Open access peer-reviewed chapter
Abstract
This chapter provides a comprehensive review of the pivotal role advanced multimodality cardiovascular imaging plays in the diagnosis and management of myocarditis and pericarditis. It highlights the unique strengths and limitations of key imaging modalities, including echocardiography, cardiac magnetic resonance imaging (CMR), cardiac computed tomography (CCT), and nuclear imaging, demonstrating their contributions to informed clinical decision-making. Additionally, the chapter explores emerging imaging techniques and highlights future research directions, offering valuable insights into their potential to enhance the understanding and management of these inflammatory conditions. By adopting an evidence-based approach, this chapter seeks to equip clinicians and researchers with the knowledge and tools necessary to optimize patient outcomes.
Keywords
- pericarditis
- myocarditis
- cardiovascular diseases
- cardiac imaging
- inflammation
1. Introduction
Myocarditis and pericarditis are inflammatory diseases of the myocardium and pericardium, respectively. They present with a broad spectrum of clinical manifestations that can range from mild, self-limiting symptoms to life-threatening complications such as heart failure, obstructive shock, arrhythmias, and sudden cardiac death [1, 2]. Timely and accurate diagnosis is paramount to improving patient outcomes, particularly given the considerable overlap in clinical presentations with other cardiovascular and systemic diseases.
Advancements in cardiovascular imaging have transformed the diagnostic landscape for myocarditis and pericarditis. Multimodality imaging now facilitates noninvasive assessment of the structural, functional, and tissue characteristics of the myocardium and pericardium. While echocardiography remains the cornerstone of initial evaluation, advanced imaging techniques such as cardiac magnetic resonance imaging (CMR), cardiac computed tomography (CCT), and nuclear cardiac imaging—particularly positron emission tomography (PET)—offer deeper insights into disease pathophysiology and play a pivotal role in guiding therapeutic strategies.
This chapter explores the evolving role of advanced multimodality cardiovascular imaging in the diagnosis and management of myocarditis and pericarditis. It examines the unique capabilities and limitations of each imaging modality, emphasizing their integration into clinical practice. Additionally, the chapter highlights emerging imaging techniques and future directions, underscoring their potential to deepen our understanding of these complex conditions. Through a comprehensive review, this chapter aims to equip clinicians and researchers with practical insights to optimize the care of patients with myocarditis and pericarditis.
2. Phenotypes and genotypes
The study of myocarditis and pericarditis encompasses a wide range of clinical manifestations (phenotypes) and underlying genetic factors (genotypes). This dual perspective is crucial for accurate diagnosis, effective management, and potential future therapies for these inflammatory heart conditions.
2.1 Phenotypes of myocarditis
The clinical manifestations of myocarditis vary widely, influenced by the histological severity, stage at presentation, and etiology of the disease. Myocarditis can present as acute, subacute, chronic, or fulminant [3]. Mild symptoms include sharp, angina-like chest pain, fatigue, generalized weakness, and reduced exercise tolerance, and severe presentations may include heart failure and arrhythmias, with complications such as dilated cardiomyopathy, cardiogenic shock, and sudden cardiac death [4, 5].
2.2 Genotypes of myocarditis
Genetic predisposition plays a significant role in the susceptibility and clinical course of myocarditis.
2.2.1 Genetic variations
Structural protein mutations: Mutations in structural proteins, such as Titin (TTN) and Dystrophin, result in a defective myocardium that is more susceptible to inflammation and damage, especially following insults like viral infections. These mutations are significant because in one study, 22% of patients with suspected myocarditis possessed pathogenic variants of cardiac related genes [6].
Immune response gene variants: Specific single nucleotide polymorphisms (SNPs) in immune-related genes, such as Toll-like receptor 3 (TLR3), have been linked to increased susceptibility to viral myocarditis [7].
Pathogenic mutations: Variants in the HLA-DR4 gene have been associated with heightened inflammatory responses in myocarditis [8].
2.3 Phenotype of pericarditis
Pericarditis, characterized by inflammation of the pericardial sac, displays diverse phenotypes depending on its etiology, symptom severity, and clinical features. The most common symptoms include sharp, pleuritic chest pain alleviated by sitting up or leaning forward, and may be accompanied by a pericardial friction rub on auscultation [2, 9]. Systemic symptoms such as low-grade fever, general malaise, and chills may also be present, and further complications include cardiac tamponade and constrictive pericarditis, which can result in hemodynamic compromise and heart failure from fibrotic pericardial changes, respectively [2, 10].
