bluuebunny/crossref_metadata_2025_split huggingface dataset:
Heart rate variability from 24-hour electrocardiography and the 2-year risk for sudden death.
Authors: Algra A , Tijssen J G , Roelandt J R , Pool J , Lubsen J 
Published: June 2012

BACKGROUND
Low heart rate variability has been implicated as a risk factor for sudden death. However, no large epidemiological studies using sudden death as an outcome event have been reported.

METHODS AND RESULTS
A total of 6,693 consecutive patients who underwent 24-hour ambulatory ECG were followed up for 2 years; of these, 245 patients died suddenly. Clinical data at the time of 24-hour ambulatory ECG were collected for all patients who died suddenly and for a random sample of 268 patients from the study cohort. In all patients in sinus rhythm with or without occasional supraventricular arrhythmias at the 24-hour ECG (193 patients who died suddenly and 230 patients from the sample), heart rate variability parameters were derived. Patients with low short-term RR interval variability (mean during 24 hours of per-minute standard deviations [SD] of RR intervals < 25 msec) had a 4.1-fold higher risk (95% confidence interval [CI], 2.6, 8.1) for sudden death than patients with high short-term variability (> or = 40 msec); after adjustment for age, evidence of cardiac dysfunction, and history of myocardial infarction, the relative risk was 2.6 (95% CI, 1.4, 5.1). The crude relative risk of long-term RR interval variability (SD during 24 hours of per-minute means of RR intervals < 8 msec) was 4.4 (95% CI, 2.6, 7.7); after adjustment for the same risk factors, it was 2.2 (95% CI, 1.2, 4.1). Patients with a minimum heart rate > or = 65 beats per minute had a double risk of sudden death compared with those with a minimum heart rate < 65 beats per minute (adjusted relative risk, 2.1; 95% CI, 1.3, 3.6).

CONCLUSIONS
These findings support the theory that patients with low parasympathetic activity (low short-term RR interval variability) have an increased risk for sudden death independent of other risk factors.
Atrioventricular nodal reentry. Clinical, electrophysiological, and therapeutic considerations.
Authors: Akhtar M , Jazayeri M R , Sra J , Blanck Z , Deshpande S , Dhala A 
Published: June 2012

BACKGROUND
Atrioventricular (AV) nodal reentry is a relatively common cause of regular, narrow QRS tachycardia. The underlying basis for this arrhythmia is functional (and anatomic) duality of pathways in the region of the AV node, although the exact boundaries of the reentrant circuit have not been convincingly defined. During the more common type of AV nodal reentry (seen in approximately 90% of cases), a slow conducting pathway is used in the anterograde direction, and a fast pathway is operative in the retrograde direction. In the uncommon form, the direction of impulse propagation within the reentrant circuit is reversed. In this article, the clinical, ECG, and electrophysiological features of AV nodal reentry as well as approaches to therapy are discussed.

METHODS AND RESULTS
Clinical diagnosis may be made from the surface ECG. In the common type of AV nodal reentry, the P wave is obscured by the QRS or may be present in its terminal portion. The P wave in the uncommon form occurs late (i.e., in or after the T wave), producing a pattern of long RP and short PR. Both forms of AV nodal reentry are controllable with various therapeutic modalities. For acute termination, adenosine is probably the ideal agent. Prevention of recurrences can be achieved with several pharmacological agents, including beta-blockers, calcium channel blockers, and class Ia, Ic, and III antiarrhythmic agents. Curative therapy is now available with a variety of nonpharmacological methods. However, the most promising therapy at the present time is catheter modification of the AV node by ablation of either the fast or slow pathway, using radiofrequency energy. Ablation of the fast pathway carries a higher risk of second- or third-degree AV block. Slow pathway ablation, by providing a high rate of success and minimal risk of AV block, seems to be a more acceptable initial approach.

