bluuebunny/crossref_metadata_2025_split huggingface dataset:
The power spectral analysis of heart rate variability in athletes during dynamic exercise—Part I
Authors: Shin Kunsoo , Minamitani Haruyuki , Onishi Shohei , Yamazaki Hajime , Lee Myoungho 
Published: February 2009

AbstractIn this study, the effects of long‐term physical training on autonomic function in athletes and the response of the autonomic nervous system to dynamic exercise were investigated in nonathletes and athletes with power spectral analysis of heart rate variability (HRV). This study was performed on 13 healthy subjects (5 athletes and 8 nonathletes). Eleclrocardiographic (ECG) signals were continuously recorded during (1) 15 min of rest in a sitting position on a bicycle ergometer, (2) the dynamic exercise test to the point of exhaustion, and (3) a 15 min postexercise period. After the recorded ECG signals were sampled at 500 samples/s, the instantaneous HRV signal was constructed from the detected R peaks and then resampled at 4 Hz in order to obtain an evenly spaced time series applicable to power spectral analysis. After linear trends were removed by the robust locally weighted regression algorithm, the power spectrum of HRV was estimated for contiguous records of 512 samples by Burg's maximum entropy method. HRV was quantified by determining the spectral area (power) in two frequency bands, low‐frequency power (LF power: 0.05–0.15 Hz) and high‐frequency power (HF power: 0.15–0.8 Hz), and their ratio. The comparison between athletes and nonathletes was performed in terms of the above‐mentioned parameters. Although both groups showed similar trends in heart rate (HR) at all stages of protocols, HR in athletes was significantly lower than that in nonathletes during rest and postexercise. In athletes and nonathletes, LF and HF powers gradually decreased with exercise. As recovery progressed, they continued to increase gradually, but remained below resting level. During rest and postexercise, HF power in athletes was significantly (p < 0.05) higher than that in non‐athletes. Also, the recovery of HR and HF power during early recovery (POI) was more rapid in athletes than in nonathletes. Both groups showed an attenuation of LF and HF powers during dynamic exercise. It is likely that, in athletes, the lower HR during rest and the more rapid recovery of HR postexercise was due to a high level of HF power, indicating that vagal activity was enhanced by the adaptive changes in neural regulation produced by long‐term physical training.
Peripheral vascular complications following coronary interventional procedures
Authors: Nasser Tony K. , Mohler Emile R. , Wilensky Robert L. , Hathaway David R. 
Published: February 2009

AbstractWe report the incidence, diagnosis, prevention, and treatment of peripheral vascular complications following coronary interventional procedures as reviewed in the English‐language literature. Peripheral vascular complications include hematomas, pseudoaneurysms, arteriovenous fistulae, acute arterial occlusions, cholesterol emboli, and infections that occur with an overall incidence of 1.5–9%. Major predictors of such complications following coronary interventional procedures include advanced age, repeat percutaneous transluminal coronary angioplasty, female gender, and peripheral vascular disease. Minor predictors include level of anticoagulation, use of thrombolytic agents, elevated creatinine levels, low platelet counts, longer periods of anticoagulation, and use of increased sheath size. Ultrasound‐guided compression repair of pseudoaneurysms and arteriovenous fistulae are discussed, as are newer methods of treatment such as hemostatic puncture closure devices. Anticipation and early recognition of possible peripheral vascular complications in conjunction with careful attention to the optimal activated clotting time for sheath removal following coronary interventional procedures may translate into fewer vascular complications as well as into shorter and less costly hospital stays.
Inotropic therapy for the failing myocardium
Authors: Shipley Joshua B. , Hess Michael L. 
Published: February 2009

AbstractCongestive heart failure (CHF) is a common clinical entity with diverse causes. Patients may present with acute decompensation or have a more indolent course, with diminishing exercise tolerance and increasing dyspnea. The management of this clinical entity traditionally has focused on restricting fluid intake, decreasing dietary sodium, decreasing afterload with vasodilatory agents, and supporting the failing myocardium with agents which produce a positive inotropic response. In the acutely decompensated patient, short‐term therapy with positive inotropics is clearly beneficial. The role of long‐term inotropic therapy for chronic CHF remains less clear. A number of clinical trials have recently evaluated the effects of long‐term therapy on morbidity and mortality, with disappointing results. For a number of the newer, nonglycocide oral positive inotropics, at doses of drug which produce measurable hemodynamic improvement, increased mortality in treatment groups has been unacceptably high. Ironically, patients with worse left ventricular dysfunction show the most clinical improvement, but have the highest increased mortality. However, as with digoxin, there is some evidence that employing lower doses of drug that do not produce measurable improvement in hemodynamic parameters may result in both improved clinical state and decreased mortality. This review discusses the role of both oral and intravenous inotropic agents, discusses the difficulty in translating short‐term hemodynamic improvement into long‐term clinical benefit, and presents a rationale for the use of lower‐dose inotropic therapy to improve long‐term clinical outcome.
Comparison of the efficacy of simvastatin and standard fibrate therapy in the treatment of primary hypercholesterolemia and combined hyperlipidemia
Authors: Bruckert E. , De Gennes J. L. , Malbecq W. , Baigts F. 
Published: February 2009

