Multimodality Cardiovascular Imaging in Long COVID

Marija Zdravkovic; Viseslav Popadic; Maja Popovic; Marija Brankovic; Milica Brajkovic; Jelica Bjekic-Macut; Tamara Trumpic; Branislava Daskalovic and
Planinka Zafirovska

doi:10.5772/intechopen.1015784

Abstract

Long COVID (LC) is a multisystem condition defined by persistent symptoms lasting at least three months after acute SARS-CoV-2 infection, affecting 10–30% of individuals. Cardiovascular manifestations – including chest pain, dyspnea, palpitations, and exercise intolerance – are frequent, and multimodality imaging has become central to the assessment of these patients, providing detailed structural, functional, and tissue-level information. This review summarizes the role of echocardiography (ECHO), cardiac magnetic resonance (CMR), coronary computed tomography angiography (CCTA), nuclear imaging, and electrocardiographic (ECG) monitoring in evaluating cardiovascular involvement in LC. Imaging findings range from subtle myocardial or right ventricular dysfunction, tissue changes such as myocardial edema or fibrosis, microvascular impairment, and pericardial involvement, to cases with minimal or no detectable structural abnormalities. Multimodality imaging guides diagnosis, phenotyping, risk stratification, and individualized follow-up, forming part of structured symptom-oriented clinical pathways. Psychosocial factors also influence how patients experience symptoms and diagnostic testing. Many individuals with persistent symptoms develop anxiety related to possible cardiac disease or the results of imaging examinations. Clear explanation of the purpose, safety, and expected findings of each imaging test can reduce patient anxiety, improve cooperation during examinations, and help contextualize borderline imaging abnormalities. Despite growing evidence, the prognostic significance of many imaging abnormalities remains uncertain. Longitudinal, outcome-based studies are needed to standardize imaging protocols, clarify clinical implications, and refine management. A multimodality imaging-guided, multidisciplinary, and psychosocially informed approach is essential for optimizing cardiovascular evaluation and care in patients with LC.

Keywords

cardiac magnetic resonance
myocardial strain
computed tomography coronarography
echocardiography
diagnosis

Author Information

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Marija Zdravkovic *
- UHMC Bezanijska Kosa, Belgrade, Serbia
- Faculty of Medicine, University of Belgrade, Belgrade, Serbia
Viseslav Popadic
- UHMC Bezanijska Kosa, Belgrade, Serbia
Maja Popovic
- UHMC Bezanijska Kosa, Belgrade, Serbia
Marija Brankovic
- UHMC Bezanijska Kosa, Belgrade, Serbia
- Faculty of Medicine, University of Belgrade, Belgrade, Serbia
Milica Brajkovic
- UHMC Bezanijska Kosa, Belgrade, Serbia
- Faculty of Medicine, University of Belgrade, Belgrade, Serbia
Jelica Bjekic-Macut
- UHMC Bezanijska Kosa, Belgrade, Serbia
- Faculty of Medicine, University of Belgrade, Belgrade, Serbia
Tamara Trumpic
- UHMC Bezanijska Kosa, Belgrade, Serbia
Branislava Daskalovic
- Kirei Medicine, Belgrade, Serbia
Planinka Zafirovska
- UHMC Bezanijska Kosa, Belgrade, Serbia
- Faculty of Medical Sciences, Goce Delcev University, Stip, North Macedonia

*Address all correspondence to: sekcija.kardioloska@gmail.com

1. Introduction

Long COVID (LC) is defined as a chronic condition that occurs after SARS-CoV-2 infection and is present for at least 3 months [1]. Available data suggest that approximately 10–30% of individuals infected with SARS-CoV-2 experience persistent symptoms beyond the acute phase, although prevalence estimates vary widely depending on study design [2]. Higher risk has been consistently observed among hospitalized patients, those with severe acute disease, older age, female sex, and individuals with preexisting comorbidities such as obesity, diabetes mellitus, and cardiovascular disease. Nevertheless, a significant proportion of affected individuals were previously young and healthy, highlighting the unpredictable nature of the syndrome. Symptoms may persist for 12 months or longer, contributing to prolonged functional impairment and significant socioeconomic consequences [3]. Cardiovascular, neurological, and musculoskeletal symptoms are the most frequently reported manifestations of LC and can significantly affect patients’ quality of life and future prognosis [4, 5]. It has been shown that patients with LC syndrome have a 1.6 times higher risk of new-onset cardiovascular disease of any type [6]. Standard clinical evaluation often reveals minimal or no abnormalities, complicating diagnosis and management.

Post-COVID syndrome is characterized by the involvement of multiple organ systems, reflecting persistent inflammation, immune dysregulation, endothelial dysfunction, microvascular injury, autonomic imbalance, and potential viral persistence [7]. These mechanisms often induce subclinical conditions that are difficult to diagnose and evaluate with routine diagnostic modalities, especially when structural changes are subtle or functional impairment is exercise-related [8]. This is why multimodality imaging plays a central role in the assessment of patients with suspected LC predominantly in those with cardiac involvement. The evaluation must provide structural, functional, and tissue-level information to allow accurate phenotyping, exclusion of alternative diagnoses, risk stratification, and guidance of individualized management strategies [9].

Post-COVID or LC care is most effectively delivered through centralized units or virtual hubs that coordinate assessment and management across multiple specialties [10]. Central coordination allows for standardized intake, minimizes overexamination, and ensures appropriate referral to specialist services based on clinical phenotype and symptom burden. Risk stratification aims to identify patients requiring urgent evaluation, such as those with progressive dyspnea, chest pain, syncope, severe neurological deficits, or evidence of organ dysfunction [11]. Digital tools and previsit questionnaires can support triage by quantifying symptom severity, functional limitation, and quality of life. Early involvement of physiotherapy, occupational therapy, and, where appropriate, speech and cognitive rehabilitation is important, particularly for patients with fatigue, exercise intolerance, and neurocognitive symptoms [12].

