A concealed carcinoid cardiac metastasis uncovered by comprehensive cardiovascular magnetic resonance-based tissue characterization: a case report.

oai:serval.unil.ch:BIB_EFAC9560DFE5Cardiac metastases of carcinoid tumours are extremely rare, and their diagnosis poses a significant challenge. A variety of techniques has been reported in the literature for this purpose, ranging from echocardiogram to the Indium-111 Octreotide, positron emission tomography using specific tracers, and biopsy. Occasionally, the diagnosis is only made post-mortem. Recently, CMR (cardiovascular magnetic resonance) has been added to the diagnostic toolkit. This case report describes the CMR sequences that can be used to characterize cardiac metastases of carcinoid tumours. A 55-year-old woman with an antecedent history of resected carcinoid tumour of the ileocecal junction underwent whole-body In-111 Octreoscan single-photon emission computed tomography in the context of her follow-up. This raised the suspicion of pericardial involvement, which prompted a CMR study. Comprehensive CMR findings were consistent with isolated carcinoid tumour metastasis embedded within the anterior papillary muscle. We describe the CMR sequences that were used to characterize the metastasis. The rarity of cardiac metastasis of carcinoid tumour makes its diagnosis challenging and warrants a high level of clinical suspicion. Cardiovascular magnetic resonance imaging proves to be an indispensable tool in the tissue characterization of such tumours

Probing the intravascular and interstitial compartments of remodeled myocardium in heart failure patients with preserved and reduced ejection fraction: a CMR study.

Recent autopsy studies found microvascular rarefaction in remodeled myocardium of patients who died of heart failure with preserved ejection-fraction (HFpEF). This condition has not been investigated so far by non-invasive methods in patients with HFpEF. The aim was to quantify the intravascular volume (IVV) compartment by CMR in HFpEF patients. In two separate CMR examinations, HFpEF patients (n = 6; 12 examinations) and post-myocardial infarction patients (post-MI; n = 6; 12 examinations) were studied with T <sub>1</sub> -mapping (MOLLI-sequence) before and after IV bolus of 0.03 mmol/Kg of the intravascular contrast-medium (CM) Gadofosveset and 0.2 mmol/Kg of the extravascular CM Gadobutrol yielding IVV and extracellular volume (ECV), respectively. Healthy controls (n = 10 with Gadofosveset only, n = 10 with Gadobutrol only) were also studied with the same protocol. IVV and ECV were measured in the basal septum (without ischemic scar in post-MI patients). In post-MI patients, ECV and IVV were also measured in the ischemic scar. Left ventricular (LV) volumes, mass, and ejection-fraction were measured by standard protocol. LV global longitudinal strain (GLS) was calculated by feature tracking on long-axis cine acquisitions. LV mass to end-diastolic volume ratio and GLS in HFpEF were higher and lower, respectively, than in healthy controls and post-MI patients, whereas the post-MI patients showed lower LV ejection-fraction. Compared to healthy myocardium of controls, IVV in scar was reduced (0.135 ± 0.018 vs 0.109 ± 0.008, respectively, p = 0.005), while ECV was increased (0.244 ± 0.037 vs 0.698 ± 0.106, respectively, p < 0.001). However, IVV did not differ among HFpEF, post-MI, and healthy controls (0.155 ± 0.033, 0.146 ± 0.038, and 0.135 ± 0.018, respectively, p = 0.413), whereas ECV was higher in HFpEF than in post-MI and healthy controls (0.304 ± 0.159, 0.270 ± 0.017, and 0.244 ± 0.037, respectively, p = 0.003). The T <sub>1</sub> -mapping technique combined with an intravascular CM shows potential to measure IVV. In infarct scar with substantially increased ECV, IVV was significantly reduced. Unlike in infarct scar, in remodeled myocardium of HFpEF patients, increased ECV was not accompanied by a reduction of IVV

Impact of bileaflet mitral valve prolapse on quantification of mitral regurgitation with cardiac magnetic resonance: a single-center study.