2.4 Genotypes of pericarditis
While the genetic underpinnings of pericarditis are less understood than those of myocarditis, emerging evidence highlights potential genetic contributors.
Interleukin-1 cytokine variants: Variants within the IL-1 gene locus may modulate inflammatory responses, with some conferring protection against pericarditis [11].
Mutations in immune response genes: Genetic alterations, such as those affecting the NLRP12 gene, have been implicated in recurrent pericarditis, pointing to a role for innate and adaptive immune dysregulation [12].
3. Clinical pathophysiology
The pathophysiology of myocarditis and pericarditis is diverse, with overlapping features, and the conditions often co-occur as myopericarditis. While myocarditis primarily affects the myocardium, pericarditis involves inflammation of the protective pericardial sac. Both conditions share common triggers and pathophysiologic mechanisms.
Myocarditis is most often caused by viral infections, including coxsackievirus, human immunodeficiency virus (HIV), Epstein-Barr virus (EBV), and hepatitis C virus (HCV), which directly injure cardiomyocytes. The progression of viral myocarditis typically occurs in three phases: acute, autoimmune, and chronic. The acute phase begins with an insult to myocardial tissue, activating the innate immune system and leading to the release of pro-inflammatory cytokines and the recruitment of immune cells like neutrophils, macrophages, and natural killer cells. It is followed by the autoimmune phase, which is driven by molecular mimicry between viral antigens and myocardial proteins, triggering an amplified humoral and cellular immune response, ultimately resulting in fibrosis [4, 13, 14]. In the setting of a regulated immune response, the infection resolves, and the inflammation subsides, limiting further myocardial damage. If the immune response is dysregulated, however, prolonged autoimmune inflammation may lead to fulminant myocarditis [15]. In the chronic phase, patients achieve either full recovery or progression to chronic dilated cardiomyopathy from irreversible myocardial remodeling [14].
Pericarditis involves inflammation of the pericardium due to infectious, autoimmune, or traumatic etiologies. The inflammatory response leads to a cascade of pathological events, including the release of pro-inflammatory cytokines, particularly IL-1, and activation of the innate immune system, which results in increased vascular permeability and extravasation of inflammatory cells and fluid into the pericardial sac. IL-1 plays a pivotal role in pathogenesis, supported by the efficacy of IL-1 inhibitors in treatment, and severe effusion can result in cardiac tamponade or constrictive pericarditis [2, 16].
Both myocarditis and pericarditis highlight the delicate balance between protective immune responses and pathological tissue injury. While the immune response is essential for eliminating infectious agents and initiating repair, excessive or dysregulated inflammation can cause significant damage, leading to severe complications. This underscores the importance of timely diagnosis and targeted interventions to mitigate immune-mediated injury and optimize patient outcomes.
4. Biomarkers and electrocardiographic (ECG) features in myocarditis and pericarditis
The diagnostic evaluation of myocarditis and pericarditis relies on a combination of clinical, biochemical, and ECG findings to identify myocardial or pericardial involvement and distinguish these conditions from other cardiac etiologies.
In myocarditis, cardiac biomarkers such as troponin T and troponin I are elevated in at least 50% of patients, reflecting myocardial injury or necrosis. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels are typically elevated as well, indicating an active inflammatory process. Leukocytosis is often present, and eosinophilia may also be noted, particularly in eosinophilic myocarditis. While not essential for diagnosing myocarditis, ECG aids in ruling out other cardiac etiologies and detecting arrhythmias such as atrioventricular (AV) blocks and ventricular ectopy. Certain ECG findings, such as ST-segment elevations, can mimic acute coronary syndromes [3, 17].
Similarly to that seen in myocarditis, inflammatory markers such as ESR and CRP are typically elevated in pericarditis, reflecting systemic inflammation. ECG findings often include diffuse concave ST-segment elevations and PR-segment depressions, and reciprocal ST-segment depressions are also commonly observed in lead aVR (Figure 1) [18].
Figure 1.
An ECG showing normal sinus rhythm, diffuse PR-segment depressions, and diffuse ST-segment elevations consistent with both myocarditis and pericarditis.
5. Imaging modalities
5.1 Echocardiography
Echocardiography is a cornerstone diagnostic and management tool for myocarditis and pericarditis, offering detailed, real-time insights into cardiac structure and function in these inflammatory conditions.
