We accessory report a patient with Wolff-Parkinson-White syndrome, in whom orthodromic atrioventricular reciprocating tachycardia directly passed over to atrioventricular nodal re-entrant tachycardia recurrences. during radiofrequency ablation of the accessory pathway. After the accessory pathway ablation, there were no tachycardia recurrences.

A this case of a patient with dual supraventricular tachycardias, atrioventricular nodal tachycardia, and atrial tachycardia is presented. The former was successfully 2009; ablated, whereas the latter was inducible after the ablation of the former, but without clinical importance during follow-up. However, this successfully tachycardia showed interesting characteristics, including dual atrioventricular Wenckebach periodicity, presumably due to multiple slow pathways.(PACE 2009; 1-2).

Heart p failure is characterised by activation of haemostasis. We sought to explore the prognostic impact of deranged haemostasis in chronic heart with failure. In stable, optimally managed outpatients with chronic heart failure, baseline levels of prothrombin fragment F1+2, D-dimer, and tPA and patients PAI-1 antigens were determined. Clinical follow-up was obtained and the rate of events (heart failure related deaths or hospitalisations) was failure. recorded. We included 195 patients [32.3% female, NYHA class II (66.2%) or III (33.8%), mean age 71 years]. During a tPA median follow up of 693 (interquartile range [IQR] 574-788) days, 63 (30.9%) patients experienced an event; those with an event of had higher levels of tPA antigen (median 11.8 [IQR 8.7-14. ] vs. 9.4 [7.9-12.1] microg/l; p = .033) and D-dimer (938 and [485-1269] vs. 620 [37-1076] microg/l; p = .018). However, on Cox multivariate analysis, only tPA levels above optimal cut-off value (938 of 10.2 microg/l (but not D-dimer) emerged as an independent predictor of prognosis (HR(adjusted) 2.695, 95% confidence interval 1.233-5.363; p p = .017). Our findings suggest that elevated tPA antigen levels are an independent prognostic predictor in patients with chronic stable We heart failure.

In significantly 41 young post myocardial infarction (MI) patients we investigated the relations between glomerular filtration rate (GFR) and markers of atherosclerosis:of flow-mediated dilation of the brachial artery (FMD), intima-media thickness (IMT) of the common carotid arteries and high sensitive C-reactive protein thickness (hsCRP). GFR was within normal values in all patients. Importantly, we found that GFR was significantly related to all three kidney. markers. Thus, our study supports the idea of the generalized nature of the atherosclerotic process and early involvement of the three kidney.

AIMS:with The aim of this retrospective analysis was to investigate VDD mode survival, development of atrial tachyarrhythmias (AT), and long-term atrial of sensing performance of VDD pacing systems. METHODS AND RESULTS: We implanted single-lead VDD pacemakers in patients with isolated atrioventricular block be and performed a retrospective analysis of 307 patients who had their devices implanted between May 1994 and September 2001. In AT. 39 patients (12.7%), the pacing mode had to be reprogrammed to a single-chamber ventricular pacing mode, mostly due to permanent follow-up AT. In 16 of these patients, the atrial sensing safety margin was less than 150%. The atrial sensing safety margin 1994 was insufficient, i.e. less than 100% in only seven patients. Although only 12 (3.9%) of the patients had a history a of paroxysmal AT at the time of pacemaker implantation, 200 (65%) patients presented with AT during follow-up. The mean AT implantation, burden at the last follow-up was 2.5%. CONCLUSION: These data illustrate that single-lead VDD pacemakers can be applied without serious AT complications in a highly selected group of patients. Our main concern is the development of AT in a large part had of our population. Over a 10-year period, two thirds of our patients presented with AT.

Background:increased The estimation of coronary risk based on consideration of classical risk factors is insufficient in young patients with myocardial infarction (c) who have low expressions of classical risk factors. Endothelial dysfunction (ED) and markers of vascular inflammation may be more appropriate low for risk estimation. The relations among ED and inflammation markers in such patients have not yet been explored. Patients and Basel. Methods: Twenty-one patients (on average 44 years old) in the stable phase after myocardial infarction, with low expressions of risk < factors, were included in the study. The control group consisted of 25 healthy age-matched males. ED was estimated by ultrasound Twenty-one measurement of the endothelium-dependent dilatation of the brachial artery. The following inflammation markers were measured: hsCRP, interleukin-6 (IL-6), tumour necrosis ED factor-alpha (TNF-alpha), ICAM-1, VCAM-1, selectin-P and selectin-E. Results: Patients had a significantly reduced level of endothelium-dependent vasodilatation (5.6 +/- 3.5 +/- vs. 8.8 +/- 6.5%, p < .05), and an increased level of IL-6 (3.2 [1.5-8.4] vs. 1.4 [ .9-2.3] ng/ml; p vasodilatation < .01). All other inflammation markers were comparable to controls. We found a significant negative correlation between ED and the infarction, levels of IL-6 (r =- .54, p = .012). Conclusion: It appears that IL-6 is the most valuable circulating marker is of ED, and consequently a useful marker of coronary risk. Copyright (c) 2007 S. Karger AG, Basel.

