Cardiomyopathy Imaging

Hassan Khalil; Talal Alzahrani

Cardiomyopathy Imaging

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Introduction

Cardiomyopathies are a heterogenic group of diseases of the myocardium, which further classify into primary “confined to the heart, “or secondary “related to systemic disease.” The primary cardiomyopathies are divided into genetic “including hypertrophic, arrhythmogenic right ventricular, left ventricular noncompaction, Danon glycogen storage disease and others”; and acquired “including acute myocarditis, stress-induced (Takotsubo), peripartum, and tachycardia-induced cardiomyopathies." The secondary cardiomyopathies occur due to systemic diseases. These include infiltrative diseases such as amyloidosis, Gaucher disease, Hunter disease, and Hurler disease. Storage diseases, medication toxicity, inflammatory disease, and endocrinology diseases can also lead to secondary cardiomyopathy.[1]

Diagnosis of the etiology of cardiomyopathy starts with a thorough history and physical exam, including obtaining detailed social and family history, a careful review of medication and substance use, and followed by diagnostic tools including electrocardiogram, laboratory testing, imaging studies, and may require a myocardial biopsy to reach the definitive diagnosis. Echocardiogram, cardiac MRI, cardiac CT, and nuclear medicine imaging are the primary imaging modalities used for both work up and follow up on patients with cardiomyopathies.

Plain Films

Chest radiograph:

A chest radiograph is usually the initial imaging study to order, especially in an acute setting, to differentiate between cardiac and pulmonary etiologies of severe respiratory symptoms. The chest radiograph can also be used to distinguish different types of cardiomyopathy although it is not a sensitive test in the workup. In dilated cardiomyopathy, the chest radiograph will show increased left and right ventricular size. The chest radiograph can show evidence of cardiomegaly and increased cephalization, pleural effusion, and Kerley B-lines in the setting of acute congestive heart failure. Cardiomegaly on chest radiograph usually reflects the decreased ejection fraction, and the increased cephalization reflects increased preload. These can be helpful to establish a diagnosis of acute heart failure but are not adequate to confirm the diagnosis.[2]

In peripartum cardiomyopathy, findings are consistent with other dilated cardiomyopathies including enlargement of the heart silhouette and increased pulmonary venous congestion with or without interstitial edema. In contrast, the chest radiograph in Chagas heart disease usually shows an enlarged cardiac silhouette, which is typically due to pericardial effusion.[3] In restrictive cardiomyopathy, the chest radiograph shows increased atrium size resulting in cardiomegaly and associated with venous congestion. The presence of pericardial calcification can be used to differentiate chronic constrictive pericarditis “present” from restrictive cardiomyopathy.

Echocardiography

Echocardiogram remains the main imaging study in the workup for cardiomyopathy and to differentiate between the different types of cardiomyopathy. The ease of use and cost efficiency of echocardiogram comparing to other imaging studies has always made it the first choice in the evaluation of new-onset cardiomyopathy and follow up on the progress of the disease. The echocardiogram helps to evaluate the systolic and diastolic dysfunction, wall motion abnormalities, and valvular abnormalities. The sensitivity of the 2D echocardiogram is 81%, and the specificity is 100% in diagnoses of left ventricular dysfunction.[4]

In dilated cardiomyopathy (DCM), the echocardiogram is an essential imaging test to make the diagnosis. The echocardiogram shows dilation with or without dysfunction of the left ventricle.[5] On 2D echocardiogram, the dilation of the left ventricle can be associated with reduced wall thickening and reduced inward systolic motion. Other common findings in DCM are reduced ejection fraction, left ventricular fractional shortening, four chambers dilation, left ventricular end diastolic volume index often exceeds 100ml/m^2 and the end systolic volume index of the left atrium usually increases to more than 50ml/m2. The enlargement of the left atrium in DCM can reflect the chronicity of the disease and can be a predictor of outcome.[6]

Abnormal global longitudinal strain (GLS) is a predictor of mortality in patients with systolic heart failure with decreased ejection fraction and is superior to other echocardiogram parameters as a prognostic measure.[7] The presence of abnormal GLS in patients who have recovered left ventricular ejection fraction is an indicator of increased risk of recurrence of decreased LVEF in the future follow up compared to patients with normal GLS.[8] Mitral regurgitation (MR) can be seen on the echocardiogram and can be primary or secondary. Primary MR can lead to increase preload on the left ventricle, and secondary MR can be a result of apical tenting of the mitral valve leaflets, annular dilatation of the valve, and ventricular dys-synchrony, which carries a poor prognosis.[5] The dilation of the right ventricle can be related to pulmonary hypertension or other pathologic involvement of the right ventricle. In idiopathic DCM, the presence of right ventricular dilation can indicate poor prognosis and higher mortality.[9] Reduced right ventricular ejection fraction is a predictor of poor survival in patients with moderate congestive heart failure.[10]

In peripartum cardiomyopathy, there is a global decrease in the left ventricular systolic function with or without evidence of dilated ventricles. A left ventricular thrombus may occur when LVEF is less than 35%.[11] Left atrium enlargement or thrombus can present in severe cases, and right ventricular dilation and hypokinesia may occur. In rare cases, there can be pericardial effusion. In ischemic cardiomyopathy, the findings in echocardiogram usually relate to left ventricular wall motion abnormality as a result of old or new infarcts. The dobutamine stress echocardiogram can distinguish between ischemic cardiomyopathy and other etiologies.[12] High left ventricular end-systolic volume index (ESVI) of 45ml/m^2 is a predictor of poor outcomes in patients with ischemic cardiomyopathy.[13] In Chagas cardiomyopathy, the left and right ventricular systolic function can be between normal and severely impaired. In moderate to severe Chagas cardiomyopathy, an echocardiogram can show left ventricular, right ventricular, or bilateral apical aneurysm.[14] Decreased LVEF in Chagas Disease on 2D echocardiogram is an important predictor of mortality.[15] Pericardial effusion and sometimes tamponade may be a feature on echocardiogram in acute Chagas disease.[16] Left ventricular and left atrial thrombus are common findings on echocardiogram in Chagas cardiomyopathy.[16]

