Obstructive Pulmonary Embolism Research Articles

Perfusion defects on dual-energy CTA in patients with suspected pulmonary embolism correlate with right heart strain and lower survival

To evaluate the utility of perfusion defects on dual-energy CT angiograms (DECTA) in assessing the clinical severity of pulmonary embolism (PE). We retrospectively reviewed 1136 consecutive diagnostic DECTA exams performed on patients with suspected PE between January 2014 and September 2014. Presence and location of obstructive and non-obstructive PE, right ventricular to left ventricular ratio (RV/LV ratio), and inferior vena cava (IVC) backflow were recorded. Iodine maps were reviewed to establish the presence of perfusion defect and its extent was determined through a score-based segmental impaired perfusion. Subsequently, the perfusion defect scores were correlated with clinical parameters including vital signs, electrocardiogram (ECG) abnormalities, echocardiogram findings, troponin, and brain natriuretic peptide (bnp) levels. Clinical information regarding primary cancer diagnosis, oncologic stage, and date of death if applicable was also recorded. Of the 1136 diagnostic iodine maps, 96 of these patients had perfusion defects on iodine maps. After uni- and multivariate analysis, significant correlation was found between the presence of a perfusion defect and RV/LV ratio (p = 0.05), IVC backflow (p = 0.03), elevated troponin (p = 0.03), and right heart dysfunction as determined on an echocardiogram (p = 0.05). The greater the perfusion defect score, the higher the likelihood of IVC backflow (p = 0.005) and obstructive PE (p = 0.002). When adjusted for oncologic stage, patients with a perfusion defect and a higher perfusion defect score had a higher mortality rate (p = 0.005). The presence of a perfusion defect correlates with several parameters evaluating PE severity. A perfusion defect and higher perfusion defect score were associated with a lower survival. • Detection of perfusion defects on dual-energy CT angiograms and its extent correlates with right heart strain in the setting of pulmonary embolism. • The presence and extent of a perfusion defect in patients with pulmonary embolism are associated with lower survival.

Diagnosis of Right Ventricular Dysfunction in Acute Pulmonary Embolism Using Helical Computed Tomography

Forty-six consecutive patients with pulmonary embolism (PE) who underwent pulmonary angiography, helical computed tomography (CT), and echocardiography in the investigators' emergency department were studied. It was determined that the CT right ventricular (RV)/left ventricular (LV) end-diastolic area ratio was correlated with PE obstruction and echocardiography. A CT RV/LV area ratio >1 had a sensitivity of 88% and a specificity of 88% in diagnosing significant PE. The present study suggests that helical CT may be used as a triage tool in acute PE for selecting high-risk patients, using calculation of the RV/LV area ratio to detect RV dysfunction.

Determinants of Right Ventricular Function and Hemodynamics after Pulmonary Embolism

The purpose of this study was to examine the relative contributions of pulmonary embolic obstruction and independent pre-embolic cardiopulmonary disease to the postembolic cardiovascular status. Of 36 patients studied, 28 had underlying heart or lung disease, while 8 patients had had neither. The extent of pulmonary embolic obstruction was determined by pulmonary angiography. No relationship could be found between the degree of cardiovascular and right ventricular functional impairment and the severity of pulmonary embolic obstruction in the group as a whole. These findings were in contrast with the dose relationship which has been shown to exist between the severity of cardiovascular impairment and the extent of embolic obstruction in patients free of pre-existing heart and rang disease. Increasingly severe impairment of right ventricular function was associated with increasing mortality within 30 days of pulmonary embolism, but no relationship between right ventricular function and the severity of embolic obstruction was found. It was concluded that: (1) the hemodynamic and right ventricular status may be very misleading as measures of the impact of pulmonary embolism in patients with pre-existing heart or lung disease; and (2) estimation of the role of pulmonary embolism in such patients must be based on a consideration of both the immediate pre-embolic cardiopulmonary status and the extent of embolic involvement. The purpose of this study was to examine the relative contributions of pulmonary embolic obstruction and independent pre-embolic cardiopulmonary disease to the postembolic cardiovascular status. Of 36 patients studied, 28 had underlying heart or lung disease, while 8 patients had had neither. The extent of pulmonary embolic obstruction was determined by pulmonary angiography. No relationship could be found between the degree of cardiovascular and right ventricular functional impairment and the severity of pulmonary embolic obstruction in the group as a whole. These findings were in contrast with the dose relationship which has been shown to exist between the severity of cardiovascular impairment and the extent of embolic obstruction in patients free of pre-existing heart and rang disease. Increasingly severe impairment of right ventricular function was associated with increasing mortality within 30 days of pulmonary embolism, but no relationship between right ventricular function and the severity of embolic obstruction was found. It was concluded that: (1) the hemodynamic and right ventricular status may be very misleading as measures of the impact of pulmonary embolism in patients with pre-existing heart or lung disease; and (2) estimation of the role of pulmonary embolism in such patients must be based on a consideration of both the immediate pre-embolic cardiopulmonary status and the extent of embolic involvement.

CHAPTER IX: Hemodynamic Results of Therapy

The hemodynamic status of patients with pulmonary embolism was essentially unaltered 24 hours after initiation of heparin therapy. However, 24 hours after initiation of urokinase therapy a significant lowering of right ventricular systolic and diastolic pressures, as well as of pulmonary arterial and right atrial mean pressures, was observed. Total pulmonary resistance also fell significantly after urokinase. These changes indicate that the resolution of pulmonary embolic obstruction was accelerated by urokinase therapy. Massiveness of embolism appeared to be a determinant of the efficacy of urokinase therapy, inasmuch as the hemodynamic treatment effect was more pronounced in patients with massive embolism than in those with submassive embolism. Patients also appeared to have a more favorable response to urokinase if their preinfusion chest roentgenogram was free of infiltrate. Previous history of cardiopulmonary disease did not appear to influence response to urokinase therapy. Therapeutic interventions other than urokinase did not influence hemodynamic responses, nor did acute bleeding complications (which were more frequent in patients treated with urokinase).

The hemodynamic response to pulmonary embolism in patients without prior cardiopulmonary disease

The hemodynamic status of 20 patients free of prior cardiopulmonary disease was related to the degree of pulmonary embolic obstruction estimated by selective pulmonary angiography. Angiographic estimation of obstruction ranged from 13 to 68 percent. Systemic arterial hypoxemia occurred in virtually all patients (95 percent) including those with only 13 percent obstruction, thus suggesting that angiographically detectable emboli virtually do not occur without producing systemic hypoxemia. Mean pulmonary arterial pressure was increased in 14 patients (70 percent) and was consistently increased when obstruction exceeded 30 percent. Elevation of the level of mean right atrial pressure was found in 10 patients (50 percent) and was usually associated with obstruction in excess of 35 percent and mean pulmonary arterial pressure in excess of 30 mm Hg. Good correlation was observed between mean pulmonary arterial pressure and angiographic estimation of obstruction (P < 0.01), mean right atrial pressure and obstruction (P < 0.01), mean pulmonary and right atrial pressures (P < 0.01), and pO 2 and obstruction (P < 0.05). Cardiac index was characteristically normal or mildly increased, being below the lower limit of normal in only 4 patients (20 percent). In patients who had not experienced cardiac failure, the cardiac index appeared to increase as systemic arterial pO 2 decreased (P < 0.01) once hypoxemia was well established. Mean pulmonary arterial pressure never exceeded 40 mm Hg, despite massive obstruction in some patients, thereby suggesting that this level approximates the maximal pressure response of the previously normal right ventricle.