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Infection with SARS-CoV-2, the virus that causes COVID, is associated with numerous potential secondary complications. Global efforts have been dedicated to understanding the myriad potential cardiovascular sequelae which may occur during acute infection, convalescence, or recovery. Because patients often present with nonspecific symptoms and laboratory findings, cardiac imaging has emerged as an important tool for the discrimination of pulmonary and cardiovascular complications of this disease. The clinician investigating a potential COVID-related complication must account not only for the relative utility of various cardiac imaging modalities but also for the risk of infectious exposure to staff and other patients. Extraordinary clinical and scholarly efforts have brought the international medical community closer to a consensus on the appropriate indications for diagnostic cardiac imaging during this protracted pandemic. In this review, we summarize the existing literature and reference major societal guidelines to provide an overview of the indications and utility of echocardiography, nuclear imaging, cardiac computed tomography, and cardiac magnetic resonance imaging for the diagnosis of cardiovascular complications of COVID.

We propose a method of quantitatively measuring drug-induced microvascular volume changes, as well as drug-induced changes in blood oxygenation using calibrated blood oxygen level-dependent magnetic resonance imaging (MRI). We postulate that for MRI signals there is a contribution to R2* relaxation rates from static susceptibility effects of the intravascular blood that scales with the blood volume/magnetic field and depends on the oxygenation state of the blood. These may be compared with the effects of an intravascular contrast agent. With 4 R2* measurements, microvascular blood volume (MBV) and tissue oxygenation changes can be quantified with the administration of a vasoactive drug.The protocol examined 12 healthy rats in a prospective observational study. R2* maps were acquired with and without infusion of adenosine, which increases microvascular blood flow, or dobutamine, which increases myocardial oxygen consumption. In addition, R2* maps were acquired after the intravenous administration of a monocrystalline iron oxide nanoparticle, with and without adenosine or dobutamine.Total microvascular volume was shown to increase by 10.8% with adenosine and by 25.6% with dobutamine ( P0.05). When comparing endocardium versus epicardium, both adenosine and dobutamine demonstrated significant differences between endocardial and epicardial MBV changes ( P0.05). Total myocardial oxygenation saturation increased by 6.59% with adenosine and by 1.64% with dobutamine ( P = 0.27). The difference between epicardial and endocardial oxygenation changes were significant with each drug (adenosine P0.05, dobutamine P0.05).Our results demonstrate the ability to quantify microvascular volume and oxygenation changes using calibrated blood oxygen level-dependent MRI, and we demonstrate different responses of adenosine and dobutamine. This method has clinical potential in examining microvascular disease in various disease states without the administration of radiopharmaceuticals or gadolinium-based contrast agents.

To characterize global and segmental circumferential systolic strain (CS) measured by cardiac MRI in athletes after SARS-CoV-2 infection.This retrospective observational cohort study included 188 soldiers and collegiate athletes referred for cardiac MRI after SARS-CoV-2 infection (C19+) between July 2020 and February 2021 and a control group of 72 soldiers, collegiate, and high school athletes who underwent cardiac MRI from May 2019 to February 2020, prior to the first SARS-CoV-2 case detected in our region (C19-). Global and segmental CS were measured by feature tracking, then compared between each group using unadjusted and multivariable- adjusted models. Acute myocarditis was diagnosed according to the modified Lake Louise criteria and the location of pathologic late gadolinium enhancement (LGE) was ascertained.Among the 188 C19+ athletes (median age, 25 years [IQR, 23-30]; 131 men), the majority had mild illness. Global CS significantly differed between C19+ and C19- groups, with a median of -24.0 (IQR -25.8, -21.4) versus. -25.0 (-28.0, -22.4), respectively (p = .009). This difference in CS persisted following adjustment for age, sex, body mass index, heart rate, and systolic blood pressure β coefficient 1.29 [95% CI: 0.20, 2.38], p = .02). In segmental analysis, the basal- and mid- inferoseptal, septal and inferolateral segments were significantly different (p.05), which had a higher frequency of post-COVID late gadolinium enhancement. The global and segmental differences were similar after exclusion of athletes with myocarditis.Among athletes, SARS-CoV-2 infection was associated with a small but statistically significant reduced CS.

