Cardiac Magnetic Resonance Studies in a Large Animal Model That Simulates the Cardiac Abnormalities of Human Septic Shock.

BACKGROUND: Septic shock is associated with increases in end-diastolic volume (EDV) and decreases in ejection fraction that reverse within 10 days. Nonsurvivors do not develop EDV increases. The mechanism is unknown. METHODS AND RESULTS: Purpose-bred beagles (n=33) were randomized to receive intrabronchial Staphylococcus aureus or saline. Over 96 hours, cardiac magnetic resonance imaging and echocardiograms were performed. Tissue was obtained at 66 hours. From 0 to 96 hours after bacterial challenge, septic animals versus controls had significantly increased left ventricular wall edema (6%) and wall thinning with loss of mass (15%). On histology, the major finding was nonocclusive microvascular injury with edema in myocytes, the interstitium, and endothelial cells. Edema was associated with significant worsening of biventricular ejection fractions, ventricular-arterial coupling, and circumferential strain. Early during sepsis, (0-24 hours), the EDV decreased; significantly more in nonsurvivors (ie, greater diastolic dysfunction). From 24 to 48 hours, septic animals' biventricular chamber sizes increased; in survivors significantly greater than baseline and nonsurvivors, whose EDVs were not different from baseline. Preload, afterload, or heart rate differences did not explain these differential changes. CONCLUSIONS: The cardiac dysfunction of sepsis is associated with wall edema. In nonsurvivors, at 0 to 24 hours, sepsis induces a more severe diastolic dysfunction, further decreasing chamber size. The loss of left ventricular mass with wall thinning in septic survivors may, in part, explain the EDV increases from 24 to 48 hours because of a potentially reparative process removing damaged wall tissue. Septic cardiomyopathy is most consistent with a nonocclusive microvascular injury resulting in edema causing reversible systolic and diastolic dysfunction with more severe diastolic dysfunction being associated with a decreased EDV and death.

Cardiovascular Magnetic Resonance Before Invasive Coronary Angiography in Suspected Non-ST-Segment Elevation Myocardial Infarction.

BACKGROUND: In suspected non-ST-segment elevation myocardial infarction (NSTEMI), this presumed diagnosis may not hold true in all cases, particularly in patients with nonobstructive coronary arteries (NOCA). Additionally, in multivessel coronary artery disease, the presumed infarct-related artery may be incorrect. OBJECTIVES: This study sought to assess the diagnostic utility of cardiac magnetic resonance (CMR) before invasive coronary angiogram (ICA) in suspected NSTEMI. METHODS: A total of 100 consecutive stable patients with suspected acute NSTEMI (70% male, age 62 ± 11 years) prospectively underwent CMR pre-ICA to assess cardiac function (cine), edema (T2-weighted imaging, T1 mapping), and necrosis/scar (late gadolinium enhancement). CMR images were interpreted blinded to ICA findings. The clinical care and ICA teams were blinded to CMR findings until post-ICA. RESULTS: Early CMR (median 33 hours postadmission and 4 hours pre-ICA) confirmed only 52% (52 of 100) of patients had subendocardial infarction, 15% transmural infarction, 18% nonischemic pathologies (myocarditis, takotsubo, and other forms of cardiomyopathies), and 11% normal CMR; 4% were nondiagnostic. Subanalyses according to ICA findings showed that, in patients with obstructive coronary artery disease (73 of 100), CMR confirmed only 84% (61 of 73) had MI, 10% (7 of 73) nonischemic pathologies, and 5% (4 of 73) normal. In patients with NOCA (27 of 100), CMR found MI in only 22% (6 of 27 true MI with NOCA), and reclassified the presumed diagnosis of NSTEMI in 67% (18 of 27: 11 nonischemic pathologies, 7 normal). In patients with CMR-MI and obstructive coronary artery disease (61 of 100), CMR identified a different infarct-related artery in 11% (7 of 61). CONCLUSIONS: In patients presenting with suspected NSTEMI, a CMR-first strategy identified MI in 67%, nonischemic pathologies in 18%, and normal findings in 11%. Accordingly, CMR has the potential to affect at least 50% of all patients by reclassifying their diagnosis or altering their potential management.

