Atrial flutter with 1:1 atrioventricular conduction caused by propafenone

We describe a case of 1:1 atrial flutter in a patient with coronary disease taking propafenone. In atrial flutter, the atrial rate is usually about 300 beats/min with 2:1 AV conduction and a ventricular rate of 150 beats/min. Class IA antiarrhythmic drugs, especially quinidine and disopyramide, may cause 1:1 AV response because they reduce atrial rate and are vagolytic. However, propafenone is a Class IC agent and has no anticholinergic properties, and the occurrence of 1:1 AV conduction at a rate of about 250 beats/min is an important side effect that, although uncommon, should be recognized.     

Phase II trial of paclitaxel and topotecan with granulocyte colony-stimulating factor support in stage IV breast cancer

PURPOSE: This multicenter phase II trial investigated the efficacy and safety of a combination of paclitaxel and topotecan in patients with pretreated metastatic breast cancer. Plasma levels of paclitaxel and topotecan were obtained during cycle 1 to correlate pharmacokinetic parameters with toxicity. PATIENTS AND METHODS: Paclitaxel was administered intravenously (i.v.) at 230 mg/m2 over 3 hours on day 1 followed by topotecan 1.0 mg/m2 i.v. over 30 minutes on days 1 to 5. Patients received an abbreviated premedication regimen that consisted of ranitidine 50 mg, diphenhydramine 50 mg, and a single 20-mg dose of dexamethasone, all administered i.v. 30 minutes before paclitaxel. Granulocyte colony-stimulating factor (GCSF) was administered at 5 micrograms/kg/d subcutaneously starting on day 6 and continuing until the absolute granulocyte count (AGC) was greater than 10,000/microL. Plasma paclitaxel and topotecan concentrations were assessed during the first cycle using limited-sampling strategies. RESULTS: Seventeen patients were treated. The majority had visceral metastases. Four patients experienced neutropenic fever and one had mild bronchospasm. Only one partial response (PR) was observed. Nadir AGC correlated strongly with both duration of paclitaxel levels greater than 0.05 mumol/L and maximum concentration (Cmax) of paclitaxel. CONCLUSION: This regimen does not produce a response rate superior to that expected with single-agent paclitaxel at doses that do not require growth factor support.     

Lipoprotein(a) and inflammation in human coronary atheroma: association with the severity of clinical presentation

OBJECTIVES: The purpose of this study was the investigation of the in vivo role of lipoprotein(a) [Lp(a)] and inflammatory infiltrates in the human coronary atherosclerotic plaque and their correlation with the clinical syndrome of presentation. BACKGROUND: Lipoprotein(a) is an atherogenic and thrombogenic lipoprotein, and has been implicated in the pathogenesis of acute coronary syndromes. Lipoprotein(a) induces monocyte chemoattraction and smooth muscle cell activation in vitro. Macrophage infiltration is considered one of the mechanisms of plaque rupture. METHODS: This study of atherectomy specimens investigated the in vivo role of Lp(a) at different stages of the atherogenic process, and its relationship with macrophage infiltration. We examined coronary atheroma removed from 72 patients with stable or unstable angina. Specimens were stained with antibodies specific for Lp(a), macrophages (KP-1), and smooth muscle cells (alpha-actin). Morphometric analysis was used to quantify the plaque areas occupied by each of the three antigens, and their colocalization. RESULTS: All specimens had localized Lp(a) staining; the mean fractional area was 58.2%. Ninety percent of the macrophage areas colocalized with Lp(a) positive areas, whereas 31.3% of the smooth muscle cell areas colocalized with Lp(a) positive areas. Patients with unstable angina (n = 46) had specimens with larger mean plaque Lp(a) areas than specimens from stable angina patients (n = 26): 64.4% versus 47.7% (p = 0.004). Unstable angina patients with rest pain (n = 28) had greater mean plaque Lp(a) area than unstable angina patients with crescendo exertional pain (n = 18): 71.1% versus 52.4% (p < 0.001). Mean KP-1 area was 31.2% in unstable rest angina versus 18.3% in stable angina (p = 0.05); alpha-actin area was greater in stable (48.5%) and crescendo exertional angina (48.8%) than in rest angina (30.4%). The strongest correlation between plaque KP-1 and Lp(a) area was in unstable rest angina (r = 0.88, p < 0.001), and between alpha-actin and Lp(a) areas in the crescendo exertional angina (r = 0.62, p < 0.01). CONCLUSIONS: Lipoprotein(a) is ubiquitous in human coronary atheroma. It is detected in larger amounts in tissue from culprit lesions in patients with unstable compared to stable syndromes, and has significant colocalization with plaque macrophages. A correlation of plaque alpha-actin and Lp(a) area suggests a role of Lp(a) in plaque growth.     

Stability of posterior spinal instrumentation and its effects on adjacent motion segments in the lumbosacral spine

STUDY DESIGN: An in vitro biomechanical analysis of three anterior instability patterns was performed using calf lumbosacral spines. Stiffness of the constructs was compared, and segmental motion analyses were performed. OBJECTIVES: To clarify the factors that alter the stability of the spinal instrumentation and to evaluate the influence of instrumentation on the residual intact motion segments. SUMMARY OF BACKGROUND DATA: Recently, many adverse effects have been reported in fusion augmented with rigid instrumentation. Only few reports are available regarding biomechanical effects of stability provided by spinal instrumentation and its effects on residual adjacent motion segments in the lumbar-lumbosacral spine. METHODS: Eighteen calf lumbosacral spine specimens were divided into three groups according to instability patterns--one-level, two-level, and three-level disc dissections. Six constructs were cyclically tested in rotation, flexion-extension, and lateral bending of intact spines, of destabilized spine, and of spines with four segmental posterior instrumentation systems used to extend the levels of instability (Cotrel-Dubousset compression hook and three transpedicular screw fixation systems). During each test, stiffness values and segmental displacements were measured. RESULTS: The rigidity of the instrumented construct increased as the fixation range became more extensive. Although application of the instrumentation effectively reduced the segmental motion of the destabilized vertebral level, the motion at the destabilized level tended to increase as the number of unstable vertebral levels increased, and the fixation range of the instrumentation became more extensive. Instrumented constructs produced higher segmental displacement values at the upper residual intact motion segment when compared with those of the intact spine. In contrast, the instrumented constructs decreased their segmental displacement values at the lower residual intact motion segment with higher magnitude of the translational (shear) motion taking place compared with the intact spine in flexion-extension and lateral bending. These changes in the motion pattern became more distinct as the fixation range became more extensive. CONCLUSIONS: As segmental spinal instrumentation progresses from one level to three levels, the overall torsional and flexural rigidity of the system increases. However, segmental displacement at the site of simulated instability becomes more obvious. Application of segmental instrumentation changes the motion pattern of the residual intact motion segments, and the changes in the motion pattern become more distinct as the fixation range becomes more extensive and as the rigidity of the construct increases.     

Survival of Taenia solium cysticerci in carcasses of pigs kept at 4 C

In the present study, the survival of cysticerci of Taenia solium in carcasses of 1 Small-Ear-Miniature and 2 Landrace Small-Ear-Miniature pigs kept in a refrigerator at 4 C was determined. The viability of the cysticerci was determined by observing evagination and active movement of the scolex under a fluorescent light after digestion in pig bile. Although no viable cysticerci were found after day 30, 58.8% cysticerci survived between day 26 and day 30. Moreover, more than 80% of the cysticerci were viable between day 1 and day 25. These findings indicate that taeniasis solium can be transmitted through eating raw or undercooked pork or viscera of pigs following refrigeration at 4 C for less than 30 days.