bluuebunny/crossref_metadata_2025_split huggingface dataset:
Electrophysiologic evaluation of sinus node dysfunction in postoperative children and young adults utilizing combined autonomic blockade–B. Marcus Et Al.: Postoperative intrinsic sinus node evaluation
Authors: Marcus B. , Gillette P. C. , Garson A. 
Published: February 2009

AbstractSinus node dysfunction is a recognized problem following surgery for congenital heart disease. Seven postoperative patients with sinus node dysfunction (5 Mustard, 1 tetralogy of Fallot, 1 Fontan) underwent electrophysiology study of sinus node function during combined autonomic blockade (CAB) utilizing propranolol 0.2 mg/kg iv and atropine 0.04 mg/kg iv to evaluate intrinsic sinus node function isolated from autonomic control. During CAB, intrinsic heart rate, intrinsic corrected sinus node recovery time, and intrinsic sinoatrial recovery time were measured. These results were compared with age‐matched normal intrinsic data from our lab [normal (n = 7, mean age 9 years) IHR 128 ± 24, intrinsic corrected sinus node recovery time 135 ± 40 ms, intrinsic sinoatrial conduction time 86 ± 19 ms]. Among postoperative Mustard patients (n = 5, mean age 13 years, mean years postoperative 11) 2 of 5 had clearly abnormal intrinsic sinus node function with nonsinus rhythm during CAB: 3 of 5 had sinus rhythm during CAB with normal or mildly abnormal intrinsic sinus node function. The postoperative case of tetralogy of Fallot (age 20 years, postoperative 14 years) had mildly abnormal intrinsic sinus node electrophysiology study. The postoperative case of Fontan (age 16 years, postoperative 1.5 years) had sinus rhythm at rest but left atrial rhythm during CAB.Different aspects of sinus node dysfunction may be expressed during resting electrophysiology study vs. electrophysiology study utilizing CAB. The pathophysiology of sinus node dysfunction among postoperative pediatric patients is not homogeneous with regard to the contribution of intrinsic sinus node dysfunction. In those patients with normal or mildly abnormal intrinsic sinus node function, an important pathophysiologic influence of the autonomic nervous system is implicated.
Transient ischemic attack‐related syncope
Authors: Davidson E. , Rotenbeg Z. , Fuchs J. , Weinberger I. , Agmon J. 
Published: February 2009

AbstractThe records of 483 patients admitted to the emergency room because of syncope were reviewed. Thirty seven patients (7.7%) were found to suffer from transient ischemic attack‐ (TIA) related syncope. This group is the subject of this report. Of these patients, 28 (76%) were men (mean age 71 years). Seven patients reported previous syncopal episodes. Past history revealed a high rate of ischemic heart disease (70%) and hypertension (68%). Concurrent neurologic symptoms, which led to the diagnosis of TIA‐related syncope, included mainly vertebrobasilar symptoms: vertigo (in 55% of the patients), ataxia (46%), parasthesia (41 %). Two patients most probably were presenting bilateral carotid artery disease. Various diagnostic tests (including electroencephalography, computed tomography, sonography, and cerebral angiography) were used to exclude other causes of syncope. During follow‐up (mean 14.5 months) four patients (11%) had an additional episode of TIA and in three of them syncope reappeared. One patient had a complete stroke. We conclude that TIA is a much more frequent explanation for syncope than has been previously argued. These patients tend to be elderly males with high incidence of ischemic heart disease and hypertension. The concurrent neurologic symptoms, leading to the diagnosis, represent mainly vertebrobasilar territory ischemia.
Pulmonary artery sarcoma: Another cause of sudden death
Authors: Waller Bruce , Varriale Philip , Chryssos Basil 
Published: February 2009

Abstractpatient hospitalized for recurrent syncope and dyspnea died suddenly before a definite clinical diagnosis could be established. At autopsy a large sarcomatous mass (undifferentiated type) was found to arise and totally occlude the pulmonary trunk without evidence of distant metastasis.
A case of cardiac amyloidosis presenting with symptoms of exertional syncope
Authors: Fujii B. , Matsuda Y. , Ohno H. , Hamada Y. , Takashiba K. , Ebihara H. , Hyakuna E. , Tani S. 
Published: February 2009

AbstractA 54‐year‐old man presented with symptoms of exertional syncope. Cardiac amyloidosis was diagnosed by endomyocardial biopsy. Exercise tolerance test revealed a failure of increased heart rate followed by sinus arrest, associated with syncope. Autopsy revealed amyloid deposits in the sinoatrial node.
The pacemaker syndrome: Old and new causes
Authors: Schüller H. , Brant J. , Camm A. J. 
Published: February 2009

