bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modification of the circadian pattern of ventricular tachyarrhythmias by beta‐blocker therapy
Authors: Behrens Steffen , Ehlers Christoph , Brüggemann Thomas , Ziss Wolfgang , Dissmann Rüdiger , Galecka Miroslawa , Willich Stefan N. , Andresen Dietrich 
Published: February 2009

AbstractBackground: Sudden cardiac death exhibits a circadian variation and predominantly occurs during morning hours. Beta‐adrenergic antagonists have shown to blunt this morning peak. However, previous reports studying the effects of beta blockers on the circadian variation did not analyze the underlying cause of sudden cardiac death. It thus remains unclear whether ventricular tachyarrhythmias are influenced by beta‐blocker therapy.Hypothesis: This study tested the hypothesis that beta‐blocking agents blunt the morning peak of life‐threatening ventricular tachyarrhythmias.Methods: In 87 patients who were treated and monitored with an implantable cardioverter defibrillator, the circadian distribution of ventricular tachyarrhythmias terminated by appropriate shocks was analyzed and compared in those receiving beta blockers versus those not receiving beta‐blocker therapy.Results: Tachyarrhythmic episodes in the absence of beta‐blocker therapy (n = 344) exhibited a circadian variation with a distinct morning peak (16, 38, 28, and 18% of episodes at 0–6, 6–12, 12–18, and 18–24 h, respectively, p<0.001). In contrast, tachyarrhythmic episodes during beta‐blocker therapy (n = 104) were equally distributed over time (22, 27, 24, and 27% of episodes at 0–6, 6–12, 12–18, and 18–24 h, respectively, p = 0.95). The circadian distribution of episodes was significantly different in patients with and those without beta blockade (p<0.05).Conclusion: Beta‐adrenergic antagonists influence the circadian distribution of malignant ventricular tachyarrhythmias in patients with an implantable cardioverter defibrillator. The blunted morning peak of tachyarrhythmic events during beta blockade supports the hypothesis that a sympathetic surge is involved in the circadian pattern of malignant arrhythmias.
Erythrocyte magnesium and prostaglandin dynamics in chronic sleep deprivation
Authors: Tanabe Kazuhiko , Osada Naohiko , Suzuki Noriyuki , Nakayama Masaru , Yokoyama Yasuhiro , Yamamoto Akiko , Oya Misa , Murabayashi Taizo , Yamamoto Masanobu , Omiya Kazuto , Itoh Haruki , Murayama Masahiro 
Published: February 2009

AbstractBackground and hypothesis: The mechanism of sudden cardiac death occurring in patients with chronic fatigue is controversial. This study was designed to define a hypothesis that coronary arterial spasm and thrombus formation can occur during chronic fatigue.Methods: For evaluating the feasibility of coronary arterial spasm, erythrocyte magnesium (Mg) was measured. Blood coagulability was evaluated by the change of prostaglandin concentration. Subjects included 16 healthy male volunteers (mean age 21.6 ± 2.5 years). Test conditions were as follows: (A) control state: a day following a night of good sleep; (B) temporary sleep deprivation: a day preceded by < 3 h of sleep; (C) chronic sleep deprivation: a day preceded by a month during which sleep lasted < 60% of that in condition (A) above. The erythrocyte Mg concentration was measured by the atomic absorption method. The plasma concentration of thromboxane B2 and 6‐keto‐prostaglandin F1α were measured in eight subjects by radioimmunoassay method.Results: (1) Mean erythrocyte Mg concentration was significantly less in chronic sleep deprivation (1.1 ±0.4 mg/dl) than in the control state (1.8 ± 0.4 mg/dl, p<0.01) or in temporary sleep deprivation (1.6 ± 0.4, p<0.01). (2) The level of thromboxane B2 was significantly higher during chronic sleep deprivation than under control conditions (104.4 ± 78.0 vs. 20.4 ± 9.0 pg/ml, p<0.05). (3) There were no significant intergroup differences in 6‐keto‐prostaglandin F1α level.Conclusion: These findings could support the hypothesis that coronary arterial spasm and thrombus formation occur in chronic sleep deprivation.
A practical approach to torsade de pointes
Authors: Roden Dan M. 
Published: February 2009