Data on medium-term outcomes in indivduals with myocarditis after mRNA COVID-19 vaccination are scarce. We aimed to assess clinical outcomes and quality of life at least 90 days since onset of myocarditis after mRNA COVID-19 vaccination in adolescents and young adults.In this follow-up surveillance study, we conducted surveys in US individuals aged 12-29 years with myocarditis after mRNA COVID-19 vaccination, for whom a report had been filed to the Vaccine Adverse Event Reporting System between Jan 12 and Nov 5, 2021. A two-component survey was administered, one component to patients (or parents or guardians) and one component to health-care providers, to assess patient outcomes at least 90 days since myocarditis onset. Data collected were recovery status, cardiac testing, and functional status, and EuroQol health-related quality-of-life measures (dichotomised as no problems or any problems), and a weighted quality-of-life measure, ranging from 0 to 1 (full health). The EuroQol results were compared with published results in US populations (aged 18-24 years) from before and early on in the COVID-19 pandemic.Between Aug 24, 2021, and Jan 12, 2022, we collected data for 519 (62%) of 836 eligible patients who were at least 90 days post-myocarditis onset: 126 patients via patient survey only, 162 patients via health-care provider survey only, and 231 patients via both surveys. Median patient age was 17 years (IQR 15-22); 457 (88%) patients were male and 61 (12%) were female. 320 (81%) of 393 patients with a health-care provider assessment were considered recovered from myocarditis by their health-care provider, although at the last health-care provider follow-up, 104 (26%) of 393 patients were prescribed daily medication related to myocarditis. Of 249 individuals who completed the quality-of-life portion of the patient survey, four (2%) reported problems with self-care, 13 (5%) with mobility, 49 (20%) with performing usual activities, 74 (30%) with pain, and 114 (46%) with depression. Mean weighted quality-of-life measure (0·91 [SD 0·13]) was similar to a pre-pandemic US population value (0·92 [0·13]) and significantly higher than an early pandemic US population value (0·75 [0·28]; p0·0001). Most patients had improvements in cardiac diagnostic marker and testing data at follow-up, including normal or back-to-baseline troponin concentrations (181 [91%] of 200 patients with available data), echocardiograms (262 [94%] of 279 patients), electrocardiograms (240 [77%] of 311 patients), exercise stress testing (94 [90%] of 104 patients), and ambulatory rhythm monitoring (86 [90%] of 96 patients). An abnormality was noted among 81 (54%) of 151 patients with follow-up cardiac MRI; however, evidence of myocarditis suggested by the presence of both late gadolinium enhancement and oedema on cardiac MRI was uncommon (20 [13%] of 151 patients). At follow-up, most patients were cleared for all physical activity (268 [68%] of 393 patients).After at least 90 days since onset of myocarditis after mRNA COVID-19 vaccination, most individuals in our cohort were considered recovered by health-care providers, and quality of life measures were comparable to those in pre-pandemic and early pandemic populations of a similar age. These findings might not be generalisable given the small sample size and further follow-up is needed for the subset of patients with atypical test results or not considered recovered.US Centers for Disease Control and Prevention.

Cardiovascular involvement following COVID-19 is heterogeneous, prevalent and is often missed by echocardiography and serum biomarkers (such as troponin I and brain natriuretic peptide). Cardiac magnetic resonance (CMR) is the gold standard non-invasive imaging modality to phenotype unique populations after COVID-19, such as competitive athletes with a heightened risk of sudden cardiac death, patients with multisystem inflammatory syndrome, and people suspected of having COVID-19 vaccine-induced myocarditis. This review summarises the key attributes of CMR, reviews the literature that has emerged for using CMR for people who may have COVID-19-related complications after COVID-19, and offers expert opinion regarding future avenues of investigation and the importance of reporting findings.

