Cognitive dysfunction in advanced heart failure and prospective cardiac assist device patients.

BACKGROUND: Extended periods of hypoperfusion in an advanced heart failure (HF) places patients at high risk for neurobehavioral compromise, which has not been studied systematically. It is also not clear how intravenous inotropic therapy and mechanical cardiac assist devices (MCAD) affect cognitive function. METHODS: This prospective cross-sectional cognitive preliminary study evaluated 252 potential heart transplant candidates assessing functions in memory, motor, and processing speed. Patients were divided into three HF groups based on severity of disease: group 1 outpatients (n = 113), group 2 in-patients requiring inotropic infusion (n = 83), and group 3 inpatients likely requiring MCAD support (n = 56). Aggregate z-scores for memory, motor, and processing speed and independent samples t tests assessed intergroup differences on 13 cognitive measures. RESULTS: A broad pattern of cognitive impairment was observed within the advanced HF group; fewer deficits were found in group 1 outpatients and more severe deficits in group 3 MCAD subjects. A difference in motor functions was observed as the earliest abnormality, with group 3 showing significant changes compared with group 1. The most dramatic changes were seen in domain mental processing speed along with specific verbal and visual memory functions, which were slower in group 3 compared with groups 1 and 2. CONCLUSIONS: Cognitive deficits are common in advanced HF and worsen with increasing severity of HF. Appropriately designed and randomized studies will be needed to demonstrate if earlier MCAD implantation is warranted to arrest cognitive dysfunction and better postimplantation adaptation.

Patent foramen ovale and stroke risk: incidental finding or causal culprit?

Between 17 and 27% of the population has a patent foramen ovale (PFO) based on autopsy studies. Given these percentages, a PFO could be considered a variant of normal cardiac anatomy and not an anomaly. As this anatomy is so prevalent in the normal population, it is likely that there are other factors involved in patients who have a PFO and a stroke. This review will evaluate the existing literature on PFO and stroke to determine what constitutes an increased risk of embolic events in patients with PFO. Given the paucity of existing literature, it is clear from this review that there is a vital need for randomized clinical trials to answer important questions, including what constitutes high-risk anatomy and optimal treatment for patients for the prevention of recurrent stroke.

The syndrome of irreversible acidosis after prolonged propofol infusion.

INTRODUCTION: Propofol infusion syndrome is described in the pediatric literature as metabolic acidosis, rhabdomyolysis, and bradycardia that results in death. The pathogenesis of this syndrome is thought to be activation of the systemic inflammatory response, which culminates in acidosis and muscle necrosis. MATERIALS AND METHODS: Retrospective chart review of three patients in the Neurological Critical Care Units at Hahnemann and Massachusetts General Hospitals between October 2001 and September 2004. RESULTS: Patient 1: A 27-year-old woman had seizures secondary to hemorrhage from an arteriovenous malformation. Propofol coma was induced for sedation. After initiation of propofol, she developed a metabolic acidosis, hypotension, and bradycardia and expired. Patient 2: A 64-year-old man presented in status epilepticus. After prolonged propofol administration, he developed metabolic acidosis, hypotension, and rhabdomyolysis and expired. Patient 3: A 24-year-old woman presented in status epilepticus secondary to encephalitis. Propofol was added for seizure control. She developed hypotension, metabolic acidosis, and bradyarrhythmias. Despite transvenous pacing, she expired. CONCLUSION: These data show an association between extended propofol use and metabolic acidosis, rhabdomyolysis, and death in adults, as well as children. Risk factors for propofol infusion syndrome in adults include lean body mass index, high dose, and administration of more than 24-hour duration. Creatine phosphokinase, lactic acid levels, electrolytes, and arterial blood gases should be monitored frequently. Both bacterial and fungal cultures should be obtained. If this syndrome is suspected, hemodialysis should be considered. In fatal cases, autopsy should include electron microscopy of cardiac and skeletal muscle to look for mitochondrial dysfunction. Further study is warranted.

Relative changes in flow velocities in vasospasm after subarachnoid hemorrhage: a transcranial Doppler study.

INTRODUCTION: Transcranial Dopplers (TCDs) have been used to monitor cerebral blood flow velocities in subarachnoid hemorrhage (SAH).The purpose of our two-part study was to compare the reliability of relative increases in flow velocities with conventionally used absolute flow velocity indices and to correct for hyperemia-induced flow velocity change. METHODS: Part 1: Charts of 50 patients admitted to Hahnemann University Hospital with aneurismal SAH were reviewed. Mean middle cerebral artery maximum flow velocities (MCA-MFV) were reviewed for initial flow velocities (IFVs) and maximal flow velocities (MFVs) that were reached during hospital course. Correlating flow velocities (SFVs) were noted in patients who developed symptomatic vasospasm. MFV/IFV and SFV/IFV ratios were calculated to evaluate relative changes in flow velocity. Part 2: Correction for hyperemia was derived from Lindegaards Ratio using extracranial internal carotid artery (ICA) flow velocity ratio (corrected MCA-MFV/observed MCA-MFV = EC-ICAFV (day1)/observed EC-ICAFV). RESULTS: Part 1: All 10 patients who developed symptomatic vasospasm exhibited a twofold increase (SFV/IFV: >2) in flow velocities prior to developing symptomatic vasospasm, and 5 patients had a threefold increase (SFV/IFV: >3). Of the 40 patients who did not develop symptomatic vasospasm, 33 patients did not have a twofold increase in their flow velocities at any time. The positive predictive value for MFV/IFV greater than 3 (n = 6) and SFV/IFV greater than 3 (n = 5) was 100%. The negative predictive value for MFV/IFV less than 2 (n = 33) was 100%. Data using relative changes (twofold increase) in flow velocity was more sensitive (100 to 90%), specific (83 to 70%), and predictive (positive predictive value [PPV]: 59 to 45%; negative predictive value [NPV]: 100 to 97%) for symptomatic vasospasm than absolute flow velocity indices using MCA-MFV greater than 120 even in combination with Lindegaards Ratio (MCA/ICA greater than 3). Part 2: Correction for hyperemia by modifying Lindegaard's Index in the 32 patients where data was available improved the PPV of absolute flow velocities from 44 to 62%. In this population, the application of this equation while evaluating relative change in flow velocities improved PPV of twofold increase from 57 to 73%. CONCLUSION: Relative changes in flow velocities in patients with aneurysmal SAH correlated better with clinically significant vasospasm than absolute flow velocity indices. Correction for hyperemia improved predictive value of TCD in vasospasm.

Diffuse cerebral air embolism treated with hyperbaric oxygen: a case report.

A 54-year-old woman presented for cardiac evaluation of atypical chest pain. Workup included coronary angiography and a left ventriculogram, during which air was inadvertently injected, resulting in the development of an acute right hemisphere syndrome. Right carotid angiography was immediately performed, yielding only a delayed diffuse venous phase without focal vessel cutoffs. Within 60 minutes, the patient underwent hyperbaric oxygen therapy for the suspected cerebral air emboli. After removal from the chamber for technical reasons, she had a generalized tonic-clonic seizure, and further hyperbaric oxygen therapy was withheld. Initial computed tomography imaging obtained approximately 8 hours after symptom onset showed signs of early right hemispheric edema. Subsequent magnetic resonance imaging studies were markedly abnormal and suggestive of diffuse bilateral but predominantly right-sided parietal lobe edema with mildly positive diffusion-weighted imaging. Follow-up magnetic resonance imaging at 6 months was normal, and the patient's neurological examination returned to normal.