AbstractThe term torsade de pointes refers to polymorphic ventricular tachycardia that occurs in the setting of an abnormally long QT interval. While the most common cause is treatment with QT prolonging drugs, torsade de pointes also occurs in the congenital long QT syndromes and in the setting of acquired heart block or severe electrolyte disturbance, notably hypokalemia. Among QT prolonging drugs that cause torsade de pointes, both antiarrhythmics and “noncardioactive” drugs have been recognized. The electrocardiographic features of torsade de pointes include labile QT intervals, prominent U waves, and a “pause‐dependent” onset of the arrhythmia. Treatment consists of recognition of the syndrome, correction of underlying electrolyte abnormalities, and withdrawal of any offending drugs. Magnesium, isoproterenol, or cardiac pacing provides specific antiarrhythmic therapy in torsade de pointes.
Atrial double potentials associated with a left‐sided accessory pathway having a single ventricular and two remote atrial insertions
Authors: Hluchy Jan , Lautermann Dirk , Sabin Georg V. 
Published: February 2009

AbstractThis paper reports the case of a 63‐year‐old female patient with Wolff‐Parkinson‐White syndrome who underwent an electrophysiologic study (EPS) and ablation using temperature‐guided radiofrequency current for atrial fibrillation with a shortest preexcited RR interval of 160 ms. Detailed EPS and mapping demonstrated an unusual, complex left‐sided accessory pathway, with the two distinct branches having two remote atrial insertions and a narrow common ventricular isthmus associated with the manifestation of atrial double potentials recorded from the coronary sinus. Simple ablation at the left lateral side from the ventricular aspect completely eliminated complex accessory pathway conduction, resulting in the disappearance of atrial double potentials.
Amiodarone in restoration and maintenance of sinus rhythm in patients with chronic atrial fibrillation after unsuccessful direct‐current cardioversion
Authors: Opolski Grzegorz , Stanislawska Jolanta , Górecki Aleksander , Świěcicka Grazyna , Kraska Tadeusz , Torbicki Adam 
Published: February 2009

AbstractBackground: When direct‐current (DC) cardioversion is used, sinus rhythm can be restored, at least temporarily, in 80–90% of patients with atrial fibrillation. However, there is a small but significant group of patients with chronic atrial fibrillation in whom DC cardioversion has failed to restore sinus rhythm. The value of antiarrhythmic drug pretreatment before DC cardioversion is still controversial.Hypothesis: The aim of our study was to assess (1) the effecti veness of repeat DC cardioversion in patients with chronic atrial fibrillation after pretreatment with amiodarone, and (2) the efficacy of amiodarone in maintaining sinus rhythm after repeat cardioversion.Methods: Forty‐nine patients with chronic atrial fibrillation after ineffective DC cardioversion were included in the study. Repeat DC cardioversion was performed after loading with oral amiodarone, 10–15 mg/kg body weight/day for a period necessary to achieve the cumulative dose of over 6.0 g.Results: Spontaneous conversion to sinus rhythm during amiodarone pretreatment was achieved in 9 of 49 patients (18%). Direct‐current cardioversion was performed in 39 patients and sinus rhythm was achieved in 23 of these patients (59%). Mean heart rate decreased from 95 beats/min before to 68 beats/min after DC cardioversion (p<0.001). Systolic blood pressure significantly (p<0.05) decreased from 126 ± 23 to 108 ± 25 mmHg. Complications occurring in four patients just after electroconversion were well tolerated and of short duration. After 12 months, 52% of patients maintained sinus rhythm on low dose (200 mg/day) amiodarone therapy.Conclusion: Pretreatment with amiodarone and repeat DC cardioversion allows for restoration of sinus rhythm in about 65% of patients with chronic atrial fibrillation after first ineffective DC cardioversion. Direct‐current cardioversion can be performed safely with the use of standard precautions in patients who are receiving amiodarone. At 12 months' follow‐up, more than 50% of patients maintain sinus rhythm on low‐dose amiodarone after successful repeat cardioversion.
Heart rate‐independent prolongation of QTc interval in women with syndrome X
Authors: Mammana Carmelo , Salomone Oscar A. , Kautzner Josef , Schwartzman Raúl A. , Kaski Juan Carlos 
Published: February 2009