Diagnostic performance of unenhanced electrocardiogram-gated cardiac CT for detecting myocardial edema.

To assess the diagnostic performance of unenhanced electrocardiogram (ECG)-gated cardiac computed tomography (CT) for detecting myocardial edema, using MRI T2 mapping as the reference standard. This retrospective study protocol was approved by our institutional review board, which waived the requirement for written informed consent. Between December 2017 to February 2019, consecutive patients who had undergone T2 mapping for myocardial tissue characterization were identified. We excluded patients who did not undergo unenhanced ECG-gated cardiac CT within 3 months from MRI T2 mapping or who had poor CT image quality. All patients underwent unenhanced ECG-gated cardiac CT with an axial scan using a third-generation, 320 × 0.5 mm detector-row CT unit. Two radiologists together drew regions of interest (ROIs) in the interventricular septum on the unenhanced ECG-gated cardiac CT images. Using T2 mapping as the reference standard, the diagnostic performance of unenhanced cardiac CT for detecting myocardial edema was evaluated by using the area under the receiver operating characteristic curve with sensitivity and specificity. Youden index was used to find an optimal sensitivity-specificity cutoff point. A cardiovascular radiologist independently performed the measurements, and interobserver reliability was assessed using intraclass correlation coefficients for CT value measurements. A P value of <.05 was considered statistically significant. We included 257 patients who had undergone MRI T2 mapping. Of the 257 patients, 35 patients underwent unenhanced ECG-gated cardiac CT. One patient was excluded from the study because of poor CT image quality. Finally, 34 patients (23 men; age 64.7 ±â€…14.6 years) comprised our study group. Using T2 mapping, we identified myocardial edema in 19 patients. Mean CT and T2 values for 34 patients were 46.3 ±â€…2.7 Hounsfield unit and 49.0 ±â€…4.9 ms, respectively. Mean CT values moderately correlated with mean T2 values (Rho = -0.41; P < .05). Mean CT values provided a sensitivity of 63.2% and a specificity of 93.3% for detecting myocardial edema, with a cutoff value of ≤45.0 Hounsfield unit (area under the receiver operating characteristic curve = 0.77; P < .01). Inter-observer reproducibility in measuring mean CT values was excellent (intraclass correlation coefficient = 0.93; [95% confidence interval: 0.86, 0.96]). Myocardial edema could be detected by CT value of myocardium in unenhanced ECG-gated cardiac CT.

Takotsubo cardiomyopathy mimicking an apical hypertrophic cardiomyopathy.

A 45-years old woman presented for dyspnea and cardiac chest pain. ECG showed deep T-wave inversion while CMR showed normal ejection fraction, hypertrophy and systolic obliteration of the apex suggesting apical HCM. Myocardial oedema was noted at the apex. Complete regression of hypertrophy and myocardial edema was observed after 2 months, and a final diagnosis of subacute Takotsubo was made.

Acute Response of the Noninfarcted Myocardium and Surrounding Tissue Assessed by T2 Mapping After STEMI.

BACKGROUND: ST-segment elevation myocardial infarction (STEMI) is associated with a systemic and local inflammatory response with edema. However, their role at the tissue level is poorly characterized. OBJECTIVES: This study aims to characterize T2 values of the noninfarcted myocardium (NIM) and surrounding tissue and to investigate prognostic relevance of higher NIM T2 values after STEMI. METHODS: A total of 171 consecutive patients with STEMI without prior cardiovascular events who underwent cardiac magnetic resonance after primary percutaneous coronary intervention were analyzed in terms of standard infarct characteristics. Edema of the NIM, liver, spleen, and pectoralis muscle was assessed based on T2 mapping. Follow-up was available for 130 patients. The primary endpoint was major adverse cardiac events (MACE), defined as cardiovascular death, myocardial infarction, unplanned coronary revascularization or rehospitalization for heart failure. The median time from primary percutaneous coronary intervention to cardiac magnetic resonance was 3 days (IQR: 2-5 days). RESULTS: Higher (above the median value of 45 ms) T2 values in the NIM area were associated with larger infarct size, microvascular obstruction, and left ventricular dysfunction and did not correlate with C-reactive protein, white blood cells, or T2 values of the pectoralis muscle, liver, and spleen. At a median follow-up of 17 months, patients with higher (>45 ms) NIM T2 values had increased risk of MACE (P < 0.001) compared with subjects with NIM T2 values ≤45 ms, mainly caused by a higher rate of myocardial reinfarction (26.3% vs 1.4%; P < 0.001). At multivariable analysis, higher NIM T2 values independently predicted MACE (HR: 2.824 [95% CI: 1.254-6.361]; P = 0.012). CONCLUSIONS: Higher NIM T2 values after STEMI are independently associated with worse cardiovascular outcomes, mainly because of higher risk of myocardial infarction.

