The structure and origin of Prydz Bay and MacRobertson Shelf, East Antarctica
1
ABSTRACTS Gregory L. Moneta, MD, Abstracts Section Editor Malignancies, prothrombotic mutations, and the risk of venous thrombosis Blom JW, Doggen CJM, Osanto S, et al. JAMA 2005;293:715-22. Conclusion: There is an increased risk of venous thrombosis in patients with cancer. The risk is greatest in the first few months after diagnosis and in the presence of distal metastasis. Patients also with Factor V Leiden and prothrombin 20210A mutations have even higher risk. Summary: This is a report of the Multiple Environmental and Genetic Assessment (MEGA) of Risk Factors for Venous Thrombosis Study. MEGA is a case controlled population based study evaluating risk of venous throm- bosis with various risk factors. This report details risk of venous thrombosis with cancer and the joint effects of cancer and selected genetic mutations predisposing to venous thrombosis. Patients were identified at 6 anticoagu- lation clinics in the Netherlands between March 1, 1999, and May 31, 2002. Patients included were those 18-70 years of age with a first time diagnosis of pulmonary embolism or lower extremity deep venous thrombosis. Control patients, (partners of the patients with venous thrombosis) were also utilized in the study. Both patients and controls received a questionnaire to evaluate acquired risk factors for venous thrombosis. Once anticoagulation therapy had been discontinued for three months, patients and controls were inter- viewed and blood taken for analysis of Factor V Leiden and prothrombin 20210A mutations. In patients with malignancy, the overall risk of venous thrombosis was increased 7 times (odds ratio [OR], 6.7; 95% CI, 5.2-8.6). The highest risk was present in patients with hematologic malignancies (OR 28.0, 95% CI, 4.0-199.7). Risk was also substantially increased in patient with gastrointes- tinal cancers (OR 18.9; 95% CI, 4.6-77.8), and patients with pulmonary malignancies (OR 24.8; 95% CI, 3.4-181.1). Risk was highest in the first several months following malignancy diagnosis (adjusted OR 53.5; 95% CI, 8.6-334.3). In patients with cancer the presence of distal metastatic disease further increased the risk of venous thromboembolism (VTE) compared to patients without metastatic disease (adjusted OR, 19.8; 95% CI, 2.6-149.1). The combination of cancer and Factor V Leiden mutation increased the risk of VTE 12 times compared to patients with Factor V Leiden mutation and no diagnosed malignancy. Results were similar for patients with and without cancer with respect to the prothrombin 20210A mutation. Comment: The data raises the question as to whether patients with cancer should be screened for Factor V Leiden and prothrombin 20210A mutation and treated with prophylactic anticoagulation therapy if a muta- tion is present. Also the question arises whether prophylactic anticoagulation is indicated in patients with malignancies associated with an especially high risk for VTE. The cost effectiveness of such strategies and the ultimate ability of such strategies to prolong life or improve quality of life is clear in patients with cancer who are undergoing surgery or active chemotherapy (ACTA Haematol 2001;106:73-80). There is currently no data to suggest routine prophylaxis for VTE in all cancer patients would be effective. However, the results of the current study suggest certain subgroups of patients with cancer should be studied more closely for potential benefit of routine VTE prophy- laxis. Complications of the Cox-II inhibitors parecoxib and valdecoxib after cardiac surgery Nussmeier NA, Whelton AA, Brown MT, et al. N Engl J Med 2005;352: 1081-91. Conclusion: Patients treated with coronary artery bypass grafting and who have Parecoxib and Valdecoxib utilized for postoperative pain control had an increased incidence of postoperative cardiovascular events. Summary: There is serious concern that, in nonsurgical settings, use of Cox-II inhibitors increases risk of thromboembolic events long-term. The authors sought to evaluate the safety of Parecoxib and Valdecoxib after coronary artery bypass grafting. This was a randomized, double-blind study. After coronary artery bypass grafting, patients were treated for ten days and followed for thirty days. The Cox-II inhibitors used in this study were Valdecoxib (Bextra, Pfizer) and its intravenous prodrug Parecoxib (Dymas- tat, Pfizer). After coronary artery bypass grafting, patients were randomly assigned to receive intravenous Parecoxib for at least three days followed by oral Valdecoxib through day ten or were assigned to be treated with intravenous placebo followed by oral Valdecoxib, or placebo, for ten days. There were 1,671 patients enrolled in the study and all patients also had access to opiate based medications. The primary endpoint was the frequency of pre-defined adverse events (cardiovascular events, renal failure or dysfunc- tion, gastroduodenal ulceration, and wound-healing complications). Compared to the group given placebo alone, the groups given Pare- coxib and Valdecoxib, placebo and Valdecoxib, and placebo and Valdecoxib, all had higher rates of confirmed adverse