AbstractThe pacemaker syndrome refers to symptoms and signs in the pacemaker patient caused by inadequate timing of atrial and ventricular contractions. The lack of normal atrioventricular synchrony may result in decreased cardiac output and venous “cannon A waves.” A sudden increase in atrial pressure at the onset of asynchrony may elicit a systemic hypotensive reflex response. A wide range of symptoms can be observed. The pacemaker syndrome is encountered in a significant number of patients with ventricular (VVI) pacemakers, mostly when 1:1 retrograde ventriculoatrial conduction is present. The risk of occurrence of the pacemaker syndrome is minimized if pacemaker systems are used which restore or maintain the normal atrioventricular contraction sequence. Hence, in sinus node disease, atrial stimulation with or without ventricular stimulation should be employed, while in high‐grade atrioventricular block dual‐chamber pacing is recommended. The pacemaker syndrome is not restricted to the VVI stimulation mode. It can be seen, though rarely, in atrial and dual‐chamber pacing, and an awareness of these new causes is necessary. An established pacemaker syndrome can often be counteracted by adjusting the pulse generator function.
Heparin‐releasable platelet factor 4 in patients with coronary artery disease
Authors: Sadayasu Takao , Nakashima Yasuhide , Yashiro Akjra , Kawashima Takashi , Kuroiwa Akio 
Published: February 2009

AbstractRecently, platelet factor 4 (PF4) release by heparin (heparin‐releasable PF4) has been examined as a useful marker of the interaction between the substances liberated from circulating platelets and the vascular endothelium. We compared the plasma levels of PF4 and β‐thromboglobulin (β‐TG) after intravenous heparin injection in patients wtih coronary artery disease (CAD) and normal control subjects. We also studied the effects of low‐dose aspirin (81 mg/day) on the plasma level of heparin‐releasable PF4 in the CAD patients. Blood samples were obtained before and 5 min after the intravenous injection of heparin (1,000 IU) from 23 patients with CAD and 15 normal control subjects. Although the plasma β‐TG level remained unchanged after heparin injection, the plasma PF4 level markedly increased in both groups. There was a significant difference in plasma PF4 levels at 5 min after heparin injection between the CAD group (100.1±38.1) and the control group (61.0±;24.0) (p<0.01). The PF4/β‐TG ratio after heparin injection was also higher in the CAD group than in the control group (p<0.01). There was a correlation between the PF4/β‐TG ratio after heparin and the Gensini CAD score, which defines the severity of coronary atherosclerosis (r = 0.489, n = 23, p<0.01). Low‐dose aspirin was administered to 11 CAD patients for 246.0 ±;28.8 days. Blood samples for the assay of PF4 and β‐TG were obtained as stated above, and platelet aggregation, thromboxane B2 (T×B2), and 6‐keto‐prostaglandin F1α (6‐keto‐PGF1α) levels were also measured before and during aspirin administration. Aspirin significantly reduced the PF4 level and the PF4/β‐TG ratio after heparin injection (p<0.05) in accoradance with the reduction in platelet aggregation (ADP induced: p<0.01, collagen‐induced: p<0.01, epinephrine‐induced: p<0.05). Although there were no statistically significant changes in T×B2 and 6‐keto‐PGF1α levels during aspirin administration, the T×B2 level was decreased by aspirin in 7 of 11 CAD patients. The decrease in the PF4/β‐TG ratio after heparin injection was significantly correlated with the changes of ADP‐ and epinephrine‐induced platelet aggregation (r = 0.717, p<0.01 and r = 0.577, p<0.05, respectively). These results suggest that heparin‐releasable PF4 (the PF4 level and/or PF4/β‐TG ratio after heparin injection) has the potential to be used as a marker of increased platelet aggregability in CAD patients.
Elevation of factor VII activity and mass in coronary artery disease of varying severity
Authors: Suzuki Toshikazu , Yamauchi Kazunobu , Matsushita Tadashi , Furumichi Takeo , Furui Hirohiko , Tsuzuki Jitsuki , Saito Hidehiko 
Published: February 2009

