Vous avez remarqu� que parfois les
troponines sont �lev�es dans l�embolie pulmonaire??
Pourrait peut-�tre �tre utile pour
la stratification de ces patients et pour guider l�agressivit� 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 J�ckle, MD; Lutz Binder, MD
From Georg-August-Universit�t G�ttingen, Abteilung
Kardiologie und Pneumologie (S.K., N.H.); Albert-Ludwigs-Universit�t Freiburg,
Abteilung Kardiologie und Angiologie (A.G., S.J.); Albert-Ludwigs-Universit�t
Freiburg, Abteilung Medizinische Biometrie und Informatik (M.O.); St Josefs
Hospital Wiesbaden, Innere Abteilung (W.K.); and Georg-August-Universit�t
G�ttingen, 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).
Logistic regression analysis confirmed that the mortality risk (OR)
was significantly 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