events (4.0% in the placebo group versus 7.4% in each of the coxib groups; risk ratio for each comparison, 1.9; 95% CI, 1.1-3.2; P .02). Cardiovascular events including myocardial infarction, cardiac arrest, stroke, and pulmonary embolism were particular more frequent among patients given Parecoxib and Valdecoxib (2.0% versus 0.5%; risk ratio 3.7; 95% CI, 1.0-13.5; P .03). Comment: Previous data on the adverse effects of Cox-II inhibitors has focused on long- term thromboembolic risk. There has been data to suggest Cox-II inhibitors could exert significant opiate sparing effects after surgical procedures. The current study, however, suggests patients with coronary artery disease who undergo CABG may be adversely impacted by the use of Cox-II inhibitors to control perioperative pain. While no such data currently exists to implicate Cox-II inhibitors and increased cardiovascular complica- tions after peripheral vascular surgery, the current data may imply Cox-II inhibitors should be avoided in patients undergoing peripheral vascular surgery as well. Intensive lipid lowering with atorvastatin in patients with stable coro- nary disease LaRosa JC, Grundy SM, Waters DD, and the Treating to New Targets (TNT) Investigators. N Engl J Med 2005;352:1425-35. Conclusion: In patients with stable coronary heart disease, intensive lipid-lowering therapy with 80mg Atorvastatin daily provides additional clinical benefit beyond that with treatment of 10mg of Atorvastatin per day. Summary: Recent trials indicate intensive lipid-lowering therapy be- yond traditionally recommended levels in patients with acute coronary syndromes provides increased benefit with respect to cardiovascular end- points compared to traditional lipid-lowering therapy in such patients (N Engl J Med 2004;50:1495-504, and J Am Col Cardiology 2004; 44:1772-9). This study investigated the safety and efficacy of lowering LDL cholesterol below 100 mg/dL in patients with stable coronary disease. Eligible patients were men and women 35-75 years of age who had clinically evident coronary heart disease. Screening of 18,469 patients took place at 256 sites in 14 countries, with 83.7% of these patients felt to be eligible to enter the open-label run in period of the study. Of these, 5,461 patients were excluded after the open label run in phase. Most exclusions were secondary to failure to meet randomization criteria. There were 10,001 patients ultimately randomized to receive double-blind treatment with either 10 mg or 80 mg daily of Atorvastatin. Primary endpoint was occurrence of a first major cardiovascular event (death from coronary heart disease, nonfatal non-procedure related myocardial infarction, fatal or nonfatal stroke, or resuscitation after cardiac arrest). Randomization took place between July 1998 and December 1999. During treatment mean LDL cholesterol levels were 77 mg/dL with 80 mg Atorvastatin daily and 101 mg/dL with 10 mg Atorvastatin daily. Persistent elevations in liver aminotransferase occurred in 1.2% of the 80 mg Atorvastatin daily group versus 0.2% in the 10 mg Atorvastatin daily group (P 0.001). Eight point seven percent (n 434) of the patients receiving 80 mg of Atorvastatin had a primary endpoint. Ten point nine percent (n 548) of the patients receiving 10mg of Atorvastatin had a primary endpoint. The absolute reduction in rate of major cardiovascular events was 2.2% with a 22% relative reduction (hazard ratio, 0.78; 95% CI, 0.69-0.89; P .001). Overall, mortality did not differ between the two groups. Discontinuation of treatment based on adverse events occurred in 7.2% of the 80 mg Atorva- statin group versus 5.3% in the 10mg Atorvastatin group (P .001). There were five cases rhabdomyolysis (2 in the 80 mg Atorvastatin group and 3 in the 10 mg Atorvastatin group). Comment: The safety data for the two doses of Atorvastatin utilized in this trial are consistent with other large scale trials of this drug (N Engl J Med 2004; 350:1495-504 and Lancet 2003; 361:1149-58). The trial was not adequately powered to detect differences in risk of death from any cause. Nevertheless, the study is part of a growing body of evidence suggesting that lowering LDL cholesterol levels significantly below traditionally recom- mended values has clinical benefit. Clinical predictors of transient ischemic attack, stroke, or death within thirty days of carotid angioplasty and stenting Kastrup A, Groschel K, Schulz JB, et al. Stroke 2005;36:787-91. Conclusion: Patients with increased age, recent stroke, or hemispheric transient ischemic attack (TIA), have higher risk of peri-procedure compli- 1242
Transcript of The structure and origin of Prydz Bay and MacRobertson Shelf, East Antarctica
OLR (1985) 32 (12) D. Submarine Geology and Geophysics 1029
deformed trench fill bounded by landward dipping thrust faults, separated by a d6collement surface from an underlying ~ l -km- th ick unit of nearly undeformed trench fill, which along with oceanic lithosphere is being underthrust to act as a buffer between offscraped sediment and oceanic basement. USGS, 345 Middlefield Rd., Menlo Park, CA 94025, USA. (hbf)
85:7155 McGinnis, L.D., R.H. Bowen, J.M. Erickson, B.J.