AbstractBackground: Cardiac syndrome X is usually diagnosed in the presence of typical exertional chest pain, a positive response to exercise testing, and normal coronary angiograms. The underlying pathogenic mechanisms are speculative, but myocardial ischemia and increased sympathetic activity have been implicated.Hypothesis: The present study examined whether QTc interval is prolonged in women with syndrome X when confounding factors such as heart rate, gender, and environmental conditions are accounted for.Methods: Maximum QTc interval and its relationship to clinical and exercise variables were evaluated in 32 women with syndrome X (exertional chest pain, positive exercise testing, and completely normal coronary arteries) and 34 normal controls.Results: Patients with syndrome X had significantly longer QTc interval (440 ± 24 ms) than normal subjects (410 ± 26 ms, p<0.004). However, this QTc prolongation appears to be heart rate‐independent as patients with syndrome X showed longer QT and QTc intervals than controls despite an identical heart rate. No relation was found between QTc prolongation and clinical or exercise test variables in patients with syndrome X.Conclusion: Although increased sympathetic drive is present in syndrome X, and this variable is likely to modulate QTc duration, the mechanism and clinical implications of QTc interval prolongation in syndrome X remain speculative.
Plasma nitrite/nitrate level is inversely correlated with plasma low‐density lipoprotein cholesterol level
Authors: Tanaka Seiya , Yashiro Akira , Ikeda Masaharu , Kuroiwa Akio , Nakashima Yasuhide , Nanri Hiroki 
Published: February 2009

AbstractBackground: Plasma nitrite/nitrate (NOx) is a stable end product of the vasodilator nitric oxide (NO). However, there are few reports about plasma NOx levels in humans.Hypothesis: The purpose of this study was to assess the availability of plasma NOx for evaluating basal endogenously‐synthesized or endothelium‐derived NO, and to examine whether NOx levels are lowered in patients with coronary artery disease (CAD) or its risk factors.Methods: Plasma NOx levels were measured using an automated system based on the Griess reaction. NOx levels for a 24‐h period reproducibly became lowest at 6 A.M. in restricted healthy volunteers, and became stable in inpatient volunteers at 6 A.M. within 4 days after admission.Results: Based on these findings, NOx levels at 6 A.M. in inpatients can be considered as the basal levels. In 40 inpatients suspected of CAD (28 men, 12 women; mean age 60 ± 11 years), the basal levels of NOx were not related to CAD and its risk factors, except for hypercholesterolemia. The NOx level of patients with hypercholesterolemia was significantly lower than that of patients with normal cholesterol (n = 16, 34 ± 16 μmol/l vs. n = 24, 49 ± 23 μmol/l, p < 0.03). Furthermore, the NOx levels correlated negatively with the total cholesterol and low‐density lipoprotein cholesterol levels (r= –0.40, p < 0.01; r = –0.47, p < 0.003, respectively), but not with other lipid fraction levels.Conclusion: The results suggest that the quantity of basal endothelium‐derived NO synthesis may be decreased in the presence of hypercholesterolemia.
Long‐term management of atrial fibrillation
Authors: John Camm A. , Gallagher Mark M. , John Camm A. 
Published: February 2009

AbstractIn the past decade, catheter ablation techniques and implantable devices have revolutionized the treatment of ventricular arrhythmias, junctional arrhythmias, and atrial flutter. For most patients presenting with atrial fibrillation (AF), the treatment available today is similar to that used a century ago, although nonpharmacologic strategies of therapy have begun to emerge for selected cases. There have been important recent advances in our understanding of the pathophysiology of AF and its complications, and it may be possible to improve patient management by refinement of the way in which current drugs are used.
Effects of imidapril therapy on endogenous fibrinolysis in patients with recent myocardial infarction
Authors: Soejima Hirofumi , Ogawa Hisao , Yasue Hirofumi , Suefuji Hisakazu , Kaikita Koichi , Nishiyama Koichi 
Published: February 2009

AbstractBackground: Treatment with an angiotensin‐con verting enzyme (ACE) inhibitor in patients with myocardial infarction has been shown to modify endogenous fibrinolysis.Hypothesis: We investigated the effects of the ACE inhibitor imidapril on endogenous fibrinolysis in association with the serum ACE activity.Methods: In a randomized, double‐blind, placebo‐controlled study beginning 4 weeks after uncomplicated myocardial infarction, 15 patients received imidapril (5 mg daily) (imidapril group) and another 15 received placebo therapy (placebo group) for 4 weeks. Blood sampling was performed before the start of administration and on Days 3, 7, and 28 after the start of administration. Serum ACE activity and plasma fibrinolytic variables [plasminogen activator inhibitor (PAI) activity, plasminogen activator inhibitor type 1 (PAI‐1) antigen level, and tissue type plasminogen activator (TPA) antigen level] were measured.Results: There was no difference between the imidapril and placebo groups in serum ACE activity or plasma fibrinolytic variables before administration. Serum ACE activity decreased significantly on Days 3, 7, and 28 in the imidapril group. The decrease of PAI activity and PAI‐1 antigen levels was significantly less on Days 7 and 28, but not on Day 3. The TPA antigen level in the imidapril group was unchanged. None of the parameters in the placebo group was changed.Conclusion: The ACE inhibitor imidapril modified fibrinolysis, but the effects occurred after the inhibition of serum ACE activity.
Abnormal Q waves on the admission electrocardiogram of patients with first acute myocardial infarction: Prognostic implications
Authors: Birnbaum Yochai , Sclarovsky Samuel , Zlotikamien Bruria , Herz Izhak , Chetrit Angela , Olmer Liraz , Barbash Gabriel I. 
Published: February 2009