All patients with suspected hypertrophic cardiomyopathy (HCM) should be evaluated with an echocardiogram, to check the LV wall thickness, systolic and diastolic function, left ventricular outflow tract (LVOT) obstruction, and presence of mitral regurgitation. Clinical diagnosis of HCM is possible with the finding of LV hypertrophy on echocardiogram.[17] In HCM, the Systolic anterior motion SAM of the mitral valve can result in obstruction in the left ventricular outflow tract. A left ventricular outflow tract gradient over 30mmHg is as common as 20 to 25% of patients. The left ventricular outflow tract obstruction is a predictor of the development of severe symptoms of heart failure and a predictor of death.[18] Other findings associated with LVOT obstruction can be asymmetric septal hypertrophy, partial early systolic closure of the aortic valve, calcification of the mitral annulus and mitral regurgitation. Symptomatic patients with HCM without evidence of LVOT obstruction at rest should undergo a stress echocardiogram to evaluate the possibility of an obstruction on exertion; this will help to start early treatment.[19] The presence of increased left atrial size is a predictor of a poor outcome in HCM and is associated with the development of atrial fibrillation.[20] Increased left atrial volume index (LAVI) and GLS are both associated with worse outcomes in HCM, and they can both be used to optimize the risk stratification in HCM patients. [21] Progression of both LAVI and GLS measures with repeated echocardiograms in non-obstructive HCM is related to the development of heart failure.[22]

Diagnosis of restrictive cardiomyopathy by echocardiogram is more difficult than the diagnosis of hypertrophic and dilated cardiomyopathies. The left ventricle usually is usually normal in size or small and associated with a normal left ventricular systolic function. These patients usually have an abnormal diastolic function with biatrial enlargement.[23],[24] Although the wall thickness is usually normal, it can increase in infiltrative diseases, such as sarcoidosis, amyloidosis, and hypereosinophilic syndrome.[25] In cardiac amyloidosis, the left ventricular wall thickness is increased, and associated with diastolic dysfunction as early findings on echocardiogram, right ventricular diastolic dysfunction can also occur. The left ventricular wall thickness in cardiac amyloidosis is symmetric, and outlet obstruction is rare.[26] One-third of the patients with cardiac amyloidosis can have diastolic dysfunction with normal left ventricular wall thickness.[27] The presence of normal ventricular wall thickness on echocardiogram cannot exclude the cardiac involvement in systemic amyloidosis.[28],[29] The presence of right ventricular dilation in cardiac amyloidosis is associated with a poor prognosis with a very low survival rate.[30]

Echocardiogram has low sensitivity when used for workup of cardiac sarcoidosis. In systemic sarcoidosis, an echocardiogram can show abnormal findings in up to 46% of patients even if they are asymptomatic for cardiac disease; findings can include: diastolic dysfunction, abnormal wall motion, and wall thickness (increased in acute cardiac sarcoidosis and decreased in chronic).[31] The presence or absence of systolic dysfunction and left ventricular dilation are mortality predictors.[31] Decreased LVEF and dilation of the left ventricle can present in up to 30% of patients.[32] In 10% of patients, an echocardiogram will show ventricular aneurysms, mainly in the septum and anterior wall.[32] Abnormal GLS can be a feature in sarcoidosis patients who have otherwise normal echocardiogram findings; the impaired GLS correlates with worse outcomes.[31] In hypereosinophilic cardiomyopathy, the echocardiogram can be normal in the acute stage, but as the disease progresses, the echocardiogram can show severe restrictive ventricular disease and intraventricular thrombus. In diabetes mellitus, an echocardiogram can show evidence of diastolic dysfunction and left ventricular hypertrophy with normal LVEF.[33]

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a cardiomyopathy that is caused by the fibrous-fatty replacement of myocardium of the right ventricle. Echocardiogram has limited sensitivity in the diagnosis of ARVC, it can show regional RV akinesia, dyskinesia, or aneurysm, [24] it can help in detection of the RV fractional area change (FAC) and tricuspid annulus plane systolic excursion (TAPSE), these two measures are strong predictors of a major advanced cardiac event.[34] An echocardiogram can be a diagnostic modality for other unclassified cardiomyopathies. In Takotsubo stress cardiomyopathy, an echocardiogram can show hypokinesia or dyskinesia with reduced left ventricular systolic function; these patients have no evidence of coronary artery obstructive disease.[35] Right ventricular dysfunction may occur in one-third of the cases and is associated with more severe disease and worse left ventricular wall motion abnormality.[36] In isolated left ventricular noncompaction (LVNC), an echocardiogram can show evidence of cardiomyopathy, the main type seen is dilated cardiomyopathy,[37] but restrictive or hypertrophic features may be visible. The echocardiogram shows numerous prominent trabeculations of the endocardium of the left ventricle.[5] Color Doppler echocardiogram may show direct blood flow into the intertrabecular recesses from the ventricle; this finding does not present in any other type of cardiomyopathy.[38]

Computed Tomography

Multidetector computed tomography can be used in the workup of cardiomyopathy to differentiate between ischemic and nonischemic dilated cardiomyopathy etiology.[39] The coronary CTA is highly sensitive and specific in the diagnosis of CAD; it can also help in predicting the prognosis of ischemic cardiomyopathy[40]. In nonischemic dilated cardiac myopathy (DCM), the cardiac CT (CCT) can be used to measure the left ventricular internal diameter and left ventricular ejection fraction. Cardiac CT can predict poor prognosis depending on the LVEF,[24] but cardiac CT cannot differentiate between different types of nonischemic DCM.[40]

In HCM, the cardiac CT can help to identify the hypertrophy of the myocardium and the LVOT obstruction and can show an enlarged mitral valve, systolic anterior motion (SAM) of the mitral valve or mitral valve regurgitation. The CCT can demonstrate the asymmetry of the ventricular hypertrophy.[24] CCT can show atypical forms of HCM including apical hypertrophy, concentric hypertrophy or sometimes mid ventricular hypertrophy.[40] On delayed iodine enhancement (DIE), images fibrosis of the myocardium can be seen, mostly focal in the right ventricle but can be diffuse. The presence of this fibrosis can be related to life-threatening arrhythmia and cardiac death.[40]

In restrictive cardiomyopathy, the CCT can show the ventricular sizes similar to the echocardiogram findings. In cardiac sarcoidosis, the cardiac CT with contrast can demonstrate the enhancement of the sub-epicardium with global or regional hypokinesia.[24]. In the acute phase, focal wall thickening is visible due to focal areas of granulomas, but in chronic cardiac sarcoidosis wall thinning is seen.[40] Fibrosis can be seen on the DIE images and can be related to poor outcomes.[40] Multidetector CT can show cardiomegaly, pericardial effusion, and ventricular aneurysms.[32] In cardiac amyloidosis, CCT is not usually used due to the low sensitivity in the detection of myocardial infiltration,[24] but it can show ventricular wall thickening and biatrial enlargement.[40] On the DIE images, a pattern of diffuse transmural or sub-endocardial enhancement may present.[40]

