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Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
Imaging con Scintigrafia
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Imaging con Scintigrafia

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imaging con scintigrafia

imaging con scintigrafia

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  • 45. Tunariu N, Gibbs SJ, Win Z, et al.Ventilation-perfusion scintigraphy ismore sensitive than multidetector CTPA in detecting chronic thromboembolicpulmonary disease as a treatablecause of pulmonary hypertension.J Nucl Med 2007;48:680–4. 46. Fedullo PF, Auger WR, Kerr KM,Rubin LJ. Chronic thromboembolicpulmonary hypertension. N EnglJ Med 2001;345:1465–72. 47. Worsley DF, Palevsky HI, Alavi A.Ventilation-perfusion lung scanningin the evaluation of pulmonary hypertension. J Nucl Med 1994;35:793– 6. 48. Reichelt A, Hoeper MM, GalanskiM, Keberle M. Chronic thromboembolicpulmonary hypertension: evaluation with 64-detector row CT versusdigital substraction angiography. Eur JRadiol 2009;71:49 –54. 49. Nikolaou K, Schoenberg SO, AttenbergerU, et al. Pulmonary arterial hypertension:diagnosis with fast perfusionMR imaging and high-spatial-resolutionMR angiography—preliminary experience. Radiology 2005;236:694 –703 60. Bergin CJ, Rios G, King MA, BelezzuoliE, Luna J, Auger WR. Accuracyof high-resolution CT in identifying chronic pulmonary thromboembolicdisease. AJR Am J Roentgenol 1996;166:1371–7.
  • gariboldi M.pierina OSM CCH a.70 Ipertensione polmonare post-embolica, in attesa TEAP
  • Conclusion : Our results demonstrate that V/Q scintigraphy has a higher sensitivity than CTPA in detecting CTEPH as a potential curable cause of PH .
  • #5214 may 11F 67 yrs PVOD : ipertensione polmonare riscontrata nel novembre 10. Scintigrafia perfusoria eseguita in altra sede nel giugno 10 compatibile con embolia polmonare. All'angio TC non difetti di carattere tromboembolico. HRCT (dott.Dore): esiti pleuritici alla base di sinistra, alterazione diffusa polmonare compatibile con sindrome veno occlusiva
  • False-Negative V/Q Scintigraphy The 2 patients from group A who had their V/Q scintigraphy interpreted as low probability did not have the diagnosis of CTEPH confirmed on pulmonary DSA. The final diagnosis was made by CTPA, which showed calcified thrombus in one patient and narrowed but patent pulmonary arterial branches in the other patient. By corroborating the patient clinical history and the CT findings, it was concluded that these patients most likely had previous PE and the pulmonary vessels had recanalized.V/Q scintigraphy that was interpreted as intermediate probability was confirmed on pulmonary DSA to be CTEPH. The CT was reported as showing severe emphysematous changes but failed to show signs of CTEPH. It was the V/Q result together with the clinical history that prompted the clinicians to request pulmonary DSA.
  • Chronic thromboembolic pulmonary hypertension (CTEPH) is a complication of venous thromboembolism. Up to 4% of patients with idiopathic pulmonary embolism may develop CTEPH.. Patients at greatest risk include those with previous episodes of venous thromboembolism, massive and sub-massive pulmonary embolism, an elevated PASP on admission or elevated pressure 2 months following initial presentation.
  • Contemporary Diagnostic Imaging Algorithm Radionuclide ventilation-perfusion scanning (V/Q) plays a key role in ruling out chronic thromboembolic pulmonary hypertension ( 44 ). Due to wider availability and more evidence, computed tomography (CT) has been ranked before cardiac magnetic resonance (CMR) ( 3 ). Center-specific use of imaging modalities may vary. CTEPH % chronic thromboembolic pulmonary hypertension.