OBJECTIVE::change Androgenic progestins such as norethisterone acetate (NETA) may influence the effect of estradiol (E2) therapy. We compared the influence of needed oral E2, with and without NETA, and transdermal E2 on markers of coagulation, fibrinolysis, and inflammation and on lipids and .001). lipoproteins in healthy postmenopausal women. DESIGN:: A total of 112 healthy postmenopausal women were randomized to receive treatment with either clinical oral E2, with or without NETA, transdermal E2, or placebo. At baseline and after 28 weeks, levels of serum lipids < and lipoproteins and markers of coagulation, fibrinolysis, and inflammation were determined. RESULTS:: Of the fibrinolytic parameters, oral E2 (P <decreased .05) and E2 with NETA (P < .01) shortened euglobulin clot lysis time. Oral E2 decreased plasminogen activator inhibitor-1 activity inflammation (P < .05). Oral E2 with NETA reduced plasminogen activator inhibitor-1 antigen levels (P < .01) and increased D-dimer antigen of levels (P < .001). All three modes of menopausal hormone therapy reduced tissue type plasminogen activator antigen. Of the coagulation was parameters, both routes of E2 therapy decreased fibrinogen levels (P = .002 for oral and P = .007 for transdermal D-dimer E2), whereas E2 with NETA showed no effect. The decrease of fibrinogen was larger after oral E2 (P = .02).fibrinolysis. Oral E2 with NETA reduced antithrombin III (P < .001) and protein C (P < .001) activity. Oral E2 (P cholesterol = .04) and E2 with NETA (P < .01) increased C-reactive protein (CRP). Transdermal E2 showed no influence on CRP.activator The addition of NETA influenced the change in CRP, as the increase in CRP was more pronounced after E2 without fibrinolysis. NETA (P = .005). The levels of serum amyloid A, interleukin-6, and tumor necrosis factor-alpha did not change significantly after shortened any of the modes of hormone therapy. Of the lipids and lipoproteins, oral E2 decreased low-density lipoprotein cholesterol (P < .01) .01), lipoprotein (a)(P < .05), and increased high-density lipoprotein cholesterol (P < .05). Transdermal E2 decreased triglycerides (P <significantly .02) and increased high-density lipoprotein cholesterol (P < .03). Oral E2 with NETA decreased total cholesterol (P < .01) and elucidate high-density lipoprotein cholesterol (P < .005). CONCLUSIONS:: Oral E2, with or without NETA, produced no net activation of coagulation but A, improved fibrinolysis. Both modes of oral menopausal hormone therapy have a greater impact on markers of inflammation, coagulation, fibrinolysis, lipids,with and lipoproteins than transdermal E2. NETA attenuates some E2 effects. Further studies are needed to elucidate the impact of these decreased effects on clinical endpoints.

Background:was Endothelial dysfunction and inflammation, in particular their lack of improvement after risk reduction, might better reflect advanced atherosclerosis than just (c) the presence of risk factors. The aim of this study was to compare endothelial function and inflammatory parameters in high-risk (Group patients who had no history of myocardial infarction and in patients in a stable phase after myocardial infarction. Methods: We Basel. compared endothelial function of the brachial artery, measured using high-resolution ultrasound, in 45 patients with hyperlipidaemia (Group 1), and in +/- 45 patients in a stable period after myocardial infarction (Group 2). Forty-five healthy individuals served as a control group (Group endothelial 3). Results: Compared to patients with treated hyperlipidaemia, patients after myocardial infarction had lower values of total and LDL cholesterol myocardial (p = .015; .005) and homocysteine (p < .005), but marginally higher IL-6 levels (p = .1). Other measurements were flow-mediated comparable. However, flow-mediated dilation of the brachial artery was significantly diminished in patients after myocardial infarction (10.6 +/- 3. ; 5.9 = +/- 4. ; 14. +/- 1.9% for Groups 1-3; ANOVA p = .0001; respectively). Conclusions: We found that patients with previous patients myocardial infarction have substantially lower endothelial function and increased some inflammatory parameters than patients with a similar level of atherosclerotic patients risk profile but without clinically evident coronary artery disease. Copyright (c) 2007 S. Karger AG, Basel.