IMPORTANCE: Vaccination against COVID-19 provides clear public health benefits, but vaccination also carries potential risks. The risks and outcomes of myocarditis after COVID-19 vaccination are unclear. OBJECTIVE: To describe reports of myocarditis and the reporting rates after mRNA-based COVID-19 vaccination in the US. DESIGN, SETTING, AND PARTICIPANTS: Descriptive study of reports of myocarditis to the Vaccine Adverse Event Reporting System (VAERS) that occurred after mRNA-based COVID-19 vaccine administration between December 2020 and August 2021 in 192 405 448 individuals older than 12 years of age in the US; data were processed by VAERS as of September 30, 2021. EXPOSURES: Vaccination with BNT162b2 (Pfizer-BioNTech) or mRNA-1273 (Moderna). MAIN OUTCOMES AND MEASURES: Reports of myocarditis to VAERS were adjudicated and summarized for all age groups. Crude reporting rates were calculated across age and sex strata. Expected rates of myocarditis by age and sex were calculated using 2017-2019 claims data. For persons younger than 30 years of age, medical record reviews and clinician interviews were conducted to describe clinical presentation, diagnostic test results, treatment, and early outcomes. RESULTS: Among 192 405 448 persons receiving a total of 354 100 845 mRNA-based COVID-19 vaccines during the study period, there were 1991 reports of myocarditis to VAERS and 1626 of these reports met the case definition of myocarditis. Of those with myocarditis, the median age was 21 years (IQR, 16-31 years) and the median time to symptom onset was 2 days (IQR, 1-3 days). Males comprised 82% of the myocarditis cases for whom sex was reported. The crude reporting rates for cases of myocarditis within 7 days after COVID-19 vaccination exceeded the expected rates of myocarditis across multiple age and sex strata. The rates of myocarditis were highest after the second vaccination dose in adolescent males aged 12 to 15 years (70.7 per million doses of the BNT162b2 vaccine), in adolescent males aged 16 to 17 years (105.9 per million doses of the BNT162b2 vaccine), and in young men aged 18 to 24 years (52.4 and 56.3 per million doses of the BNT162b2 vaccine and the mRNA-1273 vaccine, respectively). There were 826 cases of myocarditis among those younger than 30 years of age who had detailed clinical information available; of these cases, 792 of 809 (98%) had elevated troponin levels, 569 of 794 (72%) had abnormal electrocardiogram results, and 223 of 312 (72%) had abnormal cardiac magnetic resonance imaging results. Approximately 96% of persons (784/813) were hospitalized and 87% (577/661) of these had resolution of presenting symptoms by hospital discharge. The most common treatment was nonsteroidal anti-inflammatory drugs (589/676; 87%). CONCLUSIONS AND RELEVANCE: Based on passive surveillance reporting in the US, the risk of myocarditis after receiving mRNA-based COVID-19 vaccines was increased across multiple age and sex strata and was highest after the second vaccination dose in adolescent males and young men. This risk should be considered in the context of the benefits of COVID-19 vaccination.

Background Myocarditis is a potential complication after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and a known cause of sudden cardiac death. Given the athletic demands of soldiers, identification of myocarditis and characterization of post-acute sequelae of SARS-CoV-2 infection with cardiovascular symptoms (CV PASC) may be critical to guide return-to-service. This study sought to evaluate the spectrum of cardiac involvement among soldiers with cardiopulmonary symptoms in the late convalescent phase of recovery from SARS-CoV-2 compared to a healthy soldier control group, and to determine the rate of progression to CV PASC. Methods All soldiers referred for cardiovascular magnetic resonance (CMR) imaging for cardiopulmonary symptoms following COVID-19 were enrolled and matched by age, gender, and athletic phenotype 1:1 to soldiers undergoing CMR in the year prior to the first case of COVID-19 at our institution. Demographic, clinical, laboratory, and imaging parameters were compared between groups. The diagnosis of acute myocarditis was made using modified Lake Louise criteria. Wilcoxon rank sum and chi-squared tests were used for comparison of continuous and categorical variables, respectively. Results Fifty soldier cases and 50 healthy soldier controls were included. The median time from SARS-CoV-2 detection to CMR was 71 days. The majority of cases experienced moderate symptoms (N = 43, 86%), while only 10% required hospitalization. The right ventricular (RV) ejection fraction (RVEF) was reduced in soldier cases compared to controls (51.0% vs. 53.2%, p = 0.012). Four cases were diagnosed with myocarditis (8%), 1 (2%) was diagnosed with Takotsubo cardiomyopathy, and 1 (2%) had new biventricular systolic dysfunction of unclear etiology. Isolated inferior RV septal insertion late gadolinium enhancement (LGE) was present in 8 cases and 8 controls (16% vs. 24%, p = 0.09). Seven of the 19 (37%) cases that completed an intermediate-term follow-up survey reported CV PASC at a median of 139 days of follow-up. Two of the 7 soldiers (29%) with CV PASC had a pathological clinical diagnosis (myocarditis) on CMR. Conclusions Cardiovascular pathology was diagnosed in 6 symptomatic soldiers (12%) after recovery from SARS-CoV-2, with myocarditis found in 4 (8%). RVEF was reduced in soldier cases compared to controls. CV PASC occurred in over one-third of soldiers surveyed, but did not occur in any soldiers with asymptomatic acute SARS-CoV-2 infection.