  • DallaLana basale VQ 27nov03 Enfisema Angio: ostruzione completa vasi polm lobari medio e inf dx 2dec03 TEAP dx
  • DallaLana 1° ctrl 18dic03 SHIFT AL POLM DX RIPERF LOBO SUP MEDIO E INF FURTO DAL SEGM BAS ANT SN
  • Dalla Lana 2°ctrl 30mar04 3° ctrl 30nov 04
  • Dalla lana 5° ctrl 27feb07 6° ctrl 11dec07
  • FADDA Antonella Basale 24nov05
  • 2°CTRL 28MAR06
  • 3° CTRL 30GEN07 4° CTRL 5FEB08
  • Piccolomo Filippo preop V P PE 4 a fa, diatesi trombofilica, alla TC segni di PE cronica
  • bettenga
  • Quadro indicativo di fenomeni tromboembolici massivi interessanti tutti i lobi di entrambi i polmoni, lievemente più accentuati al lobo sup dx
  • bettenga
  • bettenga
  • extensive pulmonary hypertensive changes in the small distal arteries changes not detectable by routine angiography. We speculate that these changes, like those in patients with congenital right-to-left shunts, are induced bythe high flows and pressures to which the “open”vascular bed is exposed for months to years in patients with chronic thromboembolic pulmonary hypertension(C T-E PH). We further speculate that such hypertensive changes in the vascular bed that was“open” preoperatively may reduce flow to these zones postoperatively as pulmonary flow is diverted to therelatively normal microcirculation distal to endarterectomized segmental arteries. 2- A final potential explanation might exist, namely:that surgical disruption of the pulmonary vascular endothelium may induce a state of nonresponsive vasodilatation in the endarterectomized areas. Evidencefor this hypothesis is primarily circumstantial. The vascular endothelium has been shown to secretevasodilatory and vasoconstrictor substances, In the setting of experimental endothelial stripping or carotid endarterectomy, the vascular endothelium has beenshown to regenerate, forming a coherent layer in seven to ten days. However, morphologic and functional alterations in the neoendothelium have been shownto exist as late as four weeks postoperatively.} It is possible, therefore, that the neoendothelium in the operated-on segments in patients with thromboem bolic pulmonary hypertension may create an abnormally low resistance segment in endarterectomizedlung zones by its effect on vascular smooth muscle, thus shunting flow toward zones that were endarterectomized.
  • PURPOSE: To use artificial intelligence methods to determine whether quantitative parameters describing the perfusion image can be synthesized to make a reasonable estimate of the pulmonary arterial (PA) pressure measured at angiography. MATERIALS AND METHODS: Radionuclide perfusion images were obtained in 120 patients with normal chest radiographs who also underwent angiographic PA pressure measurement within 3 days of the radionuclide study. An artificial neural network (ANN) was constructed from several image parameters describing statistical and boundary characteristics of the perfusion images. With use of a leave-one-out cross-validation technique, this method was used to predict the PA systolic pressure in cases on which the ANN had not been trained. A Pearson correlation coefficient was determined between the predicted and measured PA systolic pressures. RESULTS: ANN predictions correlated with measured pulmonary systolic pressures ( r 0.846, P .001). The accuracy of the predictions was not influenced by the presence of pulmonary embolism. None of the 51 patients with predicted PA pressures of less than 29 mm Hg had pulmonary hypertension at angiography. All 13 patients with predicted PA pressures greater than 48 mm Hg had pulmonary hypertension at angiography. CONCLUSION: Meaningful information regarding PA pressure can be derived from noninvasive radionuclide perfusion scanning. The use of image analysis in concert with artificial intelligence methods helps to reveal physiologic information not readily apparent at visual image inspection. © RSNA, 2002
  • Figure 1. Example of fractal dimension calculation in (top row) a patient with pulmonary hypertension (predicted pressure, 75 mm Hg; measured PA systolic [ sys ] pressure, 80 mm Hg) and (bottom row) a normotensive patient (predicted pressure, 16 mm Hg; actual PA systolic pressure,18 mm Hg). In the top and bottom rows, the left image is the original posterior perfusion image of the right lung, the middle image shows the lung contour after subtracting 20% of the lowest count pixels, and the right image shows the lung contour after subtracting 33% of the lowest count pixels. Fractal dimension ( FD ) is shown beneath each subtracted image. The fractal dimension is higher in the patient with pulmonary hypertension and increases as more low–count density pixels are subtracted from the original image.
