We developed an animal model of coronary spasm in swine, similar to coronary spasm in patients with variant angina based on the angiographic findings. In this animal model, an impairment of endothelium-dependent dilatation appeared to play a minor role while the hypercontraction of the medial muscle cells by histamine and serotonin at the spastic site played a major role in the induction of coronary spasm. In Göttingen male miniature swine receiving focal endothelial denudation, moderate hypercholesterolemia and X-ray irradiation, the abrupt, severe and prolonged coronary spasm resulted in a sudden progression of organic coronary stenosis mainly due to intraplaque hemorrhage and also in acute myocardial infarction.
QT dispersion, a measure of inhomogenous ventricular repolarization, was measured in diabetic patients with foot ulcer. We recruited 75 patients with non-insulin-dependent diabetes mellitus : patients with neuropathic ulcer (n=15, NU group), with ischemic ulcer (n=20, IU group), with previous myocardial infarction (n=20, MI group) and without any diabetic microangiopathies (n=20, DC group). We also studied normal control subjects (n=15, NC group). The interlead variability of rate-corrected OT interval (QTc dispersion) was calculated. QTc interval in the MI group was significantly higher than that in the NC or DC but showed no difference in the NU and IU groups. QTc dispersion in the IU (54±15 msec) as well as MI (60±21 msec) group were significantly higher than the NC (36±18 msec) or DC group (39±14 msec). This may be due to complicated coronary artery disease in the IU group. Furthermore, QTc dispersion was also increased (49±14 msec) in the NU group in which cardiac autonomic nervous dysfunction was suggested. Patients with both types of diabetic ulcer demonstrated increased QT dispersion due to atherosclerosis or neurological disorder.
A 33-year-old male with no known risk factors for hypercoagulability developed a massive thrombi in the inferior vena cava (IVC). The patient had a history of both pulmonary embolism and embolism-related syncope. The thrombus which extended proximally to the level of the renal vein and distally to the left superficial femoral vein did not respond to anticoagulant therapy or thrombolysis. Thirteen days after admission, we decided to use a temporary caval filter to provide protection from migration of the thrombus while attempting invasive thrombolytic therapy, which was performed using a tissue-type plasminogen activator through a coaxial catheter of the temporary filter. This resulted in a marked decrease in the size of the thrombus, and multiple thrombi were found to be trapped in the temporary filter. Although the temporary caval filter was effective in capturing emboli, resulting in a decrease in the thrombus size, the thrombus was not completely dissolved within two weeks, which is the maximal implantation time. A permanent filter was eventually used to prevent pulmonary embolism, which could arise from the remaining thrombus. We have found placement of a temporary caval filter to be a safe and effective adjunct, in select cases, when attempting thrombolysis of massive thrombi in the IVC. Since we inserted the temporary filter 13 days after admission, use of a temporary filter during thrombolysis may have been more effective if conducted earlier in our patient's clinical course.
A patient with congenitally deficient apolipoprotein (apo) E showed numerous tuberoerutive, tendon xanthomas and severe atherosclerosis, despite a low LDL concentration. In order to study the mechanism of xanthoma formation observed in apo E-deficient patients, we evaluated the effect of VLDL and HDL from the patient on cholesterol ester (CE) accumulation in macrophages. The results showed that there was no difference in CE formation in macrophages among normal VLDL, the patient's VLDL and apo E containing VLDL, which was prepared by incubation of the patient's VLDL with recombinant apo E. On the other hand, apo E containing HDL, which was prepared by incubation of the patient's HDL with recombinant apo E, accelerated cholesterol efflux more effectively than did the patient's HDL and decreased intracellular CE content. Moreover, free apo E accelerated cholesterol efflux from lipid loaded macrophages. These results suggest that macrophages are prevented from transforming into foam cells by their secretion of apo E. This may also explain the marked atherosclerosis and xanthomatosis observed in the patient with apo Edeficiency.
The aim of this study was to evaluate the relationship between changes in abdominal fat areas and the baseline serum leptin levels of Japanese obese women during weight reduction. The study was performed on 100 obese female Japanese volunteers. We measured the BMI and abdominal fat areas (visceral, subcutaneous and total) by magnetic resonance imaging and determined the fasting serum leptin levels before and after a 3-month weight reduction program. We examined whether or not a relationship exists between the baseline leptin levels and the subsequent changes in the abdominal fat areas after a weight reduction program. Multiple linear regression analysis was performed to examine the relationship between the baseline leptin levels and changes in abdominal visceral, subcutaneous, and total fat areas, and demonstrated that the baseline leptin level was a significant predictive factor for changes in the abdominal visceral fat area in both pre-and postmenopausal Japanese obese women. We thus concluded the relatively higher baseline leptin levels in Japanese obese women to be associated with a relatively smaller reduction in the amount of abdominal visceral fat after undergoing a weight reduction program.