Chronic thromboembolic pulmonary hypertension (CTEPH) is one of the potentially curable causes of pulmonary hypertension and is definitively treated with pulmonary thromboendarterectomy.
The key benefit of imaging is the ability to demostrate the location and extent of obstructive disease which in conjunction with clinical and physiological data,
allows the experienced multidisciplinary team comprising physicians,
radiologist and surgeons to select the appropriate patients for surgical intervention.
Therefore knowledge of the conventional and less common radiologic features,
including mimics is crucial.
CTEPH is defined as a mean pulmonary arterial preassure >25mmhg that persist 3 months after acute pulmonary embolism and effective anticoagulant treatment.
It is the result of the obstruction of pulmonary vascular bed by a single or nonresolving thromoboemboli.
The reported incidence of CTEPH in patients with a previous history of pulmonary embolism (PE) varies from 2 % to 4%.
However up to 50% of patients with CTEPH have no history of documented acute PE.
The difficulties in estimating the true prevalence of CTEPH are largely due to the insidious nature of the presentation,
clinically silent acute events,
and the absence of long term follow up of all acute pulmonary emboli.
The key to the clinician making this diagnosis is to consider CTEPH in the first place and have a high index of suspicion,
specially in cases of unexplained dyspnea out of proportion or unexplained ambulatory hypoxemia,
hyperventilation or impair gas transfer.
The diagnositic criteria for CTEPH are:
1.mPAP >25mmhg,
PAWP<15 mmhg and PVR >3WU
mPAP: mean pulmonary arterial pressure.
PAWP: pulmonary arterial wedge pressure.
PVR: pulmonary vascular ressistance.
WU=wood units.
2.CT characteristics features of CTEPH.
In this poster we describe CT features of CTEPH and the most frequent disorders that can mimic CTEPH radiologically,
including malignant (primary sarcoma of the pulmonary artery),
inflamatories (fibrosing mediastinitis and takayasu arteritis),
developmental causes (proximal interruption of the pulmonary artery) and as well as idiopathic pulmonary hypertension itself.