The role of inflammation in stress cardiomyopathy.

Stress cardiomyopathy (SC) is an increasingly recognized form of acute heart failure, which has been linked to a wide variety of emotional and physical triggers. The pathophysiological mechanisms of the disease remain incompletely understood, however, inflammation has been recently shown to play a pivotal role. This review summarizes the most notable findings of myocardial inflammation, demonstrated from biopsies and cardiac magnetic resonance imaging in humans. In the acute stage macrophage infiltration appears to represent the substrate for myocardial edema, together defining the local myocardial inflammation. This appears to evolve into a low grade systemic chronic inflammation which could explain the protracted clinical course of these patients and raises hope for finding a specific SC cardiac biomarker as well as a therapeutic breakthrough. As a parallel to the human findings the review covers some of the emerging mechanistic insights from experimental models, which, albeit not proven in the human condition, highlight the possible importance in pursuing distinct paths of investigation such as the beta-receptor signaling, aberrations of nitric oxide generation and signaling and the contribution of the vascular endothelium/permeability to edema and inflammation during the acute stage.

COVID-19 in patients with heart failure: the new and the old epidemic.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has spread in nearly 200 countries in less than 4 months since its first identification; accordingly, the coronavirus disease 2019 (COVID 2019) has affirmed itself as a clinical challenge. The prevalence of pre-existing cardiovascular diseases in patients with COVID19 is high and this dreadful combination dictates poor prognosis along with the higher risk of intensive care mortality. In the setting of chronic heart failure, SARS-CoV-2 can be responsible for myocardial injury and acute decompensation through various mechanisms. Given the clinical and epidemiological complexity of COVID-19, patiens with heart failure may require particular care since the viral infection has been identified, considering an adequate re-evaluation of medical therapy and a careful monitoring during ventilation.

Clinical Importance of Myocardial T2 Mapping and Texture Analysis.

Late gadolinium enhancement (LGE) magnetic resonance imaging (MRI) is valuable for diagnosis and assessment of the severity of various myocardial diseases owing to its potential to visualize myocardial scars. T1 mapping is complementary to LGE because it can quantify the degree of myocardial fibrosis or edema. As such, T1-weighted imaging techniques, including LGE using an inversion recovery sequence, contribute to cardiac MRI. T2-weighted imaging is widely used to characterize the tissue of many organs. T2-weighted imaging is used in cardiac MRI to identify myocardial edema related to chest pain, acute myocardial diseases, or severe myocardial injuries. However, it is difficult to determine the presence and extent of myocardial edema because of the low contrast between normal and diseased myocardium and image artifacts of T2-weighted images and the lack of an established method to quantify the images. T2 mapping quantifies myocardial T2 values and help identify myocardial edema. The T2 values are significantly related to the clinical symptoms or severity of nonischemic cardiomyopathy. Texture analysis is a postprocessing method to quantify tissue alterations that are reflected in the T2-weighted images. Texture analysis provides a variety of parameters, such as skewness, entropy, and grey-scale non-uniformity, without the need for additional sequences. The abnormal signal intensity on T2-weighted images or T2 values may correspond to not only myocardial edema but also other tissue alterations. In this review, the techniques of cardiac T2 mapping and texture analysis and their clinical relevance are described.

Advanced cardiac magnetic resonance imaging in takotsubo cardiomyopathy.