To quantify mitral regurgitation (MR) with CMR, the regurgitant volume can be calculated as the difference between the left ventricular (LV) stroke volume (SV) measured with the Simpson's method and the reference SV, i.e. the right ventricular SV (RVSV) in patients without tricuspid regurgitation. However, for patients with prominent mitral valve prolapse (MVP), the Simpson's method may underestimate the LV end-systolic volume (LVESV) as it only considers the volume located between the apex and the mitral annulus, and neglects the ventricular volume that is displaced into the left atrium but contained within the prolapsed mitral leaflets at end systole. This may lead to an underestimation of LVESV, and resulting an over-estimation of LVSV, and an over-estimation of mitral regurgitation. The aim of the present study was to assess the impact of prominent MVP on MR quantification by CMR. In patients with MVP (and no more than trace tricuspid regurgitation) MR was quantified by calculating the regurgitant volume as the difference between LVSV and RVSV. LVSV <sub>uncorr</sub> was calculated conventionally as LV end-diastolic (LVEDV) minus LVESV. A corrected LVESV <sub>corr</sub> was calculated as the LVESV plus the prolapsed volume, i.e. the volume between the mitral annulus and the prolapsing mitral leaflets. The 2 methods were compared with respect to the MR grading. MR grades were defined as absent or trace, mild (5-29% regurgitant fraction (RF)), moderate (30-49% RF), or severe (≥50% RF). In 35 patients (44.0 ± 23.0y, 14 males, 20 patients with MR) the prolapsed volume was 16.5 ± 8.7 ml. The 2 methods were concordant in only 12 (34%) patients, as the uncorrected method indicated a 1-grade higher MR severity in 23 (66%) patients. For the uncorrected/corrected method, the distribution of the MR grades as absent-trace (0 vs 11, respectively), mild (20 vs 18, respectively), moderate (11 vs 5, respectively), and severe (4 vs 1, respectively) was significantly different (p < 0.001). In the subgroup without MR, LVSV <sub>corr</sub> was not significantly different from RVSV (difference: 2.5 ± 4.7 ml, p = 0.11 vs 0) while a systematic overestimation was observed with LVSV <sub>uncorr</sub> (difference: 16.9 ± 9.1 ml, p = 0.0007 vs 0). Also, RVSV was highly correlated with aortic forward flow (n = 24, R <sup>2</sup>  = 0.97, p < 0.001). For patients with severe bileaflet prolapse, the correction of the LVSV for the prolapse volume is suggested as it modified the assessment of MR severity by one grade in a large portion of patients

Relationship between CMR-derived parameters of ischemia/reperfusion injury and the timing of CMR after reperfused ST-segment elevation myocardial infarction.

To investigate the influence of cardiovascular magnetic resonance (CMR) timing after reperfusion on CMR-derived parameters of ischemia/reperfusion (I/R) injury in patients with ST-segment elevation myocardial infarction (STEMI). The study included 163 reperfused STEMI patients undergoing CMR during the index hospitalization. Patients were divided according to the time between revascularization and CMR (T <sub>revasc-CMR</sub> : Tertile-1 ≤ 43; 43 < Tertile-2 ≤ 93; Tertile-3 > 93 h). T2-mapping derived area-at-risk (AAR) and intramyocardial-hemorrhage (IMH), and late gadolinium enhancement (LGE)-derived infarct size (IS) and microvascular obstruction (MVO) were quantified. T1-mapping was performed before and > 15 min after Gd-based contrast-agent administration yielding extracellular volume (ECV) of infarct. Main factors influencing I/R injury were homogenously balanced across T <sub>revasc-CMR</sub> tertiles. T2 values of infarct and remote regions increased with increasing T <sub>revasc-CMR</sub> tertiles (infarct: 60.0 ± 4.9 vs 63.5 ± 5.6 vs 64.8 ± 7.5 ms; P < 0.001; remote: 44.3 ± 2.8 vs 46.1 ± 2.8 vs ± 46.1 ± 3.0; P = 0.001). However, T2 value of infarct largely and significantly exceeded that of remote myocardium in each tertile yielding comparable T2-mapping-derived AAR extent throughout T <sub>revasc-CMR</sub> tertiles (17 ± 9% vs 19 ± 9% vs 18 ± 8% of LV, respectively, P = 0.385). Similarly, T2-mapping-based IMH detection and quantification were independent of T <sub>revasc-CMR</sub> . LGE-derived IS and MVO were not influenced by T <sub>revasc-CMR</sub> (IS: 12 ± 9% vs 12 ± 9% vs 14 ± 9% of LV, respectively, P = 0.646). In 68 patients without MVO, T1-mapping based ECV of infarct region was comparable across T <sub>revasc-CMR</sub> tertiles (P = 0.470). In STEMI patients, T2 values of infarct and remote myocardium increase with increasing CMR time after revascularization. However, these changes do not give rise to substantial variation of T2-mapping-derived AAR size nor of other CMR-based parameters of I/R. ISRCTN03522116 . Registered 30.4.2018 (retrospectively registered)

MicroRNA-21 links epithelial-to-mesenchymal transition and inflammatory signals to confer resistance to neoadjuvant trastuzumab and chemotherapy in HER2-positive breast cancer patients

