Mentored Workstation Cases for January 12-15, 2008 Cardiac CT Angiography Course

Transcription

1 Mentored Workstation Cases for January 12-15, 2008 Cardiac CT Angiography Course Teaching TCH001 TCH002 TCH003 TCH004 TCH005 TCH006 TCH007 TCH008 /equiv The LAD is occluded. There is heavy mixed plaque. The ostial circumflex stent is patent. The circumflex is otherwise occluded in the midvessel and the obtuse marginal is occluded. The distal vessel is seen filling either from slow anterograde flow or collateral flow. The ostial RCA has significant calcified heavy plaque obstructing visualization of the lumen. There is diffuse mixed disease. The LIMA to the LAD is patent and the anastomosis is well visualized and looks fine. The SVG to the posterolateral vessel is well visualized and patent. The SVG to jump graft to the D1, D2 and obtuse marginal is patent. All limbs are patent. There is apical akinesis. Overall EF is preserved at 57%. Misregistration artifact is noted. Normal left main. Normal Cx. LAD has a severe soft plaquing noted which appears to be obstructive. Nonobstructive calcifications also noted in the LAD. Mild calcific RCA lesions also noted. Incidental findings of a right middle lobe pulmonary nodule. Mediastinal and hilar lymph nodes noted as well. (Cath Correlation) Normal EF. Heavy mitral annular calcification. Normal LM. Proximal LAD has moderate nonobstructive calcified disease. Large proximal LAD bridge. Nonobstructive calcium of D1. CX and RCA have no significant disease. Late timing due to expanded selected FOV. LM had non obstructive calcium. Critical mid LAD disease. Severe disease of several diagonals. Subtotal occlusion of circumflex/om system. Occluded RCA. Visualized portion of the left brachiocephalic and carotid arteries are fine. Visualized portion of the right carotid is fine. Right vertebral is fine. Anomolous left vertebral emanating from the aortic arch. Occluded LIMA with retrograde filling via the RIMA to LAD which is patent. The body of the RIMA is obscured in many locations by clips.there is an occluded RCA graft with an occluded stent proximally. An SVG to the PDA is patent but the PDA is severely and diffusely diseased. The native right posterolateral branch is occluded. SVG to 2 diagonals is patent. The diagonals themselves are severely diseased. There is an arterial graft from this SVG to the OM and is patent. 2 other occluded graft stumps are visualized on the aorta. Mild biatrial enlargement. Small focal apical lateral infarct noted. (Cath correlation) Normal LV function EF 60%. Normal LM. Mild soft plaque of proximal and mid LAD without obstruction. Mild ostial D4 soft plaque without obstruction. Anomalous RCA from left coronary cusp coursing between PA and Ao. The anomaly is extramural in nature. EF 61%. LIMA to D1 to LAD good contrast. Radial free graft appears patent to distal LCX. SVG to PDA appears patent. Mid RCA not evaluable. Known history of Kawasaki s Disease. Diffuse severe aneurismal dilations of all coronary arteries. Mild soft plaquing noted. (Cath correlation). EF was normal. Paradoxical septal motion due to LBBB. Heavily calcified vessels. Calcium score was 688 in LAD, 688 in Cx and 745 in RCA. Heavily calcified LAD. Lumen not visualized and thus significant disease could not be excluded. Non flow limiting mid and distal heavy LAD disease. Cx was heavily calcified and lumen could not be visualized. Obstructive lesion cannot be excluded. Heavily calcified RCA with proximal occlusion. (Cath correlation). Page 65

2 TCH009 TCH010 TCH011 TCH012 TCH013 TCH014 TCH015 TCH016 TCH017 TCH018 TCH019 TCH020 /SOB Ejection fraction was 48%. There is hypokinesis of the left ventricular apex. There is evidence of coronary artery bypass graft surgery. There is a LIMA graft which is patent to the LAD and skips to the first diagonal branch which is patent. The proximal native LAD is occluded. There is a saphenous vein graft which is patent to the obtuse marginal branch. There is a saphenous vein graft to the RCA in the area of the PDA which has a good anastomosis and is patent. All proximal native vessels are occluded. Ejection fraction is 30-35%. Inferior akinesis with scar and calcified infarct. ICD wires noted. SVG to first diagonal is occluded. Continuation of the jump graft from first diagonal to OM1 is patent. Continuation from OM to PDA is occluded. LIMA to LAD is patent. Unable to assess proximal LIMA due to ICD wires crossing. Native vessel severely diseased. Sternal malunion noted. Mild to moderate mixed disease of the LAD. Mild mixed Cx disease. Mild mixed disease of the RCA. (Cath correlation). Attenuation artifact noted. Nonobstructive calcific disease of the LAD and Cx. Misregistration artifact noted. No obstructive lesions. Anterior take off of the RCA. Ostial RCA is kinked (normal variant). Nondominant RCA with no significant disease. EF 45%. SVG to distal RCA patent. LIMA-LAD patent. SVG-Diagonal is an acute angle with narrow ostiom but patent. SVG-LCX/OM normal. RCA is free of obstructive disease. Proximal LAD has nonobstructive small calcium. Cx is normal. Markedly depressed LV systolic function. Ejection fraction 30%. Apex is dyskinetic. ICD wire noted. SVG to LAD occluded. LIMA to LAD patent. Distal anastomosis well visualized. SVG to OM has multiple stents. Stents are patent. Proximal and distal anastomosis are not well visualized. Radial graft to first diagonal patent. Continuation from first diagonal to first obtuse marginal occluded. Occluded left subclavian vein with prominant chest wall venous collaterals. Windmill artifact from pacer wires noted. Mid RCA stent is occluded likely. Mild soft plaque of the left main. Mild soft plaque of LAD. Cx has nonobstructive soft plaque lesion distal to OM. (cath correlation). Heavy RCA, LAD and Cx calcium. The proximal and mid RCA has dense calcium obscuring the lumen and a significant lesion cannot be excluded. Left main is OK. Nonobstructive LAD and Cx calcified plaquing. (Cath correlation) Nonobstructive calcified LM disease. Heavy, proximal LAD calcification. Lumen cannot be seen in places and thus a flow limiting stenosis cannot be excluded. Short myocardial bridge in mid LAD. Mid LAD stents are patent. Proximal calcifications of D1. Cx has multiple calcified plaques. OM1 has nonobstructive calcified plaques. RCA is dominant. Patent stent in proximal RCA. Second stent at origin of PDA which is patent. Large calcified plaque proximal to the second stent (nonobstructive). (Cath correlation). /equiv Normal EF. RCA is occluded proximally. SVG to RCA is patent with mild atherosclerosis noted within the graft. Nonobstructive LM plaque. LAD heavily diseased with a high grade lesion in proximal and mid segment. LIMA to LAD is patent. Anastemosis obscured by surgical clips. Distal LAD fills but is small. Severe ramus disease. Severe disease of a D1. High grade proximal Cx disease. Cx is occluded in the mid vessel. SVG to OM patent. (cath correlation) Well functioning mechanical bileaflet AVR. Absent left main with separate ostia of LAD and Cx. Mild calcified lesions of the Cx and LAD. Non dominant RCA. Page 66

