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I. Introduction
Chagas disease (ChD) is a significant public health problem in most Latin American countries. Observed mainly in rural areas, in recent decades it has spread to cities and to nonendemic countries, mostly as a result of migration of infected people. Increasing numbers of cases are now being identified in the United States, Spain, and other countries, which makes its diagnosis and management of increasing interest worldwide.
During an antimalarial campaign in Lassance (Minas Gerais, Brazil) in 1909, Carlos Chagas identified the parasite Trypanosoma cruzi , its vector for transmission (triatomine bugs, called differently in each country: kissing bug, barbeiro , vinchuca , chinche , etc.), and described the initial cases of the disease. Transmission occurs mainly through the bite of these vectors but may also occur by blood transfusion, from mother to fetus, oral ingestion of contaminated foods, organ transplantation, and laboratory accidents. Vector control programs have substantially diminished T. cruzi and ChD incidence. However, about 70 million people remain at risk for acquiring the infection.
The diagnosis of ChD is made by epidemiologic history and by two or more positive serologic tests. There are two clinical phases of T. cruzi infection: acute ChD, seen early after acquiring the infection, and chronic ChD, lasting for decades. About 70% to 80% of individuals with chronic T. cruzi infection remain asymptomatic (indeterminate form), while 20% to 30% develop cardiac and/or gastrointestinal disease. Patients with chronic Chagas heart disease (ChHD) are staged according to the severity of myocardial damage and symptoms of congestive heart failure (HF; Table 1 ). Assessment by electrocardiography is mandatory because the earliest signs of ChHD are generally conduction system defects and/or ventricular arrhythmias. The introduction of various cardiac imaging modalities, such as echocardiography, nuclear medicine, computed tomography (CT), cardiac magnetic resonance (CMR), and chest radiography, provides valuable information on cardiac structure and function.
| Acute Phase | Chronic Phase | ||||
|---|---|---|---|---|---|
| Indeterminate Form, A | Chagas Cardiomyopathy | ||||
| B1 | B2 | C | D | ||
| Infected by T. cruzi and findings of acute ChD | Positive serology Normal ECG findings No heart disease or HF | Structural cardiomyopathy (abnormal ECG or echocardiographic findings) but normal LV function No HF | LV dysfunction No HF | LV dysfunction HF (current or prior) | Refractory HF despite optimal medical therapy |
The purpose of this document is to provide recommendations for the use of cardiac ultrasound and other imaging modalities in the diagnosis, classification, and risk assessment of myocardial damage from early to advanced forms of ChHD.
II. Epidemiology of ChD: Geographic Distribution Worldwide and in the United States
ChD is caused by the protozoan parasite T. cruzi , transmitted when feces of an infected triatomine vector enters the mammalian host through the bite wound or mucous membranes. Infection is lifelong in the absence of treatment. Vector-borne transmission occurs in parts of North America, Central America, and South America, with geographic distribution determined both by the ecology of the triatomine vectors and factors such as housing conditions that govern contact between vectors and the human population. Transmission can also occur through transfusion of infected blood components, organ and bone marrow transplantation, and from mother to fetus. Outbreaks attributed to contaminated food or drink have been reported in northern South America. In addition, many T. cruzi –infected individuals have moved from endemic rural villages to Latin American cities, and hundreds of thousands now live in the United States, Spain, and other nonendemic countries outside Latin America ( Figures 1 2 and 2 9,10 ).
T. cruzi infects many mammalian species. The vector species responsible for the majority of human infections are considered domestic because they are adapted to living in cracks in mud walls and thatch roofs of rustic rural houses. Inhabitants of infested houses are repeatedly exposed to vectors and parasites over many years. In highly endemic villages, a high percentage of the adult population is infected, with the prevalence rising with increasing age. The prevalence of cardiac morbidity also increases with age. An estimated 20% to 30% of T. cruzi –infected individuals eventually develop Chagas cardiomyopathy, but in endemic or previously endemic settings, a much higher percentage of the elderly may have cardiac signs.