Takotsubo cardiomyopathy (TC) is a reversible condition in which there is transient left ventricular (LV) dysfunction characterised most commonly by basal hyperkinesis and mid-apical LV ballooning and hypokinesia. It is said to be triggered by stress and mimics, such as acute coronary syndrome (ACS) clinically. Diagnosis is usually suspected on echocardiography due to the characteristic contraction pattern in a patient with symptoms and signs of ACS but normal coronary arteries on catheter angiography. Cardiac magnetic resonance (CMR), with its latest advancements, is the diagnostic modality of choice for diagnosis, prognosis and follow-up of patients. The advances in CMR (including T1, T2, ECV mapping and threshold-based late gadolinium enhancement (LGE) measurements have revolutionised the role of CMR in tissue characterisation and prognostication in patients with TC. In this review, we highlight the current role of CMR in management of TC and enumerate the CMR findings in TC as well the current advances in the field of CMR, which could help in prognosticating these patients.

Cardiac Involvement in Patients Recovered From COVID-2019 Identified Using Magnetic Resonance Imaging.

Objectives: This study evaluated cardiac involvement in patients recovered from coronavirus disease-2019 (COVID-19) using cardiac magnetic resonance (CMR). Background: Myocardial injury caused by COVID-19 was previously reported in hospitalized patients. It is unknown if there is sustained cardiac involvement after patients' recovery from COVID-19. Methods: Twenty-six patients recovered from COVID-19 who reported cardiac symptoms and underwent CMR examinations were retrospectively included. CMR protocols consisted of conventional sequences (cine, T2-weighted imaging, and late gadolinium enhancement [LGE]) and quantitative mapping sequences (T1, T2, and extracellular volume [ECV] mapping). Edema ratio and LGE were assessed in post-COVID-19 patients. Cardiac function, native T1/T2, and ECV were quantitatively evaluated and compared with controls. Results: Fifteen patients (58%) had abnormal CMR findings on conventional CMR sequences: myocardial edema was found in 14 (54%) patients and LGE was found in 8 (31%) patients. Decreased right ventricle functional parameters including ejection fraction, cardiac index, and stroke volume/body surface area were found in patients with positive conventional CMR findings. Using quantitative mapping, global native T1, T2, and ECV were all found to be significantly elevated in patients with positive conventional CMR findings, compared with patients without positive findings and controls (median [interquartile range]: native T1 1,271 ms [1,243 to 1,298 ms] vs. 1,237 ms [1,216 to 1,262 ms] vs. 1,224 ms [1,217 to 1,245 ms]; mean ± SD: T2 42.7 ± 3.1 ms vs. 38.1 ms ± 2.4 vs. 39.1 ms ± 3.1; median [interquartile range]: 28.2% [24.8% to 36.2%] vs. 24.8% [23.1% to 25.4%] vs. 23.7% [22.2% to 25.2%]; p = 0.002; p < 0.001, and p = 0.002, respectively). Conclusions: Cardiac involvement was found in a proportion of patients recovered from COVID-19. CMR manifestation included myocardial edema, fibrosis, and impaired right ventricle function. Attention should be paid to the possible myocardial involvement in patients recovered from COVID-19 with cardiac symptoms.

Diffusion-weighted imaging in hypertrophic cardiomyopathy: association with high T2-weighted signal intensity in addition to late gadolinium enhancement.