Long COVID is a multisystem condition in which cardiovascular symptoms frequently coexist with respiratory, neurological, gastrointestinal, and autonomic disturbances. The overlap and interaction of symptoms such as dyspnea, chest pain, palpitations, fatigue, cognitive impairment, and sleep disruption make assessment complex and require a holistic, multidisciplinary approach. Equally important is the psychological component: Anxiety, fear of reinjury, postinfection trauma, and uncertainty about long-term prognosis significantly shape the patient’s perception of symptoms, health-seeking behavior, and response to clinical findings. Misinterpretation of benign physiological sensations or imaging results may intensify symptom burden and drive unnecessary healthcare utilization. For these reasons, a coordinated framework integrating cardiology, radiology, autonomic and multisystem evaluation, psychiatry, and clinical psychology is essential. Such an approach improves diagnostic accuracy, reduces patient distress, and supports more effective long-term management.

Given the fluctuating and prolonged nature of symptoms, structured reassessment allows for the monitoring of recovery, the adjustment of treatment strategies, and the timely escalation of care. In summary, a multidisciplinary approach, integrated follow-up, and dedicated post-COVID wards are important in both diagnostic pathways and therapeutic protocols, ultimately improving patient care in this complex and evolving clinical entity.

The following overview on the role of multimodality imaging in LC is primarily based on the experience of a single center, treating both patients with acute COVID infection and LC syndrome. University Hospital Medical Center Bežanijska Kosa (Belgrade, Serbia) provided extensive care during the COVID-19 pandemic between 2020 and 2023, managing more than 61,000 patients in the outpatient setting and hospitalizing over 8,000 individuals. Clinical services were organized to ensure continuous 24-hour care, early risk stratification, and intensified monitoring for patients at increased risk of developing severe forms of the disease. Laboratory assessments and, when necessary, therapeutic adjustments were performed on a daily basis, enabling timely intervention and contributing to the prevention of complications and progression to severe clinical presentations. The overall in-hospital mortality rate was comparable to that reported in large international observational studies conducted at leading tertiary centers.

Following the acute phase of the pandemic, and in light of the substantial number of treated patients, many of whom reported persistent symptoms months after the initial infection, a dedicated post-COVID outpatient clinic was established. The primary objective of this clinic was the structured evaluation and management of patients with LC syndrome. The diagnostic algorithm incorporated standardized initial assessments, including electrocardiography (ECG), chest radiography, pulmonary function testing, and comprehensive laboratory analyses. Based on clinical presentation and preliminary findings, patients were referred for more specific diagnostic procedures. Targeted therapeutic strategies were subsequently implemented according to the results obtained.

For patients requiring multiple diagnostic evaluations, a day-hospital service was organized to facilitate comprehensive assessment within a single day. This approach enabled detailed evaluation of individuals with pronounced symptoms or initial findings suggestive of cardiovascular and/or pulmonary dysfunction, thereby optimizing diagnostic efficiency and ensuring the timely initiation of appropriate management.

2. Pathophysiology of LC

Long COVID, also referred to as postacute sequelae of SARS-CoV-2 infection (PASC), encompasses a heterogeneous range of symptoms that persist for weeks to months following acute infection. Even five years after the onset of the COVID-19 pandemic, the etiology, diagnostic criteria, and optimal management of LC remain incompletely understood. [13]

The cardiovascular system is among the most frequently affected, with common patient-reported symptoms including chest pain, fatigue, and palpitations (Figure 1). The COVID Symptoms Study demonstrated a high prevalence of cardiac symptoms among individuals with LC, with most patients reporting symptom onset approximately three to four weeks after acute infection. Furthermore, a systematic review of 25 studies identified chest pain as the most prevalent cardiovascular manifestation, reported by up to 89% of participants [14].

Figure 1.
Frequent cardiovascular symptoms in long COVID patients.

Globally, the prevalence of LC is estimated to be approximately 36%, with regional peaks of up to 51% in South America. Identified risk factors include older age, female sex, severe acute SARS-CoV-2 infection, low socioeconomic status, and unvaccinated status [7, 15, 16].

The precise mechanisms underlying cardiovascular involvement in LC remain unclear. However, accumulating evidence suggests a multifactorial pathophysiology involving genetic susceptibility, direct viral toxicity, persistent inflammation, endothelial dysfunction, and autoimmune processes [17–19]. SARS-CoV-2 gains entry into host cells via the angiotensin-converting enzyme 2 (ACE2) receptor, which is widely expressed in the heart, lungs, kidneys, and vascular endothelium [20]. Viral entry into endothelial cells through ACE2 is thought to induce vascular inflammation, oxidative stress, and sustained microvascular dysfunction that may persist for months or even years following the initial infection. Histopathological findings have demonstrated viral elements within endothelial cells, accumulation of inflammatory infiltrates, and evidence of endothelial and immune cell death [1, 21].

Emerging evidence identifies endothelial dysfunction as the most important feature of COVID-19 pathophysiology [19, 21–23]. Endothelial injury appears central to both acute and postacute disease. Persistent endothelial activation promotes microvascular inflammation, oxidative stress, increased vascular permeability, platelet activation, and microthrombosis, all of which may contribute to persistent cardiovascular symptoms after SARS-CoV-2 infection.

Histopathological studies have demonstrated endothelial inflammation and immune cell infiltration, supporting sustained microvascular dysfunction beyond the acute phase [22]. This may explain persistent chest pain despite unobstructed epicardial coronary arteries and supports the role of stress perfusion cardiac magnetic resonance (CMR) and coronary computed tomography angiography (CCTA) to evaluate microvascular ischemia, further highlighting endothelial dysfunction as a potential therapeutic target.

