This consensus statement of the Multi-Society Task Force summarizes current knowledge of the medical aspects of the persistent vegetative state in adults and children. The vegetative state is a clinical condition of complete unawareness of the self and the environment, accompanied by sleep-wake cycles, with either complete or partial preservation of hypothalamic and brain-stem autonomic functions. In addition, patients in a vegetative state show no evidence of sustained, reproducible, purposeful, or voluntary behavioral responses to visual, auditory, tactile, or noxious stimuli; show no evidence of language comprehension or expression; have bowel and bladder incontinence; and have variably preserved cranial-nerve and spinal reflexes. We define persistent vegetative state as a vegetative state present one month after acute traumatic or nontraumatic brain injury or lasting for at least one month in patients with degenerative or metabolic disorders or developmental malformations. The clinical course and outcome of a persistent vegetative state depend on its cause. Three categories of disorder can cause such a state: acute traumatic and non-traumatic brain injuries; degenerative and metabolic brain disorders, and severe congenital malformations of the nervous system. Recovery of consciousness from a posttraumatic persistent vegetative state is unlikely after 12 months in adults and children. Recovery from a nontraumatic persistent vegetative state after three months is exceedingly rare in both adults and children. Patients with degenerative or metabolic disorders or congenital malformations who remain in a persistent vegetative state for several months are unlikely to recover consciousness. The life span of adults and children in such a state is substantially reduced. For most such patients, life expectancy ranges from 2 to 5 years; survival beyond 10 years is unusual.

Right ventricular infarction complicates up to half of inferior left ventricular infarctions. The term represents a spectrum of disease from mild, asymptomatic right ventricular dysfunction to cardiogenic shock, and it includes transient ischemic myocardial dysfunction as well as myocardial necrosis. Right ventricular infarction is associated with considerable morbidity and mortality, and its presence defines a high-risk subgroup of patients with inferior left ventricular infarction. Diagnosis of this condition requires a high degree of suspicion based on clinical findings and the early recording of the electrocardiogram through right precordial leads, as well as elevated right-sided filling pressures out of proportion to left-sided filling pressures. The proper management of right ventricular infarction requires sustaining adequate right ventricular preload with volume loading and maintenance of atrioventricular synchrony, reduction of right ventricular afterload (particularly when left ventricular dysfunction is present), and inotropic support of the right ventricle. Early reperfusion with fibrinolytic therapy or direct angioplasty is also warranted. Survivors of right ventricular infarction generally have a restoration of normal right ventricular function with resolution of hemodynamic abnormalities.

It is evident that cellular infiltration can affect cardiac structure and function in a variety of disease states. Myocardial contractility can be impaired by cell-mediated injury or local release of cytokines. The study of immune cardiac disease has entered a period of rapid expansion that should be characterized by delineation of the mechanisms by which immune cells and factors localize in the myocardium, modulate myocyte function, and remodel myocardial architecture (Fig. 2). This new knowledge should result in the ability to target specifically both the pathways by which cardiac contractility is impaired by chronic inflammation and the sustained immune reactivity to cardiac antigens that underlies chronic myocardial inflammation. Nonspecific therapeutic interventions directed at congestive heart failure, currently the only acceptable approach to the treatment of immune myocarditis, should then serve a more ancillary function in the context of the use of rationally designed drugs. Such drugs could, for example, be specifically targeted to inhibiting the trafficking of leukocytes into the heart or the effects of their subsequent activation within the myocardium.