3 TCH021 TCH022 TCH023 TCH024 TCH025 TCH026 Case 13 Case 16 Case 17 case 2 cath Case 20 There is heavy mixed disease of the LAD which is then occluded after the first diagonal. The circumflex has severe mixed plaque noted with significant luminal obstruction. The RCA is occluded. The SVG to the LAD is visualized nicely and is patent with the distal LAD filling nicely. There is a small LIMA to the diagonal which is patent. The body of the LIMA is obscured by clips. The distal anastomosis is not well visualized due to clips. The RIMA to the PDA is occluded. The radial to the circumflex coronary artery is occluded. The initial SVG to the circumflex and then to the PDA is occluded. The ejection fraction is approximately 50% with normal perfusion. There is aortic atherosclerosis noted /CABG LIMA to first diagonal and jump to distal LAD is patent. Distal anastomosis well visualized. No problems. Anastomosis to first diagonal not well visualized due to clip. Radial graft, proximal portion, from the aorta to OM1 is occluded. Jump graft from OM1 to OM2 to PDA is patent. Misregistration artifact is noted. CABG/ syncope Mech valve fxn Poor coronary and LV opacification. Late timing. Small, nonobstructive plaques in RCA. Normal LM. Patent proximal LAD stent. Calcified nonobstructive plaque distal to LAD stent. Calcified, nonobstructive plaque in mid LAD. Calcified, nonobstructive plaque in large diag. Anomalous Cx sharing a common ostium coming off of the right coronary sinus. The Cx passes posteriorly to the aorta and yields a large OM. Cx and OM are free of significant disease. EF was 52%. Mild anterior wall HK. RCA occluded proximally. SVG to RCA patent. Severe proximal Cx disease (mixed). LIMA to OM1 and OM2. is patent. LAD has high grade proximal disease (mixed). Distal LAD fills adequately. Occluded SVG to LAD noted. Minimal calcification of proximal LAD. Proximal LAD stant is patent. Moderate nonobstructive soft plaque prior to stent. Small amount of soft plaque distal to stent. Codominant system. OM has no significant disease. RCA has no significant disease. Normal EF. Normally functioning St. Jude Mitral valve. No significant CAD. Anomalous Left Main. LAD has common origin with RCA and courses anterior to pulmonary artery. Circumflex courses between the pulmonary artery and the aorta. Heavily calcified coronaries. Occluded mid RCA. Mid LAD has a probable significant lesion. Soft nonobstructive plaque of a large OM1. Markedly enlarged RA and RV with enlarged coronary sinus. Significant contrast in the IVC. This is consistent with significant TR. Ascending aortic aneursysm noted. Motion artifact noted in a dominant RCA. Nonobstructive soft plaque noted in RCA. LAD has mild nonobstructive disease. Cx has mild calcifications. Large right PE. Markedly enlarged right atrium. Enlarged ascending Aorta. Cardiac viens are well visualized though study was not performed specifically to look at the cardiac veins. RCA is dominant with nonobstructive ostial calcifications. Mild to moderate ostial PDA disease. Mild soft plaque in ostium of D1. Occluded LAD. D2 is likely fed from collaterals. Cx is small and free of significant disease. Calcified apical infarct noted. Large ascending aortic aneurysm. Mild calcific disease of the coronaries. Page 67