There is growing evidence that LC is characterized by persistent activation of chronic inflammatory pathways [24, 25]. In some patients, it is characterized by ongoing immune dysregulation, including upregulation of inflammatory pathways (e.g., interleukin [IL]-6 signaling, complement activation, Janus kinase–signal transducer and activator of transcription (JAK-STAT) signaling) and evidence of T-cell exhaustion. Elevated proinflammatory cytokines and altered monocyte activation profiles have been reported months after acute infection [26, 27]. Autoimmune mechanisms may also contribute, with increased autoantibody prevalence in subsets of patients [28–30]. Chronic myocardial low-grade inflammation can be detected using T1 and T2 mapping.

Direct myocardial injury represents another proposed mechanism. Viral RNA and viral particles have been identified in myocardial tissue, raising the possibility of direct cytotoxic myocardial injury. Persistent viral antigen detection in extracardiac tissues suggests that viral reservoirs may contribute to ongoing immune activation [31].

Autonomic imbalance, likely mediated by immune-related nerve injury and chronic inflammation, is increasingly recognized in LC [32–34]. Postural orthostatic tachycardia syndrome (POTS) is frequently reported and may account for palpitations, exercise intolerance, and fatigue. In this setting, structural imaging may be normal, emphasizing the importance of integrating imaging with functional assessment (e.g., tilt testing, ambulatory ECG monitoring) and avoiding unnecessary repeated structural imaging when dysautonomia is suspected.

Emerging data suggest mitochondrial impairment and metabolic dysregulation may contribute to exercise intolerance and fatigue [35]. This may explain symptoms disproportionate to structural findings and supports a multimodal diagnostic approach incorporating cardiopulmonary exercise testing (CPET) alongside imaging.

3. Overview of multimodality imaging in LC

Multimodality cardiac imaging, including echocardiography (ECHO), cardiac computed tomography (CCT), cardiac magnetic resonance (CMR), and nuclear cardiology techniques, has emerged in the twenty-first century as the standard of care for cardiovascular imaging [36]. Each modality has specific advantages and limitations: Echocardiography is widely available and cost-effective but operator-dependent; the CCT offers excellent spatial resolution for coronary anatomy but involves ionizing radiation; the CMR provides superior tissue characterization without radiation but has limited availability and longer acquisition times; nuclear imaging allows functional and perfusion assessment but is associated with radiation exposure and lower spatial resolution [36–38].

Clinical decision pathways usually start with echocardiography, with escalation to CMR or CT when findings are inconclusive or discordant with clinical suspicion. Advanced imaging is indicated when echocardiographic windows are limited, structural complexity is suspected, or further risk stratification is required, while nuclear imaging positron emission tomography/single-photon emission computed tomography (PET/SPECT) is reserved for evaluating ischemia, viability, or inflammatory activity [38, 39]. Persistent diagnostic uncertainty or symptom progression commonly prompts multimodality escalation to guide management. Multimodality imaging in LC is presented in Table 1.

Imaging modality	Strengths	Limitations/disadvantages	Pathologies best evaluated
Echocardiography (Echo)	Widely available, bedside, portableReal-time cardiac functionAssess chamber size, systolic and diastolic functionDetect pericardial effusion	Limited tissue characterizationOperator-dependentPoor acoustic window in some patientsLimited evaluation of fibrosis or microvascular injury	Ventricular dysfunctionChamber enlargementPericardial effusionWall motion abnormalities
Cardiac magnetic resonance (CMR)	Gold standard for tissue characterizationQuantitative edema, fibrosis (LGE, T1/T2 mapping, ECV)Accurate ventricular volumes and functionDetects myocarditis, pericarditis	Limited availabilityLong scan timesContraindicated with certain implants or claustrophobiaContrast limitations in cases of renal impairment	Myocarditis and pericarditisDiffuse/focal fibrosisVentricular function and volumesEdema and extracellular matrix expansion
Coronary computed tomography angiography (CCTA)	Excellent coronary anatomy resolutionNoninvasive CAD evaluationDetects high-risk plaques and coronary calcificationAssesses coronary and extracoronary vasculature	Radiation exposureLimited tissue characterization beyond coronariesContrast nephrotoxicity riskCannot detect edema or fibrosis	Obstructive and nonobstructive CADCoronary plaque morphologyCoronary calcification (CAC)Perivascular inflammation (EAT attenuation)
Nuclear imaging (SPECT/PET)	Functional myocardial perfusion assessmentQuantitative coronary flow reserve (PET)Detect microvascular dysfunction	Limited structural detailRadiation exposureLower spatial resolution than CMR/CCTALimited availability for quantitative PET	Myocardial ischemiaMicrovascular dysfunctionMyocardial viabilityInflammation (FDG-PET, research)

Table 1.

Multimodality imaging in long COVID.

4. Echocardiography in LC

Echocardiography is a widely available, safe, and cost-effective noninvasive tool for cardiac evaluation in patients with LC. Comprehensive transthoracic echocardiography (TTE), as recommended by the American Society of Echocardiography, combines two-dimensional and Doppler imaging to assess ventricular size and function, valvular hemodynamics, intracardiac pressures, and pericardial pathology [40]. The TTE offers real-time assessment without ionizing radiation and is suitable for longitudinal follow-up. However, its limitations include operator dependence, suboptimal acoustic windows, and limited tissue characterization, often necessitating complementary imaging modalities [40–42].

Left ventricular (LV) systolic function is most commonly assessed using ejection fraction (EF), which is preserved in the majority of LC patients [43–46]. However, EF may not detect subclinical dysfunction. Speckle tracking echocardiography and global longitudinal strain (GLS) frequently reveal impaired myocardial deformation despite normal EF, suggesting persistent subclinical myocardial injury or inflammation (Figure 2a). Multiple studies consistently identify abnormal LV and/or right ventricular (RV) GLS as the most common echocardiographic abnormality several months after infection, particularly following severe acute disease [44, 47–52]. Layer-specific strain analysis has revealed patterns suggestive of microvascular ischemia or transient thrombotic injury in the absence of significant coronary artery disease (CAD) [53]. Reduced GLS has also been documented in patients with mild or moderate initial infection and in those without prior cardiovascular disease, persisting up to one year or longer after COVID-19 [49, 54, 55].