Latin America has made substantial progress in decreasing T. cruzi transmission, largely through residual insecticide application to control domestic infestation. The estimated global ChD prevalence declined from 18 million in 1991, when the first regional control initiative began, to approximately 6 million in 2010. The Pan American Health Organization has certified interruption of transmission by domestic vectors in several countries of South America and Central America. T. cruzi serologic screening is conducted in most blood banks in Latin America and the United States, and some countries have systematic screening for congenital ChD. Nevertheless, ChD remains the most important parasitic disease in the Western Hemisphere.
The southern half of the continental United States has established enzootic transmission cycles, with infected vectors and mammalian hosts such as raccoons, opossums, wood rats, and domestic dogs. Nevertheless, the majority of infected residents are Latin American immigrants infected in their home countries, and infected individuals are found in nearly every state. On the basis of the Latin American immigrant population and estimates of prevalence in their home countries, an estimated 300,000 T. cruzi –infected immigrants reside in the United States. Locally acquired vector-borne infection has been documented in a handful of cases over the past 60 years and has been inferred in blood donors for whom acquisition of the infection in Latin America has been ruled out or judged unlikely. Direct assessments of prevalence in the United States are sparse and have been restricted to small-scale surveys or case series in populations chosen because of anticipated high risk (e.g., Latin American immigrants with nonischemic heart disease). Because of low provider awareness, cases of Chagas cardiomyopathy likely go unrecognized, and women at risk for vertical transmission to their infants are not screened. Thus, more work is needed to raise awareness and improve the knowledge base of providers in the United States. In addition, more extensive epidemiologic studies and better diagnostic and treatment availability are required.
- •
ChD is a vector-borne zoonotic disease endemic to the Americas, which could be underdiagnosed if aggressive screening campaigns are not pursued.
- •
Substantial progress has been made in decreasing vector- and blood-borne T. cruzi transmission through residual insecticide application and housing improvement, but there remain 6 million infected people and 70 million at risk for infection in the Americas.
- •
Zoonotic transmission occurs in the southern half of the United States, but T. cruzi –infected migrants from Latin America greatly outnumber those infected locally. Patients with ChD are found in nearly every state of the United States and in other countries outside of the Americas.
I. Introduction
Chagas disease (ChD) is a significant public health problem in most Latin American countries. Observed mainly in rural areas, in recent decades it has spread to cities and to nonendemic countries, mostly as a result of migration of infected people. Increasing numbers of cases are now being identified in the United States, Spain, and other countries, which makes its diagnosis and management of increasing interest worldwide.
During an antimalarial campaign in Lassance (Minas Gerais, Brazil) in 1909, Carlos Chagas identified the parasite Trypanosoma cruzi , its vector for transmission (triatomine bugs, called differently in each country: kissing bug, barbeiro , vinchuca , chinche , etc.), and described the initial cases of the disease. Transmission occurs mainly through the bite of these vectors but may also occur by blood transfusion, from mother to fetus, oral ingestion of contaminated foods, organ transplantation, and laboratory accidents. Vector control programs have substantially diminished T. cruzi and ChD incidence. However, about 70 million people remain at risk for acquiring the infection.
The diagnosis of ChD is made by epidemiologic history and by two or more positive serologic tests. There are two clinical phases of T. cruzi infection: acute ChD, seen early after acquiring the infection, and chronic ChD, lasting for decades. About 70% to 80% of individuals with chronic T. cruzi infection remain asymptomatic (indeterminate form), while 20% to 30% develop cardiac and/or gastrointestinal disease. Patients with chronic Chagas heart disease (ChHD) are staged according to the severity of myocardial damage and symptoms of congestive heart failure (HF; Table 1 ). Assessment by electrocardiography is mandatory because the earliest signs of ChHD are generally conduction system defects and/or ventricular arrhythmias. The introduction of various cardiac imaging modalities, such as echocardiography, nuclear medicine, computed tomography (CT), cardiac magnetic resonance (CMR), and chest radiography, provides valuable information on cardiac structure and function.
