Circulation
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Since there is considerable evidence that leukocytes contribute to tissue injury during ischemia and reperfusion, the present study was designed to: (1) determine whether reperfusion in vivo with leukopenic blood affords protection in a model of reversible hypothermic ischemia, (2) determine the duration of any protection, (3) characterize the relation between protection and duration of leukopenic perfusion, and (4) assess the effect of leukopenic reperfusion on myocardial glutathione content. ⋯ Reperfusion with leukopenic blood accelerated the rate of recovery of cardiac function after reversible myocardial injury but did not lead to a sustained increase in the eventual extent of recovery. Reperfusion with leukopenic blood for the first 10 minutes of reflow is sufficient to obtain this benefit.
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"Preconditioning" with brief episodes of coronary artery occlusion reduces infarct size caused by subsequent sustained ischemia. However, the effects of preconditioning on the coronary vasculature are poorly understood. We sought to determine whether preconditioning would attenuate "low reflow" (ie, the deterioration in resting myocardial perfusion) and blunt the loss in coronary vasodilator reserve after sustained occlusion/reperfusion in the anesthetized open-chest canine model. ⋯ The protective effects of preconditioning do not extend to the coronary vasculature in this canine model: Preconditioning neither prevented the deterioration in resting myocardial perfusion nor blunted the loss in submaximal vasodilator reserve obs
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Review
Atrioventricular nodal reentry. Clinical, electrophysiological, and therapeutic considerations.
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. ⋯ 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.
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The Pediatric Electrophysiology Society studied children with the long QT syndrome (LQTS) to describe the features of LQTS in patients less than 21 years old, define potential "low-risk" and "high-risk" subpopulations, and determine optimal treatment. ⋯ The appearance of 2:1 atrioventricular block, multiform premature ventricular contractions, and torsade de pointes are relatively more common in children with LQTS than other children and should raise the index of suspicion for LQTS. Because 9% of patients presented with cardiac arrest and no preceding symptoms, perhaps prophylactic treatment in asymptomatic children is indicated. Asymptomatic patients with normal QTc and positive family history may be a low-risk group. Patients with QTc of more than 0.60 are at particularly high risk for sudden death, and if treatment is not effective, consideration should be given to cardiac sympathetic denervation, pacemaker implantation, and perhaps implantation of a defibrillator.
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In most patients, cardiac tamponade should be diagnosed by a clinical examination that shows elevated systemic venous pressure, tachycardia, dyspnea, and paradoxical arterial pulse. Systemic blood pressure may be normal, decreased, or even elevated. The diagnosis is confirmed by echocardiographic demonstration of moderately large or large circumferential pericardial effusion and in most instances, of right atrial compression, abnormal respiratory variation in right and left ventricular dimensions, and in tricuspid and mitral valve flow velocities. ⋯ Patients with moderately large or large pericardial effusions may have echocardiographic evidence of right atrial compression without clinical signs of elevated venous pressure or pulsus paradoxus. The majority of these patients have mild or moderate tamponade and if not subjected to pericardial drainage, should be observed closely. In some of these patients, when the etiology is known and the disease can be treated effectively with medication, e.g., nonsteroidal anti-inflammatory agents or adrenal corticosteroids in Dressler's syndrome or relapsing pericarditis, pericardial drainage may not be necessary.