4 Case 19 cath Case 24 Case 25 Case 26 Case 27 Case 33 Case 36 Case 37 Case 39 Case 7 < 50% mixed prox LAD plaque. Co-dominant system with PL branch from LCX. Artifact from pacing catheter. Anomalous Left system from the right coronary cusp. Left atrium to coronary venous fistula. LV diverticulum. Apical infarct. Occluded RCA. SVG to RCA is occluded. LIMA to LAD is patent. LAD has proximal occlusive soft plaque. Occluded Cx. SVG to OM is patent and a moderate mid stenosis. Anomalous left system from RCA. Diminutive LAD. Long left main. Overall minimal diffuse disease. LIMA to LAD and RIMA to PDA are patent. LAD has a proximal severe soft plaque stenosis. Occluded SVG probably to diagonal. LIMA to LAD is patent. Patent SVG to PDA and SVG to OM. Proximal RCA has a significant stenosis. Proximal LAD and Proximal Cx are occluded. SVG to OM is atretic and diffusely diseases. LIMA to LAD, RIMA to PDA, SVG to OM are patent. Stent to distal SVG to OM is patent. Proximal calcification of LAD. RCA and OM are occluded. RCA originates from the left cusp and courses between the aorta and pulmonary artery. The artery is an intramural anomaly. RCA has nonobstructive plaque. The left system emanates from the right cusp. The LM travels to become the Cx and then a branch off of the Cx becomes the anatomic LAD. Septals emanate from the LM before it becomes the Cx. Patent proximal LAD stent. No other significant disease. Case 9 Extremely large and tortuous RCA. TCH052 TCH053 TCH054 Mild calcification of the brachiocephalic artery. Normal left carotid ostium. LIMA to LAD: proximal anastemosis is fine. Proximal portion of the LIMA is obscured by clips. LIMA is patent but multiple areas of the body of the LIMA is obscured by frequent clips. Distal anastemosis is obscured by clips. The LAD after the LIMA is not well visualized. SVG to OM: Patent. Proximal anastemosis is not visualized due to clips. Distal anastemosis is OK. The OM after the graft is patent and small. SVG to RCA. Proximal anastemosis is OK. Proximal portion of the graft and mid portion as well are obscured by clips. The distal anastemosis is also obscured by clips. The distal RCA is not visualized due to clip artifact. All 3 native vessels are occluded. Subendocardial infarct is noted in the mid inferior wall. Right dominant. Sternotomy with sternal malunion. Long proximal LAD stented segment is patent. Patent LIMA jump graft from diagonal to LAD. Diagonal anastemosis was obscured by clip artifact. LAD anastemosis was fine. Distal LAD very small. Very small Cx. Non obstructive RCA, PDA and PL disease. Right dominant. Nonobstructive calcified lesions of RCA. Significant soft plaque noted in mid RCA. Nonobstructive soft plaque noted in mid LAD. Nonobstructive disease in the ostium of the Cx. Bronchiectasis noted bilateral lower lobes. Page 68

5 TCH055 TCH056 TCH057 TCH058 TCH059 TCH060 TCH165 TCH061 TCH062 TCH063 TCH064 TCH065 h/o stent Pulm Vein Aortic Mass / syncope Cardiac compression syndrome noted. Noteable findings: Narrow AP diameter. Anterior pericardium contacting anterior chest wall and is mildly thickened. Compressed left atrium with compressed mitral annulus and posterior mitral valve prolapse. Compressed esophagus. The LAD has nonobstructive calcification. The calcification is diffuse and heavy, however. There are two patent small diagonals without significant obstruction. There is nonobstructive mixed plaque of the proximal circumflex. The RCA ostial stent is patent with no significant restenosis. The mid RCA stent is also patent but the lumen is not well visualized. There is heavy RCA calcification. The lumen is not visualized in one single plane and a tight stenosis cannot entirely be excluded at this level. The distal RCA fills normally. The probability of a tight stenosis in this location of calcium is in the 50% range. There are no other cardiac structural abnormalities. Coronary artery calcium score of 228. Left main coronary artery normal. Proximal and mid portions of the left anterior descending artery demonstrated mild mixed plaque of a nonobstructive nature. Left circumflex was a nondominant artery that demonstrated mild calcific plaque, nonobstructive. Ramus intermedius branch was normal. Right coronary artery demonstrated mild calcific plaque involving the proximal portions. Mitral valve demonstrated mild mitral prolapse. Normal left ventricular systolic function. Misregistration and breathing artifact. Small nonobstructive calcified LAD plaque. Mid myocardial bridge noted. Nonobstructive mixed disease in Cx. Nonobstructive RCA calcified plaques. Normal EF. Normal EF. Underfilled small RCA. No significant RCA disease. LM ok. LAD has 2 large diags. Distal LAD has myocardial bridge. No significant LAD or diagonal plaque. Patent proximal Cx stent. Large OM is OK. Study performed to evaluate pulmonary veins in follow up after atrial fibrillation ablation. All pulmonary veins are normal. Only proximal sections of the coronaries were visualized because of atrial fibrillation. No significant CAD noted. Case should be used to practice measuring and characterizing the pulmonary veins. Aortic tumor (path confirms myxoma). Emanates from aorta in a supravalvular location. Non obstructive calcium of LAD and diagonal and large Cx OM. Small diameter RCA is OK. Mild Ao calcium. TEE correlation. No significant disease of LAD or of diagonal system. OM2 has an ostial stent. Presumed patent but poor visualization within the stent. Patent multiple overlapping stents in RCA. Right dominant. Nonobstructive calcified lesions of RCA. Significant soft plaque noted in mid RCA. Moderate to severe mixed plaque of the mid LAD. Bronchiectasis noted bilateral lower lobes. Use dose report to calculate effective dose. Severe calcification of the pericardium with evidence of constrictive pericarditis. Cath correlation of pericarditis. MRI correlation. Intaoperative photos available. Anomalous intramural type RCA coursing between the Ao and PA. Coronary artery calcium score of 5. Left main normal. LAD has minimal calcification in the proximal/minimal portion. Left circumflex demonstrated minimal calcific plaquing, nonobstructive. The left circumflex was an anomalous vessel which arose from the diagonal branch of the LAD, but otherwise normal. Normal left ventricular systolic function. Of note, the left pulmonary vein was noted to demonstrate a single os Page 69

