(Circulation. 1997;96:716-718.)
© 1997 American Heart Association, Inc.
Articles |
Pulmonary Embolism Thrombolysis
Broadening the Paradigm for Its Administration
From the Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.
Correspondence to Samuel Z. Goldhaber, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E-mail szgoldhabe@bics.bwh.harvard.edu
Key Words: Editorials • embolism thrombolysis • heparin
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Introduction |
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Recommendations for appropriate administration of thrombolysis in PE have sparked debate and controversy for the past 30 years. Sometimes, those preparing journal symposia or national meetings have successfully enlivened their projects by inviting a "protagonist" and "antagonist" of thrombolysis for PE to pummel each other in public. Such exercises naturally tend to make the debaters focus solely on points that support their assigned positions. As a result, the audience must contend with two extreme views that rarely overlap. In contrast, consensus conferences have been convened to obtain expert opinions and then to issue guidelines on the optimal role of thrombolysis in PE management. Unfortunately, neither debates nor consensus conferences help to advance the field very much because the "take home message" is often swayed more by the articulateness and authority of a particular individual than by literature-based evidence. Ironically, the written or oral debate format and consensus guidelines are often relied on the most when data are sparse and the field of interest is murky.
Instead of becoming immolated by the heat of argument, one
should pause when considering PE thrombolysis so that
several fundamental points can be enumerated. First, PEs present
with a wide spectrum of acuity and differ markedly in size and
physiological effects. Therefore, optimal
management strategies should rely on risk stratification rather than a
"one size fits all" approach to treatment.1 Second,
PE patients are often cursorily dichotomized as having either
hemodynamic instability (with a systolic
arterial pressure <90 mm Hg) or "normal
hemodynamics." However, cardiologists
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