Allred and J.L. Kreamer, 1985. East-west Ant- arctic boundary in McMurdo Sound. Tectono- physics, 114(1-4):341-356.
Western McMurdo Sound is capped by a thin veneer of layered reflectors. The absence of deep, layered reflectors suggests the crust is made up primarily of intrusions associated with plutons generated during the Ross Orogeny. Reflection data support earlier interpretations that indicate fundamental differences in the crust beneath McMurdo Sound and the Transantarctic Mountains, perhaps due to Early Paleozoic subduction of the Ross Embayment crust beneath the Transantarctic Mountains. Orogeny has produced an over-thickened crust beneath the Ross orogenic belt which was followed by several periods of reactivation including the Jurassic thermal event and the Early Tertiary uplift of the Transantarctic Mountains. Presence of the McMurdo Volcanics and preliminary data interpretations suggest that the sound is now being thinned by extension. Dept. of Geol., Louisiana State Univ., Baton Rouge, LA 70803-4101, USA.
85:7156 Rangin, C., J.F. Stephan and C. MUller, 1985.
Middle Oligocene oceanic crust of South China Sea jammed into Mindoro collision zone (Phil- ippines). Geology, geol. Soc. Am., 13(6):425-428.
A summary is provided of the Cenozoic evolution of Mindoro, an island south of Luzon, located at the 'complex junction between the Manila Trench and the collision zone of the North Palawan block with the western Philippines mobile belt. ' The age equivalence of Amnay ophiolites and the oldest Middle Oligocene magnetic anomalies of the South China Sea Basin is cited as evidence that the ophiolites may be a piece of South China oceanic crust rotated 20 ° counterclockwise and caught between the San Jose-North Palawan block and the Mindoro-Luzon basement. LA 215, CNRS, 4 ave de Bois Preau, 92506 Rueil-Malmaison Cedex, France. (hbf)
85:7157 Srivastava, S.P., 1985. Evolution of the Eurasian
Basin and its implications to the motion of Greenland along Nares Strait. Tectonophysics, ! 14(1-4):29-53.
Analysis shows that the Eurasian Basin and Nor- wegian-Greenland Sea started to evolve at about anomaly 25 time, though active seafloor spreading did not start until anomaly 24 time. Spreading in the Eurasian Basin has been a result of motion only between the North American and Eurasian plates since the beginning, with the Lomonosov Ridge remaining attached to the North American Plate. From Late Cretaceous to Late Paleocene, Greenland moved obliquely to Ellesmere Island; most of this motion was taken up within the Canadian Arctic Islands resulting in little or no motion along Nares Strait. From anomaly 25-21 Greenland continued to move obliquely, resulting in a displacement of 125 km along and of 90 km normal to the Nares Strait. From Mid-Eocene to Early Oligocene another 100 km of motion took place normal to the Strait. Atlantic Geosci. Centre, Bedford Inst. of Oceanogr., Dartmouth, NS B2Y 4A2, Canada.
85:7158 Stagg, H.M.J., 1985. The structure and origin of
Prydz Bay and MacRobertson Shelf, East Ant- arctica. Tectonophysics, 114(l-4): 315 -340.
Multichannel seismic and magnetic data indicate that much of Prydz Bay is underlain by a sedi- mentary basin that is at least 5 km thick and probably represents a failed rift. The sediments are little disturbed by folding and faulting and contain three major unconformities of Triassic-Early Juras- sic, Early Cretaceous, and Mid-Miocene-Ear ly Pliocene age. These probably represent rift onset, margin breakup, and glacial advances, respectively. Bur. of Mineral Res., P.O. Box 378, Canberra City, ACT 2601, Australia. (amt)
85:7159 Sweeney, J.F., 1985. Comments about the age of the
Canada Basin. Tectonophysics, 114(1-4): 1-10.
The Canada Basin appears to have formed over a 60 Ma interval during the Cretaceous period. Conti- nental breakup was widespread ~131 113 Mya along what was to become the polar margin of North America, and seafloor formation was active during an extended Cretaceous interval ~118-79 Mya. Data indicate that all parts of the North American polar margin could have formed at about the same time. Relatively less/slower stretching occurred along the segment southwest of Brock Island and relatively more/faster stretching took place along the