CONCLUSIONS
AV nodal reentry is a common cause of paroxysmal supraventricular tachycardia, and a precise diagnosis can be made with intracardiac electrophysiological evaluation. Although the arrhythmia responds to a variety of antiarrhythmic agents, curative therapy can now be offered with catheter modification of the AV node using radiofrequency energy. At the time of this writing, it seems that catheter modification of the AV node is rapidly becoming the therapy of initial choice in patients with symptomatic AV nodal reentrant tachycardia requiring treatment.
Myocardial glucose uptake in patients with insulin-dependent diabetes mellitus assessed quantitatively by dynamic positron emission tomography.
Authors: vom Dahl J , Herman W H , Hicks R J , Ortiz-Alonso F J , Lee K S , Allman K C , Wolfe E R , Kalff V , Schwaiger M 
Published: June 2012

BACKGROUND
Animal studies have demonstrated reduced myocardial glucose utilization in the diabetic heart, suggesting abnormalities in glucose transport. This study was designed to evaluate myocardial glucose uptake as assessed by 2-fluoro-(fluorine-18)2-deoxy-D-glucose (FDG) and positron emission tomography (PET) in patients with insulin-dependent diabetes mellitus (IDDM) under standardized metabolic conditions.

METHODS AND RESULTS
A hyperinsulinemic-euglycemic clamp technique was used during PET data acquisition in nine healthy male volunteers and seven young male patients with a history of IDDM for less than 5 years. Oxidative metabolism was assessed with C-11 acetate, and glucose uptake was quantitatively measured with FDG using Patlak graphic analysis. Hemodynamic data and C-11 acetate kinetics were comparable. Myocardial glucose uptake averaged 0.44 +/- 0.12 mumol.g-1.min-1 in normal subjects and 0.43 +/- 0.16 mumol.g-1.min-1 in patients with IDDM (P = NS). Blood tracer clearance was also similar in both groups as determined by the ratio of peak blood tracer activity to the activity at 55 to 60 minutes after tracer injection. F-18 activity ratio between myocardium and blood pool averaged 7.2 +/- 3.4 in the normal heart and 7.5 +/- 3.0 in the diabetic heart (P = NS).

CONCLUSIONS
These data indicate that metabolic standardization and supplementation with insulin in young patients with IDDM is associated with myocardial glucose uptake similar to that observed in the normal heart. Chronic therapy with insulin may prevent the metabolic abnormalities observed in diabetic animal models.
Low-dose dobutamine echocardiography detects reversible dysfunction after thrombolytic therapy of acute myocardial infarction.
Authors: Smart S C , Sawada S , Ryan T , Segar D , Atherton L , Berkovitz K , Bourdillon P D , Feigenbaum H 
Published: June 2012

BACKGROUND
Dysfunction after thrombolytic therapy of acute myocardial infarction (MI) may be reversible. Early after myocardial infarction, both reversible and irreversible injury may be manifested by regional wall motion abnormalities. Improved wall thickening during dobutamine infusion (dobutamine-responsive wall motion) may accurately identify reversibly injured segments.

METHODS AND RESULTS
To determine whether dobutamine-responsive wall motion accurately detects reversible postischemic dysfunction irrespective of infarct location, multistage (baseline, 4 and 12 micrograms.kg-1.min-1, and peak) dobutamine echocardiography (DE) was performed within 7 days of thrombolytic therapy. Resting echocardiography was repeated > or = 4 weeks after MI, and reversible dysfunction was defined as improved wall motion. The accuracy of dobutamine-responsive wall motion was compared with that of signs of early reperfusion, non-Q-wave MI, and peak creatine kinase (CK). Sixty-three patients underwent DE without complications. Follow-up echocardiograms were done in 51 (81%) of these patients, and wall motion improved in 22 (41%). Dobutamine-responsive wall motion during all stages of DE was very specific for reversible dysfunction (90% to 93%) but sensitive (86%) only when hemodynamics were not altered (low dose, 4 micrograms.kg-1.min-1). Non-Q-wave MI and a low peak CK (< 1000 IU/mL) were also specific (89% to 93%) but less sensitive (64% [P = .16] and 55% [P < .05], respectively). Signs of early reperfusion did not identify postischemic dysfunction. Low-dose dobutamine-responsive wall motion and non-Q-wave MI independently identified reversible dysfunction, but only dobutamine-responsive wall motion was sensitive in all infarct locations. Non-Q-wave MI was sensitive only in anterior infarction.