In ARVC, cardiac CT can show dilation of the right ventricle with a bulging appearance in the right ventricular wall due to fatty deposition.[24][40] This fibro-fatty replacement in the right ventricular wall can cause thinning of the RV wall that detectable on the CCT. [41], these changes can cause RV dilation and systolic dysfunction. [40] The CCT can assess left ventricular involvement, the ventricular wall motion, and the ventricular function.[41] In Takotsubo stress cardiomyopathy (TTC), the cardiac CT can show the apical ballooning with a hyperdynamic contracting base of the left ventricle.[24][40] In 25% of patients with Takotsubo, right ventricular apex involvement is visible.[24] In LVNC, the CT can show the trabeculated to non-trabeculated myocardium in end diastole ratio to be greater than 2.3, which usually involves the anterior and inferolateral segments of the left ventricle.[24][40]

Magnetic Resonance

Cardiovascular magnetic resonance (CMR) is used in cardiomyopathy to assess ventricular volumes, ejection fraction, myocardial mass, and wall thickness. The high resolution of CMR helps in assessment of the ventricle systolic function and differentiate between ischemic and non-ischemic cardiomyopathy. Late gadolinium enhancement (LGE) can identify the fibrosis of the myocardium which helps to differentiate between types of cardiomyopathy. LGE CMR can be used to check for the arrhythmogenic substrate; this helps for future treatment options including ablation.[42]

In DCM, the dilated ventricles and decreased ejection fraction are the main findings.[43] In peripartum cardiomyopathy, CMR can be helpful to predict outcome in peripartum cardiomyopathy, an improvement in LGE can predict recovery of the systolic dysfunction.[44][45] In Chagas disease, myocardial delayed enhancement by CMR can quantify myocardial fibrosis, which is significantly helpful in early diagnosis of Chagas cardiomyopathy in asymptomatic patients. This measurement is useful as a predictor factor for disease prognosis.[46] The CMR with LGE can assess the presence of myocardial fibrosis, which is a marker of the severity of the disease and predicts the development of malignant ventricular arrhythmias, which can lead to sudden cardiac death. CMR can detect ventricular aneurysms and intraventricular thrombus in Chagas cardiomyopathy.[42] It can also detect right ventricular dysfunction which is a poor prognostic factor in Chagas cardiomyopathy.[16]

In HCM, the CMR can show the septal and left ventricular hypertrophy and helps in the assessment of variant types of HCM. CMR is more sensitive than echocardiogram to identify areas of segmental left ventricular hypertrophy. Myocardial fibrosis can be detected when using IV gadolinium.[47] The intraventricular septum is usually asymmetric on CMR, but it can be symmetric occasionally. CMR can show apical hypertrophy or mass like left ventricular hypertrophy.[42] Both mitral valve and papillary muscles are part of the etiology of the LVOT obstruction. CMR can early detect the SAM of the mitral valve, which is the main etiology for the LVOT obstruction.[48] Left ventricular papillary muscles play an important role in the LVOT obstruction. CMR can detect the mass of the papillary muscle and can be helpful in pre-op planning for septal reduction therapy.[49] CMR can also help to detect right ventricular hypertrophy in HCM.[50] In carriers and early asymptomatic HCM patients, the CMR can detect left ventricular myocardial crypts that precede myocardial wall thickening and early changes of HCM.[51]

CMR is essential in the diagnosis of restrictive cardiomyopathy and the differential diagnosis of etiology of this type of cardiomyopathies; it helps to differentiate the restrictive cardiomyopathy from the constrictive pericarditis.[42] Features of cardiac amyloidosis on CMR are concentric hypertrophy, increased septal thickness, atrial dilation bilaterally, and normal or impaired contractility.[42] In cardiac amyloidosis, LGE-CMR can detect early myocardial abnormalities in patients with normal left ventricular thickness.[52] LGE is an indicator of the severity of the cardiac amyloidosis related heart failure, and the severity is consistent with the BNP levels.[53]

In cardiac sarcoidosis, the typical findings on CMR are biventricular dilation and thinning of the septum.[42] The CMR detects cardiac sarcoidosis by identifying areas of LGE in the mid-wall, and subepicardial areas, LGE in the subendocardium is rare. These LGE areas are likely to be multifocal, especially in the anterior and inferior septum.[31] Presence of LGE was shown to be related to increased ventricular arrhythmia in cardiac sarcoidosis and can be related to cardiovascular death.[54] LGE-CMR is useful also in the evaluation of response to steroids treatment of the sarcoidosis.[42] In ARVC, the CMR can detect wall motion defects, right ventricular dilation, right ventricular dysfunction, and focal aneurysms. Right ventricular outflow tract enlargement, intramyocardial fatty infiltrates and focal wall thinning or wall hypertrophy are some of the morphological abnormalities that CMR can detect.[42]

CMR can be used as part of the workup for other unclassified cardiomyopathies. In stress cardiomyopathy, the CMR can show the left ventricular wall motion dyskinesia or akinesia in the mid and apical areas of the left ventricle in up to 75% of patients.[55] It can also show right ventricular involvement, and left ventricular thrombus.[55] LGE CMR does not show scarring of the myocardium, but CMR on the T2 weighted images shows wall edema.[42] In LVNC, the CMR can help to differentiate the true LVNC from other prominent hypertrabeculation that can present in normal individuals.[56]

Nuclear Medicine

The nuclear imaging is used to evaluate the cardiac function and myocardial perfusion to rule out ischemic cardiomyopathy. It is also useful in restrictive heart diseases, especially in cardiac sarcoidosis and amyloidosis and in the diagnosis of the hypertrophic cardiomyopathy HCM. Single-photon emission computed tomography (SPECT) and positron emission tomography (PET) are beneficial in the workup for cardiomyopathies. SPECT can help in the evaluation of wall mobility, thickness, and cardiac ischemia. PET is helpful to evaluate cardiac ischemia and inflammation.[57]

In DCM, SPECT myocardial perfusion scintigraphy (MPS) and PET can help to differentiate the ischemic versus nonischemic etiology of the cardiomyopathy. In nonischemic cardiomyopathy, the SPECT MPS shows a good distribution of the blood flow compared to the ischemic CM where there is a decrease in blood distribution due to the ischemia.[24] The SPECT sensitivity is 80 to 95% in Ischemic CM, but this reduces in three-vessel disease to 29% as there is global hypoperfusion rather than a focal defect.[24] SPECT imaging using iodine-123 labeled meta-iodobenzylguanidine (MIBG) SPECT has been the topic of study in patients with Chagas cardiomyopathy and results showed areas of denervation in the majority of the patients. These changes are visible before changes on echocardiogram and EKG.[58] The increase in myocardial denervation correlates with supraventricular tachycardia and may trigger malignant ventricular arrhythmias.[59]