  • To assess the relationship between pulmonary vascular obstruction and hemodynamic status in acute pulmonary embolism (APE)and in chronic thromboembolic pulmonary hypertension (CTEPH), perfusion lung scan and hemodynamic measurements were obtained in 31 consecutive patients with APE and in 45 with CTEPH. Methods: Lung scans were scored independently by two experienced observers who determined the percentage of vascular obstruction (PVOs). Mean pulmonary artery pressure (PAP) and total pulmonary resistance (TPR) were obtained during right heart catheterization. In patients with APE, measurements were recorded within a 1-hr interval before and 12 hours after thrombolysis. This yielded 62 paired PVOs values with concomitant PAP and TPR measurements. In patients with CTEPH, data were recorded within a 3-day interval. Results: Mean PVOs (%) values were similar in APE and CTEPH patients (59 ± 13 vs. 58 ± 15), whereas PAP and TPR were significantly higher in CTEPH patients (51 ±17 mmHg and 23 ±11U/m2, respectively) than in APE patients (23 ±8 mmHg and 9 ±5 U/m2, respectively, p < 0.001). In APE patients, significant hyperbolic correlations were found linking PVOs with PAP and TPR (r =0.75, p < 0.01 for PAP; r = 0.71, p < 0.01 for TPR). In CTEPH, there were no significant correlations between PVOs and PAP or TPR. For the same level of PVOs, patients with CTEPH had higher PAP andTPR values than patients with APE. Conclusion : In APE without prior cardiopulmonary disease, increases in PAP and TPR are correlated in a nonlinear fashion with the degree of pulmonary vascular obstruction as assessed by lung scanning. In CTEPH patients, the higher PAP and TPR values as compared to APE patients with comparable degrees of PVOs are consistent with previous reports that pulmonary hypertension in CTEPH is due not only to the obstruction of proximal pulmonary arteries but also to remodeling of small distal arteries in nonoccluded areas. Key Words: pulmonary hypertension; thromboendarterectomy; pulmonary artery pressure; pulmonary embolism J Nucl Med 1997; 38:980-983
  • TPR TOTAL PULMONARY RESISTENCE Relation between PVOs and TPR in APE (O) and chronic thromboembolic pulmonary hypertension (•F).or a given degree of obstruc tion, patients with CTEPH had higher TPR values than patients with APE.
  • Relation between PVOs and TPR in APE (O) and chronic thromboembolic pulmonary hypertension (•F).or a given degree of obstruction, patients with CTEPH had higher TPR values than patients with APE.for a comparable level of PVOs patients with CTEPH had higher PAP and TPR values than patients with APE. This result is consistent with previous reports that, contrary to APE, pulmonary hypertension in CTEPH is not due only to mechanical obstruction of proximal arteries but also to lesions of small arteries
  • Fig. 1. Functional lung images in one animal. Images are contiguous tomographic sections viewed in the cranio-caudal direction and presented from top left to bottom right. The left side in the image corresponds to left side in the animal. Tracer activity is represented in a “hot” color scale (black no activity; white maximal activity) in that frame. ( A ) Regional perfusion (Q˙ r) before embolism. ( B ) Q˙ r after embolism. There is dramatic redistribution of Q˙ r with many regions of the lungs essentially unperfused. ( C )Tracer activity remaining in the lungs at the end of the washout period after inhalational delivery of tracer. Note that higher activity corresponds to embolized areas, representing the slower washout rate of these regions.
