BACKGROUND: Inappropriate sinus tachycardia is most often treated with beta-blockers; in resistant cases, nonpharmacologic treatment has been attempted. Recent case reports have shown a favorable response to ivabradine in some patients. METHODS: A total of 13 patients (11 women, 2 men) aged from 27 to 66 years (mean 42 +/- 8) and having inappropriate sinus tachycardia were treated with ivabradine 15 mg per day. RESULTS: In 12 patients whose previous therapy could be discontinued or who did not have previous medication the mean daily heart rate decreased from 94.0 +/- 10.0 to 74.6 +/- 5.2 bpm (mean +/- SD) after ivabradine treatment. In 10 patients in whom we could reliably measure the highest and lowest daily heart rates, the highest rate decreased from 150.3 +/- 13.4 to 120.6 +/- 9.8 and the lowest from 66.7 +/- 9.6 to 54.8 +/- 6.9. All of the differences were statistically significant (P < 0.001). The percentage of heart rate reduction correlated with the initial heart rate (P < 0.005). The remaining patient, who had been treated with metoprolol 300 mg per day for more than 10 years and still had a resting heart rate of 106 bpm, switched to 15 mg of ivabradine daily without discontinuation of drug therapy. After this switch, a decrease of 4 bpm was noted in her mean daily heart rate. CONCLUSIONS: The results of our study show that patients with inappropriate sinus tachycardia can be successfully treated with ivabradine.

BACKGROUND: N-terminal pro-B-type natriuretic peptide (NT-proBNP) is increasingly used in the diagnosis and prognostic assessment of heart failure; however, the possible influence of atrial fibrillation on BNP is still a matter of controversy. We assessed the influence of atrial fibrillation on NT-proBNP levels in outpatients with signs and symptoms of heart failure. METHODS: Consecutive outpatients (n = 306) referred to a university hospital heart-failure clinic for evaluation of signs and symptoms of heart failure underwent clinical and echocardiographic assessment and had their NT-proBNP levels determined in a sandwich chemiluminescent immunoassay with two antibodies on an Elecsys analyzer. The influence of atrial fibrillation on NT-proBNP levels was assessed using a non-parsimonious linear regression model with propensity score adjustments to balance for possible confounders. RESULTS: Atrial fibrillation was associated with increased NT-proBNP levels in patients with (median concentration 1944 vs. 1390 pg/ml) and without (1093 vs. 172 pg/ml) underlying structural disease (P < 0.001). In a linear regression model with a propensity score, atrial fibrillation emerged as an independent determinant of NT-proBNP levels (P = 0.023), even after allowing for possible confounders (left ventricular ejection fraction and end-diastolic diameter, left atrial diameter, mitral insufficiency, age, sex, NYHA class or heart rate). CONCLUSIONS: Atrial fibrillation is an independent determinant of increased NT-proBNP levels. This association should be taken into account when NT-proBNP levels are used in the diagnosis of heart failure in patients with atrial fibrillation.

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

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

Heart failure is characterised by activation of haemostasis. We sought to explore the prognostic impact of deranged haemostasis in chronic heart failure. In stable, optimally managed outpatients with chronic heart failure, baseline levels of prothrombin fragment F1+2, D-dimer, and tPA and PAI-1 antigens were determined. Clinical follow-up was obtained and the rate of events (heart failure related deaths or hospitalisations) was recorded. We included 195 patients [32.3% female, NYHA class II (66.2%) or III (33.8%), mean age 71 years]. During a median follow up of 693 (interquartile range [IQR] 574-788) days, 63 (30.9%) patients experienced an event; those with an event had higher levels of tPA antigen (median 11.8 [IQR 8.7-14.0] vs. 9.4 [7.9-12.1] microg/l; p = 0.033) and D-dimer (938 [485-1269] vs. 620 [37-1076] microg/l; p = 0.018). However, on Cox multivariate analysis, only tPA levels above optimal cut-off value 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 = 0.017). Our findings suggest that elevated tPA antigen levels are an independent prognostic predictor in patients with chronic stable heart failure.

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

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

Background: The estimation of coronary risk based on consideration of classical risk factors is insufficient in young patients with myocardial infarction who have low expressions of classical risk factors. Endothelial dysfunction (ED) and markers of vascular inflammation may be more appropriate for risk estimation. The relations among ED and inflammation markers in such patients have not yet been explored. Patients and 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 measurement of the endothelium-dependent dilatation of the brachial artery. The following inflammation markers were measured: hsCRP, interleukin-6 (IL-6), tumour necrosis 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 < 0.05), and an increased level of IL-6 (3.2 [1.5-8.4] vs. 1.4 [0.9-2.3] ng/ml; p < 0.01). All other inflammation markers were comparable to controls. We found a significant negative correlation between ED and the levels of IL-6 (r =-0.54, p = 0.012). Conclusion: It appears that IL-6 is the most valuable circulating marker of ED, and consequently a useful marker of coronary risk. Copyright (c) 2007 S. Karger AG, Basel.