Figure 2.
Echocardiographic findings in long COVID: (a) mildly abnormal longitudinal segmental strain; (b) mild pericardial effusion (red arrow).

The RV function is another important focus, given the pulmonary involvement associated with COVID-19. RV systolic function is evaluated using TAPSE, fractional area change, RV S′ velocity, RV strain, and estimated systolic pulmonary artery pressure [40, 56]. While some studies report improvement in RV parameters over time, others demonstrate persistent RV dysfunction, particularly in patients with ongoing symptoms or prior moderate-to-severe disease [50, 57, 58].

Diastolic dysfunction has been reported in a subset of LC patients and may contribute to exertional dyspnea and fatigue. Echocardiographic assessment includes mitral inflow Doppler, tissue Doppler e′ velocities, E/e′ ratio, left atrial volume index, and supportive parameters such as tricuspid regurgitation velocity [59]. Studies report variable prevalence of diastolic dysfunction in the months following infection, with some evidence of increasing frequency at longer-term follow-up [52, 55, 60, 61].

Pericardial involvement is less common but includes mild pericardial effusion and pericardial thickening (Figure 2b). Symptomatic post-COVID cohorts have reported pericarditis and small effusions detectable by echocardiography, particularly in the early postinfection phase [62, 63].

Despite its clinical utility, many symptomatic LC patients have normal echocardiographic findings, reflecting the multifactorial nature of the syndrome and the contribution of noncardiac mechanisms such as autonomic dysfunction, deconditioning, and microvascular abnormalities. When present, echocardiographic abnormalities are often mild and of uncertain clinical significance, underscoring the importance of integrating imaging findings with clinical evaluation, biomarkers, functional testing, and CMR imaging.

In conclusion, echocardiography is an essential first-line tool in the evaluation of LC patients with cardiovascular symptoms. While conventional parameters are usually preserved, advanced techniques such as strain imaging can identify subtle myocardial and RV abnormalities, aiding risk stratification, guiding further diagnostic work-up, and providing reassurance when results are normal.

5. CMR in LC

Patients with persistent cardiac symptoms, such as chest pain, dyspnea, palpitations, or syncope, particularly when accompanied by abnormal biomarkers, ECG, or prior imaging, should be referred for CMR [64, 65]. The CMR enables the exclusion of myocardial ischemia and previously unrecognized cardiomyopathies and provides a comprehensive assessment of COVID-19–related myocardial inflammation, fibrosis, and pericardial involvement [64, 66].

The CMR is a noninvasive imaging modality that allows accurate evaluation of ventricular function, chamber volumes, myocardial mass, and tissue characteristics [64, 66, 67]. Its major advantage over echocardiography is the ability to characterize myocardial tissue, particularly edema and fibrosis [66, 68]. Limitations include restricted availability, longer examination times, and contraindications such as claustrophobia, noncompatible implanted devices, impaired breath-holding, renal dysfunction, or contrast hypersensitivity [67].

The CMR protocols for post-COVID evaluation include cine imaging for ventricular function and tissue characterization using T2-weighted imaging, late gadolinium enhancement (LGE), and parametric mapping (native T1, T2, and extracellular volume [ECV]) [64, 67, 68] (Figure 3). Acute myocardial injury is characterized by edema, increased capillary permeability, and myocyte necrosis, while chronic stages may show interstitial or replacement fibrosis [69]. Quantitative mapping techniques improve the detection of diffuse myocardial abnormalities that may not be apparent on LGE alone [70–74].

Figure 3.
CMR findings in patients with long COVID with chronic inflammation: (a) T2 map, mid–short axis view: borderline increased T2 values; (b) native T1 map, mid–short axis view: borderline increased native T1 values; (c) LGE, mid–short axis view: Subepicardial LGE in the mid inferolateral segment (red arrow) and pericardial effusion (blue arrow).

The LGE is highly sensitive for identifying myocardial injury. Ischemic injury presents with subendocardial or transmural enhancement in a coronary distribution, whereas nonischemic injury typically shows subepicardial or midmyocardial patchy enhancement [75–79]. Diffuse processes are better detected using T1/T2 mapping and ECV assessment [75, 80].

Stress perfusion CMR allows noninvasive assessment of myocardial blood flow (MBF) and microvascular dysfunction. Quantitative perfusion analysis enables the calculation of myocardial perfusion reserve, aiding in the differentiation between multivessel CAD and coronary microvascular dysfunction [81–85]. Persistent perfusion abnormalities and impaired myocardial strain have been demonstrated after severe COVID-19, consistent with chronic microvascular disease [84, 86].

Subclinical myocardial dysfunction can also be assessed using CMR-based strain analysis. Feature-tracking CMR is most commonly used, as it relies on standard cine images. Abnormal myocardial strain has been reported after COVID-19 and is associated with reduced quality of life [87–90].

Post-COVID-19 CMR reveals a spectrum of findings, including myocarditis, pericarditis, myocardial ischemia or infarction, and, less commonly, stress-induced cardiomyopathy [67, 91]. Despite preserved LV EF, subtle myocardial abnormalities related to edema or LGE are frequently observed two to four months after moderate-to-severe infection, while transient RV dysfunction – often related to pulmonary involvement – generally improves within six months [90–93].

Elevated troponin levels after COVID-19 are most commonly related to myocardial inflammation, reported in 14–54% of patients with severe disease [90, 91, 94]. Myocardial edema with nonischemic LGE, often involving inferolateral segments, is observed in a subset of patients [90, 94, 95]. In hospitalized patients with troponin elevation, CMR performed after recovery has demonstrated postmyocarditis scarring in approximately one-third of cases and postischemic scarring in a smaller proportion [96].