AbstractThe present study was undertaken to determine whether the extent of Factor VII elevation correlated with the severity of coronary artery disease and whether zymogen or activated Factor VII was responsible for this elevation. A group of 69 patients with coronary artery disease with old myocardial infarction was compared with 28 control subjects. The patient groups showed elevated levels of Factor VII procoagulant activity (FVII.C) and more markedly elevated Factor VII antigen (FVII:Ag) levels than the control group; therefore they had a decreased FVII:C to FVII:Ag ratio. The increased Factor VII level in the patient groups was caused by elevated Factor VII zymogen levels, and not by activated Factor VII. Since FVII:C levels strongly correlated with the titer of thrombin‐antithrombin III complexes in all patients, the hypercoagulable state accompanying severe coronary atherosclerosis seems to underlie the increase of FVII and TAT in the stable phase of myocardial infarction.
Accelerated idioventricular rhythm detected during elective surgery in a healthy man
Authors: Lew David C. , Keim Stephen G. , Curtis Anne B. 
Published: February 2009

AbstractAccelerated idioventricular rhythm (AIVR) is found most commonly in the presence of underlying heart disease. It is characterized by acceleration of a latent pacemaker that normally depolarizes slowly. We describe a 30‐year‐old man who was found to have episodes of accelerated idioventricular rhythm (AIVR) on cardiac monitoring during elective orthopedic surgery. Noninvasive evaluation including two‐dimensional echocardiography was unremarkable. No late potentials were detected on a signal‐averaged electrocardiogram. During an exercise tolerance test, AIVR was suppressed as heart rate increased. A 24‐h Holter monitor revealed that the AIVR rate was consistently 73‐76 beats/min, which appeared whenever the sinus rate slowed to this level. The patient has been asymptomatic, and the rhythm has persisted at least through a 5‐month follow‐up period.
Catheter balloon valvuloplasty of stenotic aortic valves Part I: Anatomic basis and mechanisms of balloon dilation
Authors: Waller Bruce F. , Vantassel James W. , Taliercio Charles , Howard Jane , Green Frank , Mckay Charles 
Published: February 2009

AbstractCatheter balloon valvuloplasty of stenotic aortic valves has met with generally poor short‐ and long‐term clinical results. Part of this problem resides with the lack of recognition of various etiologies of aortic stenosis. Part I of this review discusses the various etiologies of aortic stenosis and provides an anatomic basis for successful valve dilation. Results of an in vitro study indicate stenotic aortic valves are dilated by various mechanisms (cracking, stretching) based in part upon the etiology of the aortic valve stenosis.
Signal‐averaged electrocardiography: History, techniques, and clinical applications
Authors: Jarrett Jeffrey R. , Flowers Nancy C. , John A. Camm 
Published: February 2009

AbstractSignal averaging principles have been utilized since around 1875. Their application in medicine to enhance biologic signals was first made in 1947 for improved detection of electroencephalographic signals. The year 1963 marked the first application of this technique to cardiac signals. The more prevalent use in adult cardiology is in the detection of ventricular late potentials (VLPs) which correspond to areas of delayed ventricular activation as slowed conduction velocity. These VLPs have value in predicting the likelihood of malignant ventricular arrhythmias after myocardial infarction (MI). Negative predictive values on the order of 96–99% are convincing as to their ability to predict no arrhythmic event post‐MI. Positive predictive values, on the other hand, are poor (10–29%) but improve (35–62%) in combination with other parameters such as depressed left ventricular function and frequent ventricular ectopy. Additional accepted uses for the signal‐averaged electrocardiogram (SAECG) include prediction of successful ablative surgery for intractable ventricular tachycardia and facilitating evaluation of patients presenting with syncope of an unclear etiology. Potential future applications of the SAECG are (1) in following patients for rejection after cardiac transplant, (2) as a screening tool for the need for electrophysiologic study, (3) as a predictor of vessel patency after thrombolysis or percutaneous transluminal coronary angiography, and (4) as a tool to assess proarrhythmia. As the technique of signal averaging continues to evolve, its applications may become more diverse and its clinical effectiveness may improve.
Influence of exercise training soon after myocardial infarction on regional myocardial perfusion and resting left ventricular function
Authors: Beller George A. , Murray Gary C. , Erkenbrack Susan K. 
Published: February 2009

