Circulation
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Randomized Controlled Trial Comparative Study Clinical Trial
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).
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. ⋯ 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.
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There are two competing theories of the mechanism of blood flow during cardiopulmonary resuscitation. The "cardiac pump" theory postulates that blood flows because the heart is squeezed between the sternum and the spine. The "thoracic pump" theory postulates that blood flows from the thorax because intrathoracic pressure exceeds extrathoracic vascular pressure and that flow is restricted to the venous-to-arterial direction because of venous valves that prevent retrograde flow at the thoracic inlet. To determine which mechanism is operative during actual cardiopulmonary resuscitation, 20 patients were imaged with transesophageal echocardiography during resuscitation. ⋯ Transesophageal echocardiography performed during actual cardiopulmonary resuscitation showing mitral valve opening during cardiac release, reduction of ventricular cavity size with compression, and atrioventricular regurgitation support the cardiac pump theory of cardiopulmonary resuscitation. This study demonstrates the feasibility and usefulness of transesophageal echocardiography during cardiopulmonary resuscitation.
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Short-term hibernating myocardium is characterized by a decrease in contractile function in proportion to the reduced myocardial blood flow. Myocardial creatine phosphate content, initially decreased during the first minutes of ischemia, returns to near-control values, the ischemia-induced net lactate production is attenuated, and the myocardium remains viable despite ongoing hypoperfusion and contractile dysfunction. Hibernating myocardium after 85 minutes of ischemia maintains an inotropic reserve and responds to short-term intracoronary dobutamine infusion with increased work; however, this inotropic response is at the expense of metabolic recovery. We therefore hypothesized that the development of myocardial hibernation is a delicate process that is easily disturbed by unfavorable alterations in the oxygen-supply demand balance. ⋯ Both the increased severity of ischemia and the enhanced energy expenditure induced by dobutamine impair the development of myocardial short-term hibernation and precipitate myocardial infarction.
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Current knowledge of risk assessment in survivors of myocardial infarction is largely based on data gathered before the advent of thrombolysis. It must be determined whether and to what extent available information and proposed criteria of prognostication are applicable in the thrombolytic era. ⋯ A decline in 6-month mortality of myocardial infarction survivors, seen within 6 hours of symptom onset, has been observed in recent years. Ineligibility for exercise test, early left ventricular failure, and recovery-phase left ventricular dysfunction are the most powerful (RR, > 2) predictors of 6-month mortality among patients recovering from myocardial infarction after thrombolysis. Qualitative variables reflecting residual myocardial ischemia do not appear to be risk predictors. The lack of an independent adverse influence of early post-myocardial infarction angina on 6-month survival represents a major difference between this study and those of the prethrombolytic era.
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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.