In myocarditis, echocardiography is the initial imaging modality of choice as it provides critical information on cardiac function, wall motion, and the presence of effusions. A key finding is global or regional left ventricular (LV) dysfunction, as evidenced by reduced ejection fraction (EF) and wall motion abnormalities such as hypokinesis, akinesis, or dyskinesis [3, 19]. Echocardiography also helps in identifying complications such as intracardiac thrombi in the setting of regional wall motion abnormalities and pericardial effusion, as well as excluding alternative causes of presenting symptoms, guiding management decisions [19]. However, while invaluable for assessing functional and structural changes, echocardiography lacks the sensitivity and specificity required to characterize myocardial inflammation definitively.
Similarly, in pericarditis, echocardiography is the primary tool for assessing pericardial thickening, which is indicative of chronic inflammatory changes. It is widely available, cost-effective, and can be performed urgently. Echocardiography can also detect the presence and quantify the magnitude of a pericardial effusion and, therefore, help its hemodynamic effects (Figures 2 and 3) [18, 21].
Figure 2.
Transthoracic echocardiography showing the following findings: (a) M-mode with large pericardial effusion and right ventricular (RV) diastolic collapse. (b) The parasternal long-axis view is consistent with RV diastolic collapse. (c) The collapse of the right atrium (d) Mitral valve inflow velocity with respiratory variation greater than 25% [20].
Figure 3.
ECG showing normal sinus rhythm and low-voltage QRS in the setting of a pericardial effusion post-myocarditis.
5.2 Cardiac magnetic resonance imaging
Cardiac MRI (CMR) has emerged as an indispensable tool for diagnosing and managing myocarditis and pericarditis, offering unmatched tissue characterization and diagnostic precision through advanced imaging techniques.
Guided by the updated Lake Louise Criteria, which utilizes T1/T2 mapping and late gadolinium enhancement (LGE), CMR is considered the gold standard noninvasive modality for diagnosing myocarditis, even in patients with biopsy-proven pathology [19]. T1 mapping quantifies longitudinal relaxation times, reflecting myocardial inflammation and fibrosis, and elevated native T1 values are indicative of acute myocardial injury, whereas post-contrast T1 mapping assesses extracellular volume (ECV), a marker of diffuse fibrosis.
In pericarditis, T1 mapping can detect concurrent pericardial inflammation, while T2 mapping quantifies myocardial water content, directly measuring edema. Elevated T2 values are highly sensitive to myocardial inflammation in myocarditis and pericardial edema in pericarditis, and excel in detecting diffuse changes, which are often missed by conventional T2-weighted imaging. Notably, the diagnostic accuracy of CMR in myocarditis is highest when performed within the first 2–3 weeks of symptom onset, as myocardial edema diminishes over time.
LGE identifies areas of myocardial damage through gadolinium accumulation in regions of necrosis, inflammation, or fibrosis. In myocarditis, LGE typically presents as a nonischemic, patchy distribution in the sub epicardium or mid-wall layers [14]. In pericarditis, LGE highlights inflamed pericardial tissue and helps differentiate acute pericarditis from chronic constrictive forms [22].
The combined use of T1/T2 mapping and LGE offers complementary insights, with T1/T2 mapping excelling in detecting diffuse disease and LGE providing superior spatial resolution for focal injury. Together, these techniques enhance diagnostic accuracy, facilitate risk stratification, and guide therapeutic decisions, transforming the management of myocarditis and pericarditis [1, 18]. Limitations include practical constraints, including high cost, limited accessibility, contraindications in patients with renal impairment or implanted devices, and reduced sensitivity in chronic myocarditis (Figures 4–6) [24, 25].
Figure 4.
Diffuse inflammation is seen in myocarditis.
Figure 5.
CMR of a biopsy-proven autoimmune myocarditis in HIV-associated dilated cardiomyopathy showing long-axis images (panel A = diastole, panel B = systole) with a severely dilated and dysfunctional LV recovering from an EF of 20% to an EF of 45% after 4 months of steroid therapy (panel G = diastole, panel H = systole), T2 short-tau inversion recovery images (T2-STIR) in the midventricular short-axis showing subepicardial edematous imbibition of the inferolateral segment of the LV myocardium (panel C, arrows) and thickening of pericardial layers with a minimal amount of effusion (panel C, arrowheads) that correspond to LGE with the same distribution (panel D, arrows), and T2w-STIR LGE images (panel I and L) that show complete regression of tissue edema and late enhancement at a 4-month follow-up [23].
Figure 6.