AbstractBackground: Q waves developed in the subacute and persisting into the chronic phase of myocardial infarction (MI) usually signify myocardial necrosis. However, the mechanism and significance of Q waves that appear very early in the course of acute MI (<6 h from onset of symptoms), especially if accompanied by ST elevation, are probably different.Hypothesis: This study assesses the prognostic implications of abnormal Q waves on admission in 2,370 patients with first acute MI treated with thrombolytic therapy <6 h of onset of symptoms.Results: Patients with abnormal Q waves in ≥2 leads with ST‐segment elevation (n = 923) were older than patients without early Q waves (n = 1,447) (60.6 ±11.9 vs. 58.8 ±11.9 years, respectively; p = 0.0003), and had a greater incidence of hypertension (34.3 vs. 30.5% p = 0.05) and anterior MI (60.6 vs. 41.1 % p<0.0001). Time from onset of symptoms to therapy was longer in patients with Q waves upon admission (208 ± 196 vs. 183 ± 230 min; p = 0.01). Peak serum creatine kinase (2235 ± 1544 vs. 1622 ± 1536 IU; p<0.0001), prevalence of heart failure during hospitalization (13.8 vs. 7.0%, p<0.0002), hospital mortality (8.0 vs. 4.6% p = 0.02), and cardiac mortality (6.6 vs. 4.5%, p = 0.11) were higher in patients with anterior MI and with abnormal Q waves than in those without abnormal Q waves upon admission. There was no difference in peak creatine kinase, prevalence of heart failure, in‐hospital mortality, and cardiac mortality between patients with and without abnormal Q waves in inferior MI. Multivariate regression analysis confirmed that mortality is independently associated with presence of Q waves on admission (odds ratio 1.61; 95% CI 1.04–2.49; p = 0.04 for all patients; odds ratio 1.65; 95% CI 0.97–2.83; p=0.09 for anterior wall MI.Conclusion: Abnormal Q waves on the admission electrocardiogram (ECG) are associated with higher peak creatine kinase, higher prevalence of heart failure, and increased mortality in patients with anterior MI. Abnormal Q waves on the admission ECG of patients with inferior MI are not associated with adverse prognosis.
The effect of iron overload in the hearts of patients with beta‐thalassemia
Authors: Brili Stella V. , Castelanos Stamatis S. , Aggeli Constadina J. , Tentolouris Costas A. , Pitsavos Christos E. , Toutouzas Pavlos K. , Tzonou Anastasia I. 
Published: February 2009

AbstractBackground and hypothesis: An important complication of beta‐thalassemia is iron deposition in cardiac tissues resulting in fibrosis and dysfunction. Our aim was the investigation of the possible clinical effect of iron loading in the heart of patients with beta‐thalassemia prior to the appearance of symptoms of depressed systolic function.Methods: Thirty‐five patients with beta‐thalassemia, of whom 24 had the major type (Group 1) and 11 had the intermedia type (Group 2) were studied. Eleven age‐ and gender‐matched controls were also studied (Group 3). All patients were evaluated echocardiographically and were shown to have normal left ventricular systolic function and dimensions. Serum ferritin, atrial natriuretic peptide (ANP), left atrial diameter (LAD), peak early mitral inflow velocity (E), peak late mitral inflow velocity (A), E/A ratio, deceleration time of the mitral inflow E wave (DT), and isovolumic relaxation time (IVRT) were measured.Results: Univariate analysis showed that both groups of patients had similarly increased LAD and ANP plasma levels. Group 1 had a higher E/A ratio (2.27 ± 0.88) SS than Group 2 (1.69 ± 0.47, p = 0.05) and Group 3(1.50 ± 0.38, p = 0.01). Serum ferritin was significantly higher in Group 1 (3.526 ± 0.352) than in Group 2 (2.808 ± 0.288, p < 10–5) and Group 3 (2.139 ± 0.124, p<10–5). Multivariate analysis showed that ANP is a factor that is affected by the LAD and E/A ratio and that serum ferritin levels affect the LAD and E/A ratio.Conclusions: Although LAD and ANP levels are increased in patients with beta‐thalassemia, the increased serum ferritin levels of patients seem to affect left atrial size and E/A ratio. ANP secretion is consecutively affected by these factors.
Left atrial size is the major predictor of cardiac death and overall clinical outcome in patients with dilated cardiomyopathy: A long‐term follow‐up study
Authors: Modena Maria Grazia , Muia Nicola , Sgura Fabio Alfredo , Molinari Rosella , Castelli Annadele , Rossi Rosario 
Published: February 2009

