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Biomedical subjects

Samuel Z Goldhaber

Publications and source records attributed to Samuel Z Goldhaber.

At least 19 recordsLinked to original sources
PubMed2006

Comparison of a single end point to determine optimal initial warfarin dosing (5 mg versus 10 mg) for venous thromboembolism.

There remains considerable controversy regarding optimal initial warfarin dosing in patients with acute venous thromboembolism. Therefore, an open-label, randomized trial comparing 2 warfarin initiation nomograms (5 vs 10 mg) was conducted in patients with acute venous thromboembolism. All participants received fondaparinux for > or = 5 days as a "bridge" to warfarin. The primary end point was defined as the number of days necessary to achieve 2 consecutive international normalized ratio laboratory test values > 1.9. A total of 50 patients were enrolled and randomly assigned to each of the treatment arms. The median time to 2 consecutive international normalized ratios was 5 days in the 2 groups. There was no statistical difference in achieving the primary end point using either the 5- or the 10-mg nomogram (p = 0.69). These results should provide clinicians with increased warfarin dosing options in patients presenting with acute venous thromboembolism.

Acute Disease↗
PubMed2006

Comparison of bleeding in patients with nonvalvular atrial fibrillation treated with ximelagatran or warfarin: assessment of incidence, case-fatality rate, time course and sites of bleeding, and risk factors for bleeding.

BACKGROUND: Ximelagatran is a novel direct thrombin inhibitor that can be administered as a fixed oral dose, without the need for anticoagulant monitoring. METHODS: We undertook a pooled analysis of 7329 patients with nonvalvular atrial fibrillation from the Stroke Prevention Using Oral Thrombin Inhibitor in Atrial Fibrillation III and V trials to compare bleeding outcomes in patients who received ximelagatran, 36 mg twice daily, or warfarin sodium (target international normalized ratio, 2.0-3.0). We determined annual risk of bleeding (any, major), case-fatality rate, time course and anatomic sites of major bleeding, and risk factors for major bleeding with ximelagatran and warfarin treatment. RESULTS: Annual incidence of any bleeding was 31.75% with ximelagatran and 38.82% with warfarin (relative risk reduction, 18.2%; 95% confidence interval [CI], 13.0-23.1; P<.001). Annual incidence of major bleeding was 2.01% with ximelagatran and 2.68% with warfarin (relative risk reduction, 25.1%; 95% CI, 3.2-42.1; P = .03). Case-fatality rate of bleeding was comparable in ximelagatran- and warfarin-treated patients (8.16% vs 8.09%; P = .98). Cumulative incidence of major bleeding was higher with warfarin than ximelagatran after 24 months of treatment (4.7% vs 3.7%; P = .04). Anatomic sites of bleeding were comparable with both treatments. Risk factors for bleeding with ximelagatran were as follows (hazard ratios and 95% CIs in parentheses): diabetes mellitus (1.81; 1.19-2.77; P = .006), previous stroke or transient ischemic attack (1.78; 1.16-2.73; P = .008), age 75 years or greater (1.70; 1.33-2.18; P<.001), and aspirin use (1.68; 1.08-2.59; P = .02). Risk factors for bleeding in warfarin-treated patients were previous liver disease (4.88; 1.55-15.39; P = .007); aspirin use (2.41; 1.69-3.43; P<.001); and age 75 years or greater (1.26; 1.03-1.52; P = .02). CONCLUSIONS: Treatment with ximelagatran, 36 mg twice daily, is associated with a lower risk of bleeding than warfarin in patients with nonvalvular atrial fibrillation. Aspirin use and increasing age were associated with an increased risk of bleeding in ximelagatran- and warfarin-treated patients.

Adolescent↗
PubMed2006

The probability of pulmonary embolism is a function of the diagnoses considered most likely before testing.