Background Myocarditis is a leading cause of sudden cardiac death among competitive athletes and may occur without antecedent symptoms. COVID-19-associated myocarditis has been well-described, but the prevalence of myocardial inflammation and fibrosis in young athletes after COVID-19 infection is unknown. Objectives This study sought to evaluate the prevalence and extent of cardiovascular involvement in collegiate athletes that had recently recovered from COVID-19. Methods We conducted a retrospective cohort analysis of collegiate varsity athletes with prior COVID-19 infection, all of whom underwent cardiac magnetic resonance (CMR) prior to resumption of competitive sports in August 2020. Results Twenty-two collegiate athletes with prior COVID-19 infection underwent CMR. The median time from SARS-CoV-2 infection to CMR was 52 days. The mean age was 20.2 years. Athletes represented 8 different varsity sports. This cohort was compared to 22 healthy controls and 22 tactical athlete controls. Most athletes experienced mild illness (N=17, 77%), while the remainder (23%) were asymptomatic. No athletes had abnormal troponin I, electrocardiograms, or LVEF < 50% on echocardiography. Late gadolinium enhancement was found in 9% of collegiate athletes and one athlete (5%) met formal criteria for myocarditis. Conclusions Our study suggests that the prevalence of myocardial inflammation or fibrosis after an asymptomatic or mild course of ambulatory COVID-19 among competitive athletes is modest (9%), but would be missed by ECG, Ti, and strain echocardiography. Future investigation is necessary to further phenotype cardiovascular manifestations of COVID-19 in order to better counsel athletes on return to sports participation., Condensed Abstract COVID-19-associated myocarditis has been well-described, but the prevalence of myocardial inflammation and fibrosis in athletes after COVID-19 is unknown. We conducted a retrospective cohort analysis of 22 collegiate athletes with prior COVID-19 infection who underwent electrocardiography, troponin I, echocardiography with strain, and CMR. The median time from SARS-CoV-2 infection to CMR was 52 days. All athletes experienced mild illness or were asymptomatic. Late gadolinium enhancement was found in 9%. This suggests the prevalence of myocardial inflammation or fibrosis after an asymptomatic or mild course of COVID-19 among competitive athletes is modest, but would be missed without CMR screening.

Innovation plays an important role in the advancement of nuclear cardiology, meeting the need for reduced exposure to radiation, and maintaining and improving image quality. As we innovate, it is important to understand the impact of these improvements on the clinical and research knowledge base that has made nuclear cardiology such a powerful clinical tool. The need for comparative studies insuring stability in the clinical applicability of our current guidelines and use of the prognostic power of radionuclide myocardial perfusion imaging in clinical practice is essential for new and innovative techniques. The existing data demonstrating the significant differences that can occur with the innovative techniques is explored. The need for tools to insure comparable data is available as we begin to utilize registries to inform our clinical practice and research will be an important part of the future of nuclear cardiology.