6 TCH066 TCH067 TCH068 TCH069 TCH070 TCH071 TCH072 TCH073 TCH074 TCH075 Assess Venous anatomy Suspected Cor Anomaly Cong. Dz Prosthetic valve function Patient is s/p ASD closure with correction of anomalous pulmonary venous return. Normal LV. RV is dilated. RA is dilated. Epicardial pacer leads noted. Tricuspid annuloplasty ring noted. Persistent left SVC draining into a markedly dilated coronary sinus. LAD has mild calcified disease. Normal left ventricular size and function. Ejection fraction 63%. Annuloplasty ring noted. This is in the mitral position. Pacemaker wires noted. Bicuspid aortic valve without stenosis. LAD and RCA, nonobstructive disease. Mid circumflex, obstructive soft plaque. There is patent-free left internal mammary artery to posterolateral branch. Both anastomoses are patent. Normal EF. LM originates from the right coronary sinus. Separate LM ostium. The LM courses posterior to the Aorta. No significant plaquing noted. Calcium score of 19. Apical hypertrophy noted with hyperdynamic apex (consider Yamaguchi type HOCM). Mild Calcium and mixed LAD dz. EF normal. RCA is OK. Cx has mild calcific plaque. LAD has proximal heavy calcifications where obstructive lesion cannot be excluded. Misregistration artifact noted. (Cath correlation). Normal EF. Anomalous LM arising from the posterior moste aspect of the left coronary cusp. Mild calcified plaque of the proximal LAD. No significant RCA disease. Sinus venosis ASD with anomalous right upper pulmonary vein into the superior vena cava. Severely enlarged RA and RV. Functional analysis possible. Normal EF. Paradoxical septal motion. Mildly dilated RV. Right atrial and right ventricular pacing wires noted. Normal coronaries. Normally functioning Starr Edwards mitral valve Normal LV function. Diffuse 3 vessel nonobstructive calcific plaquing. Large right atrial mass extending from the IVC. There is also a left lower lobe lung mass noted. Multiple pulmonary emboli are seen. MRI correlation available. Possible left renal cyst noted. Stent in SVC. Mild coronary calcifications noted. TCH076 TCH077 Moderate LV dysfunction with EF of 30%. Global hypokinesis. Dominant RCA without significant disease. Bentall procedure with Cabral modification. Mechanical (ST. Jude) aortic valve. There is a repaired aortic dissection noted. Severe breathing and cardiac motion artifact noted. Severe attenuation artifact. These artifacts markedly limit scan interpretation. Surgical report notes jump graft of SVG to OM1 to OM2 to OM3 to distal RCA. All limbs are probably patent but the quality of the scan precludes a confident interpretation. Distal anastemoses are not visualized nor is the distal vessels visualized after the grafts. Patent LIMA to LAD noted by the anastemoses are not well visualized. The distal LAD after the graft fills but is not seen well. The native LAD is not well visualized due to motion. The RCA is not visualized due to motion. Right ventricular enlargement is noted. Apical aneurysm is noted on functional analysis with EF overall of 60%. Page 70

7 TCH078 TCH079 TCH080 TCH081 TCH082 TCH083 TCH084 TCH085 TCH086 TCH087 TCH088 Page 71 /CHF CM /equiv S/P CABG /equiv There is four-chamber dilatation. There is a dilated mitral annulus as well as papillary muscle dysfunction. There is severe generalized hypokinesis throughout the left ventricle. There is a biventricular ICD present. There is no significant coronary artery disease seen. History: 25 yo male with new onset CHF. Markedly dilated LV divided into a superior and inferior LV with isolated left ventricular noncompaction. EF by CT overestimated compared to MRI. MRI correlation available. Outside read of CTA reports a dominant RCA supplying most of the Cx territory as well. Cx is very small and arises from the anomalous LM. Left main coronary arises from the proximal RCA and courses posterior to the aorta and then gives rise to the LAD and Cx. Severe soft plaque of the LM. Moderate soft plaque of the LM prior to the Cx and LAD bifurcation. Distal LAD is occluded. RCA had proximal mid mild soft plaque. A stent is present in the proximal 3rd of the RCA and is well deployed and patent. (Cath correlation). EF 45%. Extensive apical infarct. Dual chamber pacer noted. Mitral annuloplasty ring noted. No sig. RCA disease. LM ok. CX ok. Small nonobstructive proximal LAD calcified plaque. Distal LAD is occluded. D1 is ok. Small Ramus ok. Mid and distal LAD myocardial bridge. Bridge also seen in the major OM branch. Mild calcium of the ascending and proximal descending aorta. LVH. Normal EF. Inferoposterior LV pseudoaneurysm with clot present. Right dominant. RCA is without significant disease. Cx is without disease. Mild mixed plaque in LAD. Prosthetic AV. Flecks of calcium in proximal LAD. Ancillary findings include: bronchiectasis in both lower lobes and lingula. Dilated main pulmonary artery. Ground glass appearance in patchy distribution of both lungs. Small bilateral pleural effusions. 4.4 cm ascending aortic aneurysm. Enlarged LV (58mm). Nonobstructive mixed plaque in the distal LM and proximal LAD. The proximal LAD is subtotally occluded. There is filling of the LAD distal to the occlusion (collaterals or antegrade trickling of dye cannot be distinguished). The LAD proximal plaquing involves the septal and D1 which do fill. >75% mixed plaque of proximal Cx. Proximal RCA occlusion with mixed plaque. RCA demonstrates distal filling (antegrade or collateral cannot be distinguished). Subendocardial inferior infarct is noted. Apex is extremely thin suggesting infarct. Mild ascending aorta calcium. Soft plaque noted in the descending aorta. EF was 29 % with apical thinning and akinesis of the apex and segmental hypokinesis in the inferior wall. Other walls are less severely hypokinetic globally. (cath correlation) EF 40%. Global HK. LM no sig. disease. LAD occluded proximally. RCA occluded proximally. Heavy distal RCA disease with small PDA. D1 is patent. D2 is small with an ostial stenosis. Cx has proximal severe stenosis. LIMA to LAD patent. Distal anastemosis obscured by clips. CX graft patent. No disease of left main. Proximal LAD is heavily calcified an the lumen could not be evaluated (significant stenosis could thus not be excluded). Mid Cx stent is patent. No significant Cx disease. Dominant RCA with heavy calcium but no obstructive lesions. Mid RCA stent is patent. Distal RCA calcifications without obstructive lesions. Large saddle pulmonary embolus. LAD has heavy calcification. A circumflex stent is noted and is patent. RCA is heavily calcified. Calcium score of 0. Normal coronaries. Excess IVC contrast suggestive of significant TR. Normal EF. LAD with stent is patent. LCX stent appears patent but can not visualize inside stent. OM nonobstructive calcific plaque. Example of sharp filter to evaluate stent.