CONCLUSIONS
Multistage dobutamine echocardiography can be performed safely early after thrombolytic therapy. Low-dose dobutamine-responsive wall motion accurately detected reversible dysfunction in all infarct locations. Dobutamine-responsive wall motion and non-Q-wave infarction may be very useful for accurately identifying reversible dysfunction early after thrombolytic therapy for acute MI.
Can further benefit be achieved by adding flosequinan to patients with congestive heart failure who remain symptomatic on diuretic, digoxin, and an angiotensin converting enzyme inhibitor? Results of the flosequinan-ACE inhibitor trial (FACET).
Authors: Massie B M , Berk M R , Brozena S C , Elkayam U , Plehn J F , Kukin M L , Packer M , Murphy B E , Neuberg G W , Steingart R M 
Published: June 2012

BACKGROUND
Angiotensin converting enzyme inhibitors, diuretics, and digoxin are each effective in treating congestive heart failure, but many patients remain symptom-limited on all three medications. This trial was designed to determine whether the addition of oral flosequinan, a new direct-acting arterial and venous vasodilator with possible dose-dependent positive inotropic effects, improves exercise tolerance and quality of life in such patients.

METHODS AND RESULTS
In a randomized, double-blind multicenter trial, 322 patients with predominantly New York Heart Association class II or III congestive heart failure and left ventricular ejection fractions of 35% or less, who were stabilized on a diuretic, angiotensin converting enzyme inhibitor, and digoxin, were treated with 100 mg flosequinan once daily, 75 mg flosequinan twice daily, or matching placebo. Efficacy was evaluated with serial measurements of treadmill exercise time, responses to the Minnesota Living With Heart Failure Questionnaire (LWHF), and clinical assessments during a baseline phase and a 16-week treatment period. After 16 weeks, 100 mg flosequinan once daily produced a significant increment in median exercise time (64 seconds at 16 weeks) compared with placebo (5 seconds), whereas the higher-dose flosequinan group did not show a statistically significant increase. Flosequinan (100 mg once daily) also improved the overall LWHF score significantly compared with placebo; both active therapies decreased the physical component, but 75 mg flosequinan twice daily was associated with a trend toward worsening of the emotional component. Most clinical assessments tended to improve on active therapy.

CONCLUSIONS
These results indicate that additional symptomatic benefit can be attained by adding flosequinan to a therapeutic regimen already including a converting enzyme inhibitor. Because in the future most patients will fall into this category, flosequinan is a potential adjunctive agent in the management of severe congestive heart failure. However, because recent evidence indicates that the flosequinan dose studied in the present trial has an adverse effect on survival, the benefit-to-risk ratio must be assessed in individual patients.
Contrast echocardiography for evaluation of left ventricular flow dynamics using densitometric analysis.
Authors: Mizushige K , DeMaria A N , Toyama Y , Morita H , Senda S , Matsuo H 
Published: June 2012

BACKGROUND
Few data exist regarding intraventricular flow patterns in the presence of left ventricular dysfunction. Therefore, we examined the relation between intracavitary left ventricular flow dynamics and the presence of ventricular contractile abnormalities using videodensitometric analysis of transpulmonary contrast echocardiography.

METHODS AND RESULTS
Two-dimensional echocardiography was performed before, during, and after intravenous injection of sonicated albumin in 8 normal subjects, 22 patients with infarction, and 6 patients with dilated cardiomyopathy. Time-intensity curves were recorded, and disappearance half-times (in cardiac cycles) were measured for regions of interest at the mitral orifice (Ta) and mid-left ventricular cavity (Tb). We observed contrast enhancement of the left ventricular cavity in 28 of 36 patients. Ta and Tb were identical (19 beats) in all normal patients, but Tb was greater than Ta (19 versus 22 beats, P < .001) in patients with dyssynergy. Patients with dyssynergy were divided in three groups: group A, in whom Tb-Ta < or = 3; group B, in whom Tb-Ta > or = 4; and group C, which was composed of patients without contrast enhancement. Left ventricular end-diastolic dimension was similar in normal patients (46.1 mm) and group A patients (50.3 mm) but was less in each cohort than in groups B (58.7 mm) and C (64.1 mm) (all P < .01). Significant correlation was observed between Tb-Ta and both ejection fraction (r = -.67, P < .001) and wall motion index (r = .62, P < .001).