Diagnosis of myocarditis by CMR relies on the 2018 updated Lake Louise criteria, incorporating T1- and T2-based mapping techniques. Fulfillment of both edema and injury criteria improves diagnostic specificity, while supportive findings include pericardial involvement and regional systolic dysfunction [97–99]. Pericardial effusion and pericardial LGE have been associated with poorer post-COVID quality of life [65, 100].

The CMR also identifies acute myocardial infarction by characteristic LGE patterns with corresponding edema and wall motion abnormalities and can detect inducible ischemia even in patients without known CAD [66, 101]. During the pandemic, stress-induced (Takotsubo) cardiomyopathy occurred more frequently, likely related to heightened psychosocial stress [102–104].

Finally, rare cases of vaccine-associated myopericarditis – predominantly following mRNA vaccines in adolescent and young adult males – have been reported. The incidence is low, the clinical course is typically mild, and CMR findings resemble nonischemic myocarditis with preserved ventricular function. Most patients recover fully, and effective immunization is achieved despite these rare adverse events [105–110].

6. Coronary computed tomography angiography in LC

Clinical evaluation of COVID-related cardiac involvement is challenging because symptoms are nonspecific, and cardiac biomarker elevation does not reliably distinguish ischemic from nonischemic causes [111, 112]. Given the high prevalence of chest pain, advanced imaging – particularly coronary computed tomography angiography (CCTA) – plays a central role in evaluating potential coronary etiologies [111–113]. The CCTA has excellent negative predictive value for both acute and chronic chest pain and is widely used as a first-line modality for excluding or detecting CAD [112, 114, 115]. In patients with cardiovascular postacute sequelae of SARS-CoV-2 infection (CV-PASC), CCTA helps correlate symptoms, troponin elevation, and ECG abnormalities with underlying mechanisms such as obstructive or nonobstructive CAD, thromboembolism, or perimyocardial inflammation [111]. Referral for CCTA should be guided by the pretest probability of CAD, particularly in patients with low to intermediate risk of acute coronary syndrome [116]. Notably, invasive angiography has shown no obstructive disease in a substantial proportion of COVID-19 patients presenting with STEMI, supporting a role for noninvasive coronary imaging [117].

With high spatial and temporal resolution, CCTA allows detailed assessment of coronary anatomy, plaque burden, and stenosis severity [111]. It also provides prognostic information through the identification of high-risk plaque features, which are important for risk stratification and the selection of patients for invasive evaluation [112, 115, 118, 119]. Prior SARS-CoV-2 infection has been associated with accelerated plaque progression and a higher prevalence of vulnerable plaque characteristics, correlating with increased cardiovascular event risk [120]. Beyond atherosclerosis, coronary CT can identify features suggestive of coronary vasculitis and assess perivascular inflammation using epicardial adipose tissue (EAT) attenuation, with higher values reflecting increased inflammatory activity and plaque instability [111, 121].

Coronary artery calcium (CAC) scoring is another important CT-based tool for cardiovascular risk assessment. Higher CAC scores, particularly above 400 Agatston units, are associated with worse outcomes in COVID-19 patients and enable detection of subclinical atherosclerosis, improving early risk stratification [122–125]. The CAC burden also correlates with hypertension, a common comorbidity associated with more severe disease [126]. The CT imaging additionally provides prognostic information from extracoronary calcifications, including aortic valve and thoracic aortic calcium, which reflect systemic atherosclerosis and further refine cardiovascular risk assessment [123, 127, 128] (Figure 4).

Figure 4.
CT coronary angiography – Agatston calcium score 790: calcified plaques in the left main (LM) coronary artery (yellow arrow), left anterior descending (LAD) coronary artery (red arrow), left circumflex (LCX) coronary artery (blue arrow), and right coronary artery (RCA) (black arrow).

Finally, CCTA allows evaluation of extracardiac findings, such as pericardial effusion and pulmonary abnormalities, as well as alternative diagnoses that may explain persistent symptoms in patients with LC [111, 112].

7. Nuclear imaging in LC

Nuclear imaging methods play an important complementary role in the evaluation of cardiovascular involvement in LC syndrome. It is mainly used in patients with persistent symptoms and inconclusive findings on conventional cardiac imaging modalities [128]. Bearing in mind that endothelial and microvascular dysfunction, as well as chronic low-grade inflammation, contribute to LC pathophysiology, nuclear techniques offer a comprehensive functional evaluation that extends beyond structural assessment. Myocardial perfusion imaging using SPECT or PET allows for the evaluation of regional and global MBF and the detection of ischemia in the absence of obstructive CAD, which is a common pathological substrate in LC patients [129]. In those presenting with chest pain, exertional dyspnea, or reduced exercise tolerance, these techniques are especially valuable for identifying coronary microvascular dysfunction [130]. The PET, similar to CMR, enables absolute quantification of MBF and coronary flow reserve, providing high sensitivity for diffuse microvascular impairment. The PET imaging with fluorodeoxyglucose (PET-FDG) is significant in evaluating ongoing myocardial or vascular inflammation [131]. This is particularly relevant in selected LC patients, especially when CMR findings are equivocal or contraindicated. Additionally, in patients with both cardiovascular and respiratory manifestations, nuclear imaging can contribute to the evaluation of pulmonary vascular involvement through ventilation–perfusion scintigraphy, aiding in the detection of chronic thromboembolic disease or perfusion abnormalities in patients with persistent dyspnea [132]. These findings suggest that nuclear imaging primarily contributes to functional and pathophysiological assessment in LC. As part of a multimodality imaging strategy, nuclear techniques help clarify symptom mechanisms, establish diagnoses, and guide targeted management. Although it is a valuable tool for comprehensive cardiovascular evaluation, its usage should be individualized due to its limited approach and associated radiation exposure.

