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Acute Occlusion (acute + occlusion)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Restored Atrial Excitability After Late Recanalization in a Patient with Atrial Standstill and Acute Myocardial Infarction

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2002
TAKA-AKI KOSHIMIZU
KOSHIMIZU, T-A., et al.: Restored Atrial Excitability After Late Recanalization in a Patient with Atrial Standstill and Acute Myocardial Infarction. Atrial standstill is electrophysiologically characterized by the loss of spontaneous excitation in atrial muscle and the inability to cause action potential firing upon electrical stimulation. Clinical diagnosis of transient standstill of the right atrium was made in a patient with acute occlusion of the right coronary artery and acute renal failure. Percutaneous coronary intervention, performed 5 days after the onset, restored the coronary blood flow and resulted in full recovery of electrical activity and regular sinus rhythm. [source]

,-Adrenergic inhibition increases collateral circuit conductance in rats following acute occlusion of the femoral artery

THE JOURNAL OF PHYSIOLOGY, Issue 6 2008
Jessica C. Taylor
This study evaluated whether ,-adrenergic activation contributes to collateral circuit vascular resistance in the hindlimb following acute unilateral occlusion of the femoral artery in rats. Blood pressures (BPs) were measured above (caudal artery) and below (distal femoral artery) the collateral circuit. Arterial BPs were reduced (15,35 mmHg) with individual (prazosin, rauwolscine) or combined (phentolamine) ,-receptor inhibition. Blood flows (BFs) were measured using microspheres before and after , inhibition during the same treadmill speed. ,1 inhibition increased blood flow by ,40% to active muscles that were not affected by femoral occlusion, whereas collateral-dependent BFs to the calf muscles were reduced by 29 ± 8.4% (P < 0.05), due to a decrease in muscle conductance with no change in collateral circuit conductance. ,2 inhibition decreased both collateral circuit (39 ± 6.0%; P < 0.05) and calf muscle conductance (36 ± 7.3%; P < 0.05), probably due to residual ,1 activation, since renal BF was markedly reduced with rauwolscine. Most importantly, inhibiting ,2 receptors in the presence of ,1 inhibition increased (43 ± 12%; P < 0.05) collateral circuit conductance. Similarly, non-selective , inhibition with phentolamine increased collateral conductance (242 ± 59%; P < 0.05). We interpret these findings to indicate that both ,1 - and ,2 -receptor activation can influence collateral circuit resistance in vivo during the high flow demands caused by exercise. Furthermore, we observed a reduced maximal conductances of active muscles that were ischaemic. Our findings imply that in the presence of excessive sympathetic activation, which can occur in the condition of intermittent claudication during exertion, an exaggerated vasoconstriction of the existing collateral circuit and active muscle will occur. [source]

Extraction of previously deployed stent by an entrapped cutting balloon due to the blade fracture

CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 2 2002
Akio Kawamura MD
Abstract During treatment for in-stent restenosis, entrapment of cutting balloon occurred because of the blade fracture. Removal of the balloon caused stent extraction, inducing acute occlusion of the coronary artery. Application of cutting balloon for in-stent restenosis requires every caution against such type of complications. Cathet Cardiovasc Intervent 2002;57:239,243. © 2002 Wiley-Liss, Inc. [source]

Epidemiology and stratification of risk for sudden cardiac death

CLINICAL CARDIOLOGY, Issue S1 2005
Philip J. Podrid M.D.
Abstract Sudden cardiac death (SCD) is a major cause of mortality in the United States. Approximately 65% of cases of SCD occur in patients with underlying acute or chronic ischemic heart disease. The incidence of SCD increases 2- to 4-fold in the presence of coronary disease and 6- to 10-fold in the presence of structural heart disease. Ventricular fibrillation (VF) precipitated by ventricular tachycardia (VT) is a common mechanism of cardiac arrest leading to SCD. Triggers for SCD include electrolyte disturbances, heart failure, and transient ischemia. Although a large percentage of patients with out-of-hospital SCD do not survive, successful resuscitation to hospitalization has improved in recent years. One of the challenges for preventing SCD lies in identifying individuals at highest risk for SCD within a lower-risk population. The progression from conventional risk factors of coronary artery disease to arrhythmogenesis and SCD can be represented as a cascade of changes associated with levels of increasing risk. At the first level is atherogenesis, followed by changes in atherosclerotic plaque anatomy, which may be mediated by inflammatory processes. Disruption of active plaque formed during a transitional state initiates the thrombotic cascade and acute occlusion, after which acute changes in myocardial electrophysiology become the immediate trigger for arrhythmogenesis and SCD. Each level of the cascade offers different opportunities for risk prediction. Among the classes of risk predictors are clinical markers, such as ECG measures and ejection fraction. Transient risk markers, such as inflammatory markers, are potentially useful for identifying triggers for SCD. In the future, genetic profiling is expected to allow better assessment of individual risks for SCD. [source]