We observed abrupt changes in sympathovagal balance in the last 5 minutes preceding an episode of atrial fibrillation. This can be related to a double behavior in the neurogenic drive: in Type A episodes there is an increase of the LF spectrum, LF:HF ratio, and a decrease of the HF spectrum consistent with an increase of neurogenic sympathetic drive; in Type B episodes there is a reduction of the LF spectrum, LF/HF ratio, and an increase of HF spectrum consistent with an enhancement of the neurogenic parasympathetic drive. In some patients, we found that the two mechanisms operate during different hours of the day and that sometimes there is an increase of sympathetic tone, and in the same instances an increase of parasympathetic tone. Heart-rate variability measures fluctuation in autonomic inputs to the heart rather than the mean level of autonomic impulse; autonomic imbalance is probably more important than the vagal or sympathetic drive alone.
A 58-year-old man with chronic renal failure developed severe muscle pain and tenderness 1 week after starting bezafibrate 400 mg daily. Serum creatine kinase was 32,280 U/l. Muscle biopsy revealed scattered necrotic fibers and mild type 2b atrophy. Muscle total and free carnitine were at the upper limits of the normal range. Biochemical investigations of muscle homogenate showed normal carnitine pelmityl transferase (CPT) as well as normal individual glycolytic and mitochondrial enzyme activities. Withdrawal of the drug was followed by rapid clinical improvement. Our study casts doubt on the hypothesis that bezafibrate is able to affect muscle metabolic pathways. It is likely that the drug acts on cholesterol constituents of the muscle membrane, producing discontinuities of the sarcolemma and initiating cell necrosis.
We present a case of Loëffler endocarditis in a 45-year-old man. This syndrome is characterized by unexplained prolonged and marked hypereosinophilia (>1500 eosinophils/mm), absence of a primary cause of hypereosinophilia and evidence of eosinophil-mediated organ damage. Detection of cardiac damage is based on electrocardiography, echocardiography, cardiac MRI and endomyocardial biopsy. Two-dimensional echocardiography is an essential tool for diagnosis. In this case, a transthoracic echocardiogram revealed a complete obliteration of the apex of both ventricles associated with a restrictive left ventricular filling pattern.
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