Vous
avez remarqué que parfois les troponines sont élevées
dans l�embolie pulmonaire??
Pourrait
peut-être être utile pour la stratification de ces patients
et pour guider l�agressivité de nos traitements??
Voir
l�abstract ci-joint :
(Circulation.
2002;106:1263.)
© 2002 American Heart
Association, Inc.
|
Clinical
Investigation and Reports
|
Importance
of Cardiac Troponins I and T in Risk Stratification of Patients With Acute
Pulmonary Embolism
Stavros
Konstantinides, MD; Annette Geibel, MD; Manfred
Olschewski, PhD; Wolfgang Kasper, MD; Nadine
Hruska, MD; Sebastian Jäckle, MD; Lutz Binder,
MD
From
Georg-August-Universität Göttingen, Abteilung Kardiologie und
Pneumologie (S.K., N.H.); Albert-Ludwigs-Universität Freiburg, Abteilung
Kardiologie und Angiologie (A.G., S.J.); Albert-Ludwigs-Universität
Freiburg, Abteilung Medizinische Biometrie und Informatik (M.O.); St Josefs
Hospital Wiesbaden, Innere Abteilung (W.K.); and Georg-August-Universität
Göttingen, Abteilung Klinische Chemie (L.B.), Germany.
Correspondence
to Stavros Konstantinides, MD, Department of Cardiology and Pulmonary Medicine,
Georg August University of Goettingen, Robert Koch Strasse 40, D-37075
Goettingen, Germany. E-mail [EMAIL PROTECTED]
Background�
Assessment of risk and appropriate management of patients with
acute pulmonary embolism (PE) remains a challenge. Cardiac troponins
I (cTnI) and T (cTnT) are reliable indicators of myocardial
injury and may be associated with right ventricular dysfunction
in PE.
Methods
and Results� The present
prospective study included 106 consecutive patients with confirmed
acute PE. cTnI was elevated (
0.07
ng/mL) in 43 patients (41%), and cTnT (
0.04
ng/mL) was elevated in 39 (37%). Elevation of cTnI or cTnT was
significantly associated with echocardiographically detected
right ventricular dysfunction (P=0.001
and P<0.05, respectively).
Moreover, a significant correlation was found between elevation
of cTnI or cTnT and the two major end points overall mortality
and complicated in-hospital course. The negative predictive
value of cardiac troponins for major clinical events was 92%
to 93%. Importantly, there was obvious escalation of in-hospital
mortality, the rate of complications, and the incidence of recurrent
PE, when patients with high troponin concentrations (cTnI >1.5;
cTnT >0.1 ng/mL) were compared with those with only moderately
elevated levels (cTnI, 0.07 to 1.5; cTnT, 0.04 to 0.1 ng/mL).
Logisticregression analysis confirmed that the mortality risk (OR) wassignificantly
elevated only in patients with high cTnI (P=0.019)or
cTnT (P=0.038) levels. Furthermore,
the risk of a complicated in-hospital course was almost 5 times
higher (15.47 versus 3.16) in the high-cTnI group compared with
patients with moderate cTnI elevation.
Conclusions�
Our results indicate that cTnI and cTnT may be a novel, particularly
useful tool for optimizing the management strategy in patients
with acute PE.
J.
Levasseur