In HCM, the perfusion Imaging can demonstrate thickened asymmetric septum or apex, and shows fixed reversible defects without evidence of coronary artery disease. The Thallium-201 can help to detect reversible exercise-induced defects in the left ventricle.[60] PET is better than SPECT to quantify the myocardial blood flow and to measure the transmural differences in perfusion. In patients lacking evidence of coronary artery disease, PET shows that even if the blood flow to the myocardium is normal, there is impaired blood flow after the use of maximal pharmacological vasodilation “ dipyridamole,” this is due to increased resistance of the intramyocardial arterioles; this is considered to have a poor prognosis in patients with HCM.[60]

In cardiac sarcoidosis cardiac, fluorodeoxyglucose (FDG) PET scan is considered an important test to establish the diagnosis. FDG PET can show focal areas of increased uptake which represents areas of inflammation. These appear as patchy infiltrates on the scan.[32] Combination of PET with a perfusion scan (99m Tc SPECT or Th SPECT) can help to differentiate cardiac sarcoidosis form ischemic cardiomyopathy.[32] FDG PET helps to predict poor outcome; an abnormal PET can predict sustained ventricular tachycardia and cardiac death.[61] The presence of focal FDG uptake in the right ventricle is associated with increased risk of death and ventricular tachycardia.[61] Nuclear imaging is useful in monitoring progress in the treatment of cardiac sarcoidosis, after steroid therapy.[24] FDG PET can be used as a serial follow up testing to guide immunosuppression treatment and to decrease the need for steroids treatment in cardiac sarcoidosis.[62]

In cardiac amyloidosis, the MIBG SPECT helps for early detection of the myocardium denervation before the incidence of amyloid deposition that leads to heart disease. The use of PET is still limited in the use of work up for cardiac amyloidosis.[63] But some studies showed that the use of (18)F-Florbetapir PET could help to diagnose both AL "light chain" and TTR "transthyretin" cardiac amyloidosis.[64] It is important to differentiate between the AL (light-chain) and TTR (transthyretin-related) cardiac amyloidosis subtypes as the LA type carries the worst prognosis.[65] The 99mTc-3,3-diphosphono-1,2-propanodicarboxylic acid (99mTc-DPD) can be used to differentiate between AL and TTR amyloidosis,[66] it can also be used as a predictor of outcome in TTR amyloidosis.[67] SPECT scan using (99m) Tc PYP 'pyrophosphate" imaging has a high sensitivity to diagnose TTR amyloidosis cardiomyopathy and is helpful to differentiate it from the AL type.[68] SPECT using (99m) MDP "methylene diphosphonate" and (99m) HMDP "hydroxymethylene diphosphonate" is also effective in detecting the TTR deposition in the myocardium.[65]

In arrhythmogenic right ventricular cardiomyopathy (ARVC), abnormal 123I-MIBG SPECT uptake is related to increased risk of life-threatening ventricular arrhythmias.[69] The MIBG SPECT is sensitive to detect the left ventricular involvement in ARVC, the extent of MIBG distribution abnormalities can help to assess the severity of left ventricular involvement in patients with ARVC.[70] In TTC, the I-123 MIBG SPECT is specific in diagnosis. If combined with myocardial perfusion imaging, they both help to differentiate TTC from ischemic cardiomyopathy.[71]

Clinical Significance

Diagnosis of cardiomyopathy requires multiple diagnostic tests. Imaging tests play a primary role in the workup. Echocardiogram remains the first test to order; it helps in establishing the diagnosis and provides an easy and cheap tool for routine follow up on disease progression and response to treatment. Cardiac MR provides an excellent evaluation of the myocardial function and is considered to be the definitive imaging test to diagnose hypertrophic and infiltrative diseases of the myocardium. It is useful for predicting prognosis in multiple types of cardiomyopathy. Cardiac CT is essential in the workup of ischemic heart disease and helps in the workup of hypertrophic and restrictive cardiomyopathies. Nuclear imaging is helpful on the evaluation of metabolism and function of the myocardium, and it is an excellent tool for the diagnosis of ischemic cardiomyopathy and has value in the workup of infiltrative cardiomyopathies especially cardiac sarcoidosis and TTR amyloidosis.

Details

References

[1]

Maron BJ, Towbin JA, Thiene G, Antzelevitch C, Corrado D, Arnett D, Moss AJ, Seidman CE, Young JB, American Heart Association, Council on Clinical Cardiology, Heart Failure and Transplantation Committee, Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups, Council on Epidemiology and Prevention. Contemporary definitions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation. 2006 Apr 11:113(14):1807-16 [PubMed PMID: 16567565]

Level 2 (mid-level) evidence

[2]

Badgett RG, Mulrow CD, Otto PM, Ramírez G. How well can the chest radiograph diagnose left ventricular dysfunction? Journal of general internal medicine. 1996 Oct:11(10):625-34 [PubMed PMID: 8945695]

[3]

Parada H, Carrasco HA, Añez N, Fuenmayor C, Inglessis I. Cardiac involvement is a constant finding in acute Chagas' disease: a clinical, parasitological and histopathological study. International journal of cardiology. 1997 Jun 27:60(1):49-54 [PubMed PMID: 9209939]

[4]

Erbel R, Schweizer P, Krebs W, Meyer J, Effert S. Sensitivity and specificity of two-dimensional echocardiography in detection of impaired left ventricular function. European heart journal. 1984 Jun:5(6):477-89 [PubMed PMID: 6745290]

[5]

Thomas DE, Wheeler R, Yousef ZR, Masani ND. The role of echocardiography in guiding management in dilated cardiomyopathy. European journal of echocardiography : the journal of the Working Group on Echocardiography of the European Society of Cardiology. 2009 Dec:10(8):iii15-21. doi: 10.1093/ejechocard/jep158. Epub [PubMed PMID: 19889654]

[6]

Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L, Flachskampf FA, Foster E, Goldstein SA, Kuznetsova T, Lancellotti P, Muraru D, Picard MH, Rietzschel ER, Rudski L, Spencer KT, Tsang W, Voigt JU. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography. 2015 Jan:28(1):1-39.e14. doi: 10.1016/j.echo.2014.10.003. Epub [PubMed PMID: 25559473]

[7]

Sengeløv M, Jørgensen PG, Jensen JS, Bruun NE, Olsen FJ, Fritz-Hansen T, Nochioka K, Biering-Sørensen T. Global Longitudinal Strain Is a Superior Predictor of All-Cause Mortality in Heart Failure With Reduced Ejection Fraction. JACC. Cardiovascular imaging. 2015 Dec:8(12):1351-1359. doi: 10.1016/j.jcmg.2015.07.013. Epub 2015 Nov 11 [PubMed PMID: 26577264]

[8]