  • Transcript

    • 1. Carlo Aprile SC Medicina Nucleare Fond.Policlinico S.Matteo,IRCCS Pavia IMAGING MEDICO-NUCLEARE
    • 2. Identification of CTEPH as the cause of PH is facilitated by several imaging techniques: <ul><li>Ventilation–Perfusion (V/Q) scintigraphy, </li></ul><ul><li>multidetector CT Pulmonary Angiography (CTPA), </li></ul><ul><li>High-Resolution CT (HRCT), </li></ul><ul><li>pulmonary Digital Subtraction Angiography (DSA), </li></ul><ul><li>Magnetic Resonance Angiography </li></ul>
    • 3. <ul><li>CTPA-large multicenter study Stein PD, et al. Multidetector computed tomography for acute pulmonary embolism . N Engl J Med. 2006;354:2317 </li></ul><ul><li>sensitivity of 83% </li></ul><ul><li>specificity of 96%, </li></ul><ul><li>with even a lower sensitivity for segmental (68%) and subsegmental (25%) branches </li></ul><ul><li>Pitton MB, et al. Chronic thromboembolic pulmonary hypertension : diagnostic impact of multislice-CT and selective pulmonary-DSA. Rofo. 2002;174:474. </li></ul><ul><li>Multidetector CTPA </li></ul><ul><li>sensitivity of 70.4% for segmental and </li></ul><ul><li>63.6% for subsegmental branches </li></ul><ul><li>when compared with pulmonary DSA </li></ul>
    • 4. Accuracy of Various Imaging Methods Against Pulmonary Angiography as the Reference Method to Diagnose CTPH
    • 5. SCINTIGRAFIA POLMONARE DI PERFUSIONE
    • 6. SCINTIGRAFIA POLMONARE VENTILATORIA <ul><ul><ul><ul><ul><li>1. Sc VENTILATORIA CON AEROSOL : test diagnostico che visualizza la distribuzione broncopolmonare di un radioaerosol inalato </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Sc. VENTILATORIA CON GAS RADIOATTIVI : test diagnostico che visualizza la distribuzione polmonare di un gas radioattivo inalato, durante le manovre respiratorie </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>3. Sc VENTILATORIA CON PSEUDOGAS (Technegas), range 60-160nm (media 97nm) </li></ul></ul></ul></ul></ul>
    • 7. Limite dimensionale di valutazione del circolo periferico della metodica scintigrafica e TC.
    • 8. F a.70 Ipertensione polmonare post-embolica, in attesa TEAP
    • 9. SOSPETTA PE IN COPD
    • 10. J Nucl Med 2007; 48:680–684
    • 11. 500 patients with PH referred to Hammersmith Hospital, London, between 2000 and 2005: 227 elegible pts <ul><li>V/Q Images were interpreted according to the modified PIOPED criteria </li></ul><ul><li>A high-probability scan : suggestive of chronic thromboembolic pulmonary disease, </li></ul><ul><li>2. l ow-probability scan : suggestive of nonchronic thromboembolic pulmonary disease etiology. </li></ul><ul><li>For intermediate-probability scans: 2 separate datasets </li></ul><ul><ul><li>In one as suggestive of chronic thromboembolic pulmonary disease and, </li></ul></ul><ul><ul><li>in the other dataset, not suggestive of chronic thromboembolic pulmonary disease </li></ul></ul>
    • 12. Multidetector CTPA - A report was considered as suggestive of chronic thromboembolic pulmonary disease if: <ul><li>visualization of the thrombus, </li></ul><ul><li>calcified thrombus, </li></ul><ul><li>recanalization, </li></ul><ul><li>sudden change in vessel caliber, </li></ul><ul><li>strictures, </li></ul><ul><li>poststenotic dilatation, </li></ul><ul><li>webs, or perfusion abnormality </li></ul>
    • 13. Pulmonary DSA: indications (61/78 pts) <ul><li>(a) clinical suspicion of CTEPH, </li></ul><ul><li>(b) at least one positive imaging modality for chronic thromboembolic pulmonary disease,and </li></ul><ul><li>(c) whether the patient was being assessed for pulmonary thrombendarterectomy. </li></ul>
    • 14. Summary of V/Q Scans and CTPA Results with CTEPH (group A, n 78 patients), with non-CTEPH (group B, n 149 patients) MP: Mosaic Perfusion V/Q scan CTPA Group Low probability Intermediate probability High probability Negative Positive A ( n 78) 2 FN 1 75 38 FN 40 B ( n 149) 134 7 8 FP 148 1 MP 43 10
    • 15. Summary of False-POSITIVE V/Q Scans IPAH = idiopathic pulmonary arterial hypertension; ASD = atrial septal defect; PVOD = pulmonary venoocclusive disease; APAH = associated pulmonary arterial hypertension V/Q Diagnosis Intermediate probability ( n = 7) IPAH ( n = 4) IPAH and emphysema ( n = 1) ASD and pulmonary fibrosis ( n = 1) Pulmonary fibrosis ( n = 1) High probability ( n = 8) IPAH ( n = 3) PVOD ( n = 1) APAH and ASD ( n = 2) Scleroderma and pulmonary fibrosis ( n = 1) Apical bullae: apical mismatch on V/Q ( n = 1)
    • 16.  