OBJECTIVES: To determine the frequency of pulmonary embolism (PE) diagnosis when different alternative diagnoses were considered most likely before testing, because the relationship between specific alternative diagnoses and the diagnosis of PE has not been explored. METHODS: This study was a preplanned secondary analysis of a prospective study of the diagnosis of pulmonary embolism conducted in the emergency department (ED) of an urban university hospital. Physicians were queried as to their most likely pretest diagnosis when they ordered any of the following tests to evaluate possible PE: D-dimer, contrast-enhanced computed tomography of the chest, ventilation-perfusion lung scan, or pulmonary angiogram. To compare the frequency of PE diagnosis across alternative diagnoses, risk ratios, 95% confidence intervals (CI), and p-values using Fisher's exact test were calculated. RESULTS: Six hundred seven patients were enrolled, and 61 had PE. Physicians thought PE was the most likely pretest diagnosis in 162 (26.7%) patients, and 20.4% (95% CI = 14.4% to 27.4%) of these patients had PE. For four alternative diagnoses, PE was diagnosed less frequently than when PE was considered most likely: musculoskeletal pain (2.2%, 95% CI = 0.4% to 6.2%), anxiety (1.7%, 95% CI = 0.0 to 9.2%), asthma or chronic obstructive pulmonary disease (0, 95% CI = 0.0 to 10.9%), and viral syndrome (0, 95% CI = 0.0 to 14.3%). CONCLUSIONS: The frequency of PE is related to the most likely pretest alternative diagnosis. PE is diagnosed infrequently when anxiety, asthma or chronic obstructive pulmonary disease, musculoskeletal pain, or viral syndrome is the most likely alternative diagnosis.

Diagnosis, Differential↗
PubMed2006

Massive pulmonary embolism.

BACKGROUND: Acute massive pulmonary embolism (PE) carries an exceptionally high mortality rate. We explored how often adjunctive therapies, particularly thrombolysis and inferior vena caval (IVC) filter placement, were performed and how these therapies affected the clinical outcome of patients with massive PE. METHODS AND RESULTS: Among 2392 patients with acute PE and known systolic arterial blood pressure at presentation, from the International Cooperative Pulmonary Embolism Registry (ICOPER), 108 (4.5%) had massive PE, defined as a systolic arterial pressure <90 mm Hg, and 2284 (95.5%) had non-massive PE with a systolic arterial pressure > or =90 mm Hg. PE was first diagnosed at autopsy in 16 patients (15%) with massive PE and in 29 patients (1%) with non-massive PE (P<0.001). The 90-day mortality rates were 52.4% (95% CI, 43.3% to 62.1%) and 14.7% (95% CI, 13.3% to 16.2%), respectively. In-hospital bleeding complications occurred in 17.6% versus 9.7% and recurrent PE within 90 days in 12.6% and 7.6%, respectively (P<0.001). In patients with massive PE, thrombolysis, surgical embolectomy, or catheter embolectomy were withheld in 73 (68%). Thrombolysis was performed in 33 patients, surgical embolectomy in 3, and catheter embolectomy in 1. Thrombolytic therapy did not reduce 90-day mortality (thrombolysis, 46.3%; 95% CI, 31.0% to 64.8%; no thrombolysis, 55.1%; 95% CI, 44.3% to 66.7%; hazard ratio, 0.79; 95% CI, 0.44 to 1.43). Recurrent PE rates at 90 days were similar in patients with and without thrombolytic therapy (12% for both; P=0.99). None of the 11 patients who received an IVC filter developed recurrent PE within 90 days, and 10 (90.9%) survived at least 90 days. IVC filters were associated with a reduction in 90-day mortality (hazard ratio, 0.12; 95% CI, 0.02 to 0.85). CONCLUSIONS: In ICOPER, two thirds of the patients with massive PE did not receive thrombolysis or embolectomy. Counterintuitively, thrombolysis did not reduce mortality or recurrent PE at 90 days. The observed reduction in mortality from IVC filters requires further investigation.

Aged↗
PubMed2006

Low intensity warfarin anticoagulation is safe and effective as a long-term venous thromboembolism prevention strategy.