AbstractFive multicenter, randomized, double‐blind, placebo‐controlled studies were conducted in France to compare the efficacy and safety of once‐daily simvastatin treatment (10–40 mg/day) with conventional therapy with gemfibrozil 900 mg/day, ciprofibrate 100 mg/day, bezafibrate 400 mg/day, and fenofibrate 300 or 400 mg/day in a total of 800 patients with hypercholesterolemia. Simvastatin was associated with statistically significantly greater (p ≪ 0.01) mean percent reductions in plasma low‐density lipoprotein (LDL) cholesterol compared with each of the five fibrate regimens, even when administered at its recommended starting dose of 10 mg/day. Furthermore, approximately 90% of patients treated once daily with simvastatin experienced an at least 20% decrease in plasma LDL cholesterol compared with only 36 to 68% of patients treated with the individual fibrate agents (p ≪ 0.05). The effectiveness of simvastatin in reducing LDL cholesterol did not differ as a function of the baseline plasma concentrations of total cholesterol or triglycerides. In contrast, the effectiveness of fibrate therapy in lowering plasma LDL cholesterol levels was significantly diminished (p ≪ 0.05) among patients with triglyceride concentrations > 1.7 mmol/1. Plasma highdensity lipoprotein (HDL) cholesterol levels were increased by approximately 10% after treatment with simvastatin or the fibrates. Although fibrate therapy was more effective overall in lowering plasma triglyceride levels, the effectiveness of simvastatin in reducing plasma triglyceride levels was generally 2‐ to 4‐fold greater in patients with hypercholesterolemia associated with triglyceride levels ≫ 2.3 mmol/1 than in those with hypercholesterolemia associated with triglyceride levels < 2.3 mmol/1. The results of these studies confirm the superiority of simvastatin to standard fibrate therapy in reducing plasma levels of total and LDL cholesterol. They further indicate that once‐daily treatment with simvastatin is effective in patients with isolated hypercholesterolemia or hypercholesterolemia associated with elevated triglyceride levels.
Plasma concentrations and coronary vasodilation after sublingual and intracoronary administration of isosorbide dinitrate
Authors: Hoshio Akira , Shirota Kinya , Sasaki Norihito , Doi Tetsuya , Sawada Yoshihiro , Fukuki Masaharu , Miyakoda Hiroyuki , Kotake Hiroshi , Mashiba Hiroto 
Published: February 2009

AbstractTo investigate the relationship between plasma levels and coronary vasodilation after administration of isosorbide dinitrate (ISDN), the plasma concentration and diarneters of six segments of the left coronary artery were measured before and after sublingual (SL) ISDN (5 mg) and left intracoronary (IC) administration of ISDN (3 mg) in 12 patients. After SL‐ISDN, the systolic aortic pressure decreased with no significant concomitant changes in heart rate or diastolic aortic pressure. After IC‐ISDN, all hemodynamic parameters showed significant changes, and these were greater after IC‐ISDN than those after SL‐ISDN. The individual mean vasodilation of six segments induced by SL‐ and IC‐ISDN, were 23± 9 and 35± 11% (p<0.01), respectively. Before SL‐ISDN, ISDN was not detected in plasma. After SL‐ and IC‐ISDN, however, the plasma values of the ISDN were 36.1± 53.3 and 101.5± 90.0 ng/ml (p<0.01), respectively. Thus, both coronary vasodilative responses and plasma ISDN levels after IC‐ISDN were significantly greater than those after SL‐ISDN. However, neither the individual mean coronary vasodilation nor the hemodynamic changes correlated significantly with plasma ISDN levels. Consequently, with administration of the same dose, the coronary vasodilative response to ISDN did not correlate with plasma levels. Furthermore, IC‐ISDN dilates coronary arteries more effectively than SL‐ISDN.
Treatment of silent ischemia in unstable angina: A randomized comparison of sustained‐release verapamil versus metoprolol
Authors: Singh Narendra , Mironov Dmitry , Goodman Shaun , Morgan Christopher D. , Langer Anatoly 
Published: February 2009

