Cardiac Imaging Answers (PDF)

CARDIAC IMAGING ANSWERS FROM THE ARTICLES The coronary artery that gives rise to the PDA and posterolateral branch is referred to as the “dominant” artery. RCA being dominant in approximately 70% of cases The LCA is dominant in approximately 10% of cases, supplying the entire LV, accompanied by the...

CARDIAC IMAGING ANSWERS FROM THE ARTICLES The coronary artery that gives rise to the PDA and posterolateral branch is referred to as the “dominant” artery. RCA being dominant in approximately 70% of cases The LCA is dominant in approximately 10% of cases, supplying the entire LV, accompanied by the PDA and posterolateral branches from the LCx artery. Dominate coronary artery In the remaining cases, the RCA and LCA are codominant; that is, portions of the LV diaphragmatic wall are supplied by both the RCA and the LCx artery. The length of the distal RCA is inversely proportional to the length of the LCA along the inferior aspect of the heart. The RCA is typically diminutive compared with the LCx artery in patients with left-dominant systems. RA and RV anatomy Feature of the RV: the moderator band, a muscular band extending from the interventricular septum to the base of the anterior papillary muscle, trabeculated apex are distinct features of the RV, well-developed infundibulum, septal papillary muscles, and lack of fibrous continuity of the AV valve and outflow tract are key to differentiating the RV from the LV. Congenital heart disease to distinguish the LV from the RV may be of paramount importance. Coarc ation of aorta Congenital maldevelopment aorta. Hypoplasia of the distal aortic arch and focal narrowing of the proximal descending aorta almost invariably at the junction of the ductus arteriosus and aorta. Presents in childhood or adulthood Associated with: 1 in 25-50% often associated with bicuspid aortic valve PDA VSD Turner Transposition of the great vessels (rare) Shone syndrome (rare) Retain HTN risk even after surgery Fatal complications occur such as bacterial aortitis On CXR: Rib notching (lateral and middle part of posterior ribs) Medial notching can be normal Bulging aortic notch Prominent left subclavian artery Indentation of paraaortic stripe Collateral circulation to the post-coarctation segment usually originates from branches of the proximal subclavian arteries (the internal mammary arteries and thyrocervical trunk). Blood flow is around the shoulder or anterior chest wall and retrograde through the intercostal arteries to the post-coarctation segment of the proximal descending aorta. Occasionally, CoA may be associated with an aberrant subclavian artery. In such circumstances, the aberrant artery originating downstream from the coarctation (thus, at low pressure with respect to the ascending aorta), is unable to provide collateral flow to the post-coarctation aorta. Cardiac CT examination of patients with CoA is directed toward demonstration of the location, caliber, and length of the coarctation segment, the status of the aortic isthmus and the degree of arterial collateralization present. Furthermore, the relationship of the coarctation to the origins of the left and right subclavian arteries (especially in cases with an aberrant subclavian artery) must be demonstrated. Thes changes are usually best appreciated in oblique sagittal or parallel to the axis of the ascending and descending aorta. However, the small caliber of the aorta or aortic tortuosity may necessitate reconstruction in additional oblique sections. 2 3 Arrhythmogenic Right Ventricular Dysplasia.— (ARVD) Structural and functional anomaly of right ventricle wall -> ventricle arrhythmias and progressive right ventricular failure. Associated with sudden death. Diagnosis based on major and minor criteria: family history, genetic factors, conduction and repolarization anomaly, biopsy, abnormal right ventricle. + (67%), delayed myocardial enhancement of the right ventricle. An increasing number of enhancing segments of the right ventricle correlates with a decreased right ventricular ejection fraction and increasing end-diastolic volume. 