Diffusion-weighted imaging (DWI) has been confirmed to be associated with late gadolinium enhancement (LGE) in hypertrophic cardiomyopathy (HCM). In this context, we aimed to study whether DWI could reflect the active tissue injury and edema information of HCM which were usually indicated by T2 weighted images. Forty HCM patients were examined using a 3.0 T magnetic resonance scanner. Cine, T2-weighted short tau inversion recovery (T2-STIR), DWI and LGE sequences were acquired. T1 mapping was also included to quantify the focal and diffuse fibrosis. Cardiac troponin I (cTnI) was tested to assess the recently myocardial injury. Student's t-test, Mann-Whitney U test, One-way analysis, Kruskal-Wallis analysis, the Spearman correlation analysis, and multivariable regression were used in this study. The apparent diffusion coefficient (ADC) was significantly elevated in the cTnI positive group (P = 0.01) and correlated with LGE (ρ = 0.312, P = 0.049) and HighT2 extent (ρ = 0.443, P = 0.004) in the global level. In the segmental analysis, the ADC significantly differentiated the segments with and without HighT2/LGE presence (P = 0.00). The average ADC values were higher in segments with HighT2 and LGE coexistence than in those with only LGE presence (P < 0.05). Multivariable regression indicated that segmental HighT2 and LGE were both contributing factors to the ADC values. In this study of HCM, we confirmed that ADC as a molecular diffusion parameter reflects the replacement fibrosis of myocardium. Moreover, it also reveals edema extent and its association with serum cTnI.

Echocardiographic two-dimensional speckle tracking identifies acute regional myocardial edema and sub-acute fibrosis in pediatric focal myocarditis with normal ejection fraction: comparison with cardiac magnetic resonance.

The aim here was to describe the role of speckle tracking echocardiography (STE), in identifying impairment in systolic function in children and adolescents with focal myocarditis and without reduction in ejection fraction. We describe data from 33 pediatric patients (age 4-17 years) admitted for focal myocarditis, confirmed by cardiac magnetic resonance (CMR), and without impaired ejection fraction and/or wall motion abnormalities. All children underwent Doppler echocardiography examination with analysis of global (G) and segmental longitudinal strain (LS) and CMR for the quantification of edema and myocardial fibrosis. Reduction in LS was defined according to age-specific partition values. At baseline, impaired GLS was present in 58% of patients (n = 19), albeit normal ejection fraction. LS was also regionally impaired, according to the area of higher edema at CMR (i.e. most impaired at the level of the infero-lateral segments as compared to other segments (p < 0.05). GLS impairment was also moderately correlated with the percentage edema at CMR (r = - 0.712; p = 0.01). At follow-up, GLS improved in all patients (p < 0.001), and normal values were found in 13/19 patients with baseline reduction. Accordingly persistent global and regional impairment was still observed in 6 patients. Patients with persistent LS reduction demonstrated residual focal cardiac fibrosis at follow-up CMR. Both global and regional LS is able to identify abnormalities in systolic longitudinal mechanics in children and adolescents with focal myocarditis and normal ejection fraction. The reduction in LS is consistent with edema amount and localization at CMR. Furthermore, LS identifies regional recovery or persistent cardiac function impairment, possibly related to residual focal fibrosis.

Letter to the editor: is it time for imaging to level with pathology?

CMR provides pathology-like insights of myocardial abnormality, such as hyperemia, edema, necrosis and fibrosis, which is in-vivo, non-invasive and real-time. Hence, it is most likely to become one alternative tool for mimicking pathology, so-called pathologicalized imaging due to its extraordinary tissue characteristics. This article aims to call for a wider clinical application of CMR with more attention on its tissue characterization value.

Performance of two Methods for Cardiac MRI Edema Mapping: Dual-Contrast Fast Spin-Echo and T2 Prepared Balanced Steady State Free Precession.

PURPOSE: To compare true positive and false negative results of myocardial edema mapping in two methods. Myocardial edema may be difficult to detect on cardiac MRI. MATERIALS AND METHODS: 76 patients (age 59 ±â€Š11 years, 15 female) with acute myocardial infarction (MI) and 10 healthy volunteers were prospectively included in this single-center study. 1.5 T cardiac MRI was performed in patients 2.5 days after revascularization (median) for edema mapping: Steady State Free Precession (SSFP) mapping sequence with T2-preparation pulses (T2prep); and dual-contrast Fast Spin-Echo (dcFSE) signal decay edema mapping. Late gadolinium enhancement (LGE) was used as the reference for expected edema in acute MI. RESULTS: 311 myocardial segments in patients were acutely infarcted with mean T2 73 ms for T2prep SSFP vs. 87 ms for dcFSE edema mapping. In healthy volunteers the mean T2 was 56 ms for T2prep SSFP vs. 50 ms for dcFSE edema mapping. Receiver operating characteristic (ROC) curve for T2prep SSFP show area under the curve (AUC) 0.962, p < 0.0001, Youden index J 0.8266, associated criterion > 60 ms, sensitivity 94 %, specificity 89 %. dcFSE ROC AUC 0.979, p < 0.0001, J 0.9219, associated criterion > 64 ms, sensitivity 93 %, specificity 99 %. CONCLUSION: Both edema mapping methods indicate high-grade edema with high sensitivity. Nevertheless, edema in acute infarction may be focally underestimated in both mapping methods. KEY POINTS: · Sensitivity for edema detection is high for both methods.. · Edema may be focally underestimated by T2prep SSFP edema mapping and dcFSE mapping.. CITATION FORMAT: · Krumm P, Martirosian P, Rath D et al. Performance of two Methods for Cardiac MRI Edema Mapping: Dual-Contrast Fast Spin-Echo and T2 Prepared Balanced Steady State Free Precession. Fortschr Röntgenstr 2020; 192: 669 - 677.