| Acute Phase | Chronic Phase | ||||
|---|---|---|---|---|---|
| Indeterminate Form, A | Chagas Cardiomyopathy | ||||
| B1 | B2 | C | D | ||
| Infected by T. cruzi and findings of acute ChD | Positive serology Normal ECG findings No heart disease or HF | Structural cardiomyopathy (abnormal ECG or echocardiographic findings) but normal LV function No HF | LV dysfunction No HF | LV dysfunction HF (current or prior) | Refractory HF despite optimal medical therapy |
The purpose of this document is to provide recommendations for the use of cardiac ultrasound and other imaging modalities in the diagnosis, classification, and risk assessment of myocardial damage from early to advanced forms of ChHD.
II. Epidemiology of ChD: Geographic Distribution Worldwide and in the United States
ChD is caused by the protozoan parasite T. cruzi , transmitted when feces of an infected triatomine vector enters the mammalian host through the bite wound or mucous membranes. Infection is lifelong in the absence of treatment. Vector-borne transmission occurs in parts of North America, Central America, and South America, with geographic distribution determined both by the ecology of the triatomine vectors and factors such as housing conditions that govern contact between vectors and the human population. Transmission can also occur through transfusion of infected blood components, organ and bone marrow transplantation, and from mother to fetus. Outbreaks attributed to contaminated food or drink have been reported in northern South America. In addition, many T. cruzi –infected individuals have moved from endemic rural villages to Latin American cities, and hundreds of thousands now live in the United States, Spain, and other nonendemic countries outside Latin America ( Figures 1 2 and 2 9,10 ).
T. cruzi infects many mammalian species. The vector species responsible for the majority of human infections are considered domestic because they are adapted to living in cracks in mud walls and thatch roofs of rustic rural houses. Inhabitants of infested houses are repeatedly exposed to vectors and parasites over many years. In highly endemic villages, a high percentage of the adult population is infected, with the prevalence rising with increasing age. The prevalence of cardiac morbidity also increases with age. An estimated 20% to 30% of T. cruzi –infected individuals eventually develop Chagas cardiomyopathy, but in endemic or previously endemic settings, a much higher percentage of the elderly may have cardiac signs.
Latin America has made substantial progress in decreasing T. cruzi transmission, largely through residual insecticide application to control domestic infestation. The estimated global ChD prevalence declined from 18 million in 1991, when the first regional control initiative began, to approximately 6 million in 2010. The Pan American Health Organization has certified interruption of transmission by domestic vectors in several countries of South America and Central America. T. cruzi serologic screening is conducted in most blood banks in Latin America and the United States, and some countries have systematic screening for congenital ChD. Nevertheless, ChD remains the most important parasitic disease in the Western Hemisphere.
The southern half of the continental United States has established enzootic transmission cycles, with infected vectors and mammalian hosts such as raccoons, opossums, wood rats, and domestic dogs. Nevertheless, the majority of infected residents are Latin American immigrants infected in their home countries, and infected individuals are found in nearly every state. On the basis of the Latin American immigrant population and estimates of prevalence in their home countries, an estimated 300,000 T. cruzi –infected immigrants reside in the United States. Locally acquired vector-borne infection has been documented in a handful of cases over the past 60 years and has been inferred in blood donors for whom acquisition of the infection in Latin America has been ruled out or judged unlikely. Direct assessments of prevalence in the United States are sparse and have been restricted to small-scale surveys or case series in populations chosen because of anticipated high risk (e.g., Latin American immigrants with nonischemic heart disease). Because of low provider awareness, cases of Chagas cardiomyopathy likely go unrecognized, and women at risk for vertical transmission to their infants are not screened. Thus, more work is needed to raise awareness and improve the knowledge base of providers in the United States. In addition, more extensive epidemiologic studies and better diagnostic and treatment availability are required.
- •
ChD is a vector-borne zoonotic disease endemic to the Americas, which could be underdiagnosed if aggressive screening campaigns are not pursued.
- •
Substantial progress has been made in decreasing vector- and blood-borne T. cruzi transmission through residual insecticide application and housing improvement, but there remain 6 million infected people and 70 million at risk for infection in the Americas.
