We reviewed a series of 17 consecutive patients demonstrated to have persistent pulmonary hypertension after acute massive, submassive, or recurrent PE between January 2005 and July 2006. None of these patients had significant cardiopulmonary disease or evidence of malignancy at the time of diagnosis of PE and thereafter. All patients remained on warfarin or low-molec-ular-weight heparin (LMWH) since their last episode of PE. The study was performed retrospectively after approval by the Toronto Academic Health Sciences Network (http://www.tahsn.ca/) Institutional Research Ethics Board.
Two patients presented with acute massive and submassive PE during the same time period but had normalization of their pulmonary artery pressures on echocardiography at 3 months follow-up and were therefore not included in this study. Six patients presented with acute submassive PE while undergoing chemotherapy or radiation therapy for malignancy and were therefore also excluded from the study.
PE was diagnosed using ventilation/perfusion (V/Q) scan or CTPA, and was classified as acute if symptoms began 2 weeks before diagnosis. Patients were also classified as to whether they had a documented history of PE or not. PE was considered documented if confirmed by V/Q scan, CTPA, or pulmonary angiography. Patients in cardiogenic shock were considered to have massive PE, and those with RV dysfunction only were considered to have submassive PE.
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All patients were evaluated after at least 12 weeks of anticoagulation (median, 18 weeks; range, 12 to 30 weeks) with echocardiography, a V/Q scan, and CTPA, and every 6 to 12 months thereafter. If patients had dyspnea (New York Heart Association [NYHA] class II or higher) after > 12 weeks of anticoagulation and persistently abnormal perfusion scan and/or CTPA, right-heart catheterization and pulmonary angiography were performed. Total pulmonary resistance (TPR) was calculated as follows: (mean pulmonary artery pressure/cardiac output) X 80. Preoperative TPR was calculated based on the last measurement before PEA, and postoperative TPR was calculated after PEA before removing the Swan-Ganz catheter (Edwards Lifesciences; Mississauga, ON, Canada).
Patients with CTEPH were evaluated for PEA, and surgical candidates then completed the preoperative evaluation with duplex vascular Doppler of the carotid and femoral vessels as well as coronary angiography in patients > 40 years old. Pulmonary function tests and arterial blood gas analysis were also systematically performed. PEA was performed according to the standardized technique previously described, with a period of circulatory arrest under deep hypothermia (18° to 20°C) for the right side and the left side.
All follow-up echocardiograms were performed by experienced cardiologists in our institution. The estimated pulmonary artery systolic pressure (PAsP) was calculated from the tricuspid regurgitation (TR) jet obtained under color flow imaging guidance. In all patients, the TR Doppler signal was obtained from the apical or modified low left parasternal four-chamber view. The simplified Bernoulli formula (peak gradient = 4-v2, where v is the peak TR velocity into the right atrium) was used to obtain the PAsP by adding the peak TR gradient to the estimated right atrial pressure. Right atrial pressure was estimated based on the degree of inspiratory collapse of the inferior vena cava.
Pulmonary hypertension was defined as PAsP > 35 mm Hg. Patients were classified into three groups based on the degree of residual pulmonary hypertension after at least 12 weeks of anticoagulation: (1) PAsP 35 to 40 mm Hg, (2) PAsP 41 to 50 mm Hg, and (3) PAsP > 50 mm Hg.
Data are expressed as mean ± SD or as median and range. Student t test was used to test differences between continuous variables, and x2 was used for categorical variables. Statistical software (Graphpad; San Diego, CA) was used for all analyses; p < 0.05 was considered significant.Tags: acute pulmonary emboli, chronic thromboembolic pulmonary hypertension, pulmonary thromboendarterectomy