    • 17. Summary of False-NEGATIVE V/Q Scans V/Q Diagnosis 2 patients from group A with low probability scan CTPA  1. calcified thrombus in one patient and 2. narrowed but patent pulmonary arterial branches 1 patient from group A with intermediate probability scan CT  severe emphysematous changes without signs of CTEPH DSA  CTEPH
    • 18. Summary of Performance Indicators for V/Q Scintigraphy and CTPA * Intermediate with high-probability scans as indicative of CTEPH.    Only high-probability scans as indicative of CTEPH. scan Indicator V/Q (1) * V/Q (2)  CTPA Sensitivity (%) 97.4 96.2 51.3 Specificity (%) 90 94.6 99.3 Accuracy (%) 92.5 95.2 82.8 NPV (%) 98.5 97.9 79.7 PPV (%) 83.5 90.3 97.6
    • 19. PISAPED Q J Nucl Med 2001; 45: 281 <ul><li>Perfusione da sola, criteri interpretativi “nuovi”, risposta SI/NO: </li></ul><ul><li>1) scintigrafia normale; </li></ul><ul><li>2) scintigrafia anormale con aspetto non embolico; </li></ul><ul><li>3) scintigrafia anormale con aspetto embolico </li></ul>
    • 20. PISAPED Q J Nucl Med 2001; 45: 281 <ul><li>890 pazienti </li></ul><ul><li>SENSIBILITA’: 92% </li></ul><ul><li>SPECIFICITA’: 87% </li></ul>Miniati (Am J Respir Crit Care Med 1996; 154: 1387 ; Am J Respir Crit Care Med 1999; 159: 864) Interpretazione Casistica CRITERI SENS SPEC Sostman (PIOPED) PISAPED PISAPED 91 90 Miniati (PISAPED ) PIOPED PISAPED 80 83
    • 21. DECT vs. V/Q scan IRCCS S.Matteo -Pavia Stoppa D. Tesi Laurea aa.2009-10 DECT V/Q scan tot PE+ PE+ e altro Altre pat NEG A-operati Q dif. 50 15 0 0 65 Q unif 0 0 0 0 0 A- non operati Q dif. 9 3 2 0 14 Q unif 0 0 0 0 0 B Q dif. 0 2 1 0 3 Q unif 2 0 2 3 7 tot 61 20 5 3 89
    • 22. VENTILATION–PERFUSION IN CTEPH • Tunariu et al. J Nucl Med 2007; 48:680 <ul><li>normal V/Q scintigraphy practically rules out the presence of CTEPH, </li></ul><ul><li>whereas normal CTPA does not exclude the presence of CTEPH. </li></ul><ul><li>high probability V/Q scintigraphy makes CTEPH the most likely diagnosis, although other conditions—including pulmonary venoocclusive disease—may result in similar findings. </li></ul><ul><li>grouping intermediate- with low-probability V/Q scans as indicative of non-CTEPH etiology would maintain a high sensitivity and improve specificity, NPV,and PPV. </li></ul>
    • 23. V/Q Scanning for Pulmonary Hypertension Worsley DF et al. JNM 1994;35:793
    • 24. National Pulmonary Hypertension Centres of the UK and Ireland Consensus statement on the management of pulmonary hypertension in clinical practice in the UK and Ireland Heart 2008;94;1-41