- •
Zoonotic transmission occurs in the southern half of the United States, but T. cruzi –infected migrants from Latin America greatly outnumber those infected locally. Patients with ChD are found in nearly every state of the United States and in other countries outside of the Americas.
III. Pathophysiology Related to Imaging and Clinical Presentation
The pathophysiology of myocardial damage in chronic ChHD is complex and multifactorial. ChHD is an acquired inflammatory cardiomyopathy caused by three key pathologic processes: inflammation, cell death, and fibrosis. A consensus is now emerging that parasite persistence and parasite-driven adverse immune response play a pivotal role in the pathogenesis of ChHD.
Because of these underlying pathogenic mechanisms, a variety of structural and functional cardiovascular abnormalities have been shown in patients with ChHD. Cardiac structural cells affected by the inflammatory process include the myocytes, leading to myocytolysis and contraction band necrosis and irreversible lesions of the specialized conduction system and cardiac neural cells. The progressive destruction of normal cardiac constituents leads to a marked reparative and reactive fibrosis, characterized by a dense interstitial accumulation of collagen that encloses fibers or groups of myocardial fibers. This explains the frequent occurrence of atrioventricular and intraventricular blocks, sinus node dysfunction, malignant ventricular arrhythmias, and sudden death in patients with ChHD. Recent studies in the experimental model of chronic T. cruzi infection have shown that at early stages, the coalescence of focal areas of myocardial inflammation, necrosis, and fibrosis typically results in the appearance of left ventricular (LV) segmental wall motion abnormalities, a hallmark of ChHD. At later stages, these regional derangements gradually cause progressive impairment of global myocardial contractile function. The ultimate consequence of is dilated cardiomyopathy with biventricular dysfunction and congestive HF.
Derangements of the coronary microcirculation, including increased platelet activity, microthrombi, microvascular spasm, and endothelial dysfunction, have been reported in animal models of T. cruzi infection and in studies of humans with ChD. These phenomena precede and may be causally related to the development of segmental wall motion abnormalities. Abnormal reactivity to vasodilator and vasoconstrictor stimuli has also been reported in the epicardial coronary arteries of patients with ChD. Overall, these derangements in the coronary microcirculation are likely to cause ischemic myocytolic necrosis and reparative fibrosis that are clinically expressed as ischemic-like symptoms, electrocardiographic changes, and perfusion defects described in ChHD patients with angiographically normal coronary arteries. In the advanced stages of ChHD, ventricular aneurysms are detected mostly in watershed zones between principal coronary artery branches, such as regions between the left anterior descending and posterior descending coronary arteries and the right coronary and left circumflex coronary arteries, which supply the apex and the basal-posterior wall of the left ventricle, respectively.
Virtually all pathophysiologic aspects of chronic ChHD can be detected using various imaging modalities, which are discussed in the following sections.
IV. Special Features of Electrocardiography and Each Imaging Modality in Relation to ChD
IV.a. Electrocardiography and Continuous Rhythm Monitoring
Electrocardiographic (ECG) abnormalities are often the first indicator of cardiac involvement in ChD. Electrocardiography remains a cost-effective diagnostic test that should be performed routinely once serologic confirmation is obtained. Recent regional guidelines provide a class I recommendation with level of evidence C for the indication of 12-lead electrocardiography in the diagnosis and risk stratification of patients with ChD.
By and large, the acute presentation of ChD is usually mildly symptomatic and manifests as a flu-like event. In approximately 5% of cases, acute myocarditis may clinically manifest with a wide range of ECG abnormalities. The most frequent findings are nonspecific and common to any myocarditis and include sinus tachycardia, diffuse abnormal repolarization, low QRS voltage, and atrioventricular block. With severe myocarditis, higher degrees of atrioventricular block and intraventricular conduction disturbances (bundle branch and fascicular blocks) may occur. In a series of acute Chagas myocarditis cases, ECG alterations were documented in 66% of the patients. Abnormal repolarization was the most common finding (37%), and the most frequent arrhythmia was inappropriate sinus tachycardia (9%), followed by atrial premature complexes (8%). In this series, only 2% developed right bundle branch block. Abnormal ECG findings during the acute phase may have prognostic implications, as reported by Porto in a classic series of patients presenting with acute Chagas myocarditis.