8 TCH089 TCH090 TCH091 Significant obstructive soft plaque lesion in proximal LAD. Nonobstructive calcifications noted in LAD as well. Mild soft plaque in ramus intermedius. RCA and CX are without significant obstructions. (cath correlation). RCA occluded proximally. RCA reconstitutes distally (collaterals vs slow antegrade flow). Mixed plaque in poorly filled distal RCA. LAD has proximal, nonobstructive plaques (mixed). Nonobstructive small diags. CX has a high grade stenosis in the proximal portion (mixed plaque). (Cath correlation). Normal LV. Non obstructive LAD calcified disease. TCH092 TCH093 TCH094 TCH095 TCH096 TCH097 TCH098 TCH099 TCH100 /SOB EF 60%. Mid, Distal and Anterior septum is hypokentic. LIMA-D1 clip obscures anstomosis but appears patent. LIMA-LAD appears patent. Radial T-graft LIMA to PL branch appears patent but limb to PDA appears occluded. RCA occluded proximally. Proximal LAD nonobstructive (<50%) lesion of soft plaque. Nonobstructive mid LAD calcified plaque just before major diagonal. The diagonal itself is OK. Tiny ramus intermedius noted. Anterior take off of RCA from right coronary cusp. Secundum ASD noted. RA and RV enlargement noted. EF 51%. Mildly thickened anterior pericardium. Left middle accessory pulmonary vein. Non obstructive calcific disease of a high OM. Mild soft plaque in the proximal RCA. Moderate to severe mixed mid LAD disease. Nonobstructive calcified LM disease. LAD is occluded proximally. LIMA to mid LAD with patent distal anastemosis and no significant stenoses. Distal LAD beyond graft is patent but small. Non obstructive calcified Cx disease. RCA is proximally occluded. SVG to RCA is occluded near aortic anastemosis. /equiv /equiv Late timing. Poor coronary filling. Normal LV. Normal pericardium. LM has heavy, nonobstructive calcification. Mid LAD is heavily calcified with subtotal occlusion. Diffuse nonobstructive, calcified RCA disease. LIMA to LAD is patent. Body of LIMA obscured by multiple clips. Marked misregistration artifact. LM normal. LAD calcium noted proximally proximal stent is patent. Mid LAD cannot exclude possiblity of lesion due to misregistration. RCA is dominant and nonobstructed. LCX and OM are normal. Late timing so suboptimal contrast opacification. Mild aortic calcification. Mitral annular calcification. Mild calcium in LM. LAD heavily calcified nonobstructive disease. Mid RCA difficult to visualize due to heavy calcification. RCA occlusion cannot be ruled out. Focal inferior hypokinesis noted. (cath correlation) Mild calcium of LM. Mild soft plaque of proximal RCA. Significant soft plaque seen in proximal LAD. Use dose report to calculate the effective dose. Patent LIMA to LAD with no distal LAD obstructions. Reported radial free graft arising from the LIMA was not visualized and presumed occluded. Heavy RCA calcification. Obstructive lesion could not be excluded. Heavy circumflex calcification. Obstructive lesion could not be excluded. (cath correlation). Page 72

9 TCH101 TCH102 TCH103 TCH104 TCH105 TCH106 TCH107 TCH108 TCH109 TCH110 TCH111 /CABG /equiv CHF Thickened posterior pericardium. Distal left main has nonobstructive calcifications. Nonobstructive diffuse proximal LAD calcified disease. Motion artifact is noted in distal and mid LAD. D1 has nonobstructive mixed disease. Cx has mild calcified disease with mild luminal irregularities. Proximal RCA has nonobstructive mixed disease. Mild calcification of the ascending aorta. Severe calcifications of the descending aorta with soft plaque seen as well. Ejection fraction is 49% with lateral wall hypokinesis. Native vessel, LAD, circumflex and RCA are occluded. LIMA to LAD are patent with good visualization of the proximal portion and distal anastomosis. SVG to distal RCA is patent. Jump graft SVG to D1, D2, OM1, OM2 patent. Anastomosis well visualized Normal left ventricular size and function. Ejection fraction 65%. Calcium score zero. There is proximal nonobstructive LAD soft plaque; otherwise, normal vessels. Normal EF. Misregistration artifact noted. No significant RCA disease. LAD and Ramus have no significant disease. Cx is free of significant disease. Normal EF. LAD has proximal, nonobstructive calcifications. Large tortuous OM without significant disease. Moderate, soft plaque in RCA. The calcium score is 206 total. Function parameters indicate an ejection fraction of 42%. Left main, there appears to be significant soft plaque with small islands of calcium in the left main coronary artery. LAD, there is a mild ostial lesion. There is a large calcified plaque in the mid LAD which appears nonobstructive. The RCA is a dominant vessel and appears unremarkable. The left circumflex is unremarkable and free of significant obstructions. (cath correlation) Ejection fraction is 60%. Apical hypokinesis. Paradoxical septal motion. LIMA to LAD patent. Distal left main heavily calcified. Native LAD is occluded. RCA heavily diseased. Radial graft to distal RCA is patent with good visualization of anastomosis. Right internal mammary artery to obtuse marginal is patent. Distal anastomosis was very well visualized. Body of radial graft was not visualized due to proximity of sternal wires. Pacer wires in RV and RA. Bi-atrial enlargement. Increased attenuation of small area in mid interatrial septum consistent with prior ASD repair. RCA dominance. No significant CAD. Occluded SVC at right atrial junction. Severely dilated coronary sinus and IVC, hepatic viens and azygous vein. Persistent left SVC noted. Significant contrast in hepatic veins and IVC consistent with significant tricuspid regurgitation. (Cath correlation). Non obstructive distal LM. LAD stent noted and patent but lumen of stent cannot be reliably visualized. Ramus is fine. Cx and OM system are fine. Diagonal stent is large and cannot exclude mild focal in stent stenosis. Diagonal vessels are otherwise ok. RCA is dominant with mild nonobstructive calcific disease. Apical infarct with apical and septal hypokinesis. Calcium score of 68 in the RCA, LAD and Circumflex. Mild mixed RCA disease. Non obstructive calcific LAD disease. RV and RA enlargement. RV volume overload with flattening of the interventricular septum in diastole only. Contrast seen in IVC suggesting significant tricuspid regurgitation. Normal EF. LM ok. LAD has diffuse non flow-limiting disease. Mild Ramus disease. Cx has mild disease. Ostial RCA not well visualized due to motion artifact in all phases. Atleast moderate concentric soft plaque suspected. Severe disease cannot be excluded. (Cath correlation). Page 73