Adamo L, Perry A, Novak E, Makan M, Lindman BR, Mann DL. Abnormal Global Longitudinal Strain Predicts Future Deterioration of Left Ventricular Function in Heart Failure Patients With a Recovered Left Ventricular Ejection Fraction. Circulation. Heart failure. 2017 Jun:10(6):. doi: 10.1161/CIRCHEARTFAILURE.116.003788. Epub [PubMed PMID: 28559418]

[9]

Sun JP, James KB, Yang XS, Solankhi N, Shah MS, Arheart KL, Thomas JD, Stewart WJ. Comparison of mortality rates and progression of left ventricular dysfunction in patients with idiopathic dilated cardiomyopathy and dilated versus nondilated right ventricular cavities. The American journal of cardiology. 1997 Dec 15:80(12):1583-7 [PubMed PMID: 9416940]

[10]

de Groote P, Millaire A, Foucher-Hossein C, Nugue O, Marchandise X, Ducloux G, Lablanche JM. Right ventricular ejection fraction is an independent predictor of survival in patients with moderate heart failure. Journal of the American College of Cardiology. 1998 Oct:32(4):948-54 [PubMed PMID: 9768716]

[11]

Sliwa K, Hilfiker-Kleiner D, Petrie MC, Mebazaa A, Pieske B, Buchmann E, Regitz-Zagrosek V, Schaufelberger M, Tavazzi L, van Veldhuisen DJ, Watkins H, Shah AJ, Seferovic PM, Elkayam U, Pankuweit S, Papp Z, Mouquet F, McMurray JJ, Heart Failure Association of the European Society of Cardiology Working Group on Peripartum Cardiomyopathy. Current state of knowledge on aetiology, diagnosis, management, and therapy of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology Working Group on peripartum cardiomyopathy. European journal of heart failure. 2010 Aug:12(8):767-78. doi: 10.1093/eurjhf/hfq120. Epub [PubMed PMID: 20675664]

[12]

Vigna C, Russo A, De Rito V, Perna GP, Testa M, Lombardo A, Lanna P, Langialonga T, Salvatori MP, Fanelli R, Loperfido F. Regional wall motion analysis by dobutamine stess echocardiography to distinguish between ischemic and nonischemic dilated cardiomyopathy. American heart journal. 1996 Mar:131(3):537-43 [PubMed PMID: 8604635]

[13]

White HD, Norris RM, Brown MA, Brandt PW, Whitlock RM, Wild CJ. Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction. Circulation. 1987 Jul:76(1):44-51 [PubMed PMID: 3594774]

[14]

Acquatella H. Echocardiography in Chagas heart disease. Circulation. 2007 Mar 6:115(9):1124-31 [PubMed PMID: 17339570]

[15]

Salles G, Xavier S, Sousa A, Hasslocher-Moreno A, Cardoso C. Prognostic value of QT interval parameters for mortality risk stratification in Chagas' disease: results of a long-term follow-up study. Circulation. 2003 Jul 22:108(3):305-12 [PubMed PMID: 12835217]

[16]

Acquatella H, Asch FM, Barbosa MM, Barros M, Bern C, Cavalcante JL, Echeverria Correa LE, Lima J, Marcus R, Marin-Neto JA, Migliore R, Milei J, Morillo CA, Nunes MCP, Campos Vieira ML, Viotti R. Recommendations for Multimodality Cardiac Imaging in Patients with Chagas Disease: A Report from the American Society of Echocardiography in Collaboration With the InterAmerican Association of Echocardiography (ECOSIAC) and the Cardiovascular Imaging Department of the Brazilian Society of Cardiology (DIC-SBC). Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography. 2018 Jan:31(1):3-25. doi: 10.1016/j.echo.2017.10.019. Epub [PubMed PMID: 29306364]

[17]

American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, Society of Thoracic Surgeons, Gersh BJ, Maron BJ, Bonow RO, Dearani JA, Fifer MA, Link MS, Naidu SS, Nishimura RA, Ommen SR, Rakowski H, Seidman CE, Towbin JA, Udelson JE, Yancy CW. 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. The Journal of thoracic and cardiovascular surgery. 2011 Dec:142(6):1303-38. doi: 10.1016/j.jtcvs.2011.10.019. Epub [PubMed PMID: 22093712]

Level 1 (high-level) evidence

[18]

Maron MS, Olivotto I, Betocchi S, Casey SA, Lesser JR, Losi MA, Cecchi F, Maron BJ. Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy. The New England journal of medicine. 2003 Jan 23:348(4):295-303 [PubMed PMID: 12540642]

Level 2 (mid-level) evidence

[19]

Maron MS, Olivotto I, Zenovich AG, Link MS, Pandian NG, Kuvin JT, Nistri S, Cecchi F, Udelson JE, Maron BJ. Hypertrophic cardiomyopathy is predominantly a disease of left ventricular outflow tract obstruction. Circulation. 2006 Nov 21:114(21):2232-9 [PubMed PMID: 17088454]

[20]

Nistri S, Olivotto I, Betocchi S, Losi MA, Valsecchi G, Pinamonti B, Conte MR, Casazza F, Galderisi M, Maron BJ, Cecchi F. Prognostic significance of left atrial size in patients with hypertrophic cardiomyopathy (from the Italian Registry for Hypertrophic Cardiomyopathy). The American journal of cardiology. 2006 Oct 1:98(7):960-5 [PubMed PMID: 16996883]

[21]

Hiemstra YL, Debonnaire P, Bootsma M, van Zwet EW, Delgado V, Schalij MJ, Atsma DE, Bax JJ, Marsan NA. Global Longitudinal Strain and Left Atrial Volume Index Provide Incremental Prognostic Value in Patients With Hypertrophic Cardiomyopathy. Circulation. Cardiovascular imaging. 2017 Jul:10(7):. pii: e005706. doi: 10.1161/CIRCIMAGING.116.005706. Epub [PubMed PMID: 28679523]

[22]

Hiemstra YL, Debonnaire P, van Zwet EW, Bootsma M, Schalij MJ, Bax JJ, Delgado V, Marsan NA. Development of and Progression of Overt Heart Failure in Nonobstructive Hypertrophic Cardiomyopathy. The American journal of cardiology. 2018 Aug 15:122(4):656-662. doi: 10.1016/j.amjcard.2018.04.038. Epub 2018 Jun 20 [PubMed PMID: 30205890]

[23]

Habib G, Bucciarelli-Ducci C, Caforio ALP, Cardim N, Charron P, Cosyns B, Dehaene A, Derumeaux G, Donal E, Dweck MR, Edvardsen T, Erba PA, Ernande L, Gaemperli O, Galderisi M, Grapsa J, Jacquier A, Klingel K, Lancellotti P, Neglia D, Pepe A, Perrone-Filardi P, Petersen SE, Plein S, Popescu BA, Reant P, Sade LE, Salaun E, Slart RHJA, Tribouilloy C, Zamorano J, EACVI Scientific Documents Committee, Indian Academy of Echocardiography. Multimodality Imaging in Restrictive Cardiomyopathies: An EACVI expert consensus document In collaboration with the "Working Group on myocardial and pericardial diseases" of the European Society of Cardiology Endorsed by The Indian Academy of Echocardiography. European heart journal. Cardiovascular Imaging. 2017 Oct 1:18(10):1090-1121. doi: 10.1093/ehjci/jex034. Epub [PubMed PMID: 28510718]