    • 25. Diagnostic approach to chronic thromboembolic pulmonary hypertension (CTEPH). National Pulmonary Hypertension Centres of the UK and Ireland Heart 2008;94;1-41
    • 26. ESC/ERS GUIDELINES FOR THE DIAGNOSIS AND TREATMENT OF PULMONARY HYPERTENSION Eur Respir J 2009; 34: 1219–1263
    • 27. Contemporary Diagnostic Imaging Algorithm
    • 28. Caso 1 - DLS
    • 29. V Q DLS ♂ 68 a. Angio : ostruzione completa rami polmonari lobari medio e inf. Dx EAP dx & CABG V / Q BASALE
    • 30. DLS +16 d ANT POST RAO LPO LAO RPO
    • 31. DLS +4m DLS +9m ANT POST LAO RPO RAO LPO ANT POST RAO LPO LAO RPO
    • 32. DLS +38m DLS +26m ANT POST RAO LPO LAO RPO ANT POST LAO RPO RAO LPO
    • 33. DLS +48m RPO ANT POST LAO
    • 34. Caso 2 -FA
    • 35. FA ♀ 44 a , PE in gravidanza a 26 a.,dai 43 a. dispnea da sforzo, NYHA III, CT trombosi bilat aa. Polmonari, PAPs 105mmHg, ECO-Doppler DVT aa.inf. EAP sn sup,lingula, inf dx sup, inf - lobect inf dx V/Q BASALE ANT POST RAO LPO LAO RPO
    • 36. FA +9 d ANT POST RAO LPO LAO RPO
    • 37. FA +3 m ANT POST RAO LPO LAO RPO FA +3 m
    • 38. FA +13 m FA +26 m ANT POST RAO LPO LAO RPO
    • 39. P.F.#1166 basale V/P
    • 40. P.F.#1166 TEAP bilat : Dx S,M,I ; Sn S, Li, I 8 d - 3mo
    • 41. P.F.#1166 TEAP bilat : Dx S,M,I ; Sn S, Li, I
    • 42. BL#1903 basale VP: PAPs 80mmHg. Angio-CT embolia ramo principale a polm dx e coinvolgimento ramo lobare inf, difetto di un ramo segmentario LIS
    • 43. BL #1903 TEAP DX (S,M,I) 8 d - 200 d
    • 44. BL #1903 TEAP DX (S,M,I)
    • 45. CM #1895  46 a. VP basale
    • 46. CM #1895  46 a. DX (S,M,I) Sn (S,Li,I)
    • 47. “ Steal” after PEA 1 <ul><li>The incidence of new defects was increased tenfold in segments that had </li></ul><ul><li>normal preoperative angiographic findings, </li></ul><ul><li>normal preoperative radionuclide perfusion, and </li></ul><ul><li>not been entered at the time of surgery. </li></ul>Olman MA et al. Chest. 1990 ;98:1430-4.
    • 48. “ Steal” after PEA 2 1- hypertensive changes induced by the high flows and pressures to which the “open” vascular bed is exposed for months to years, may reduce flow to these zones postoperatively as pulmonary flow is diverted to the relatively normal microcirculation distal to endarterectomized segmental arteries. 2- the neoendothelium in the operated-on segments may create an abnormally low resistance segment in endarterectomized lung zones by its effect on vascular smooth muscle, thus shunting flow toward zones that were endarterectomized. Olman MA et al. Chest. 1990 ;98:1430-4.