AbstractHypothesis: This study was undertaken to determine whether echo‐derived left atrial dimension and other echocardiographic, clinical, and hemodynamic parameters detected at the time of entry into the study may influence prognosis in patients with dilated cardiomyopathy during a long‐term follow‐up.Methods: This was a prospective cohort analysis of 123 patients with dilated cardiomyopathy. Clinical evaluation, chest x‐ray, M‐mode and two‐dimensional echocardiogram, exercise test, 72‐h ambulatory electrocardiogram monitoring, and cardiac catheterization study were performed in all patients. The study was divided into two phases: in the first phase, patients were divided into two groups according to the left atrial size (≥45 mm; <45 mm), with cardiac death as the end point. In the second phase, all patients were further divided into two groups according to their clinical course. A multivariate analysis was performed to determine independent correlated parameters of cardiac mortality and overall clinical outcome.Results: Cardiac mortality rate was 47.9%: 29% in the group without left atrial dilation and 54.3% in the group with dilated left atrium. Multivariate analysis revealed that left atrium ≥45 mm, New York Heart Association functional classes III/IV, and the presence of one or more episodes of ventricular tachycardia at Holter monitoring were independent predictors of cardiac mortality, while left atrium ≥45 mm, left ventricular end‐diastolic pressure >17 mmHg, and exercise tolerance ≤ 15 min were independent predictors of poor clinical outcome.Conclusions: Our results revealed that left atrial size is the principal independent predictor of prognosis in patients with dilated cardiomyopathy in that patients with left atrial dilation had an increase in mortality and a worse clinical outcome compared with those without left atrial dilation.
Antihypertensive effects of mibefradil: A double‐blind comparison with diltiazem CD
Authors: Massie Barry M. , Chrysant Steven G , Jain Adesh , Weir Matthew , Weiss Robert , Kobrin Isaac 
Published: February 2009

AbstractBackground and hypothesis: Mibefradil is the first compound of a new class of calcium antagonists with a unique chemical structure and mechanism of action. This trial compared mibefradil with diltiazem CD, a widely prescribed calcium antagonist for the treatment of hypertension.Methods: In all, 201 patients with uncomplicated, mild‐to‐moderate essential hypertension with a baseline sitting diastolic blood pressure (SDBP) of ≥95 and ≤ 114 mmHg were evenly randomized to receive either mibefradil (100 mg) or diltiazem CD (360 mg) daily for 12 weeks. To determine whether antihypertensive effects persisted after 12 weeks, patients then entered a 4‐week withdrawal period during which they remained on active treatment or were switched to placebo.Results: Efficacy variables were the changes from baseline in SDBP to the end of the treatment period (Week 12) and during the randomized withdrawal period (Week 16). At Week 12, the reduction from baseline in SDBP at trough was significantly greater (p<0.001) in the mibefradil group (–14.0 ± 7.8 mmHg) than in the diltiazem CD group (–9.5 ± 7.5 mmHg). Significantly more patients (72%) on mibefradil achieved SDBP normalization by Week 12 than did patients on diltiazem (51%) (p<0.01). Patients maintained on mibefradil or diltiazem CD during the withdrawal period had a significantly larger reduction in trough SDBP at Week 16 than those switched to placebo. The incidence of side effects was similar in both treatment groups.Conclusions: Once‐daily mibefradil was equally well tolerated as diltiazem CD, but was more effective in lowering blood pressure at the doses studied than the extended‐release formulation of diltiazem.
Myocardial bridging in a young patient with sudden death
Authors: Cutler David , Wallace John M. 
Published: February 2009

AbstractSystolic compression of a coronary artery is considered to be a benign phenomenon, although numerous case reports have suggested an association between bridging and sudden death or ischemia in certain patients without other abnormalities on cardiovascular evaluation. We present the case of a young patient with two episodes of spontaneous ventricular fibrillation and electrocardiographic evidence of ischemia, whose only primary abnormality on extensive workup was a long segment of left anterior descending systolic compression. This case adds to the growing body of anecdotal evidence that myocardial bridging may be associated with significant cardiac events.