AbstractSilent ischemia is a frequent finding in patients with unstable angina and portends a poor prognosis. We compared the efficacy of sustained‐release (SR) verapamil and metoprolol in reducing silent ischemia in patients with unstable angina and assessed whether detection of silent ischemia was related to unfavorable outcomes in the contemporary setting of concurrent therapy with heparin and aspirin. Holter monitoring (leads a VF, V2, V5) for the first 72 h was used to assess the frequency and duration of ST‐shift episodes. There were 37 patients in the verapamil‐SR group and 40 patients in the metoprolol group, with both groups having similar baseline characteristics. There were more episodes of angina in the verapamil‐SR group (29 vs. 12, p = 0.05). There was no difference between the two groups in the frequency (51 vs. 49 episodes, p = 0.9) or duration (23± 48 vs. 18± 50 min, p = 0.6) of ST‐shift episodes. There were 20 unfavorable in‐hospital outcomes distributed equally between the two groups (p = 0.9). Patients with unfavorable outcomes had ST shift more often (50 vs. 28%, p = 0.07) and for a longer duration (40± 69 vs. 13± 38 min, p = 0.03). Patients with ST shift > 60 min had a 60% probability of unfavorable outcome compared with 33% for ST shift of 1–59 min duration and 20% for no ST shift (p = 0.04). We conclude that metoprolol appears to reduce symptoms better than verapamil‐SR, but no difference in silent ischemia or unfavorable outcomes was seen. Silent ischemia remains a common occurrence in these patients despite heparin and aspirin therapy and its detection continues to have prognostic value.
Cardiovascular effects of dobutamine stress testing in healthy women
Authors: Blomstrand Peter , Thulesius Olav , Wranne Bengt 
Published: February 2009

AbstractDobutamine echocardiography is frequently used for detection of coronary artery disease. The circulatory response in patients is known to some extent, but studies in normals are lacking. Hypotensive response during the test is a common side effect, the cause of which is unclear. The aim of this study was, therefore, to investigate the hemodynamic response to dobutamine in women without cardiovascular disease and interfering medications. Eleven healthy women, age 53–71 years, were investigated with Doppler echocardiography and venous occlusion plethysmography during intravenous infusion of increasing doses of dobutamine according to a standardized protocol. An average peak dose of 22 ± 7.5 μMu kg‐1min‐1was administered. Cardiac output increased by 93%, heart rate by 68%, and stroke volume by 15%, while peripheral vascular resistance decreased by approximately 50%. Systolic blood pressure remained unchanged and diastolic blood pressure decreased by 21%. One subject demonstrated a decreased systolic blood pressure exceeding 10 mmHg. Outflow obstruction from the left ventricle was seen in two subjects, one of whom had a slight decrease of 10 mmHg in systolic blood pressure. Subjects > 65 years demonstrated a less pronounced increase in heart rate, cardiac output, and decrease in peripheral vascular resistance compared with those < 65 years.
Intracardiac thrombi: Frequency, location, etiology, and complications: A morphologic review—Part IV
Authors: Waller Bruce F. , Grider Larry , Rohr Todd M. , Mclaughlin Todd , Taliercio Charles P. , Fetters Julie 
Published: February 2009

AbstractIntracardiac thrombus may develop as a consequence of multiple underlying cardiac disorders. Valvular heart disease, in particular, rheumatic mitral stenosis is frequently associated with intracardiac thrombus. Pant IV of this 5‐part article on intracardiac thrombus focuses on the frequency and consequences of thrombus in valvular heart disease.
The role of prolonged thrombolytic infusions and transesophageal echocardiography in thrombosed prosthetic heart valves: Case Report and review of the literature
Authors: Puleo John A. , Fontanet Hector L. , Schocken Douglas D. 
Published: February 2009

AbstractThrombolytic therapy for prosthetic heart valve thrombosis has recently been receiving increased attention and is now frequently used an alternative to high‐risk surgery. A case is presented describing a novel thrombolytic therapy regimen with emphasis on the role of transesophageal echocardiography in diagnosis and management. A complete review of the literature is presented.
Invtracardiac thrombi: Frequency, location, etiology, and complications: A morphologvic review—Part V
Authors: Waller Bruce F. , Rohr Todd M. , Mclaughlin Todd , Grider Larry , Taliercio Charles P. , Fetters Julie 
Published: February 2009