CONCLUSIONS
Clearance of contrast from the mid-left ventricular cavity is prolonged in patients with left ventricular dysfunction. This prolongation may be related to increased left ventricular diastolic volume, impaired intracavitary mixing, or paradoxical systolic flow. Delayed left ventricular contrast washout may have implications regarding the formation of left ventricular thrombi.
Regional entrainment of atrial fibrillation studied by high-resolution mapping in open-chest dogs.
Authors: Kirchhof C , Chorro F , Scheffer G J , Brugada J , Konings K , Zetelaki Z , Allessie M 
Published: June 2012

BACKGROUND
It recently has been demonstrated that during atrial fibrillation, a short and variable excitable gap exists, allowing regional control of atrial fibrillation by local stimulation. In the present study, we visualized the process of excitation during regional entrainment of atrial fibrillation by rapid pacing.

METHODS AND RESULTS
In six open-chest dogs, the excitation of the left atrial free wall was mapped using a spoon-shaped mapping electrode (248 points). Episodes of atrial fibrillation were induced by burst pacing (50 Hz, 2 seconds). During atrial fibrillation, the electrograms showed rapid irregular activity with a median cycle length of 98 +/- 16 ms (mean +/- SD, n = 6). Rapid pacing in the center of the mapping electrode at intervals slightly shorter or longer than the median atrial fibrillation interval resulted in regional capture of atrial fibrillation. The window of entrainment was 16 +/- 5 ms. Mapping of atrial fibrillation showed that the left atrium was activated by fibrillatory wavelets coming from different directions. During entrainment, a relatively large area with a diameter of about 4 cm was activated by uniform wave fronts propagating away from the site of stimulation. The area of entrainment was limited by intra-atrial conduction block and by collision with fibrillation waves. Regional control of atrial fibrillation was lost by pacing either too slowly or too rapidly. In the first case, retrograde invasion of the area of entrainment by fibrillatory waves resulted in depolarization of the pacing site prior to the stimulus. Pacing too rapidly caused acceleration of atrial fibrillation by induction of local intra-atrial reentry circuits with a revolution time shorter than the pacing interval.

CONCLUSIONS
During atrial fibrillation, an area with a diameter of about 4 cm can be entrained by local pacing. The resulting reduction in fibrillating tissue mass was not sufficient to terminate atrial fibrillation. Extension of the area of entrainment was limited by intra-atrial conduction block, whereas entrainment at a too high rate resulted in acceleration of atrial fibrillation by induction of local microreentry.
Right ventricular-vascular interaction in congestive heart failure. Importance of low-frequency impedance.
Authors: Kussmaul W G , Altschuler J A , Matthai W H , Laskey W K 
Published: June 2012

BACKGROUND
Vasodilator agents are widely used in congestive heart failure. These agents may have important effects on the pulsatile aspects of right ventricular hydraulic load.

METHODS AND RESULTS
Fifteen patients with severe congestive heart failure were studied during cardiac catheterization by use of high-fidelity pressure transducers and a catheter-mounted flow velocity probe. Three graded doses of nitroprusside were infused as pulmonary artery (PA) pressure and flow were continuously recorded. From Fourier transforms of signal-averaged waves, PA impedance, hydraulic power, and wave reflection indices were derived. At the highest dose of nitroprusside (66 +/- 41 micrograms/min), cardiac output was significantly improved, whereas PA mean and wedge pressure, resistance, impedance at the first harmonic, characteristic impedance, and wave reflection amplitude were all reduced. At the dose (32 +/- 20 micrograms/min) at which cardiac output first showed improvement, only PA mean pressure and first-harmonic impedance were significantly reduced. Hydraulic power cost per unit of forward flow was also lowered at this dose, despite lack of significant change in pulmonary vascular resistance. At the lowest dose of nitroprusside (11 +/- 4 micrograms/min), six patients experienced a decrease in stroke volume, whereas the other nine were either unchanged (n = 1) or showed an increase (n = 8). Multiple regression revealed that only the change in first-harmonic impedance correlated with this effect, increasing when stroke volume decreased and decreasing when stroke volume increased (P = .02). The change in first-harmonic impedance at this dose appeared to be caused by alterations in the amplitude of PA wave reflections. At higher doses, changes in mean PA pressure (but not in pulmonary vascular resistance) correlated with changes in stroke volume.