AbstractThere is scant information regarding the effect of exercise training begun soon after hospital discharge for myocardial infarction (MI) with respect to subsequent improvement in exercise tolerance, enhancement of regional myocardial perfusion, or left ventricular function. Accordingly, 19 post‐MI patients (mean age 53 ± 7 years) underwent treadmill exercise quantitative thallium‐201 (Tl‐201) scintigraphy and rest radionuclide angiography (RNA) prior to and after 12 weeks of thrice‐weekly exercise training which was targeted to 70–85% of maximum exercise heart rate achieved. Training was begun at 25 ± 3 days after hospital discharge. Eight Tl‐201 scan segments were each scored from 1–6 points based upon uptake and washout criteria with 6 being the most severe defect (>50% reduction in Tl‐201 events with no delayed redistribution). When matched to the pretraining peak workload on exercise testing, 12 weeks of training significantly lessened heart rate (120±4 to 97±4, p<0.001), peak systolic blood pressure (142±6 to 129±5 mmHg, p<0.01), and significantly reduced double product [17.2±10.8 to 12.7±9 (×103), p<0.001]. Training was associated with a reduction of exercise‐induced ST depression or angina (42 to 16%) which was not statistically significant. The mean resting by RNA ejection fraction was 50±3% prior to training and 51±3% after training. There was no significant change in overall Tl‐201 defect score or the number of defect regions per patient scan comparing pre‐ and post‐training scintigrams. Of the 5 patients who had elimination of exercise‐induced angina or ischemic ST depression after training, none showed an improvement in the Tl‐201 defect score between the two studies. Thus, 3 months of exercise conditioning begun soon after acute MI is associated with a significant training effect without an improvement in resting left ventricular function or myocardial perfusion at peak exercise.
The postcardiac injury syndromes
Authors: Khan Abdul Hakim 
Published: February 2009

AbstractLate pericarditis following myocardial infarction, cardiac surgery, or trauma is referred to as postmyocardial infarction syndrome (PMIS) or postcardiotomy syndrome (PCS), respectively. The term postcardiac injury syndrome (PCIS) is used to encompass both these entities. PCIS is characterized by fever, pleuropericardial pain, pericarditis, and pulmonary involvement. Abnormal laboratory findings include leukocytosis, high sedimentation rate, and chest x‐ray abnormalities of pleural effusion with or without pulmonary infiltrates. Evidence supports an immunopathic etiology; viruses may play a contributing role. The course is benign but rare complications include tamponade, constriction, anemia, and coronary bypass graft occlusion. Anti‐inflammatory agents are helpful; indo‐methacin and steroids are preferably avoided. Rarely, PMIS‐like syndrome may occur following pulmonary embolism. Anticoagulation and steroids have been used successfully in the latter situation.
Coronary hemodynamic effects of systemic thrombolysis in patients with unstable angina
Authors: Pozzati Andrea , Bugiardini Raffaele , Ottani Filippo , Morgagni Gian Luigi , Puddu Paolo 
Published: February 2009

AbstractIntracoronary (i.c.) thrombus is a frequent finding in patients with unstable angina (UA). Accordingly, thrombolytic treatment could be beneficial, as resolution of thrombus might result in increased delivery of blood flow to the ischemic regions. To test this hypothesis, we studied 13 patients with active UA and ST‐segment shift in the anterior leads. Coronary angiography was performed and great cardiac vein blood flow (GCVF; thermodilution) was measured in all patients 25 ± 14 h after the last chest pain episode. Following angiography, patients received i.v. urokinase (UK: 1,000,000 IU/30 min); aortic pressure and GCVF were measured before and every 10 min following drug infusion, for a total time of 90 min. At baseline angiography, 5 of 13 patients (Group 1) had evidence of i.c. thrombus (intraluminal filling defect or thrombotic subocclusion) in the ischemia‐related left coronary artery, whereas 8 patients (Group 2) did not. Group analysis showed that UK increased GCVF and decreased anterior coronary resistance in Group 1 (respectively, from 86±33 to 114±41 ml/min: p<0.005; and from 1.37±0.68 to 1.01±0.44 mmHg/ml/min: p<0.05) but not in Group 2 (both: p=NS). In conclusion, UK has been shown to increase regional coronary blood flow in selected patients presenting with active UA, as well as evidence of i.c. thrombus at early angiography. Heterogeneity of angiographic findings could explain controversies in trials dealing with thrombolysis in UA.
Effect of diuretic therapy on the electrocardiographic response to exercise
Authors: Pascual Eduardo E. , Cintron Guillermo B. , Valdez Michael G. , Clark Pamela I. 
Published: February 2009