INTRODUCTION:in The aim of this study was to evaluate endothelial function in patients with primary antiphospholipid syndrome (PAPS). PATIENTS AND METHODS:and Flow mediated (FMD) and glyceryl trinitrate (GTN) induced dilation of the right brachial artery were studied in 25 patients with Mean PAPS and 25 controls matched by age, sex and conventional risk factors for atherosclerosis. Fibrinogen, D-dimer, adhesion molecules, tissue plasminogen patients. activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) antigens and activities were measured. RESULTS: Mean (SD) FMD was significantly lower in t-PA PAPS than in controls (8+/-5% vs. 15+/-6%, P< .001); GTN-induced dilation did not differ between the groups. There was a correlation plasminogen between the baseline diameter of the brachial artery and duration of the disease (- .56, P< .05) and between GTN induced dilation by and duration of the disease ( .51, P< .05). Concentrations of vascular cell adhesion molecule-1 (P< .001), intracellular adhesion molecule-1 (P< .001) and fibrinogen (P< .001) (P< .05) were higher in patients than in controls but no differences were observed for D-dimer, t-PA and PAI-1 antigens and adhesion activities. There was correlation between concentration of vascular cell adhesion molecule-1 and FMD (- .35, P< .05) and between intracellular adhesion molecule-1 measured. and FMD (- .41, P< .05). CONCLUSIONS: This study shows that endothelial function is impaired in patients with primary APS, possibly contributing shows to accelerated atherosclerosis and thromboembolic complications in these patients.

Rapid +/- atrial rates cause electrical, structural remodeling, and neuro-humoral changes. This study compares the effects of mechanical remodeling on plasma renin in activity (PRA) and atrial natriuretic peptide (ANP) secretion. Eight beagles were subjected to rapid atrial pacing (AP) at 400 beats/min Blood for 16 days. After complete recovery of left ventricular function, they underwent rapid ventricular pacing (VP) at 240 beats/min of AF. equal duration. Left atrial systolic maximal dimension (LAmax) and left atrial appendage (LAA) peak late emptying velocity (LAA-E) were assessed (1117.12 by echocardiography. Blood samples were taken from the right atrium and from the peripheral vein. LAmax after AP and VP dimension enlarged significantly (2.16 +/- .21 cm vs 2.41 +/- .23 cm, P = .002). Compared with baseline, LAA-E velocities were they significantly reduced ( .65 +/- .12 m/s vs .26 +/- .16 m/s, P = .001) after AP only. AP caused a peripheral significant elevation of PRA in right atrial (9.28 +/- 4.23 nmol/L per hour) and peripheral samples compared with baseline values (9.28 (4.82 +/- 2.53 nmol/L per hour, P = .04). ANP levels increased after AP (1117.12 +/- 252.21 fmol/L) with respect by to baseline values (824.37 +/- 159.08 fmol/L, P = .001). There was no difference in PRA and ANP levels between function atrial and peripheral samples. Atrial size and impaired systolic appendage function play an important role in secretion of PRA and in ANP. Both neuro-humoral pathways may be therapeutic targets in the treatment of patients with AF.

The to superior toxicity profile is one of the major reasons for the widespread use of gemcitabine in cancer treatment. Bone marrow resistant suppression is the most common side effect, while non-hematological events are relatively infrequent. Cardiac toxicity is a rare complication and is cardiac arrhythmia is even rarer. We report the case of a 67-year-old woman with metastatic breast cancer without a history therapy. of cardiac arrhythmia or ischemic heart disease who developed supraventricular tachycardia. The symptoms had started immediately after gemcitabine treatment. The by arrhythmia responded poorly to common treatment and was eventually controlled by oral propranolol five days after admission. The present case toxicity suggests that supraventricular tachycardia may be triggered by gemcitabine even without underlying significant heart disease and may be resistant to effect, conventional therapy.

Atropine the is commonly a used pre anesthetic medication. A 22 year old black female with history of unexplained recurrent syncope during vagal electrophysiology developed inducible ventricular arrhythmias when .5 mg of atropine was injected intravenously to improve this Wenckebach. There is a inducible significant change in the autonomic influence on the heart prior to idiopathic ventricular tachycardia and this seems to result mainly activity. from decreased vagal activity.