Level 3 (low-level) evidence

[24]

Gunaratnam K, Wong LH, Nasis A, Ellims A, Nandurkar D, Soo G, Cameron J, Troupis J. Review of cardiomyopathy imaging. European journal of radiology. 2013 Oct:82(10):1763-75. doi: 10.1016/j.ejrad.2013.05.041. Epub 2013 Jul 2 [PubMed PMID: 23827801]

[25]

Seward JB, Casaclang-Verzosa G. Infiltrative cardiovascular diseases: cardiomyopathies that look alike. Journal of the American College of Cardiology. 2010 Apr 27:55(17):1769-79. doi: 10.1016/j.jacc.2009.12.040. Epub [PubMed PMID: 20413025]

[26]

Klein AL, Hatle LK, Burstow DJ, Taliercio CP, Seward JB, Kyle RA, Bailey KR, Gertz MA, Tajik AJ. Comprehensive Doppler assessment of right ventricular diastolic function in cardiac amyloidosis. Journal of the American College of Cardiology. 1990 Jan:15(1):99-108 [PubMed PMID: 2295749]

[27]

Lee GY, Kim K, Choi JO, Kim SJ, Kim JS, Choe YH, Grogan MA, Jeon ES. Cardiac amyloidosis without increased left ventricular wall thickness. Mayo Clinic proceedings. 2014 Jun:89(6):781-9. doi: 10.1016/j.mayocp.2014.01.013. Epub 2014 Apr 3 [PubMed PMID: 24702732]

[28]

Bellavia D, Pellikka PA, Abraham TP, Al-Zahrani GB, Dispenzieri A, Oh JK, Bailey KR, Wood CM, Lacy MQ, Miyazaki C, Miller FA Jr. Evidence of impaired left ventricular systolic function by Doppler myocardial imaging in patients with systemic amyloidosis and no evidence of cardiac involvement by standard two-dimensional and Doppler echocardiography. The American journal of cardiology. 2008 Apr 1:101(7):1039-45. doi: 10.1016/j.amjcard.2007.11.047. Epub 2008 Feb 1 [PubMed PMID: 18359328]

[29]

Baccouche H, Maunz M, Beck T, Gaa E, Banzhaf M, Knayer U, Fogarassy P, Beyer M. Differentiating cardiac amyloidosis and hypertrophic cardiomyopathy by use of three-dimensional speckle tracking echocardiography. Echocardiography (Mount Kisco, N.Y.). 2012 Jul:29(6):668-77. doi: 10.1111/j.1540-8175.2012.01680.x. Epub 2012 Apr 4 [PubMed PMID: 22486396]

[30]

Patel AR, Dubrey SW, Mendes LA, Skinner M, Cupples A, Falk RH, Davidoff R. Right ventricular dilation in primary amyloidosis: an independent predictor of survival. The American journal of cardiology. 1997 Aug 15:80(4):486-92 [PubMed PMID: 9285663]

[31]

Blankstein R, Waller AH. Evaluation of Known or Suspected Cardiac Sarcoidosis. Circulation. Cardiovascular imaging. 2016 Mar:9(3):e000867. doi: 10.1161/CIRCIMAGING.113.000867. Epub [PubMed PMID: 26926267]

[32]

Jeudy J, Burke AP, White CS, Kramer GB, Frazier AA. Cardiac sarcoidosis: the challenge of radiologic-pathologic correlation: from the radiologic pathology archives. Radiographics : a review publication of the Radiological Society of North America, Inc. 2015 May-Jun:35(3):657-79. doi: 10.1148/rg.2015140247. Epub [PubMed PMID: 25969930]

[33]

Galderisi M. Diastolic dysfunction and diabetic cardiomyopathy: evaluation by Doppler echocardiography. Journal of the American College of Cardiology. 2006 Oct 17:48(8):1548-51 [PubMed PMID: 17045886]

[34]

Saguner AM, Vecchiati A, Baldinger SH, Rüeger S, Medeiros-Domingo A, Mueller-Burri AS, Haegeli LM, Biaggi P, Manka R, Lüscher TF, Fontaine G, Delacrétaz E, Jenni R, Held L, Brunckhorst C, Duru F, Tanner FC. Different prognostic value of functional right ventricular parameters in arrhythmogenic right ventricular cardiomyopathy/dysplasia. Circulation. Cardiovascular imaging. 2014 Mar:7(2):230-9. doi: 10.1161/CIRCIMAGING.113.000210. Epub 2014 Feb 10 [PubMed PMID: 24515411]

[35]

Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. American heart journal. 2008 Mar:155(3):408-17. doi: 10.1016/j.ahj.2007.11.008. Epub 2008 Jan 31 [PubMed PMID: 18294473]

[36]

Singh K, Neil CJ, Nguyen TH, Stansborough J, Chong CR, Dawson D, Frenneaux MP, Horowitz JD. Dissociation of early shock in takotsubo cardiomyopathy from either right or left ventricular systolic dysfunction. Heart, lung & circulation. 2014 Dec:23(12):1141-8. doi: 10.1016/j.hlc.2014.06.010. Epub 2014 Jun 27 [PubMed PMID: 25043578]

[37]

Biagini E, Ragni L, Ferlito M, Pasquale F, Lofiego C, Leone O, Rocchi G, Perugini E, Zagnoni S, Branzi A, Picchio FM, Rapezzi C. Different types of cardiomyopathy associated with isolated ventricular noncompaction. The American journal of cardiology. 2006 Sep 15:98(6):821-4 [PubMed PMID: 16950194]

[38]

Jenni R, Oechslin E, Schneider J, Attenhofer Jost C, Kaufmann PA. Echocardiographic and pathoanatomical characteristics of isolated left ventricular non-compaction: a step towards classification as a distinct cardiomyopathy. Heart (British Cardiac Society). 2001 Dec:86(6):666-71 [PubMed PMID: 11711464]

[39]

Andreini D, Pontone G, Pepi M, Ballerini G, Bartorelli AL, Magini A, Quaglia C, Nobili E, Agostoni P. Diagnostic accuracy of multidetector computed tomography coronary angiography in patients with dilated cardiomyopathy. Journal of the American College of Cardiology. 2007 May 22:49(20):2044-50 [PubMed PMID: 17512361]

