itself had no further detectable effect.

[Endothelial function and ischemic heart disease]. / Endothelfunkció és ischaemiás szívbetegség.

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.

Five-year outcomes of staged percutaneous coronary intervention in the SYNTAX study.

AIMS: The SYNTAX study compared PCI with TAXUS Express stents to CABG for the treatment of de novo 3-vessel and/or left main coronary disease. This study aimed to determine patient characteristics and five-year outcomes after a staged PCI strategy compared to single-session PCI. METHODS AND RESULTS: In the SYNTAX trial, staged procedures were discouraged but were allowed within 72 hours or, if renal insufficiency or contrast-induced nephropathy occurred, within 14 days (mean 9.8±18.1 days post initial procedure). A total of 125 (14%) patients underwent staged PCI. These patients had greater disease severity and/or required a more complex procedure. MACCE was significantly increased in staged patients (48.1% vs. 35.5%, p=0.004), as was the composite of death/stroke/MI (32.2% vs. 19%, p=0.0007). Individually, cardiac death and stroke occurred more frequently in the staged PCI group (p=0.03). Repeat revascularisation was significantly higher in staged patients (32.8% vs 24.8%, p=0.035), as was stent thrombosis (10.9% vs. 4.7%, p=0.005). CONCLUSIONS: There is a higher incidence of MACCE in patients undergoing staged compared to single-session PCI for 3-vessel and/or left main disease over the first five years of follow-up. However, these patients had more comorbidities and more diffuse disease.

Simple, quantitative body surface potential map parameters in the diagnosis of remote Q wave and non-Q wave myocardial infarction.

BACKGROUND: 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. OBJECTIVE: To identify quantitative body surface potential mapping parameters that could enable a computer-based diagnosis. METHODS: 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. RESULTS: 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. CONCLUSIONS: Time-shift and max/min are two new, simple, powerful parameters for infarction diagnosis and may also be suitable for automated, computer-based processing.

Ventricular tachycardia induced by a pacemaker lead.

The authors present a case of symptomatic non-sustained ventricular tachycardia induced by mechanical irritation of the outflow tract of the right ventricle by a loop in a permanent ventricular pacing lead. Reposition of the lead eliminated the rhythm disturbance.