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A 57-year-old woman presented to the Emergency Department with symptoms of worsening heart failure (HF). She had a past medical history of breast cancer treated with surgery and chemotherapy with anthracyclines and no family history of cardiomyopathy (CMP). In the last year, she received a diagnosis of HF with normal coronary arteries, during hospitalization for acute onset of dyspnea and was treated with medical therapy. After several months, few days before admission to our hospital, an echocardiography (ECHO) showed features of left ventricular noncompaction (LVNC), not described in previous ECHO and further confirmed by cardiac magnetic resonance. This case highlights the current uncertainties regarding the pathogenesis of LVNC and the clinical challenge of cardiologists facing LVNC morphology to decide if they are observing a genetic CMP, a phenotype overlapping with dilated or hypertrophic CMP, or a variant of the left ventricular (LV) wall anatomy. No consensus exists among scientific communities regarding diagnostic criteria of LVNC and in most cases; the key element in the diagnostic decision is not the LVNC by itself, but the associated LV dilation and/or dysfunction, hypertrophy, arrhythmias, and embolic events., (© 2019 S. Karger AG, Basel.)

The epoxide hydrolase activity with styrene oxide as substrate was investigated in the nuclear fraction of human fetal and adult liver specimens. All investigated liver fractions catalyzed the hydration of styrene oxide and the average epoxide hydrolase activities were 0.37 and 1.90 nmol/min/mg protein in fetal and adult specimens, respectively. The enzyme followed Michaelis-Menten kinetics in fetal nuclear fraction and biphasic kinetics in adult livers. The nuclear/microsomal enzyme activity ratios of epoxide hydrolase were 0.09 and 0.11 for fetal and adult livers, respectively.

Sulfotransferase with 2-naphthol as substrate was investigated in the cytosolic fraction of human fetal liver, lungs, kidneys, adrenal glands, intestine and placenta and also in liver, lungs, kidneys, intestinal and urinary bladder mucosa from human adult subjects. All tissue specimens assayed catalyzed the sulfation of 2-naphthol at a significant rate. The activity (expressed as pmole per minute per milligram protein; mean +/- SD) was 211 +/- 197 (n = 46) fetal liver; 22 +/- 12 (n = 29) placenta; 625 +/- 205 (n = 42) human adult liver. In fetal kidneys (576 +/- 177; n = 6) and gut (558 +/- 293; n = 6) the activity was twice as high as in liver. In the lungs (273 +/- 125; n = 6) and in the adrenals (174 +/- 119; n = 19) the sulfotransferase activity was comparable with the hepatic one. In human adult extrahepatic tissues the highest activity was found in the intestinal mucosa (153 +/- 49; n = 4) and the lowest one in the urinary bladder mucosa (16 +/- 4; n = 4). This paper shows that the sulfotransferase has a wide distribution in the human fetus and the distribution pattern of this enzyme is different in the human fetus and adult subject.