AbstractIntracardiac thrombus may develop as a consequence of multiple underlying cardiac disorders. Other systemic disorders may predispose formation of thrombus within the heart, or the heart may be the site of emboli in transitthrombus originating elsewhere and traveling through the heart to the pulmonary or arterial circulation. Part V of this five‐port series on intracardiac thrombus will focus on “migrating thrombi,” miscellaneous systemic conditions associated with intracardiac thrombi, and echocardiographic detection of intracardiac thrombus.
Dobutamine‐induced transmural myocardial ischemia in a patient with mild coronary lesions
Authors: Kardaras Fotis G. , Bonou Maria S. , Kardara Dimitra F. , Kranidis Athanasios I. , Sioras Elias P. , Anthopoulos Lambros P. 
Published: February 2009

AbstractA 70‐year‐old man was admitted for evaluation of retrosternal pain at rest. During infusion of dobutamine (25 μg/kg/min) the patient developed angina, ST‐segment elevation in the inferior leads, and echocardiographic hypokinesia in the inferior‐basal myocardial wall. Coronary angiography revealed insignificant (20‐30%) stenosis of the right coronary artery and a normal remaining tree. This case suggests that dobutamine may induce transmural myocardial ischemia in patients with mild coronary lesions, probably by producing occlusive coronary spasm on a substrate of arterial endothelial dysfunction.
Resolution of an aortic mobile mass with anticoagulation without evidence of arterial embolism
Authors: Pasierski T. , Jasek S. , Firek B. , Przbylski A. , Szwed H. , Sadowski Z. 
Published: February 2009

AbstractThe prognostic significance of aortic mobile debris detected by transesophageal echocardiography (TEE) in patients without history of embolism has not been established. A mobile aortic arch mass was found by TEE in a 59‐year‐old man with coronary artery disease, and with rheumatic mitral valve disease, and with no embolic symptoms. The patient was anticoagulated for 6 weeks and the mass was no longer seen on repeated TEE. He had no embolic symptoms during 9 months of follow‐up. Different therapeutic approaches to mobile aortic debris are discussed and anticoagulant treatment of asymptomatic cases is advocated.
Manifestation of severe coronary heart disease after anabolic drug abuse
Authors: Mewis C. , Spyridopoulos I. , Kühlkamp V. , Seipel L. 
Published: February 2009

AbstractAnabolic steroids are frequently abused, thus increasing the risk of cardiovascular disease, despite the known unfavorable influence on lipid profiles. We report on a young bodybuilder who presented with ventricular tachycardia as the first manifestation of severe underlying coronary heart disease. Coronary angiogram revealed severe stenotic lesions in the right coronary artery and the left descending coronary artery, and hypokinetic regions corresponded to posterolateral and anterior myocardial infarctions. This young patient had a history without any coronary risk factors, but with a 2‐year abuse of the anabolic steroid stanazolol. No report published so far has shown possible atherogenic consequences of long‐term abuse of stanazolol.
Retinal artery embolization: A rare presentation of calcific aortic stenosis
Authors: Reimers Carl D. , Berger Marvin , Williams Richard J. , Tranbaugh Robert F. , Jay Wisnicki H. 
Published: February 2009

AbstractRetinal artery embolization is an unusual but serious complication of calcific aortic stenosis. However, it is rare for retinal embolization to be the presenting feature of aortic stenosis. This report describes a young patient who presented with an acute retinal artery occlusion secondary to calcific aortic valve disease, and discusses the rationale for early surgical intervention.
Postpericardiotomy syndrome and cardiac tamponade following transvenous pacemaker placement
Authors: Miller Gregory L. , Coccio Elizabeth B. , Sharma Satish C. 
Published: February 2009

AbstractThis is the first reported case of cardiac tamponade presumed to be caused by postpericardiotomy syndrome (PPS) following endocardial pacemaker placement. An 84‐year‐old woman developed fever and dyspnea 3 weeks after pacemaker placement. Physical examination revealed hypotension, tachycardia, and pulsus paradoxus. Auscultation revealed clear lungs and diminished heart sounds. The sedimentation rate was 60 mm/h. Echocardiography revealed a large pericardial effusion with signs of cardiac tamponade. Surgical drainage of the pericardial space resulted in complete resolution of symptoms. The pericardial fluid was culture‐ and cytologically negative. PPS is a common complication of cardiothoracic surgery and chest trauma. It rarely occurs after percutaneous procedures such as percutaneous transluminal coronary angioplasty and transvenous pacemaker placement. While usually having a benign, self‐limited course, PPS can cause a serious complication as illustrated in this case report.
An unusual case of cyanotic heart disease in a patient with patent foramen ovale and right ventricular hypertrophy
Authors: Will Peter M. , Serrian John L. , Dawson John T. 
Published: February 2009