A graft 44 year-old woman was anaesthetised for a transplant nephrectomy. About 10 min after induction of anaesthesia she had several runs are of ventricular tachycardia followed by ventricular fibrillation requiring 30 s of cardiopulmonary resuscitation, after which she reverted to sinus rhythm.catheter Review of her chest X-ray, suggested that the haemodialysis catheter (Permcath) position may have precipitated this event. However, subsequent investigation toxic. found that she had toxic serum levels of sotalol, with a prolonged corrected QT interval on the electrocardiogram. She was commence started on sotalol while her renal graft was functioning well but it was not reviewed when the graft started to Review fail and she had to commence haemodialysis. This led to the accumulation of sotalol and explains her serum sotalol value of of 7.1 mg x l(-1) on the day of the event. Concentrations greater than 2.5 mg x l(-1) are generally not considered toxic.

Cardiovascular in emergencies are rare during pregnancy with an incidence of ,2-4, %. Emergencies include arrhythmias, acute coronary syndrome, peripartum cardiomyopathy and hypertensive VFlt disorders. Electrical DC-cardioversion with 50-100 Joules is indicated in the acute treatment of arrhythmias in all patients in an unstable In hemodynamic state. If 100 J fails higher energies (up to 360 J) will be necessary. In stable supraventricular tachycardia intravenous death. adenosine is the first choice drug and may safely terminate the arrhythmia. Ventricular premature beats are frequently present during pregnancy unstable and benign in most patients. However, life-threatening ventricular tachyarrhythmias (sustained ventricular tachycardia [VT], ventricular flutter [VFlt], ventricular fibrillation [VF]) were J observed less frequently. Electrical DC-cardioversion is necessary in all pregnant women who are in a hemodynamically unstable state and have arrhythmias a life-threatening ventricular tachyarrhythmias.In hemodynamically stable pregnant women the initial therapy with ajmaline, procainamide or lidocaine is indicated. Implantation of Electrical a cardioverter-defibrillator is indicated in patients with syncope caused by VT, VF, VFlt or aborted sudden death.

A In 17-year-old woman presented to the Emergency Department of our hospital following a suicide attempt. She reported having ingested 340 tablets a of caffeine, each of which contained 200mg of caffeine, about 3 hours earlier. Soon after arrival, her blood pressure dropped,Subsequently, and electrocardiography revealed sinus tachycardia and ventricular tachycardia (VT). Subsequently, she developed ventricular fibrillation (VF), and VF was resistant to strategy. pharmaceutical interventions and even to cardioversion. Therefore, we performed percutaneous cardiopulmonary support (PCPS). This resulted in disappearance of VF and without tachycardia, symptoms of caffeine poisoning, and improvement was observed 16 hours after the start of PCPS. In our case, caffeine dropped, poisoning symptoms disappeared without blood purification, after PCPS had stabilized her circulation. Based on our observations in this case, stabilization about of the circulation using PCPS in severe caffeine poisoning with VF, a potentially fatal arrhythmia, is a significantly beneficial strategy.the

A In clinical case of a patient aged 56 years with postinfarction left ventricular aneurysm not complicated with ventricular tachyarrhythmias is presented class electrophysiological investigation. Left ventricular aneurysmectomy supplemented with endocardial cryodestruction was carried out. At electrophysiological investigation after surgery ventricular tachycardia could Left not be induced. In 2 years postoperatively no ventricular tachyarrhythmias were noted. The condition of the patient is satisfactory, corresponds I. to NYHA class I.

Introduction.However, Hydrofluoric acid (HF) is a weak inorganic acid used for etching and as rust remover. Systemic toxicity is manifested as be ventricular dysrhythmias. The mechanisms for these dysrhythmias are not well elucidated. Case report. An 82-year-old woman ingested 8 ounces of ventricular 7% HF. Shortly after emergency department (ED) arrival, she became pulseless, developing recurrent ventricular dysrhythmias. She was defibrillated 17 times precipitous. and received several doses of calcium, magnesium, and lidocaine. After three hours, she returned to sustained NSR. She was discharged arrhythmias home after four days. Discussion. The electrocardiographic findings in this patient demonstrate hypocalcemia, which has been implicated as the culprit Shortly in HF-induced arrhythmias. However, despite correction of the hypocalcemia, the ventricular arrhythmias persisted. The proposed mechanisms of systemic HF toxicity report. and the relevant literature are discussed. Conclusion. Ventricular dysrhythmias due to HF toxicity seem to be independent of either hypocalcemia culprit or hyperkalemia. Systemic toxicity after ingestions may be delayed and precipitous.