10 TCH112 TCH113 TCH114 TCH115 TCH116 TCH117 TCH118 TCH119 SOB /equiv /equiv Normal LV function. Mild LM calcification. Proximal LAD heavy calcification which is nonobstructive. Heavy ostial D1 calcium which is nonobstructive. CX hs nonobstructive ostial disease and mild calcification throughout. RCA subtotally occluded proximallly with mixed disease. Distal vessel is visualized. (cath correlation) Severe attenuation artifact. Venous plexus/collaterals noted suggestive of subclavian vein stenosis Hx of HOCM noted. EF 50 to 55% (visual). LAD myocardial bridge noted. No significant CAD. Chordal SAM with hyperdynamic mid LV noted. Apical akinesis noted with LVH. (MRI correlation) Occluded LM. Proximal LAD has a high grade stenosis versus a total occlusion. The mid LAD is patent. Cx OM1 is large and without obstructive disease. Dominant RCA with no ostial disease. Proximal mid RCA has heavy, nonobstructive calcium. The Distal RCA is free of significant disease. LIMA to LAD patent. Distal anastomosis is patent. SVG to OM1 is patent and without disease. But the limb to OM2 is occluded. Anterior take off of the RCA traversing between the aorta and the pulmonary artery. Mild calcium of LAD. Mild mixed plaque of proximal LAD. Cx is OK. (Cath correlation) Use dose report to calculate effective dose. Non obstructive calcified LM disease. Heavy mixed disease proximal LAD. Patent LIMA to LAD. Heavily calcified mixed disease of proximal Cx. SVG to OM was patent. Heavily calcified RCA with heavy significant disease. SVG to distal RCAwas patent. Calcium score of 0. Normal coronaries. Excess IVC contrast suggestive of significant TR. Calcium score of 0 with nonobstructive CAD. TCH120 TCH121 TCH122 TCH123 TCH124 Dominant RCA. Moderate, nonobstructive, concentric soft plaque proximal to RCA stent. RCA mid vessel stent was patent. Non obstructive calcified LM plaque. Moderate, non-flow limiting soft plaque in LAD. Mid LAD stent was patent but the inside of the stent was not visualized. Diffuse nonobstructive D1 disease. No significant Cx and OM disease. Example of 2 filter types to evaluate stents. LM arises from the proximal RCA or from a common trunk from the right coronary sinus. The LM courses anterior to the PA and give rise to the LAD and Cx. No significant CAD. Hepatic cyst noted. (cath correlation). Mixed plaquing of the LAD with greater than 75% ostial LAD soft plaque stenosis. Mild diffuse left main plaque. Late timing of the scan is noted thus the distal LAD is difficult to visualize. D1 has an proximal significant stenosis (mixed) versus occlusion. Nonobstructive calcified plaque of the dominant main Cx. Nondominant RCA with obstructive soft plaque in the ostium. Nonobstructive calcified plaque of the distal RCA. Mild aortic valve calcification is noted. No perfusion abnormalities. (Cath correlation) Coronary anomaly noted. The RCA has an anterior take off from the right coronary cusp traversing between the great vessels (intramural course), likely malignant potential. Significant misregistration artifact. Patient demonstrated SVT during scan. No significant CAD. Page 74

11 TCH125 TCH126 TCH127 TCH128 TCH129 TCH130 TCH131 TCH132 TCH133 TCH134 TCH135 Mech valve fxn Eval LAA in Afib The RCA contains an ostial stent. The proximal portion of the stent protrudes into the aorta. There appears to be a mild degree of in-stent restenosis, but the stent is patent. There is calcification of the proximal RCA. There is mild to moderate soft plaque in the mid RCA. The remainder of the RCA is patent. LAD contains calcification and soft plaque proximally. The left circumflex contains proximal soft plaque but is patent. No significant obstructive disease. 2 filters available to evaluate stents. The circumflex arises from the RCA and courses posterior to the aorta. Mild calcifications of the RCA. Mild calcified plaques of the LAD. Obstructive soft plaque noted in mid LAD. 50 to 75% diagonal stenosis noted. Anomalous Cx is free of significant disease. Bronchiectasis noted. (Cath correlation). Use dose report to calculate effective dose. Normal EF. Non obstructive calcified LAD plaque noted. 2 myocardial bridges in proximal and distal LAD. RCA and CX are without significant disease. Normal EF. Paradoxical septal motion noted. Normally functioning mechanical St Jude MVR. Mild calcified RCA plaque. Cx has nonobstructive calcified plaques. LAD has no obstructive disease. Late timing so poor opacification of LV and coronaries. LM is normal. Stent in prox LAD is patent. D1 and D2 are patent. LIMA to LAD occluded. Cx has occluded proximal stent. Graft to OM is patent. RCA is poorly opacified and underfilled, cannot exclude obstructive disease. Sternal malunion noted. (cath correlation) Left main has mild nonobstructive plaque. The LAD has a long tight mixed lesion proximally. Nonobstructive disease in the Cx. LIMA sequentially to LAD and to D1 is patent. The distal anastomosis is poorly visualized. (Pre CABG cath available). RV dilation noted. LV is ok. LAE. RAE. RV and RA pacer noted. Dilated IVC and coronary sinus with reflux of contrast suggesting sig. TR. LAA had no clot. Nonobstructive coronary disease. CATH CORRELATION Mild RV enlargement. RA enlargement (5.2 X 4.5). Nonobstructive calcified plaque in LAD, Cx and RCA. Mild soft plaque in proximal RCA. Mild soft plaque in proximal LAD. Normal perfusion. Heavy misregistration due to sudden tachycardia during scan. No significant coronary artery disease. LIMA to LAD patent with good distal LAD flow and well visualized clean anastomoses. Patent SVG to Diag with well visualized and clean anastomoses. Distal diag after the graft is fine. Patent SVG to OM with well visualized and clean anastomoses. Distal OM after the graft is fine. Patent SVG to RCA but the RCA is poorly filled and while the distal anastomosis is patent it is poorly visualized. Native RCA occlusion. Left main has heavy calcification encompassing the entire lumen. This calcification involves the bifurcation of the LAD and Cx. The native LAD has severe disease with mixed plaque and is occluded in the mid vessel. OM1 is grafted with nonobstructive calcifications noted. Nonobstructive calcification of the main Cx. The D1 is grafted and severely diseased. Perfusion is normal. Descending aorta calcifications noted. Mild calcification of the ascending aorta. Normal EF. LAD arises from the proximal RCA and courses between the aorta and the pulmonary artery. The circumflex arises from the proximal RCA as well separate from the LAD and courses posteriorly behind the aorta. The RCA, LAD and Cx have no significant atherosclerosis. (Cath correlation) Page 75