Electrocardiography is instrumental in classifying the stage of disease in patients in the chronic phase of ChD. The lack of ECG abnormalities stages T. cruzi carriers in the indeterminate phase of the disease (stage A; Table 1 ). Normal ECG findings are rare in the presence of moderate or severe LV dysfunction, while a greater number of ECG alterations correlates with worse LV function, especially if left bundle branch block is present. Of note, ECG abnormalities were strongly associated with ChHD in the Retrovirus Epidemiology Donor Study II, with a high negative predictive value (95%) for Chagas cardiomyopathy. This finding suggests that in rural areas with very limited resources, normal ECG findings without other imaging modalities (such as echocardiography) could be sufficient screening in asymptomatic T. cruzi –infected individuals.
The earliest ECG abnormalities of ChHD usually involve the conduction system, manifesting most frequently as right bundle branch block and/or left anterior fascicular block. Second- and third-degree atrioventricular block have also been strongly related with Chagas cardiomyopathy in endemic populations. Sinus node dysfunction may present as episodes of sinoatrial block with bradycardia or ectopic atrial tachycardia ( Figure 3 ). Complex ventricular arrhythmias such as ventricular tachycardia occur even in patients without overt HF but tend to be associated with more advanced stages of ChHD and worse prognosis.
Electrocardiography is also a useful tool for risk stratification. The presence of premature ventricular contractions, increased QT-interval dispersion, low-voltage QRS, QRS fragmentation, and prolonged QRS duration have all been associated with a worse prognosis. Once ECG abnormalities arise, they imply disease progression (stage B; Table 1 ), preceding the appearance of HF symptoms (stages C and D). ECG abnormalities are frequent and related primarily with nonspecific repolarization alterations (30%–40%), right bundle branch block in conjunction with left anterior fascicular block (20%–35%), premature ventricular ectopic beats (5%–10%), and atrial fibrillation (5%–10%). These findings have been recently supported by Echeverría et al. , who by using electrocardiography for Chagas cardiomyopathy staging predicted disease progression as determined by elevation in N-terminal pro–brain natriuretic peptide and high-sensitivity troponin.
Twenty-four-hour ambulatory ECG monitoring (Holter) is recommended in patients with symptoms suggestive of cardiac arrhythmias (palpitations, presyncope, or syncope) or the presence of certain ECG findings, such as sinus bradyarrhythmias (heart rate < 40 beats/min and/or prolonged sinus pauses), second-degree atrioventricular block, or frequent and/or repetitive (bursts of) ventricular extrasystoles.
Holter monitoring may identify patients at risk for sudden death and unmask early signs of cardiac autonomic dysfunction with reduced heart rate variability. In asymptomatic patients or those with rare symptoms, Holter monitoring will have a low diagnostic yield and is usually not routinely indicated. An implantable cardiac monitor may be considered in patients with other markers of risk such as depressed LV or right ventricular (RV) function, regional wall motion abnormalities, or syncope with frequent premature ventricular complexes or palpitations.
In summary, electrocardiography should be performed in all patients identified with positive T. cruzi serology. The rationale for this strategy is based on the cost-effectiveness and wide availability of this diagnostic test, in addition to high negative predictive value to rule out cardiomyopathy in T. cruzi –infected individuals. Electrocardiography serves two purposes: staging and prediction of disease progression. The appropriate timing and frequency for performing electrocardiography during follow-up remains debatable and is not evidence based. It seems reasonable that in individuals with a normal baseline ECG findings, follow-up ECG testing may be performed at least every 5 to 10 years. Further screening with biomarkers and cardiac imaging may be selectively performed, depending on baseline ECG findings. Patients with frequent premature ventricular complexes, nonsustained ventricular tachycardia, and other bradytachyarrhythmias identified by Holter monitoring should undergo further assessment of LV systolic function.