4 Cardiac MRI FOR Acute MI 5 Prognostic factor for risk stratification: -LV ejection fraction, - MVO, - Infarct size. MVO and intramyocardial hemorrhage - severe myocardial damage. late MVO is the best prognostic marker of LV remodeling, associated with increased medium-term hospitalization, major adverse cardiac events and cardiovascular death independent from infarct size. Perfusion and EGE are more sensitive than LGE for detection of MVO. RCA Arisa from RC sinus, cross in the right AV groove. 50-60% thr first branch is conus artery. Conus artery supplies the RV outflow and form circle of Vieussens. MRI differention of constriction from restrictive cardiomyopathy. Constriction with normal-thickness pericardium (Rajiah, 2011) 6 Pericardial thickening (> 4 mm) is an indicator of constriction, more in the right side. Elevated cardiac filling pressure - biatrial enlargement. Narrow atrioventricular groove; Dilated SVC, IVC, and hepatic veins; Pleural effusion and ascites. In the SVC, systolic flow is decreased, absent, or reversed, but in diastole, forward flow is increased with increased late backflow Respiratory variation in septal movement is a pathognomonic feature of pericardial constriction. In 18% normal thickness, but noncompliant pericardium. Effusive constrictive pericarditis, rare syndrome cause tamponade. Cause – malignancy, post radiation. Pericardial constriction is caused by thickened, fibrotic or calcified, nonelastic pericardium -> impaired left ventricle diastolic filling -> elevated systemic venous pressures and low cardiac output. Usually affect parietal pericardium. Retrospective ECG-gating For young patients. 1. Coverage of the entire cardiac cycle. 2. Flexibility with ECG-editing. 3. Dose modulation is used to decrease the radiation exposure with peak tube current (toc) applied during at least systole. 4. Tube current outside of the peak acquisition window to a level for aortic annulus and valve evaluation. Coronary CT angiography 1. first-line investigation in known or suspected CAAs. 2. evaluation of anomalous coronary arteries. Pericardial diverticulum 1. Origin similar to that of a pericardial cyst 2. Pericardial diverticulum communicates with the pericardial cavity; due to the wall is incomplete on the medial aspect. 3. Other common lesions that mimic a pericardial cyst include enlarged lymph nodes, loculated fluid collection, hematoma, and necrotic tumor. 4. Less common: bronchogenic cyst, cystic teratoma, cystic neurogenic tumor, cystic lymphangioma. Pericardial Cyst Developmental abnormality -blindly ending parietal pericardial recess. 1. asymptomatic 2. may produce chest pain or dyspnea if compressed the heart. 3. most common location - right cardiophrenic angle. 4. MRI: well-defined, homogeneus, low on T1, high on T2 with no contrast. 5. may be high on T1 because on protein content. Role of MRI in acute setting The Lake Louise Criteria are based on the detection of two 7 - evaluation of chest pain of uncertain diagnosis. - risk stratification in patients with coronary artery disease. - identification of patients at high risk of future cardiac events (ie, reinfarction or heart failure. Myocardial edema on T2. T1 hyperemia with contrast. Fibrosis (late enhancment on LGE) of three characteristic feature of Myocarditis. Nonischemia pattern –midwall or subepicardial. Do not follow a coronary distribution. DDX myocarditis from MI MI – LGE subendocardial or transmural in a coronary distribution. Myocarditis - not correspond to any particular coronary artery distribution and midwall distribution. Myocarditis predominantly in the lateral free wall and originate from the epicardial quartile of the ventricular wall. MVO ddx with thrombus Thrombus is intracavitary. MVO – intramyocardial. Subendocardial enhancement. Transmural extent that follows coronary artery distribution. STEMI in 25-35% Thrombus cause total vessel occlusion - > reperfusion therapy. Partial or intermittent occlusion ->collateral circulation (unstable angina or NSTEMI). T2 for ddx of acute from chronic MI and sensitive for acute myocardial damage. Ischemic LGE pattern Acute myocardial infarction Coronary artery anomalies Congenital and relatively uncommon. Origin LCX from LAD – benign coronary variant. 