AbstractFor nearly 30 years clinicians have assumed that diuretic therapy, per se, even in the absence of clinical hypokalemia, can cause false‐positive exercise ST‐segment responses. The precept has stubbornly persisted in the literature and in the day‐to‐day interpretation of exercise tests in clinical settings. The assumption probably originated with very early studies of patients on diuretics, in which other causes of false‐positive tests were not excluded. This study was undertaken to show that diuretic therapy alone is not sufficient to cause ST depression. Twenty healthy male volunteers, aged 18 to 35, with normal history and physical examinations, echocardiograms, electrocardiograms, serum electrolytes, renal function tests and exercise tests, took 50 mg of hydrochlorothiazide daily for four weeks. Exercise tests, serum electrolytes, and renal function tests were repeated at Weeks 2 and 4. The administration of the diuretic resulted in a statistically significant reduction in serum potassium (from 4.37±0.37 to 3.96±0.28, and 3.94 ±0.31 mEq/1 at 2 and 4 weeks, respectively). There were no abnormal ST‐segment shifts on any of the exercise tests. It is concluded that exercise‐induced ST‐segment shifts in otherwise healthy young male normokalemic subjects who are taking diuretics should not be ascribed to a false‐positive response to diuretics.
Combination Therapy with Nicardipine and Beta‐Adrenergic Blockade for Angina Pectoris
Authors: Lambert Charles R. 
Published: February 2009

AbstractNicardipine a second‐generation dihidropyridine calcium antagonist, has been approved in oral formulation for use in the United States, and is under review for parenteral use. Nicardipine is the most vascular‐selective a‐gent of this class currently approved and should, on theoretical grounds, be ideal for combination therapy with beta‐adrenergic blocking agents. Studies have shown that the combination of nicardipine and beta‐blocking agents offers additional efficacy over monotherapy with either agent alone. The hemodynamic profile of combination therapy appears to be especially favorable in patients with diminished left ventricular function needing therapy with agents of both classes. Adverse effects are few and may be improved compared with other agents of the dihidropyridine class.
Effects of diltiazem, propranolol, and their combination in the control of atrial fibrillation
Authors: Dahlström C.G. , Bertil Olsson S. , Edvardsson Nils , Nasheng Cai 
Published: February 2009

AbstractThe effect of the combined treatment with propranolol 20 mg tid and diltiazem 60 mg tid in patients with chronic atrial fibrillation treated with digoxin was evaluated. Thirteen patients entered a double‐blind, three‐phase crossover study. Heart rate was significantly reduced during rest and at maximal exercise (p < 0.05) during combined treatment compared with treatment with any single drug. No significant changes in maximal work load, exercise time, systolic blood pressure at maximal work load, or subjective sensation of well‐being could be demonstrated during combined drug treatment. The RR distribution pattern was unaffected by the addition of propranolol, diltiazem, or their combination to the chronic digoxin treatment. It is concluded that the combination of diltiazem and propranolol has no advantages over any of these drugs singly, in the moderation of heart rate in patients with atrial fibrillation even combined with basic digitalis treatment, and that the intrinsic AV nodal function is unaffected by these drugs or their combination.
Does juxtamesenteric placement of intra‐aortic balloon interrupt superior mesenteric flow?
Authors: Shimamoto Hiroyuki , Kawazoe Kohei , Kito Hiroyuki , Fujita Tsuyoshi , Shimamoto Yoriko 
Published: February 2009

AbstractTo assess influences of intra‐aortic balloon pumping (IABP) on superior mesenteric flow, 15 postoperative patients were examined, in whom distal aspects of balloons were distal to the superior mesenteric artery. Superior mesenteric flow velocity‐time integral in systole (IntS), that in diastole (IntD), and the sum of IntS and IntD (IntS+IntD) were determined on and off IABP (IABP ON‐OFF test). The same parameters were obtained with balloon inflating on every other beat (IABP 1:2 test). The cardiac cycle with balloon inflation during diastole was defined as “1:2 ON,” and the cardiac cycle without balloon inflation during diastole was defined as “1:2 OFF.” (1) IABP ON‐OFF test. IABP increased IntS (p<0.01), IntD (p<0.01), IntS+IntD (p<0.01), and cardiac output (p<0.05). The increments in IntS, IntD and IntS+IntD on IABP are attributed largely to an increase in cardiac output. (2) IABP 1:2 test. IntS during 1:2 OFF was greater than IntS during 1:2 ON (p<0.01), whereas IntD during 1:2 OFF was smaller than IntD during 1:2 ON (p<0.01). There was no significant difference in IntS+IntD between 1:2 ON and 1:2 OFF. These data suggest that juxtamesenteric balloon placement did not interrupt the arterial inflow of a superior mesenteric artery.