12 TCH136 Normal LV. No significant CAD. Large hiatal hernia. TCH137 TCH138 TCH139 TCH140 TCH141 TCH142 TCH143 TCH144 TCH145 TCH146 /CABG Aortic Aneurysm Large aortic root pseudo aneurysm originating from lateral aspect of ascending thoracic aorta, measuring 3 cm in diameter. Heavy mitral annular calcification, bioprosthesis in aortic position. Circumflex is diffusely diseased but no significant obstruction. Proximal LAD diffuse disease. LIMA-LAD patent. RCA diffusely diseased and occluded in mid portion. Radial T-graft to distal RCA is patent. Normal left ventricular size and function. Mechanical aortic prosthesis (On-X). Normal function of mechanical prosthesis. Normal coronary vessel. A dominant circumflex. Ascending aortic graft. (Not a composite graft). Normal LV. Ascending aortic aneursym measuring 5.3 by 5.6 cm. Normal coronaries. Bisuspid AV with calcifications. No significant AS noted. Ascending aortic aneurysm measuring 5.2 cm. Scattered mild calcifications of LAD. Less than 50% soft plaque lesion in LAD at bifurcation with diagonal. Cx has mild calcifications. RCA has scattered nonobstructive calcifications. Diffuse bronchitis. Mild peripheral pulmonary fibrosis. Cirrhosis of liver. Coronary artery calcium score 25. Left main coronary artery normal. Left anterior descending artery demonstrated mild calcification proximally with no obstructive lesions. Left circumflex normal. Right coronary artery normal. The chest wall was noted to have a reduced anteroposterior diameter with close proximity of the right ventricle to the sternum. This would be consistent with cardiac compression syndrome with mild compression of left atrium. LM has heavy nonobstructive calcium. LIMA sequentially to the D2 and LAD. The LIMA origin is not visualized. SVG sequentially to the OM1 and PDA is patent. Aortic anastomosis was obscured by a clip. The LAD has proximal heavy calcifications with distal LAD occlusion. There is a patent proximal LAD stent. Ostial plaque of a D2. Diffuse distal LAD disease with probable distal occlusion. Cx is diffusely diseased with a significant lesion in the OM. RCA is diffusely diseased without significant obstructive disease. (Cath correlation) No significant coronary artery disease by CTA. Patient later had cath and Ostial RCA was in appropriately stented due to spasm. (Cath correlation). L transposition with dextrocardia. Systemic ventricle (morphologically right ventricle) severely depressed with ejection fraction of 25% and global hypokinesis. Pulmonic ventricle (morphologically left ventricle) pacemaker wire not at normal function. Markedly dilated main pulmonary artery measuring 6 cm. Mildly dilated aortic root. Normal coronary vessels. Mild ascending aortic calcification. Calcium score of 113 all in distal LM and ostial LAD. LM was nonobstructive. Nonobstructive ostial LAD disease with mild associated soft plaque but no obstructive disease. Ramus was tortuous but no sig. disease. Otherwise no significant disease. RCA dominant. Normal EF. LVH. Patent LIMA to LAD. Distal anastemosis not well visualized due to clips. High grade lesion in proximal LAD. Occluded SVG to RCA. Distal RCA not visualized. High grade D1 and Cx disease. Patent SVG to D1 and patent SVG to OM. Banding artifact noted. Page 76