8. ECG monitoring and arrhythmia evaluation in LC

The unexpectedly high prevalence of cardiac arrhythmias in LC patients, ranging from 10 to 20%, requires comprehensive evaluation and timely treatment [133]. Palpitations, dizziness, syncope, and exercise intolerance are among the most frequently reported persistent cardiovascular symptoms, which is why ECG monitoring and systematic arrhythmia evaluation play a crucial role in the assessment [134]. As these symptoms may be present in those without prior cardiovascular disease or severe acute illness, careful ECG-based evaluation is essential to identify rhythm disturbances, establish their clinical relevance, and guide management. Although frequently normal, a standard 12-lead ECG represents the initial step in cardiovascular assessment. It may reveal sinus tachycardia or bradycardia, atrial or ventricular ectopy, conduction abnormalities, QT interval prolongation, or repolarization changes suggestive of prior myocardial involvement. It is important to underline that comparison with previous ECGs, when available, can be particularly informative. However, ECG alone has limited sensitivity for detecting paroxysmal arrhythmias or autonomic dysfunction, which are particularly common in LC patients [135]. Short-term Holter monitoring (24–48 hours) can identify frequent premature atrial or ventricular complexes, nonsustained supraventricular or ventricular tachycardia, and heart rate variability abnormalities. In patients with less frequent or episodic symptoms, extended monitoring using patch-based recorders (7–14 days) or external loop recorders substantially increases diagnostic yield [136]. Implantable loop recorders may be considered in selected patients with unexplained syncope or suspected clinically significant arrhythmias despite negative prolonged noninvasive ECG monitoring [137]. Inappropriate sinus tachycardia and POTS are commonly reported as part of the autonomic dysfunction spectrum, especially in younger individuals. ECG monitoring, combined with orthostatic testing and heart rate variability analysis, helps differentiate autonomic-mediated tachycardia from primary arrhythmias [138]. Exercise ECG testing may further evaluate chronotropic competence, heart rate recovery, and symptom–rhythm correlation, while also excluding ischemia. According to various observational studies, the overall burden of malignant arrhythmias in LC syndrome appears to be low [139]. However, careful risk stratification remains essential, especially in patients with evidence of myocardial injury, myocarditis, or fibrosis on cardiac imaging. In those cases, ECG monitoring is important in decisions regarding physical activity, further management, and follow-up intensity. Integration of ECG findings with laboratory markers, echocardiography, and CMR allows a more comprehensive understanding of the underlying pathophysiological substrate. In conclusion, systematic and tailored ECG assessment in patients with LC syndrome is crucial for symptom correlation, exclusion of clinically significant arrhythmias, reassurance of patients, and guidance of individualized treatment strategies.

9. The overview of published LC study methodology

Considering the echo and CMR findings in particular, the heterogeneity of available studies and the clinical significance of subclinical alterations should be addressed. First, study populations differ markedly in sample size and selection strategy. Many early investigations were single-center, observational cohorts with relatively small numbers, frequently enriched with previously hospitalized or symptomatic individuals. Conversely, community-based cohorts often included milder cases with lower event rates. This variability introduces potential selection bias when comparing results across studies. Hospital-based studies tend to overestimate the prevalence of myocardial abnormalities (reduced GLS or LGE), whereas population-based studies may underestimate subtle changes due to less systematic imaging. Furthermore, control groups are inconsistently defined, ranging from healthy volunteers to patients with non-COVID viral illnesses, limiting comparative validity.

Second, the diagnostic criteria for LC are not uniform across studies. While most definitions require symptoms persisting ≥ 3 months after acute infection, operationalization varies considerably with respect to symptom clusters, severity thresholds, and the requirement for laboratory confirmation. Some cohorts include self-reported infection without virological proof, whereas others rely strictly on polymerase chain reaction (PCR)-confirmed cases. Heterogeneity also extends to the timing of imaging, ranging from a few weeks to more than one year after infection, which affects the detection of transient edema versus chronic fibrosis. These inconsistencies complicate pooled prevalence estimates and make cross-study comparisons of imaging biomarkers problematic.

Methodological variability in imaging acquisition and interpretation further contributes to inconsistency. For echocardiography, vendor-dependent strain software, differing GLS cutoff values, and a lack of standardized reference ranges may yield divergent abnormality rates. Similarly, CMR protocols differ in field strength, mapping sequences, thresholds for native T1/T2 elevation, and criteria for LGE positivity. Nuclear imaging studies vary in quantitative versus qualitative perfusion assessment and in the definition of microvascular dysfunction. Without standardized imaging protocols, it is difficult to determine whether reported abnormalities reflect true biological changes or differences in acquisition and analysis methods.

10. Clinical significance of subclinical alterations: Echo and CMR findings in focus

Beyond methodological heterogeneity, the clinical significance of subclinical alterations requires cautious interpretation. Reduced GLS in the setting of preserved LV EF is frequently reported months after SARS-CoV-2 infection. However, the magnitude of impairment is often mild (e.g., − 16% to − 18%), and longitudinal data linking such findings to hard outcomes (heart failure hospitalization, arrhythmia, cardiovascular mortality) are sparse. In non-COVID populations, mildly reduced GLS has prognostic implications in specific contexts (e.g., chemotherapy cardiotoxicity), but extrapolation to LC remains speculative. Similarly, small areas of nonischemic LGE or borderline elevation of native T1/T2 values may represent residual inflammation or limited fibrosis, yet their long-term arrhythmic or functional consequences are unknown. Current evidence suggests that malignant arrhythmias and progressive systolic dysfunction are uncommon, indicating that many of these findings may have limited adverse prognostic weight.

Importantly, the psychological impact of reporting “abnormal” but clinically indeterminate findings should not be underestimated. Overemphasizing minor imaging abnormalities may increase patient anxiety and lead patients to attribute ongoing symptoms to clinically insignificant findings, particularly in a syndrome already characterized by autonomic dysregulation and increased interoceptive awareness.