8 CTA for TAVI Anatomy 3 chamber view Sarcoidosis 9 CT is gold standard tool for annular sizing. determination of risk of annular injury coronary occlusion coplanar fluoroscopic angle prediction in advance of the procedure. Follow-up of TAVI/TAVR for assessment of postprocedural complications including identification of leaflet thickening. Oblique long-axis view: LV, LA, aortic root, MV, and aortic valve. The posteromedial papillary muscles from the LV free (lateral) wall on this view. These muscles are connected to the MV by chordae tendineae, which are linear fibrous bands. During systole, the LV myocardium contracts. The papillary muscles likewise contract, tugging on the MV leaflets to ensure complete closure of the MV and prevent regurgitation. Focal internsity on T2 and early GE because of edema and inflammation. Usually septum, LV wall/ LGE – may also be.nFocal myocardial thickening may mimic hypertophic cardiomyopathy. Acute MI Early perfusion: lack of SUBENDOCARDIAL enhancement LAD territory due to MVO. LGE – transmural enhancement, persistent MVO. Cardiac CT (Rajiah, 2011) Retrospective study is associated with a higher radiation dose ther ECG gated study. ECG gated study with a dose lower than a typical dose chest CT (nor good for arrhyphmia or unstabel patints). The Agatston score (Gupta et al., 2022) Amount of calcified lesions, accounting for the total area and maximal attenuation of calcification. “-“ Affected by small variations in image noise Strict adherence to protocol Limited interscan reproducibility Aortic dissection: disruption of the intima, tracking of the blood in the meida. Intramural hematoma: intramural haemorrhage from vasa vasorum or bleeding at the base of penetrating ulcer. Penetratinf atherosclerotic ulcer (PAU): ukcerating atherosclerotic lesion that penetrates into media. Left-to-right shunt (e.g. ASDs, VSDs, PDA). -> PULMONARY HYPERTENSION. Compromised systemic perfusion (e.g. critical aortic stenosis). Pulmonary venous congestion (e,g, obstructed TAPVD). Low pulmonary blood flow (e,g, tetralogy of Fallot). Parallel circulation (e,g, transposition of the great arteries). Intracardiac mixing (e,g, truncus arteriosus). Congenital anomaly of the tricuspid valve and right ventricle. 1. Adherent leaflets of the tricuspid valve to myocardium. 2. Anterior and apical displacment of functional annulus. 3. Dilatation, aterialisation of RV with hyperthropy and thickening of the wall. Acuter aortic syndrome Major Modes of Clinical Presentation of Congenital Heart Disease Granger, 7th (2015) Ebstein Anomaly of the Tricuspid Valve Granger, 7th 10 4. Dilation of the right AV junction (the true tricuspid annulus); 5. Variable ventricular myocardial dysfunction. Sarcoma (Sparrow et al., 2005) Most common primary tumor of the heart. 40% angiosarcoma. Rare in children May mts to lungs. May be intramural, intracavitary with hemorrhage component, and necrosis. Predominant in the RIGHT ATRIUM. Cardiac thrombus 11 Intracavitary up to 7% with acute MI. 96% in anterior STEMI. Risk factors: anterior STEMI, LV dysfunction (LV ejection fraction fibroma. Metastatic is 40 times is more common. Direct spread – bronchus and breast. Transvenous – RCC, Hepatoma. Hematologic – melanoma, lymphoma, leukemia. Primary – rare, angiosarcoma in adults. Rhabdomiosarcoma in children. 14 1. 2. Fibroma Transthoracic echo. MRI is gold standart. Second most common in children. 15% in adolescent. May mimic hypertrophy. Ass with Gorlin syndrome. CT – well defined, homogeneus, left ventricle myocard. Mild enhancement. MTI – iso to myocardium on T1, T2 hypo die to fibrosis. Avascular – no enhancement on perfusion. Mild LGE. Myxoma (Sparrow et al., 2005) Benign Carney complex: hyperpigmented skin lesions. Pituitary adenoma, Breast adenoma, schwannoma. Triad: cardiac obstruction syndrome, embolic events, constitutional symptoms. T1 hypo, T2 hyper (water content). 90% - Left atrium. 10-20% right atrium. May be hypo on T1 and T2 due to hemorrhage. 15 Lipoma the second most common. May be incidental, manifestation due to obstruction of blood flow or compression of the ventricles. Epicardial or endocardial location. Most SUBEPICARDIAL. T1 high, less high in T2. May have septations, no enhancement. Papillary Fibrielastoma 90% on cardiac valves. Asymptomatic, symptoms related to the emboly. Left