OBJECTIVE:: Androgenic progestins such as norethisterone acetate (NETA) may influence the effect of estradiol (E2) therapy. We compared the influence of oral E2, with and without NETA, and transdermal E2 on markers of coagulation, fibrinolysis, and inflammation and on lipids and lipoproteins in healthy postmenopausal women. DESIGN:: A total of 112 healthy postmenopausal women were randomized to receive treatment with either 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 < 0.05) and E2 with NETA (P < 0.01) shortened euglobulin clot lysis time. Oral E2 decreased plasminogen activator inhibitor-1 activity (P < 0.05). Oral E2 with NETA reduced plasminogen activator inhibitor-1 antigen levels (P < 0.01) and increased D-dimer antigen levels (P < 0.001). All three modes of menopausal hormone therapy reduced tissue type plasminogen activator antigen. Of the coagulation parameters, both routes of E2 therapy decreased fibrinogen levels (P = 0.002 for oral and P = 0.007 for transdermal E2), whereas E2 with NETA showed no effect. The decrease of fibrinogen was larger after oral E2 (P = 0.02). Oral E2 with NETA reduced antithrombin III (P < 0.001) and protein C (P < 0.001) activity. Oral E2 (P = 0.04) and E2 with NETA (P < 0.01) increased C-reactive protein (CRP). Transdermal E2 showed no influence on CRP. The addition of NETA influenced the change in CRP, as the increase in CRP was more pronounced after E2 without NETA (P = 0.005). The levels of serum amyloid A, interleukin-6, and tumor necrosis factor-alpha did not change significantly after any of the modes of hormone therapy. Of the lipids and lipoproteins, oral E2 decreased low-density lipoprotein cholesterol (P < 0.01), lipoprotein (a)(P < 0.05), and increased high-density lipoprotein cholesterol (P < 0.05). Transdermal E2 decreased triglycerides (P < 0.02) and increased high-density lipoprotein cholesterol (P < 0.03). Oral E2 with NETA decreased total cholesterol (P < 0.01) and high-density lipoprotein cholesterol (P < 0.005). CONCLUSIONS:: Oral E2, with or without NETA, produced no net activation of coagulation but improved fibrinolysis. Both modes of oral menopausal hormone therapy have a greater impact on markers of inflammation, coagulation, fibrinolysis, lipids, and lipoproteins than transdermal E2. NETA attenuates some E2 effects. Further studies are needed to elucidate the impact of these effects on clinical endpoints.

Background: Endothelial dysfunction and inflammation, in particular their lack of improvement after risk reduction, might better reflect advanced atherosclerosis than just the presence of risk factors. The aim of this study was to compare endothelial function and inflammatory parameters in high-risk patients who had no history of myocardial infarction and in patients in a stable phase after myocardial infarction. Methods: We 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 3). Results: Compared to patients with treated hyperlipidaemia, patients after myocardial infarction had lower values of total and LDL cholesterol (p = 0.015; 0.005) and homocysteine (p < 0.005), but marginally higher IL-6 levels (p = 0.1). Other measurements were comparable. However, flow-mediated dilation of the brachial artery was significantly diminished in patients after myocardial infarction (10.6 +/- 3.0; 5.9 +/- 4.0; 14.0 +/- 1.9% for Groups 1-3; ANOVA p = 0.0001; respectively). Conclusions: We found that patients with previous myocardial infarction have substantially lower endothelial function and increased some inflammatory parameters than patients with a similar level of atherosclerotic risk profile but without clinically evident coronary artery disease. Copyright (c) 2007 S. Karger AG, Basel.

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

Atropine is commonly a used pre anesthetic medication. A 22 year old black female with history of unexplained recurrent syncope during electrophysiology developed inducible ventricular arrhythmias when 0.5 mg of atropine was injected intravenously to improve this Wenckebach. There is a significant change in the autonomic influence on the heart prior to idiopathic ventricular tachycardia and this seems to result mainly from decreased vagal activity.

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

Cardiovascular emergencies are rare during pregnancy with an incidence of 0,2-4,0%. Emergencies include arrhythmias, acute coronary syndrome, peripartum cardiomyopathy and hypertensive disorders. Electrical DC-cardioversion with 50-100 Joules is indicated in the acute treatment of arrhythmias in all patients in an unstable hemodynamic state. If 100 J fails higher energies (up to 360 J) will be necessary. In stable supraventricular tachycardia intravenous adenosine is the first choice drug and may safely terminate the arrhythmia. Ventricular premature beats are frequently present during pregnancy and benign in most patients. However, life-threatening ventricular tachyarrhythmias (sustained ventricular tachycardia [VT], ventricular flutter [VFlt], ventricular fibrillation [VF]) were observed less frequently. Electrical DC-cardioversion is necessary in all pregnant women who are in a hemodynamically unstable state and have a life-threatening ventricular tachyarrhythmias.In hemodynamically stable pregnant women the initial therapy with ajmaline, procainamide or lidocaine is indicated. Implantation of a cardioverter-defibrillator is indicated in patients with syncope caused by VT, VF, VFlt or aborted sudden death.

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

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

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