[40]

Kalisz K, Rajiah P. Computed tomography of cardiomyopathies. Cardiovascular diagnosis and therapy. 2017 Oct:7(5):539-556. doi: 10.21037/cdt.2017.09.07. Epub [PubMed PMID: 29255695]

[41]

Clayton B, Roobottom C, Morgan-Hughes G. Assessment of the myocardium with cardiac computed tomography. European heart journal. Cardiovascular Imaging. 2014 Jun:15(6):603-9. doi: 10.1093/ehjci/jeu028. Epub 2014 Feb 26 [PubMed PMID: 24578413]

[42]

Karamitsos TD, Francis JM, Myerson S, Selvanayagam JB, Neubauer S. The role of cardiovascular magnetic resonance imaging in heart failure. Journal of the American College of Cardiology. 2009 Oct 6:54(15):1407-24. doi: 10.1016/j.jacc.2009.04.094. Epub [PubMed PMID: 19796734]

[43]

Bello D, Shah DJ, Farah GM, Di Luzio S, Parker M, Johnson MR, Cotts WG, Klocke FJ, Bonow RO, Judd RM, Gheorghiade M, Kim RJ. Gadolinium cardiovascular magnetic resonance predicts reversible myocardial dysfunction and remodeling in patients with heart failure undergoing beta-blocker therapy. Circulation. 2003 Oct 21:108(16):1945-53 [PubMed PMID: 14557364]

[44]

Fett JD, The role of MRI in peripartum cardiomyopathy. International journal of cardiology. 2009 Oct 2; [PubMed PMID: 18684520]

[45]

Marmursztejn J, Vignaux O, Goffinet F, Cabanes L, Duboc D. Delayed-enhanced cardiac magnetic resonance imaging features in peripartum cardiomyopathy. International journal of cardiology. 2009 Nov 12:137(3):e63-4. doi: 10.1016/j.ijcard.2009.04.028. Epub 2009 May 12 [PubMed PMID: 19439378]

[46]

Rochitte CE, Oliveira PF, Andrade JM, Ianni BM, Parga JR, Avila LF, Kalil-Filho R, Mady C, Meneghetti JC, Lima JA, Ramires JA. Myocardial delayed enhancement by magnetic resonance imaging in patients with Chagas' disease: a marker of disease severity. Journal of the American College of Cardiology. 2005 Oct 18:46(8):1553-8 [PubMed PMID: 16226184]

[47]

Rickers C, Wilke NM, Jerosch-Herold M, Casey SA, Panse P, Panse N, Weil J, Zenovich AG, Maron BJ. Utility of cardiac magnetic resonance imaging in the diagnosis of hypertrophic cardiomyopathy. Circulation. 2005 Aug 9:112(6):855-61 [PubMed PMID: 16087809]

Level 3 (low-level) evidence

[48]

Silbiger JJ. Abnormalities of the Mitral Apparatus in Hypertrophic Cardiomyopathy: Echocardiographic, Pathophysiologic, and Surgical Insights. Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography. 2016 Jul:29(7):622-39. doi: 10.1016/j.echo.2016.03.003. Epub 2016 Apr 14 [PubMed PMID: 27146120]

[49]

Harrigan CJ, Appelbaum E, Maron BJ, Buros JL, Gibson CM, Lesser JR, Udelson JE, Manning WJ, Maron MS. Significance of papillary muscle abnormalities identified by cardiovascular magnetic resonance in hypertrophic cardiomyopathy. The American journal of cardiology. 2008 Mar 1:101(5):668-73. doi: 10.1016/j.amjcard.2007.10.032. Epub 2007 Dec 21 [PubMed PMID: 18308018]

[50]

Maron MS, Hauser TH, Dubrow E, Horst TA, Kissinger KV, Udelson JE, Manning WJ. Right ventricular involvement in hypertrophic cardiomyopathy. The American journal of cardiology. 2007 Oct 15:100(8):1293-8 [PubMed PMID: 17920373]

[51]

Germans T, Wilde AA, Dijkmans PA, Chai W, Kamp O, Pinto YM, van Rossum AC. Structural abnormalities of the inferoseptal left ventricular wall detected by cardiac magnetic resonance imaging in carriers of hypertrophic cardiomyopathy mutations. Journal of the American College of Cardiology. 2006 Dec 19:48(12):2518-23 [PubMed PMID: 17174192]

[52]

Syed IS, Glockner JF, Feng D, Araoz PA, Martinez MW, Edwards WD, Gertz MA, Dispenzieri A, Oh JK, Bellavia D, Tajik AJ, Grogan M. Role of cardiac magnetic resonance imaging in the detection of cardiac amyloidosis. JACC. Cardiovascular imaging. 2010 Feb:3(2):155-64. doi: 10.1016/j.jcmg.2009.09.023. Epub [PubMed PMID: 20159642]

[53]

Ruberg FL, Appelbaum E, Davidoff R, Ozonoff A, Kissinger KV, Harrigan C, Skinner M, Manning WJ. Diagnostic and prognostic utility of cardiovascular magnetic resonance imaging in light-chain cardiac amyloidosis. The American journal of cardiology. 2009 Feb 15:103(4):544-9. doi: 10.1016/j.amjcard.2008.09.105. Epub 2008 Dec 25 [PubMed PMID: 19195518]

[54]

Hulten E, Agarwal V, Cahill M, Cole G, Vita T, Parrish S, Bittencourt MS, Murthy VL, Kwong R, Di Carli MF, Blankstein R. Presence of Late Gadolinium Enhancement by Cardiac Magnetic Resonance Among Patients With Suspected Cardiac Sarcoidosis Is Associated With Adverse Cardiovascular Prognosis: A Systematic Review and Meta-Analysis. Circulation. Cardiovascular imaging. 2016 Sep:9(9):e005001. doi: 10.1161/CIRCIMAGING.116.005001. Epub [PubMed PMID: 27621357]

Level 1 (high-level) evidence

[55]

Sharkey SW,Windenburg DC,Lesser JR,Maron MS,Hauser RG,Lesser JN,Haas TS,Hodges JS,Maron BJ, Natural history and expansive clinical profile of stress (tako-tsubo) cardiomyopathy. Journal of the American College of Cardiology. 2010 Jan 26 [PubMed PMID: 20117439]

[56]

Peritz DC, Vaughn A, Ciocca M, Chung EH. Hypertrabeculation vs left ventricular noncompaction on echocardiogram: a reason to restrict athletic participation? JAMA internal medicine. 2014 Aug:174(8):1379-82. doi: 10.1001/jamainternmed.2014.1066. Epub [PubMed PMID: 24911984]

[57]