IV.b. Echocardiography
IV.b.i. M-Mode and Two-Dimensional Echocardiography
ChHD is an inflammatory cardiomyopathy that may affect the myocardium in a segmental or regional manner. On imaging, the heart may appear normal, have localized segmental ventricular abnormalities (wall motion, thinning, aneurysms, etc.), or manifest as a globally dilated cardiomyopathy with associated valvular heart disease (mainly functional mitral and tricuspid regurgitation). In general, echocardiographic evaluation should be performed as suggested by the American Society of Echocardiography (ASE) guidelines on chamber quantification, with a special emphasis on LV function and morphology, RV function, and valvular disease. As previously mentioned, the absence of ECG abnormalities mostly rules out significant cardiomyopathy. However, it is reasonable to perform at least a single echocardiographic examination (baseline evaluation) on every patient with positive serology for ChD and repeat during follow-up if the ECG findings become abnormal to document disease progression ( Table 1 ). Patients with symptomatic ChHD (HF) may present with predominantly hypokinetic, dilated left ventricles with diminished LV ejection fraction (LVEF), or biventricular dilatation ( Figure 4 ). Although infrequent, even asymptomatic subjects may display subtle abnormalities by two-dimensional (2D) and three-dimensional (3D) echocardiography, such as small aneurysms or wall motion abnormalities.
Global LV Function
Initial rural surveys using basic M-mode and 2D echocardiography were useful for clinical staging by estimating anatomic and functional damage and assessing LV function. Current ASE guidelines recommend routine clinical evaluation using 2D and 3D echocardiography to estimate LV, RV, left atrial (LA) and right atrial volumes and dimensions and for assessment of LV and RV function. Global LV systolic function should be addressed on 2D echocardiography by calculation of LVEF through the biplane method of disks (the Simpson rule). The endocardial border should be traced at the interface of the compacted myocardium and the LV cavity at end-systole and end-diastole in the apical four- and two-chamber views. Although the accuracy of LV volumes and LVEF is higher when using 3D echocardiography (which is therefore preferred whenever available), 2D echocardiography has the advantage of easiness and wider availability. However, the presence of apical LV aneurysms present a challenge to the use of the method of disks, as apical aneurysms frequently cannot be included within the ultrasound field ( Figure 5 ).
Regional Wall Motion Abnormalities
LV segmental abnormalities are common in ChHD at any stage of the disease. These are located mainly at the LV apex ( Figure 6 , Videos 1 and 2, available at www.onlinejase.com ) and inferior and inferolateral walls ( Figures 7 and 8 ) but may also affect other LV or RV segments. Technically, it is important to perform a comprehensive examination from multiple windows, as wall motion abnormalities should be demonstrated in at least two different views to avoid false-positive results. The use of ultrasound contrast agents for LV opacification ( Figure 9 ) and wall motion evaluation is recommended when images are suboptimal in at least two contiguous segments. In addition, contrast could be particularly useful for the detection of small aneurysms and thrombus, typical of ChHD. In a review of 2D echocardiographic series of patients with ChHD, among 920 asymptomatic patients with mild cardiac damage, the prevalence of LV aneurysm was 8.5%, while it increased to 55% in patients with more advanced cardiac disease. Similarly, LV apical abnormalities had a low prevalence in those with normal ECG findings but increased to 24% in those with abnormal ECG findings. Other common contractile abnormalities involve the inferolateral or inferior walls, with prevalence of up to 23% in symptomatic patients.
Valvular Disease
A comprehensive evaluation in patients with ChD should include careful examination of the cardiac valves. Two-dimensional echocardiography is used to evaluate valvular and subvalvular structure and, together with a thorough Doppler examination, provide a good understanding of the severity and etiology of different valvular diseases and dysfunction. Functional incompetence of the mitral and tricuspid valves is common as ChHD advances ( Figure 10 ). Ventricular remodeling with progressive dysfunction, dyssynchrony, valvular annular dilation, tethering of the subvalvular apparatus, fibrosis, and atrial enlargement may induce various degrees of valve dysfunction. An understanding of these alterations will help in determining the need and proper strategy for therapeutic interventions.
