Assessment of myocardial triglyceride oxidation with PET and 11C-palmitate

Background  The goal of this study was to test whether myocardial triglyceride (TG) turnover including oxidation of TG-derived fatty acids (FA) could be assessed with PET and ¹¹C-palmitate. Methods and Results  A total of 26 dogs were studied fasted (FAST), during Intralipid infusion (IL), during a hyperinsulinemic-euglycemic clamp without (HIEG), or with Intralipid infusion (HIEG + IL). ¹¹C-palmitate was injected, and 45 minutes were allowed for labeling of myocardial TG pool. 3D PET data were then acquired for 60 minutes, with first 15 minutes at baseline followed by 45 minutes during cardiac work stimulated with constant infusion of either phenylephrine (FAST, n = 6; IL, n = 6; HIEG + IL, n = 6) or dobutamine (FAST, n = 4; HIEG, n = 4). Myocardial ¹¹C washout during adrenergic stimulation (AS) was fitted to a mono-exponential function (Km(PET)). To determine the source of this ¹¹C clearance, Km(PET) was compared to direct coronary sinus-arterial measurements of total ¹¹C activity, ¹¹C-palmitate, and ¹¹CO₂. Before AS, PET curves in all groups were flat indicating absence of net clearance of ¹¹C activity from heart. In both FAST groups, AS resulted in negligible net ¹¹C activity and ¹¹CO₂ production higher than net ¹¹C-palmitate uptake. AS with phenylephrine resulted in net myocardial uptake of total ¹¹C activity and ¹¹C-palmitate in IL and HIEG + IL, and ¹¹CO₂ production lower than ¹¹C-palmitate uptake. In contrast, AS with dobutamine in HIEG resulted in net clearance of all ¹¹C metabolites (total ¹¹C activity, ¹¹C-palmitate and ¹¹CO₂) with ¹¹CO₂ contributing 66% to endogenous FA oxidation. The AS resulted in significant Km(PET) in all the groups, except HIEG + IL. However, positive correlation between Km(PET) and ¹¹CO₂ was observed only in HIEG (R ² = 0.83, P = .09). Conclusions  This is the first study to demonstrate that using PET and pre-labeling of intracardiac TG pool with ¹¹C-palmitate, noninvasive assessment of myocardial TG use is feasible under metabolic conditions that favor endogenous TG use such as increased metabolic demand (β-adrenergic stimulation of cardiac work) with limited availability of exogenous substrate (HIEG).     

Speech-controlled generation of radiology reports

Voice entry has been successfully employed to generate radiology reports with a word recognizer with a 1,000-word lexicon capacity. About 50% of reports were able to be dictated with a single 900-word lexicon. This was split into five sections by anatomic or subspecialty application. Each was augmented to 900 words. By switching from one lexicon to another, it was possible to dictate more than 70% of reports. With exclusive use of three lexicons in subspecialty areas (gastrointestinal radiology, neuroradiology, and mammography), and with further modification of the respective vocabulary, it has been possible to employ the system 88% of the time. Twelve percent of cases included wording that was beyond the scope of the lexicon. Computer subsets that allow different translations of some words when used in different contexts have been used. Some of these are used as triggers that will print whole lines, sentences, or even complete reports. Dictation times with voice entry take about 20% longer. Recognition reliability has been greater than 95%.     

Motor Axonal Neuropathy During Treatment With Simvastatin

Simvastatin is a cholesterol-lowering drug that acts by inhibiting hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol synthesis. Abnormal laboratory findings include transient increases in serum creatine kinase (CK) due to a myopathic syndrome. Rarely, neurological side effects include axonal sensory-motor peripheral neuropathy, characterized in some cases by a prevalent motor involvement accompanied by subclinical sensory damage. We report a case of purely motor axonal neuropathy associated with simvastatin. A 72-year-old woman, after five years of treatment with simvastatin, developed progressive weakness, cramps and fasciculations mainly involving proximal muscles in the lower limbs, though without sensory symptoms or signs. Deep reflexes were lost in the lower limbs. There was no sign of upper motor-neuron involvement. CK was elevated (up to 2000 U/l). EMG showed marked neurogenic damage with fibrillations and fasciculations in the lower limbs. ENG showed motor fiber loss within the lower limb nerves without involvement of sensory fibers. CSF examination was normal. Deltoid muscle biopsy showed neurogenic changes and some ragged-red fibers. One year after simvastatin withdrawal the patient's state of weakness improved and the cramps resolved. The CK level dropped to 700 U/l.