    • 49. Role of V/Q scan in CTEPH DIAGNOSIS High accuracy established EARLY CHANGES AFTER PEA sensitive Prompt visualization of Q changes LATE CHANGES AFTER PEA Clinical impact? FOLLOW-UP Detection of recurrent PE established
    • 50. Longitudinal analysis of perfusion lung scan of patients with unoperated CTEPH Skoro-Sajer N et al Thromb Haemost 2004; 92: 201 Perfusion scan at (A) baseline and (B) 3 yrs after <ul><li>A decrease in the crosssectional area of the pulmonary vessels leads to a loss of the functional capillary bed and vascular remodeling similar to nonthromboembolic PAH. </li></ul><ul><li>Within the observation period cardiac index decreased, reflecting RV decline. </li></ul><ul><li>Thus, the data suggest that the diagnostic V/Q scan pattern of CTEPH is lost over time, and may be misleading as the disease progresses. </li></ul>
    • 51. Pulmonary Perfusion Patterns and Pulmonary Arterial Pressure Scott JA. Radiology 2002; 224:513–518
    • 52. Scott JA 2002 <ul><li>Higher total peripheral resistances were seen with chronic PE than with acute for a given degree of vascular obstruction </li></ul><ul><li>This difference was attributed to small-vessel disease in the patients with chronic PE, which was inapparent at subjective evaluation of the Q scan. </li></ul><ul><li>Changes in the peripheral small vessels may thus be an important parameter in determining the PA pressure. </li></ul><ul><li>Patients with primary pulmonary hypertension and CTEPH  medial hypertrophy and intimal proliferation in the small distal arteries of the lung . </li></ul><ul><li>This small-vessel component may alter the appearance of the lung periphery on Q scans. Although the scans of most patients with primary pulmonary hypertension lack segmental perfusion defects, the images obtained in some of these patients show a nonspecific “patchiness” that may be related to small-vessel disease </li></ul>
    • 53. Fractal dimension calculation in (top row) a patient with pulmonary hypertension (predicted pressure, 75 mm Hg; measured PA systolic [ sys ] pressure, 80 mm Hg) and (bottom row) a normotensive patient (predicted pressure, 16 mm Hg, actual18 mm Hg).
    • 54. Scatterplot of ANN-predicted PA systolic pressures versus those measured at angiography in patients with and in those without pulmonary embolism ( r 0.846, P < .001).
    • 55. Lung Perfusion Scans and Hemodynamics in Acute and Chronic Pulmonary Embolism Réza Azarian, Myriam Wartski, Marie-Anne Collignon, Florence Parent, Philippe Hervé,Hervé Sors and Gerald Simonneau J Nucl Med 1997; 38:980-983
    • 56. Relation between PVOs and TPR in APE A strong hyperbolic correlation was found between PVOs and TPR (y = 1578/(530 - 5.88x)). J Nucl Med 1997; 38:980
    • 57. Relation between PVOs and TPR in APE (  ) and CTEPH (  ). For a given degree of obstruction, patients with CTEPH had higher TPR values than patients with APE. J Nucl Med 1997; 38:980
    • 58. Pulmonary Vascular Obstruction and Hemodynamics in Acute and Chronic PE Values are expressed as means mean±s.d. (range). APE = acute pulmonary embolism; CTEPH = chronic thromboembolic pulmonary hypertension; PVOs = pulmonary vascular obstruction scoreassessed by perfusion lung scanning; PAP = mean pulmonary artery pressure; TPR = total pulmonary resistance. J Nucl Med 1997; 38:980
    • 59. <ul><li>In CTEPH patients, the higher PAP and TPR values as compared to APE patients with comparable degrees of PVOs are consistent with previous reports that </li></ul><ul><li>PH in CTEPH is due not only to the obstruction of proximal pulmonary arteries but also to remodeling of small distal arteries in nonoccluded areas. </li></ul>J Nucl Med 1997; 38:980
    • 60. PET & LUNG
    • 61. ( A ) Regional perfusion (Q˙ r) before embolism. ( B ) Q˙ r after embolism: dramatic redistribution of Q˙ r with many regions of the lungs essentially unperfused. ( C )Tracer activity remaining in the lungs at the end of the WO after inhalational delivery of tracer. Note that higher activity corresponds to embolized areas, representing the slower washout rate of these regions.
    • 62. Grazie dell’attenzione
    • 63.  
    • 64.  
    • 65. The 4th WHO Symposium on Pulmonary Hypertension Dana Point, California, 2008 <ul><li>group 1 as pulmonary arterial hypertension (PAH), </li></ul><ul><li>group 2 as pulmonary hypertension due to left heart disease, </li></ul><ul><li>group 3 as pulmonary hypertension due to lung diseases and/or hypoxia, </li></ul><ul><li>group 4 as chronic thromboembolic pulmonary hypertension , </li></ul><ul><li>group 5 as pulmonary hypertension of othercauses. </li></ul>

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