13 TCH147 TCH148 TCH149 TCH150 TCH151 TCH152 TCH153 TCH154 CHF Dyspnea History: 77 yo with emergent LM stent 3 years prior to CTA. Suffered 3 episodes of pulmonary edema and most recent prevented extubation. Continued pulmonary edema episodes with every extubation attempt. Two prior caths misssed LM restenosis. Third Cath available for review. RCA not found on this third cath. Patient underwent emergent cardiac CTA due to worsening symptoms. For cardiac CTA she was intubated, paralyzed and apnea was induced for 10 sec for the scan. Still misregistration artifact noted. Anomalous RCA was identified with good distal target. Emergent CABG performed and patient had an uneventful recovery. Cardiac CTA findings: Motion artifact noted. The ostial vessels are difficult to assess. Anomalous RCA originating from left coronary cusp. Heavy calcification of RCA. Patent PDA. Left coronary cusp calcium noted and LM. Degree of LM stenosis cannot be assessed due to artifact. Proximal LAD stent which is patent. Ostial and proximal Cx calcium with a severe ostial Cx stenosis. Mid LAD calcification. Pulmonary nodule in right middle lobe. Bilateral atelectasis. Normal LV function. Mildly dilated RV. Normally functioning bileaflet mechanical AVR. Mitral annuloplasy ring noted. Tricuspid annuloplasty ring noted. Mild nonobstructive LAD calcified disease. Minimal calcified Cx disease. RCA is dominant and normal. RCA proximal portion of stent is patent. Mid RCA stent appears patent but unable to visualize inside. LCX proximal has 2 tandem stents that appear to be patent but again can not visualize inside stent, there is calcific plaque beyond the stent. LAD is heavily calcified but patent. Mid LAD myocardial bridge. D1 unobstrucive calcific plaque. D2 normal. 2 filters available for stent review. RCA is small and normal. LAD and Cx have common trunk. Mild LAD calcification. Dominant Cx without significant disease. EF 52%. Ascending thoracic aorta is dilated (4.6 cm). Left subclavian port present. Left lower lobe calcified granuloma. Moderate paraesophageal hiatal hernia. Severe dehiscence of aortic bioprosthesis. TEE, and cath correlation noted. Heavy calcium throughout. Tight circumflex (mixed). Severe calcium of proximal LAD occluding lumen (48% chance for tight stenosis). Tight soft plaque mid LAD. Non obstructive calcified plaque of RCA. Cath correlation present. Mixed disease of LAD. 50 to 75% proximal LAD soft plaque and greater than 75% soft plaque stenosis of LAD after the first septal. Prominent ramus branch with < 50% soft plaque. Cx has a large calcification (probably nonobstructive). Heavy calcium in all vessels with previous stents noted. Pacer wired are seen. Pacer streak artifact obscures parts of the coronaries. Old calcified granulomas noted. RCA has diffuse mixed disease. The stenosis grade is 50 to 75%. Mild to moderate mixed plaque of proximal and ostial LAD. Large ramus intermedius noted with nonobstructive calcified plaque. 2 LAD stents one proximally and one after D1. Lumen of the stents are poorly seen. Mid vessel LAD between the stents has a 50 to 75% soft plaque lesion. Pacer noted. Practice effective dose calculation using dose report. Mild soft plaque of RCA. Ramus and Cx OK. Moderate to severe OM1 disease. Normal LM. LAD stent is patent but a tight stenosis distal to the stent cannot be excluded. Inside the stent cannot be well visualized. Page 77

14 TCH155 TCH156 /AVR/ MVR /CABG S/P multiple valve replacements for endocarditis with reconstruction of the aortic root and reimplantation of the mechanical aortic valve superior in the root and ligation of the native coronaries (LM and RCA) with bypass of RCA and LM. Findings: Ligated RCA and LM. SVG to LAD is patent with good distal anastemosis with back filling the proximal LAD and Circumflex retrograde through the LAD. The distal LAD looks good. Patent SVG to RCA with back filling of RV marginals and antegrade flow to distal RCA, which looks good. 4.3 X 4.2 mm aneurysm of the native circumflex. Markedly enlarged left ventricle measuring 6.3 cm. Well functioning bileaflet mechanical AVR and MVR. Moderate left atrial enlargement (4.6 X 4.5 cm). Global hypokinesis of the LV with akinesis of the apex and akinesis to dyskinesis of the septum. EF estimated by the computer to be 42%. Visually it appears in the 35% range. RCA is occluded. SVG-RCA is occluded. SVG-OM patent. High grade stenosis proximal to stent in LAD. Proximal LAD stent appears patent. LIMA-LAD limb occluded. RIMA-Tgraft-D1 small vessel. TCH157 TCH159 TCH160 TCH161 TCH162 Attenuation artifact noted. Misregistration artifact noted as well. Thus a technically difficult study. Normal dominant RCA. No significant LAD disease. Cx has no significant disease. RCA poorly visualized in mid section but no significant disease noted. Minimal LAD calcium. Normal EF. Paradoxical septal motion. LCX is dominant. Artifact in left chest wall. Non obstructive calcified LM disease. Heavily calcified proximal LAD with significant disease. In places the LAD lumen is completely obscured by calcium and significant lesion cannot be excluded. LIMA to mid LAD patent. Small LAD distal to graft. Cx is nondominant. Heavily calcified nonobstructive Cx disease. RCA is occluded in midsection. SVG to mid RCA patent with no significant disease distal to graft. RCA and Cx are without sig. disease. Nonobstructive calcium of LAD noted. Possible moderate lesion of mid LAD. LIMA to LAD patent but small. Distal anastemosis not well seen due to clips. Apical infarct noted with apical dyskinesis. Calcified pulmonary lymph nodes noted. Late timimg. LAD: patent with anastemoses well seen and OK. Distal LAD fills but is poorly visualized due to late scan timing. 1 graft stump is seen (occluded), probably an RCA graft.. Anterior take off of the RCA and proximal occlusion is noted. Main Cx poorly visualized. OM is occluded. Apical infarct noted. Persistent left SVC noted with drainage into rigth SVC which connects to the hemiazygous vein and then to the azygous vein and then again to the IVC from below. Page 78

15 TCH163 Calcium score only. Score is 2251 with diffuse calcium of all vessels. TCH164 Calcium score of 1426 diffusely. Ascending aortic calcium noted. Mild RA enlargement. Heavy left main calcium with visualized lumen (probably nonobstructive). Heavy calcification of the LAD at the bifurcation of a major diagonal. The lesion in part covers the entire lumen and a significant, obstructive lesion cannot be excluded. Non obstructive calcium is present throughout the LAD and diagonal system. Cx has multiple diffuse areas of nonobstructive calcified plaques with some areas covering the entire lumen with no visualized lumen (obstructive plaques cannot be excluded in these areas). RCA has nonobstructive calcified plaquing diffusely with a proximal calcified area that obscures the entrire lumen and an obstructive plaque cannot be ruled out. (cath correlation) Page 79