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Biomedical subjects

D Massel

Publications and source records attributed to D Massel.

36 records · Page 2Linked to original sources
PubMed1998

A systematic review of the cost-effectiveness of noncardiac transitional care units.

OBJECTIVE: To critically appraise and summarize the studies examining the cost-effectiveness of noncardiac transitional care units (TCUs). DATA SOURCES: We conducted a computerized literature search using MEDLINE, and Current Contents from January 1, 1986 to December 31, 1995 and HealthSTAR from January 1, 1989 to December 31, 1995 with the key words intermediate care unit, respiratory care unit, and step-down unit. Bibliographies of all selected articles and review articles were examined. Personal files were also reviewed. STUDY SELECTION: (1) POPULATION: patients in a noncardiac TCU of an acute-care institution; (2) intervention: addition of a noncardiac TCU to the institution; and (3) outcomes: patient outcome-survival and associated costs. DATA EXTRACTION: The necessary data were abstracted and study validity was evaluated by two independent reviewers using a modification of previously published criteria. DATA SYNTHESIS: The studies were summarized qualitatively; upon inspection, they were too heterogeneous to allow quantitative analysis. While the studies all claimed that their TCUs were cost-effective, the economic evaluation designs were flawed to such an extent that the validity of the conclusions is suspect. CONCLUSIONS: To date, the evidence in the literature is insufficient to determine under which circumstances, if any, TCUs are a cost-effective alternative technology to the traditional institution with only ICU and general ward beds.

Humans↗
PubMed1996

PROTECT (Prospective Reinfarction Outcomes in the Thrombolytic Era Cardizem CD Trial): a randomized, double-blind clinical trial of diltiazem versus atenolol in secondary prophylaxis post non-Q wave myocardial infarction.

OBJECTIVE: To describe the rationale and design of the Prospective Reinfarction Outcomes in the Thrombolytic Era Cardizem CD Trial (PROTECT). DESIGN: A multicentre, randomized, double-blind, parallel-group comparison of once daily beta-therapy versus heart rate lowering calcium channel blocker therapy, in the reduction of one-year nonfatal reinfarction and cardiovascular death (combined primary end-point) initiated 24 to 96 h post non-Q wave myocardial infarction. SETTING: One hundred and twenty hospitals across Canada. PATIENTS: Over 7500 women and men aged 21 years or older with enzyme-confirmed non-Q wave infarction and without significant left ventricular systolic dysfunction will be recruited over two years. INTERVENTIONS: Once daily beta-blocker therapy (oral atenolol, 50 to 200 mg) versus once daily calcium channel blocker therapy (oral diltiazem 120 to 360 mg) with follow-up for up to three years. CONCLUSIONS: The PROTECT will be the largest all-Canadian cardiovascular trial to date and will compare two commonly prescribed agents for secondary prophylaxis following non-Q wave infarction. The scientific question addressed by the PROTECT is of major public health importance and the results of the study will directly affect current clinical practice.

Adrenergic beta-Antagonists↗
PubMed1995

Maximizing the benefits of thrombolytic therapy for acute myocardial infarction.

Thrombolytic therapy is a huge advance in the management of acute myocardial infarction (AMI). The results of large clinical trials over the past 9 years have unequivocally demonstrated its benefit: of every 1000 patients treated 30 will be saved, at a cost of two cases of nonfatal cerebral hemorrhage and seven of noncerebral major hemorrhage. The concurrent use of acetylsalicylic acid increases the benefit of thrombolytic therapy. Sales figures for thrombolytic agents indicate that their use in Canada is less than optimal and lags behind that in several European countries. Major educational efforts are needed to promote awareness of the efficacy of thrombolytic therapy and of optimal approaches for maximizing its potential benefit for patients with AMI.

Clinical Trials as Topic↗
PubMed1991

Report of the Canadian Cardiovascular Society's consensus conference on the Management of the Postmyocardial Infarction Patient.

In October 1989, the Canadian Cardiovascular Society announced a program to achieve consensus on important issues in the care of patients with cardiovascular disease. This report on the management of the postmyocardial infarction patient represents the first in a series of these consensus conferences. The process for establishing consensus recommendations involved several steps. A primary panel of 11 experts from various fields was selected to review the available clinical evidence and to make a list of recommendations about management decisions in the postmyocardial infarction period. The initial report was distributed to a secondary panel of 16 reviewers* representing allied health care constituencies from across Canada. On the basis of the critical reviews and feedback from these reviewers, a revised report was distributed to all members (over 800) of the Canadian Cardiovascular Society for further review and feedback. This iterative approach resulted in a penultimate report that was presented at a plenary session of the annual scientific meeting of the Canadian Cardiovascular Society on Oct. 18, 1990, in Halifax, NS. On the basis of discussion and feedback from this symposium, the consensus review was completed.