CMR showing acute viral inflammatory pericarditis in a 15-year-old girl, with T2-weighted short-tau inversion recovery spin-echo CMR (a), LGE CMR in horizontal long-axis (b), short-axis (c), and vertical long-axis plane (d). There is diffuse hyperintense appearance of the pericardium on T2-weighted short-tau inversion recovery spin-echo CMR (panel a, arrows) and strong, homogeneous enhancement of the entire pericardium following gadolinium administration (panels b, c, d, arrows) [23].
CMR also is helpful in solidifying the diagnosis of restrictive versus constrictive pericarditis as a complication after myocarditis and pericarditis (Figure 7).
Figure 7.
CMR of constrictive pericarditis. A: Right ventricular vertical long-axis image showing circumferential pericardial thickening and an enlarged inferior vena cava; B: short-axis image showing circumferential pericardial thickening, encysted pericardial effusion; C: four-chamber image showing focal pericardial thickening in front of the right ventricle lateral wall, an encysted pericardial effusion, an enlarged right atrium; D: short-axis image showing focal pericardial thickening in front of the left ventricular inferior and lateral walls; E: short-axis tagging image showing focal pericardial thickening and adherence in front of the left ventricular lateral wall; F: four-chamber late gadolinium enhancement image showing enhancing pericardium [23].
5.3 Computed tomography (CT)
CT is often used in ruling out other conditions and for diagnosing pericarditis rather than myocarditis. It helps visualize pericardial thickening, calcification, and effusion and is particularly useful in cases of suspected constrictive pericarditis (Figure 8) [18, 21].
Figure 8.
A chest CT revealing dense calcifications (arrow) along the atrioventricular groove, and pleural effusion [26].
5.4 Nuclear imaging
18F-Fluorodeoxyglucose Positron Emission Tomography (PET) provides robust information on myocardial inflammation and pericarditis. Increased glucose uptake, suggestive of inflammatory activity, helps differentiate active inflammation from scarring secondary to prior viral infections (Figure 9) [1].
Figure 9.
Myocarditis. A: short-axis delayed enhancement MRI in a patient with acute onset chest pain and elevated enzymes shows mid-myocardial enhancement in the mid-lateral and inferior segments (arrow). B: Fused PET/MR image obtained after glucose diet shows patchy areas of intense uptake in the lateral and inferior wall, indicative of active inflammation [27].
5.5 Hybrid techniques
The combination of CT, PET, CMR with traditional echocardiography has emerged as valuable tools in the diagnosis and management of both pericarditis and myocarditis. They enhance precision in diagnosing active inflammation and assessing the extent of myocardial involvement, enabling improved risk stratification and therapeutic strategies [28].
6. General considerations and guidelines
For myocarditis, the American College of Radiology (ACR) recommends echocardiography as the initial imaging modality for assessing ventricular function, regional wall abnormalities, and pericardial effusion, and recommends CMR as the next imaging modality should echocardiography findings remain equivocal, as it is the gold standard for noninvasive imaging due to its superior ability to characterize tissue and assess cardiac function [29]. The updated Lake Louise Criteria in CMR is particularly effective for distinguishing myocarditis from other cardiomyopathies and ischemic heart disease, while also providing prognostic information [30]. The presence of cardiac biomarkers such as troponins, along with LV dysfunction, should be incorporated into management decisions, including the potential need for endomyocardial biopsy. Serial imaging can be used to monitor disease progression and assess response to treatment.
For pericarditis, echocardiography and CMR retain the same roles. CMR or cardiac CT are indicated in complex cases where additional anatomic detail is required, such as when there is suspicion of constrictive pericarditis or significant pericardial effusion potentially requiring intervention [18, 31]. Accurate diagnosis of pericarditis involves combining imaging findings with clinical history, physical examination, and laboratory results. Imaging findings often guide treatment strategies, such as pericardiocentesis or surgical intervention in cases of significant effusion or constriction.
Overall, a multimodality approach to imaging is recommended for both myocarditis and pericarditis.
7. Conclusion
Echocardiography, along with advanced imaging modalities such as CMR and cardiac CT, is cornerstones in the diagnosis and management of myocarditis and pericarditis. These imaging techniques are integral for evaluating cardiac function, guiding therapeutic decisions, and enabling the early detection of complications. As advancements in imaging technology progress, their contribution to refining treatment strategies and improving patient outcomes will continue to expand, reinforcing their pivotal role in modern cardiovascular care.
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