CONCLUSIONS
Nitroprusside vasodilation at low doses alters PA hemodynamics in congestive heart failure primarily through changes in low-frequency impedance. In some patients, this effect is associated with decreased stroke output. At higher doses, favorable alterations in resistance, low- and high-frequency impedance, and wave reflections all contribute to increased forward flow and decreased power requirement per unit forward flow. These findings show that ventricular-vascular interaction is importantly affected by pulmonary vasodilation and that appreciation of pulsatile properties is required to understand the effects of pulmonary vasodilation on cardiac output.
Influence of implantable cardioverter-defibrillators on the long-term prognosis of survivors of out-of-hospital cardiac arrest.
Authors: Powell A C , Fuchs T , Finkelstein D M , Garan H , Cannom D S , McGovern B A , Kelly E , Vlahakes G J , Torchiana D F , Ruskin J N 
Published: June 2012

BACKGROUND
Survivors of out-of-hospital cardiac arrest not associated with acute myocardial infarction are at high risk for recurrent cardiac arrest and sudden cardiac death. The impact of the implantable cardioverter-defibrillator on long-term prognosis in these patients is uncertain.

METHODS AND RESULTS
Three hundred thirty-one survivors of out-of-hospital cardiac arrest (age, 56 +/- 13.7 years) underwent electrophysiologically guided therapy. Implantable defibrillators were placed in 150 patients (45.3%), and 181 patients (54.7%) received pharmacological and/or surgical therapy alone. Left ventricular ejection fraction was 35.2 +/- 16.6% in defibrillator recipients and 45.3 +/- 18.2% in nondefibrillator patients. Median patient follow-up was 24 months in the defibrillator group and 46 months in the nondefibrillator group. In a proportional hazards model, the independent predictors of total cardiac mortality were left ventricular ejection fraction of less than 0.40 (relative risk, 4.55; 95% confidence interval, 2.44 to 8.33; P = .0001), absence of an implantable defibrillator (relative risk, 2.70; confidence interval, 1.41 to 5.00; P = .017), and persistence of inducible sustained ventricular tachycardia (relative risk, 1.84; 95% confidence interval, 0.97 to 3.49; P = .045). The 1- and 5-year probabilities of survival free of cardiac mortality in patients with left ventricular ejection fraction of less than 0.40 were 94.3% and 69.6% with a defibrillator and 82.1% and 45.3% without a defibrillator, respectively. For patients with left ventricular ejection fraction of 0.40 or more, the 1- and 5-year probabilities of survival free of cardiac mortality were 97.7% and 94.6% with a defibrillator and 95.4% and 86.9% without a defibrillator, respectively.

CONCLUSIONS
In survivors of out-of-hospital cardiac arrest, the implantable defibrillator is associated with a reduction in cardiac mortality, particularly in patients with impaired left ventricular function.
Transcatheter occlusion of patent ductus arteriosus with adjustable buttoned device. Initial clinical experience.
Authors: Rao P S , Sideris E B , Haddad J , Rey C , Hausdorf G , Wilson A D , Smith P A , Chopra P S 
Published: June 2012

BACKGROUND
Several devices are available for transcatheter occlusion of patent ductus arteriosus. Most of these devices either require complicated intracardiac maneuvering, have not been tried in humans, or need a large-sized sheath for implantation of the device.

METHODS AND RESULTS
During a 26-month period ending November 1992, 14 patients underwent transcatheter closure of patent ductus arteriosus with an adjustable buttoned device delivered via a 7F sheath under an institutional review board-approved custom-made device protocol. The children were 15 months to 8 years of age with weight range of 7.2 to 19 kg. The patent ductus arteriosus measured from 2 to 7.5 mm (median, 3 mm) at the narrowest diameter and was conical, short, or tubular. They were occluded with devices measuring 15 to 20 mm. The ratio of pulmonary to systemic flow decreased (P < .01) from 1.9 +/- 0.6 (mean +/- SD; range, 1.3 to 3.2) to 1.05 +/- 0.1 (1 to 1.3). Continuous murmur of patent ductus arteriosus disappeared in all except 1 patient. Small residual shunts were detected by color Doppler studies in 4 of 14 patients (29%). All patients were followed for 1 to 24 months (mean, 6 +/- 7 months). The device was intact in all patients, and no breakage of the wires was noted. No shunts were seen in 12 of 14 patients (86%), and minute residual shunts were seen in 2 children. No major complications were encountered.

CONCLUSIONS
It is concluded that transcatheter closure of patent ductus arteriosus with the adjustable buttoned device is feasible and effective and can be accomplished via small 7F sheaths; a 7F sheath is adequate for all ductal sizes; and the adjustable length of the loop accommodated all types of patent ductus arteriosus. Clinical trials on a larger number of patients are warranted.