11. Psychological impact of cardiac symptoms and imaging anxiety in the clinical pathway of LC

11.1 Anxiety triggered by cardiac symptoms

Patients with LC frequently report chest pain, palpitations, tachycardia, or shortness of breath, even when structural heart disease cannot be demonstrated. Increased awareness of bodily sensations may lead patients to interpret otherwise benign symptoms as signs of serious cardiac pathology. Anxiety can further intensify autonomic responses such as tachycardia, rapid breathing, and muscle tension, creating a cycle in which symptoms and fear reinforce each other [140–143].

In addition, some patients experienced severe illness during the acute phase of COVID-19, including dyspnea, hospitalization, or prolonged isolation. These experiences may increase emotional sensitivity to physical symptoms and contribute to disproportionate concern during physical activity or minor symptom recurrence [144]. These mechanisms can significantly reduce daily functioning, leading to activity avoidance and social withdrawal. Sleep difficulties are common as well – either due to nocturnal palpitations or persistent fear that “something might happen during sleep.” Over time, this pattern contributes to emotional exhaustion, health anxiety, and a reduced overall quality of life.

Recognizing the interaction between psychological and physiological mechanisms is, therefore, important during clinical assessment, as anxiety-related autonomic activation may mimic or aggravate cardiovascular symptoms.

11.2 Anxiety related to imaging and diagnostic procedures

Cardiovascular imaging itself may also provoke anxiety in some patients. Examinations such as echocardiography, CMR, computed tomography, or nuclear imaging may raise concerns about possible heart damage, exposure to radiation, or discomfort during the procedure [145–147]. Claustrophobia during CMR and uncertainty regarding imaging results are commonly reported sources of distress.

Anxiety may influence heart rate and blood pressure, which can occasionally affect patient cooperation and image acquisition. For this reason, addressing procedural anxiety is not only supportive for patients but may also contribute to optimal examination conditions [148, 149]

Healthcare professionals play a central role in mitigating this anxiety. A clear explanation of why a specific imaging modality is chosen, what diagnostic question it addresses, and how it contributes to the overall clinical plan helps patients perceive the investigation as purposeful rather than alarming.

Providing simple information about the procedure – such as expected duration, breath-holding instructions, contrast administration, and possible sensations during the examination – can improve patient comfort and reduce uncertainty. Maintaining communication during the examination and ensuring patient comfort are simple measures that often help reduce anxiety.

11.3 Diagnostic communication and management of uncertainty

Effective communication is particularly important when discussing imaging results in LC patients. Borderline or subtle abnormalities may occasionally be detected, including small areas of LGE or mild reductions in GLS [150–152]. In many cases, it remains uncertain whether these findings are directly related to persistent symptoms or represent incidental or preexisting changes, especially in patients with comorbidities such as hypertension or metabolic disease [153].

It is, therefore, important that clinicians explain that minor imaging abnormalities do not necessarily indicate active myocardial injury or progressive cardiac disease. Using clear and understandable language when discussing results can help prevent misinterpretation and unnecessary concern while supporting shared decision-making [154].

Imaging findings should always be interpreted in the broader clinical context, including symptom severity, functional capacity, laboratory markers, and coexisting conditions. When abnormalities are identified, patients should receive clear information about their clinical relevance, whether additional monitoring is required, and the expected follow-up strategy.

11.4 Postdischarge psychological management and avoidance of overtesting

Structured follow-up can help reduce uncertainty and prevent anxiety related to repeated testing. Establishing clear timelines for reassessment and defining indications for repeat imaging may limit unnecessary investigations.

Clinicians should remain attentive to persistent psychological stress. In some patients, targeted psychological interventions, including cognitive-behavioral approaches, may be helpful, and collaboration with a psychologist or psychiatrist may be appropriate in more complex cases.

Repeated investigations for small imaging findings of unclear clinical relevance should be carefully reconsidered, as they may increase patient anxiety. For this reason, imaging should primarily be guided by clinical symptoms and objective findings, while clear communication with patients remains essential.

12. Multisystem considerations in LC

12.1 Liver injury in LC

Long COVID refers to the persistence of symptoms after the acute SARS-CoV-2 infection. Liver injury in LC is multifactorial, resulting from systemic inflammation, endothelial dysfunction, microvascular and metabolic disorders, and sometimes medications used to treat COVID-19, including antivirals, antibiotics, corticosteroids, and IL-6 receptor antagonists. While usually mild to moderate, liver damage can affect diagnostics and prognosis, particularly in patients with preexisting chronic liver disease [155–161].

Imaging can help detect liver changes beyond laboratory abnormalities. Ultrasound and elastography assess steatosis and fibrosis, while CT and MRI provide detailed analysis of the parenchyma and vascular structures [156, 162, 163]. Liver abnormalities are often linked to cardiovascular complications. Congestive liver disease can result from right-sided heart failure or pulmonary hypertension, and increased portal or mesenteric vein thrombosis in LC reflects a systemic procoagulant state and heightened cardiovascular risk [9, 157, 164, 165].

Contrast-enhanced CT scans, often used to assess lung damage, are generally safe for LC patients with liver injury due to the renal excretion of iodinated contrast; however, renal function should be evaluated in patients with additional chronic diseases [161, 165].

12.2 Respiratory manifestations of LC

Long COVID is characterized by persistent respiratory issues after acute SARS-CoV-2 infection, including ongoing abnormalities in lung function, structure, and gas exchange [166, 167]. Common symptoms are exertional dyspnea, chronic cough, reduced exercise tolerance, and fatigue (50–70%), often due to deconditioning, impaired oxygen use, or microvascular dysfunction [166–168]. Other symptoms, such as chest tightness and wheezing, may mimic asthma or interstitial lung disease [166, 167].