AbstractAn unusual case of cyanosis and patent foramen ovale/atrial septal defect with right‐sided septal hypertrophy is presented. Mild right ventricular dysfunction led to predominant right‐to‐left shunting. The atrial defect was surgically closed. The patient is from a family with hypertrophic cardio‐myopathy;she is negative for the gene abnormality.
Nonatherosclerotic causes of coronary artery narrowing—Part II
Authors: Waller Bruce , Waller Bruce F. , Fry Edward T. A. , Hermiller James B. , Peters Thomas , Slack John D. 
Published: February 2009

AbstractPart II of this three‐part article on nonatherosclerotic causes of coronary heart disease focuses on myocardial bridges, coronary artery aneurysms, emboli, coronary dissection, and spasm as causes of luminal narrowing.
Possible mechanisms of mitral regurgitation in dilated hearts: A study using transesophageal echocardiography
Authors: Oki Takashi , Fukuda Nobuo , Iuchi Arata , Tabata Tomotsugu , Yamada Hirotsugu , Fukuda Kazuyo , Manabe Kazuyo , Ito Susumu 
Published: February 2009

AbstractHypothesis: This study was undertaken to clarify the mechanisms of mitral regurgitation (MR) in dilated hearts.Methods: in all, 68 patients with dilated heart and MR, including 26 patients with dilated cardiomyopathy (DCM), 24 with prior anterior myocardial infarction (A‐MI), and 18 with prior posteroinferior myocardial infarction (I‐MI), as well as 25 normal subjects were examined by transesophageal two‐dimensional and color Doppler echocardiography.Results: The maximum area of the MR signal in the DCM group correlated positively with the anteroposterior diameter of the mitral annulus at late systole. Although the coaptation edge length of the anterior and posterior mitral leaflets appeared shorter in dilated hearts than in the hearts of controls, a significant difference did not exist. The length of the coaptation edge correlated negatively with the maximum area of the MR signal in all dilated hearts, and characteristic systolic displacement of the coaptation point of both mitral leaflets occurred. The MI groups demonstrated anterior and posterior displacement in the direction of the short axis of the left ventricle in the A‐MI and I‐MI groups, respectively. However, the DCM group demonstrated inferior displacement toward the long axis of the left ventricle; its magnitude correlated positively with the maximum area of the MR signal.Conclusion: A major cause of MR in dilated hearts is mitral malcoaptation due to displacement of the coaptation point of the mitral leaflets along the long or short axis of the left ventricle. This is caused by left ventricular enlargement and/or asynergy of the left ventricular wall, rather than by a decrease in mitral coaptation edge length due to mitral annular dilation.
Atrial Fibrillation in the Elderly
Authors: Reardon Michael , John Camm A. 
Published: February 2009

AbstractThe prevalence of atrial fibrillation is 11 % in persons older than 70 years and rises to 17% in those aged 84 years or more. One‐year mortality ranges from 0.2 to 16%, being highest in elderly patients, and is associated with a 4.8‐fold increased risk of stroke. Atrial fibrillation can be cardioverted to normal sinus rhythm electrically or pharmacologically and rapid ventricular rate can be controlled with drugs. While anticoagulation prevents embolic events in those with atrial fibrillation, the decision to anticoagulate should be based on an assessment of the risk/benefit ratio.
The role of magnesium therapy in acute myocardial infarction
Authors: Rabbani Llroy E. , Antman Elliott M. 
Published: February 2009

AbstractMagnesium possesses numerous salutary effects for the treatment of acute myocardial infarction (AMI). It is a coronary vasodilator, calcium antagonist, afterload reducer, antiarrhythmic, and antiplatelet drug that modulates autonom‐ic function and limits reperfusion injury when administered early in infarction. Various clinical trials of magnesium therapy for AMI have proffered conflicting results as to the efficacy of magnesium therapy because of significant differences in the timing of magnesium administration. Additional clinical trials that focus on early administration of magnesium are warranted to delineate the role of magnesium therapy for AMI.