MODERN CARDIAC MR imaging has shown the ability to reveal information beyond simple anatomy. Current techniques include evaluations of cardiac mass (1–4), measures of ejection fraction and contractility (5,6), as well as susceptibility-based contrast methods to assess myocardial perfusion and viability using exogenous contrast agents including gadolinium chelates (3,7–9) or by taking advantage of the BOLD effect using stress-inducing compounds such as dobutamine (10) or dipyridamole (10–12). Several cardiac imaging groups have reported large static field inhomogeneities in and near the heart (11–18) giving rise to a characteristic “bite”-shaped artifact. The artifact is seen as a highly focal, “bite”-shaped signal void along the infero-apical margin of the heart (Fig. 1). Pulse sequences that are highly sensitive to susceptibility differences such as many gradient echo methods, scans with echo planar readouts, and several other fast imaging techniques are most affected (14). The presence of this artifact can affect the interpretation of cardiac MR images. Figure 1 Human cardiac MR image at 3T. TFE black blood technique. θ = 25°, TR = 25 ms, TE = 11.53 ms, FOV = 290 mm, BW = 543 Hz. This is the third image of a four image set used to map T2* decay. Note the loss of signal in the inferoapical region ... Previous studies into the cause of this artifact have agreed that it is caused by magnetic susceptibility gradients but the relative influence of the various gradients around the heart has not been agreed upon. One study noted that the artifacts appeared near large epicardial veins, specifically the posterior vein of the left ventricle (PVLV) and, in some subjects, the great cardiac vein (17). The authors suggested that areas of high field inhomogeneity in measured field maps were generated by the difference in susceptibility between the deoxygenated blood flowing in large epicardial veins and the susceptibility of surrounding myocardium. In another study, experiments with a porcine model were conducted to examine several possible causes for the artifact (14). The study showed that there was very little dependence of the artifact on lung volume. The authors did note there was a slight improvement in the end-inspiratory images and attributed this to a shift in the artifact to a more apical position. The authors found that the artifact was not dependent on the oxygenation of the blood in the coronary sinus (14), apparently contradicting the conclusions of the human study (17). The porcine study also showed that surgical resection of the lungs away from the myocardium removed the artifact. When the chest was opened, the lungs partially collapsed. Significant artifacts were still seen near the “points” of the now collapsed, triangular lungs. When the lungs were resected out of the chest, and the cavity was filled with copper sulfate solution, the artifacts were removed. Furthermore, the artifact was removed independent of the position of the diaphragm, reducing the likelihood that sub-diaphragmatic structures are responsible. The authors of this study concluded lung tissue is the most likely source of the susceptibility artifacts although they noted that structural differences in heart and lung anatomy between pigs and humans prevent making this conclusion unequivocally for humans (14). An earlier report by the same group showed that free air in the chest after lung resection also did not produce the artifact, leading to the conclusion that the packaging of air into alveoli and small bronchioles rather than the extreme susceptibility difference between air and soft tissue is the source of the artifact (13). The results and conclusions of the previous studies (13,14,17) lead to some interesting questions. If the large epicardial veins are the primary cause of the artifact, as suggested in the human study, why did increasing the oxygen saturation of the vessels and thus reducing the susceptibility difference between the blood and the myocardium not lead to a reduction in the artifact in the porcine study? Second, if the heart–lung interface is the primary source of the susceptibility gradient, why does the artifact appear so focally rather than along the entirety of the heart–lung interface? It is the purpose of this study to assess by means of rigorous simulations the specific contributions of the PVLV and coronary sinus (CS) versus the heart–lung interface to the formation of static field inhomogeneities in the heart and thus imaging artifacts, with particular emphasis on the focal “bite”-shaped artifact. Simulating experiments allows control over the experiment such as setting blood oxygenation levels, changing the susceptibility of an entire organ, and eliminating motion, things not possible in real life. The simulations also provide the ability to completely remove or change internal structures without disrupting the rest of the body as would be required with surgical preparation of an in vivo study.

[Figure][1] [![Graphic][3] ][3][![Graphic][4] ][4] Magnetic resonance venography was performed to better understand venous anatomy in a woman with failed pacemaker implantation. Compared with a healthy subject (A) , her maximal intensity projection images (B) showed an absent