High-resolution CT often shows ground-glass opacities, reticular changes, and parenchymal bands in 20–40% of patients at three to six months. Severe cases may exhibit bronchiectasis, residual consolidation, or air trapping, mostly in the lower lobes. Fibrotic-like changes are rare (<5%) but may progress in some patients over 12 months [169–172]. Expiratory CT helps identify small airway disease.

Pulmonary function tests frequently reveal restrictive defects (reduced FVC/TLC) in 30–50% of patients, while impaired diffusing capacity (DLCO) affects 20–40% and may persist longer. Obstructive defects are less common [167, 169, 171]. Pathophysiology involves alveolar damage, organizing pneumonia, fibrosis, inflammation, endothelial dysfunction, microvascular thrombosis, viral persistence, and immune-mediated injury [166, 167, 172]. Risk factors include older age, female sex, obesity, and severe initial illness [166, 168, 172].

Management requires a multidisciplinary approach. Pulmonary rehabilitation improves dyspnea and functional capacity. Symptom-directed pharmacologic therapy includes bronchodilators and inhaled corticosteroids; antifibrotics are under investigation. Long-term oxygen therapy is used for persistent hypoxemia. Follow-up with CT and pulmonary function tests at 3, 6, and 12 months is recommended [166, 167, 173]. Most patients gradually improve within a year, but 10–20% develop persistent pulmonary impairment, especially after severe disease or fibrotic changes [168, 172, 173].

13. Integrating cardiovascular imaging into clinical pathways

As previously mentioned, a structured decision-making algorithm integrating multimodality imaging across clinical phenotypes would provide a timely evaluation and therapeutic management. According to the most common clinical presentations and multimodality imaging findings, a phenotype-driven framework may be conceptualized as follows:

Chest pain phenotype
The initial assessment would include ECG, troponin levels, and risk stratification. In patients with low to intermediate risk, CT coronary angiography could be used to exclude obstructive CAD. In patients with elevated troponin levels that can point to myocardial injury, CMR with tissue characterization (myocardial mapping and LGE) should be considered. In patients without obstructive CAD and with persistent angina symptoms, stress CMR or PET should be considered to assess coronary microvascular dysfunction. If both epicardial and microvascular CAD are excluded, and there is no clinical evidence of myocardial injury, other noncardiac causes of chest pain should be evaluated.
Dyspnea phenotype
Initial evaluation should include chest X-ray, pulmonary function tests, natriuretic peptides, and transthoracic echocardiography. If abnormal RV function or pulmonary hypertension is observed, a targeted cardiopulmonary work-up should be considered, including right heart catheterization. In patients with unexplained symptoms and normal echocardiographic findings, CMR with tissue characterization to evaluate inflammation or fibrosis should be considered. Additionally, perfusion imaging is recommended if ischemia is suspected.
Palpitations phenotype
Initial evaluation should include a mandatory 12-lead ECG, Holter, or extended rhythm monitoring. The findings should be correlated with echo results suggesting potential structural abnormalities, or in those with elevated biomarkers, a CMR exam could provide a more detailed examination and stratification of the patients. In patients with predominant autonomic features, autonomic testing, especially in the absence of structural abnormalities, should be considered.

This kind of stepwise diagnostic algorithm can allow the avoidance of redundant testing and provide clear criteria for follow-up imaging (Figure 5).

Figure 5.
A structured decision-making algorithm integrating multimodality imaging across clinical phenotypes in long COVID patients.

It is important to avoid overtesting, balancing thorough evaluation with minimizing patient anxiety and unnecessary exposure to radiation or contrast agents. Practical algorithms support this process, offering stepwise guidance for imaging selection, interpretation, and follow-up. Multidisciplinary collaboration, particularly between cardiology and radiology teams, ensures appropriate modality choice and efficient use of resources. Patient education about the rationale for each test helps address fear, improves adherence, and reinforces shared decision-making. It is also important to provide information about potential pathological findings and how they affect further management. Ultimately, integrating imaging into clinical pathways enhances diagnostic accuracy, improves outcomes, and allows patient-centered care.

14. Knowledge gaps and future directions

Future research should focus on longitudinal studies that correlate imaging abnormalities with clinical outcomes. Standardization of imaging protocols and reporting criteria would improve comparability between studies, while identification of reliable biomarkers may enhance risk stratification. In addition, outcome-based clinical trials are needed to determine whether targeted therapeutic strategies can modify disease progression in LC.

15. Conclusion

Long COVID represents a complex, multisystem syndrome in which cardiovascular symptoms are common, yet frequently disproportionate to structural findings. Multimodality imaging – including echocardiography, CMR, CCTA, nuclear techniques, and ECG monitoring – plays a central role in phenotyping, exclusion of alternative diagnoses, risk stratification, and guidance of management. Structured, symptom-oriented decision pathways support appropriate modality selection while minimizing unnecessary investigations.

Equally important is the psychological dimension of care. Anxiety related to cardiac symptoms and diagnostic procedures can enhance symptom perception and influence healthcare utilization. Clear, empathetic, and patient-centered communication by healthcare professionals is crucial for helping patients understand their results, navigate uncertainty, avoid unnecessary medical interventions, and minimize distress related to medical care.

Future research should prioritize longitudinal and outcome-based studies to determine the prognostic value of imaging alterations, establish standardized imaging protocols, and refine risk stratification models.

Multidisciplinary collaboration and structured diagnostic pathways remain important for the appropriate evaluation and follow-up of patients with LC.

Acknowledgments

The authors acknowledge the use of the Jenni AI platform for language polishing of the chapter.

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Multimodality Cardiovascular Imaging in Long COVID

Long COVID - From Pathophysiology to Rehabilitation [Working Title]

Abstract

Keywords

Author Information

Marija Zdravkovic *

Viseslav Popadic

Maja Popovic

Marija Brankovic

Milica Brajkovic

Jelica Bjekic-Macut

Tamara Trumpic

Branislava Daskalovic

Planinka Zafirovska