Canada↗
PubMed1991

Anaphylactoid reaction during an infusion of recombinant tissue-type plasminogen activator for acute myocardial infarction.

Potentially life-threatening immediate hypersensitivity reactions are extremely rare among patients treated with thrombolytic agents for suspected acute myocardial infarction. A patient who developed a severe reaction during an infusion of recombinant tissue-type plasminogen activator is described. Potential causal mechanisms for the reaction could be related either to nonmedicinal additives or complement activation. Implications for treatment in the setting of acute myocardial infarction are discussed.

Aged↗
PubMed1990

Management of the patient following coronary thrombolysis.

Myocardial salvage can be maximized by the early institution of thrombolytic therapy and aspirin. Certain patients may benefit from the administration of intravenous heparin, beta blockers, or nitroglycerin. The routine use of percutaneous transluminal coronary angioplasty (PTCA) or calcium-channel blockers does not appear to be warranted. Recurrent myocardial ischemia should be vigorously treated with medical therapy and there may be value in cardiac catheterization, followed by PTCA or bypass surgery, depending upon the extent of myocardium at risk and the underlying coronary anatomy. Long-term morbidity and mortality may be reduced by instituting aspirin and beta blockers as well as by modifying risk factors. There is no evidence for the long-term benefit from any calcium-channel blocker. Oral anticoagulation may be warranted in those patients with a mural thrombus, congestive heart failure, or atrial fibrillation. ACE inhibitors may be of value in the presence of left ventricular dysfunction and certainly in the presence of symptomatic congestive heart failure. Antiarrhythmic therapy is generally indicated only for symptomatic or life-threatening arrhythmias. Residual myocardial ischemia should be sought by exercise testing, and those patients with poor exercise tolerance generally warrant cardiac catheterization in consideration for revascularization.

Coronary Disease↗
PubMed1990

Clot-bound thrombin is protected from inhibition by heparin-antithrombin III but is susceptible to inactivation by antithrombin III-independent inhibitors.

Propagation of venous thrombi or rethrombosis after coronary thrombolytic therapy can occur despite heparin administration. To explore potential mechanisms, we set out to determine whether clot-bound thrombin is relatively protected from inhibition by heparin-antithrombin III but susceptible to inactivation by antithrombin III-independent inhibitors. Using plasma fibrinopeptide A (FPA) levels as an index of thrombin activity, we compared the ability of thrombin inhibitors to block FPA release mediated by fluid-phase thrombin with their activity against the clot-bound enzyme. Incubation of thrombin with citrated plasma results in concentration-dependent FPA generation, which reaches a plateau within minutes. In contrast, there is progressive FPA generation when fibrin clots are incubated with citrated plasma. Heparin, hirudin, hirudin dodecapeptide (hirugen), and D-phenylalanyl-L-prolyl-L-arginyl chloromethyl ketone (PPACK) produce concentration-dependent inhibition of FPA release mediated by fluid-phase thrombin. However, heparin is much less effective at inhibiting thrombin bound to fibrin because a 20-fold higher concentration is necessary to block 70% of the activity of the clot-bound enzyme than is required for equivalent inhibition of fluid-phase thrombin (2.0 and 0.1 U/ml, respectively). In contrast, hirugen and PPACK are equally effective inhibitors of fluid- and solid-phase thrombin, while hirudin is only 50% as effective against the clot-bound enzyme. None of the inhibitors displace bound 125I-labeled thrombin from the clot. These studies indicate that (a) clot-bound thrombin is relatively protected from inhibition by heparin, possibly because the heparin binding site on thrombin is inaccessible when the enzyme is bound to fibrin, and (b) clot-bound thrombin is susceptible to inactivation by antithrombin III-independent inhibitors because the sites of their interaction are not masked by thrombin binding to fibrin. For these reasons, antithrombin III-independent inhibitors may be more effective than heparin in certain clinical settings.

Amino Acid Chloromethyl Ketones↗