García-Orta R, Mahía-Casado P, Gómez de Diego JJ, Barba-Cosials J, Rodriguez-Palomares JF, Aguadé-Bruix S, Candell-Riera J. Update on cardiac imaging techniques 2013. Revista espanola de cardiologia (English ed.). 2014 Feb:67(2):127-34. doi: 10.1016/j.rec.2013.10.003. Epub 2014 Jan 6 [PubMed PMID: 24795120]

[58]

Simões MV, Pintya AO, Bromberg-Marin G, Sarabanda AV, Antloga CM, Pazin-Filho A, Maciel BC, Marin-Neto JA. Relation of regional sympathetic denervation and myocardial perfusion disturbance to wall motion impairment in Chagas' cardiomyopathy. The American journal of cardiology. 2000 Nov 1:86(9):975-81 [PubMed PMID: 11053710]

[59]

Miranda CH, Figueiredo AB, Maciel BC, Marin-Neto JA, Simões MV. Sustained ventricular tachycardia is associated with regional myocardial sympathetic denervation assessed with 123I-metaiodobenzylguanidine in chronic Chagas cardiomyopathy. Journal of nuclear medicine : official publication, Society of Nuclear Medicine. 2011 Apr:52(4):504-10. doi: 10.2967/jnumed.110.082032. Epub [PubMed PMID: 21441532]

[60]

Shirani J, Dilsizian V. Nuclear cardiac imaging in hypertrophic cardiomyopathy. Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology. 2011 Feb:18(1):123-34. doi: 10.1007/s12350-010-9279-2. Epub [PubMed PMID: 20737262]

[61]

Blankstein R, Osborne M, Naya M, Waller A, Kim CK, Murthy VL, Kazemian P, Kwong RY, Tokuda M, Skali H, Padera R, Hainer J, Stevenson WG, Dorbala S, Di Carli MF. Cardiac positron emission tomography enhances prognostic assessments of patients with suspected cardiac sarcoidosis. Journal of the American College of Cardiology. 2014 Feb 4:63(4):329-36. doi: 10.1016/j.jacc.2013.09.022. Epub 2013 Oct 16 [PubMed PMID: 24140661]

[62]

Ning N, Guo HH, Iagaru A, Mittra E, Fowler M, Witteles R. Serial Cardiac FDG-PET for the Diagnosis and Therapeutic Guidance of Patients With Cardiac Sarcoidosis. Journal of cardiac failure. 2019 Apr:25(4):307-311. doi: 10.1016/j.cardfail.2019.02.018. Epub 2019 Feb 27 [PubMed PMID: 30825644]

[63]

Noordzij W, Glaudemans AW, Longhi S, Slart RH, Lorenzini M, Hazenberg BP, Rapezzi C. Nuclear imaging for cardiac amyloidosis. Heart failure reviews. 2015 Mar:20(2):145-54. doi: 10.1007/s10741-014-9463-6. Epub [PubMed PMID: 25424887]

[64]

Dorbala S, Vangala D, Semer J, Strader C, Bruyere JR Jr, Di Carli MF, Moore SC, Falk RH. Imaging cardiac amyloidosis: a pilot study using ¹⁸F-florbetapir positron emission tomography. European journal of nuclear medicine and molecular imaging. 2014 Sep:41(9):1652-62. doi: 10.1007/s00259-014-2787-6. Epub 2014 May 20 [PubMed PMID: 24841414]

Level 3 (low-level) evidence

[65]

Andrikopoulou E, Bhambhvani P. Nuclear imaging of cardiac amyloidosis. Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology. 2019 Apr:26(2):505-508. doi: 10.1007/s12350-017-1028-3. Epub 2017 Aug 18 [PubMed PMID: 28822085]

[66]

Perugini E, Guidalotti PL, Salvi F, Cooke RM, Pettinato C, Riva L, Leone O, Farsad M, Ciliberti P, Bacchi-Reggiani L, Fallani F, Branzi A, Rapezzi C. Noninvasive etiologic diagnosis of cardiac amyloidosis using 99mTc-3,3-diphosphono-1,2-propanodicarboxylic acid scintigraphy. Journal of the American College of Cardiology. 2005 Sep 20:46(6):1076-84 [PubMed PMID: 16168294]

[67]

Rapezzi C, Quarta CC, Guidalotti PL, Pettinato C, Fanti S, Leone O, Ferlini A, Longhi S, Lorenzini M, Reggiani LB, Gagliardi C, Gallo P, Villani C, Salvi F. Role of (99m)Tc-DPD scintigraphy in diagnosis and prognosis of hereditary transthyretin-related cardiac amyloidosis. JACC. Cardiovascular imaging. 2011 Jun:4(6):659-70. doi: 10.1016/j.jcmg.2011.03.016. Epub [PubMed PMID: 21679902]

[68]

Bokhari S, Castaño A, Pozniakoff T, Deslisle S, Latif F, Maurer MS. (99m)Tc-pyrophosphate scintigraphy for differentiating light-chain cardiac amyloidosis from the transthyretin-related familial and senile cardiac amyloidoses. Circulation. Cardiovascular imaging. 2013 Mar 1:6(2):195-201. doi: 10.1161/CIRCIMAGING.112.000132. Epub 2013 Feb 11 [PubMed PMID: 23400849]

[69]

Paul M, Wichter T, Kies P, Gerss J, Wollmann C, Rahbar K, Eckardt L, Breithardt G, Schober O, Schulze-Bahr E, Schäfers M. Cardiac sympathetic dysfunction in genotyped patients with arrhythmogenic right ventricular cardiomyopathy and risk of recurrent ventricular tachyarrhythmias. Journal of nuclear medicine : official publication, Society of Nuclear Medicine. 2011 Oct:52(10):1559-65. doi: 10.2967/jnumed.111.088997. Epub 2011 Sep 9 [PubMed PMID: 21908389]

[70]

Takahashi N, Ishida Y, Maeno M, Hirose Y, Kawano S, Fukuoka S, Hayashida K, Kuribayashi S, Hamada S, Yamada N, Takamiya M, Shimomura K, Ohe T. [Significance of 123I-metaiodobenzylguanidine SPECT for detecting left ventricular involvement in patients with arrhythmogenic right ventricular dysplasia]. Kaku igaku. The Japanese journal of nuclear medicine. 1996 Jan:33(1):57-67 [PubMed PMID: 8819715]

[71]

Cimarelli S, Imperiale A, Ben-Sellem D, Rischner J, Detour J, Morel O, Ohlmann P, Constantinesco A. Nuclear medicine imaging of takotsubo cardiomyopathy: typical form and midventricular ballooning syndrome. Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology. 2008 Jan-Feb:15(1):137-41. doi: 10.1007/BF02976903. Epub 2007 Dec 21 [PubMed PMID: 18242491]