IV.b.ii. Three-Dimensional Echocardiography
Cardiac chambers are 3D structures with complex anatomy and variable shape. Therefore, the accuracy of 2D echocardiography for evaluation of cardiac structure, shape, and dimensions is limited, as it requires some degree of reconstruction and geometric assumptions. Three-dimensional echocardiography, on the other hand, allows visualization of cardiac chambers in their entirety without geometric assumptions. Creation of 3D echocardiographic images requires specialized transducers for acquisition of a volume (pyramid) of data rather than a slice (2D echocardiography). The 3D volume could be acquired through a single heartbeat or by stitching together smaller volumes in consecutive beats. Although 3D echocardiography has significant advantages over 2D echocardiography, as mentioned above, there are limitations, related mostly to lower temporal and spatial resolution or stitching artifact with multibeat acquisition. Nevertheless, by direct visualization of the entire left ventricle, 3D echocardiography avoids foreshortening of the left ventricle from the apical windows and facilitates measurement of LV volumes and LVEF by direct endocardial contour tracing, rather than assumptions of LV shape from 2D apical views with the single or biplane method of disks ( Figure 11 ). Three-dimensional echocardiography is currently well validated compared with other 3D imaging techniques such as CMR and cardiac CT. This concept also applies to visualization and volume measurements of other cardiac chambers, such as the left atrium and right ventricle ( Figure 12 ). As with patients with other forms of cardiomyopathy, 3D echocardiography should be used in patients with ChD to evaluate cardiac chamber size and ventricular function. Currently, LV volumes and LVEF can be measured using a variety of semiautomated software that are less time-consuming and improve reproducibility. In patients with ChHD presenting with HF, it is important to have information concerning RV size and function, which is particularly challenging with 2D echocardiography. The use of 3D echocardiography allows an accurate analysis of RV volumes and RV ejection fraction (RVEF; Figure 12 ). In addition, the use of 3D or 3D-derived 2D images (biplane, Xplane, etc.) could help in detecting small LV aneurysms that would otherwise be overlooked by 2D echocardiography because of foreshortening.
The analysis of mitral regurgitation severity in patients with chronic Chagas cardiomyopathy should include 3D echocardiography as part of the comprehensive mitral valve evaluation to assess the structure and morphology of the leaflets and subvalvular apparatus. Although a dilated annulus with tethering of the leaflets from a dilated left ventricle (functional or secondary mitral regurgitation) is the most common finding in ChHD, the examination should evaluate other coexisting valvular abnormalities. Therefore, careful attention should be paid to valvular and subvalvular function and structure to evaluate for presence, location, and extent of prolapse, redundant tissue, clefts, rheumatic changes, annular dimensions, cusp separation, and other abnormalities that are not specific for ChHD. Color 3D echocardiography may be used to identify multiple or noncircumferential jets, measure the vena contracta area, or, in combination with continuous-wave Doppler echocardiography, calculate regurgitant orifice area or regurgitant volume and fraction using the proximal isovelocity surface area method. Comprehensive analysis with information derived from 2D, 3D, and Doppler echocardiography may be useful for the prediction of success in future attempts at mitral valve repair (surgical or percutaneous), similar to other etiologies of functional mitral regurgitation.
IV.b.iii. Strain and Speckle-Tracking Echocardiography
Myocardial deformation imaging is a relatively new technique for quantitative assessment of myocardial contractility. Strain is a measure of myocardial deformation, defined as the change in length of the myocardium relative to the original length. Strain rate is the rate of change in strain. Myocardial deformation imaging with echocardiography can be measured using Doppler tissue imaging and 2D and 3D speckle-tracking echocardiography ( Figures 13 and 14 ). Tissue Doppler–derived strain has several limitations, particularly in relation to angle dependency and noise interference. Therefore, strain measurement based on speckle-tracking, which is not angle dependent, has become a method of choice to assess myocardial deformation.
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