Lung Ultrasound for the Diagnosis and Management of Acute Respiratory Failure.

For critically ill patients with acute respiratory failure (ARF), lung ultrasound (LUS) has emerged as an indispensable tool to facilitate diagnosis and rapid therapeutic management. In ARF, there is now evidence to support the use of LUS to diagnose pneumothorax, acute respiratory distress syndrome, cardiogenic pulmonary edema, pneumonia, and acute pulmonary embolism. In addition, the utility of LUS has expanded in recent years to aid in the ongoing management of critically ill patients with ARF, providing guidance in volume status and fluid administration, titration of positive end-expiratory pressure, and ventilator liberation. The aims of this review are to examine the basic foundational concepts regarding the performance and interpretation of LUS, and to appraise the current literature supporting the use of this technique in the diagnosis and continued management of patients with ARF.

Acute impact of an endurance race on cardiac function and biomarkers of myocardial injury in triathletes with and without myocardial fibrosis.

AIMS: The aim of this study was to investigate the occurrence of myocardial injury and cardiac dysfunction after an endurance race by biomarkers and cardiac magnetic resonance in triathletes with and without myocardial fibrosis. METHODS AND RESULTS: Thirty asymptomatic male triathletes (45 ± 10 years) with over 10 training hours per week and 55 ± 8 ml/kg per minute maximal oxygen uptake during exercise testing were studied before (baseline) and 2.4 ± 1.1 hours post-race. Baseline cardiac magnetic resonance included cine, T1/T2, late gadolinium enhancement (LGE) and extracellular volume imaging. Post-race non-contrast cardiac magnetic resonance included cine and T1/T2 mapping. Non-ischaemic myocardial fibrosis was present in 10 triathletes (LGE+) whereas 20 had no fibrosis (LGE-). At baseline, LGE + triathletes had higher peak exercise systolic blood pressure with 222 ± 21 mmHg compared to LGE- triathletes (192 ± 30 mmHg, P < 0.01). Post-race troponin T and creatine kinase MB were similarly increased in both groups, but there was no change in T2 and T1 from baseline to post-race with 54 ± 3 ms versus 53 ± 3 ms (P = 0.797) and 989 ± 21 ms versus 989 ± 28 ms (P = 0.926), respectively. However, post-race left atrial ejection fraction was significantly lower in LGE + triathletes compared to LGE- triathletes (53 ± 6% vs. 59 ± 6%, P < 0.05). Furthermore, baseline atrial peak filling rates were lower in LGE - triathletes (121 ± 30 ml/s/m2) compared to LGE + triathletes (161 ± 34 ml/s/m2, P < 0.01). Post-race atrial peak filling rates increased in LGE- triathletes to 163 ± 46 ml/s/m2, P < 0.001), but not in LGE + triathletes (169 ± 50ml/s/m2, P = 0.747). CONCLUSION: Despite post-race troponin T release, we did not find detectable myocardial oedema by cardiac magnetic resonance. However, the unfavourable blood pressure response during exercise testing seemed to be associated with post-race cardiac dysfunction, which could explain the occurrence of myocardial fibrosis in triathletes.