Longitudinal studies indicate a high rate of recurrence of venous thromboembolism after an episode of deep venous thrombosis or pulmonary embolism. Extended anticoagulant therapy will decrease the recurrence rate, but there is controversy as to the optimal intensity of therapy that will be effective, yet safe. The PREVENT trial addresses the question of whether long-term low intensity therapy (INR 1.5-2.0) will effectively prevent recurrence compared to placebo treatment, yet be safe without a significant increase in major bleeding. The results of this trial show a significant reduction in recurrent venous thromboembolism with a major bleeding rate that is no different than the placebo arm of the study (0.9 vs 0.4 per 100 patient years; p = 0.25). Although the ELATE trial showed greater effectiveness with no increase in bleeding in the standard intensity arm vs the low intensity arm, the question remains whether such safety can be obtained in the real world management of oral anticoagulation.

Anticoagulants↗
PubMed2006

Risk stratification of acute pulmonary embolism.

Acute pulmonary embolism (PE) is a potentially life-threatening condition, with an overall 3-month mortality rate of 15% and with right ventricular failure as the most common cause of early death. Risk stratification facilitates identification of high-risk patients and may be helpful in guiding the initial and long-term management. In patients with massive PE and hemodynamic instability, rapid risk assessment is paramount and bedside echocardiography and multislice chest computed tomography (CT) are useful for identifying patients who may benefit from thrombolysis or embolectomy. Cardiac biomarkers, including troponin and the natriuretic peptides, are sensitive markers of right ventricular function. Low levels of troponin, B-type natriuretic peptide (BNP), and NT-terminal proBNP are all highly sensitive assays for identifying patients with an uneventful clinical course. Multislice chest CT is not only useful to diagnose or exclude PE; it also is useful for risk assessment. A right-to-left ventricular dimension ratio > 0.9 on the reconstructed CT four-chamber view identifies patients at increased risk of early death. This article focuses on risk stratification tools, including the clinical examination, electrocardiography, echocardiography, cardiac biomarkers, and chest CT.

Biomarkers↗
PubMed2006

Acute pulmonary embolism: risk stratification.

The death rate from acute pulmonary embolism (PE) exceeds the mortality rate for acute myocardial infarction. Risk stratification helps optimize the selection of those patients who will benefit from more aggressive therapy, such as thrombolysis or embolectomy, in addition to anticoagulation. The classic paradigm was to observe patients deteriorate and to attempt to maintain acceptable hemodynamics by starting vasopressors. If hemodynamics failed to improve or if cardiogenic shock persisted, thrombolysis or surgical embolectomy was considered. Sadly, this "watch and wait" approach often resulted in irreversible cardiogenic shock and multisystem organ failure. The new approach hinges upon rapid and accurate risk stratification. There are four features of this strategy: 1) clinical evaluation, 2) bedside nonimaging tests-electrocardiography and pulse oximetry, 3) imaging tests-echocardiography and chest computed tomography,and 4) cardiac biomarkers-such as the troponin level. When high-risk patients are identified,they can be triaged for urgent or emergent therapy, usually prior to developing overt hypotension and cardiogenic shock.

Acute Disease↗
PubMed2006

Risk factors for the assessment of patients with pulmonary embolism.

Pulmonary embolism (PE) occurs frequently among cancer patients, with a spectrum ranging from small, clinically insignificant thrombi to life-threatening massive PE. It is fatal in as many as 14% of cancer patients, primarily by producing right ventricular heart failure and cardiogenic shock. PE diagnosis is difficult because the signs and symptoms imitate other commonly occurring diseases. Clinicians must be able to integrate a wide array of diagnostic imaging tools and laboratory tests to ensure rapid assessment and diagnosis. Risk stratification with the use of cardiac biomarkers and imaging tests to evaluate right ventricular function will identify treatment options. Hemodynamically stable patients can be treated effectively with anticoagulation alone, whereas those with right ventricular dysfunction require an aggressive strategy with thrombolysis, surgical embolectomy, or a catheter-based intervention. When anticoagulation is contraindicated, a vena caval filter may be deployed. PE treatment must be customized to the individual and consider the existing thrombus burden, presence of underlying cardiopulmonary disease and right side heart dysfunction, and cancer status of the patient. Clinicians should focus on providing adequate thromboprophylaxis in hospitalized cancer patients to avoid PE treatment.

Humans↗