Patients with primary HER2-positive breast cancer benefit from HER2-targeted therapies. Nevertheless, a significant proportion of these patients die of disease progression due to mechanisms of drug resistance. MicroRNAs (miRNAs) are emerging as critical core regulators of drug resistance that act by modulating the epithelial- to-mesenchymal transition (EMT) and cancer-related immune responses. In this study, we investigated the association between the expression of a specific subset of 14 miRNAs involved in EMT processes and immune functions and the response to neoadjuvant trastuzumab and chemotherapy in 52 patients with HER2-overexpressing breast tumors. The expression of only a single miRNA, miR-21, was significantly associated with residual disease (p = 0.030) and increased after trastuzumab-chemotherapy (p = 0.012). A target prediction analysis coupled with in vitro and in vivo validations revealed that miR-21 levels inversely correlated with the expression of PTEN (rs = -0.502; p = 0.005) and PDCD4 (rs = -0.426; p = 0.019), which differentially influenced the drug sensitivity of HER2-positive breast cancer cells. However, PTEN expression was only marginally associated with residual disease. We further demonstrated that miR-21 was able to affect the response to both trastuzumab and chemotherapy, triggering an IL-6/STAT3/NF-\u3baB-mediated signaling loop and activating the PI3K pathway. Our findings support the ability of miR-21 signaling to sustain EMT and shape the tumor immune microenvironment in HER2-positive breast cancer. Collectively, these data provide a rationale for using miR-21 expression as a biomarker to select trastuzumab-chemotherapy-resistant HER2-positive breast cancer patients who may benefit from treatments containing PI3K inhibitors or immunomodulatory drugs

A concealed carcinoid cardiac metastasis uncovered by comprehensive cardiovascular magnetic resonance-based tissue characterization: A case report

Background: Cardiac metastases of carcinoid tumours are extremely rare, and their diagnosis poses a significant challenge. A variety of techniques has been reported in the literature for this purpose, ranging from echocardiogram to the Indium-111 Octreotide, positron emission tomography using specific tracers, and biopsy. Occasionally, the diagnosis is only made post-mortem. Recently, CMR (cardiovascular magnetic resonance) has been added to the diagnostic toolkit. This case report describes the CMR sequences that can be used to characterize cardiac metastases of carcinoid tumours. Case summary: A 55-year-old woman with an antecedent history of resected carcinoid tumour of the ileocecal junction underwent whole-body In-111 Octreoscan single-photon emission computed tomography in the context of her follow-up. This raised the suspicion of pericardial involvement, which prompted a CMR study. Comprehensive CMR findings were consistent with isolated carcinoid tumour metastasis embedded within the anterior papillary muscle. We describe the CMR sequences that were used to characterize the metastasis. Discussion: The rarity of cardiac metastasis of carcinoid tumour makes its diagnosis challenging and warrants a high level of clinical suspicion. Cardiovascular magnetic resonance imaging proves to be an indispensable tool in the tissue characterization of such tumours. © 2020 The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology

Blood flow assessment by transit time flow measurement and its prognostic impact in coronary bypass surgery.

The competitive coronary flow is influenced by the severity of the stenosis and may affect graft patency. Transit time flow measurement (TTFM) enables intraoperative graft evaluation and cardiac magnetic resonance (MRI) allows for graft evaluation during follow-up. Competitive flow and target vessel diameters were determined in 35 patients undergoing off-pump coronary bypass graft surgery (CABG) and correlated to TTFM. Cardiac function, ischemia, and graft flow were evaluated using cardiac MRI during the follow-up period to determine the impact of above-mentioned parameters on graft patency. Competitive flow led to reduced mean graft flow (MGF) and increased pulsatility index (PI) in arterial grafts. This effect to was not observed in veins. Smaller target coronary arteries (<1.5 mm) were associated with reduced MGF, more pronounced in veins, which presented increased PI and shortened diastolic flow fraction (DF). No death and no re-hospitalization for acute coronary syndrome occurred. Borderline values of TTFM (mean MGF 13±4 mL/min; PI 3.8±1) in left internal mammary artery (LIMA) were mainly observed due to increased native anterior descending artery (LAD) flow. These LAD's collateralized occluded right coronaries (RCA). The corresponding LIMA to LAD grafts showed a bypass flow increase at cardiac MRI follow-up. Two graft occlusions occurred: one in LIMA-to-LAD bypass with borderline TTFM, which did not collateralize the RCA and one in a vein graft with borderline TTFM bypassed on a narrow vascular target. Competitive flow has an impact on arteries contrary to veins. Veins are at risk for occlusion when grafted to smaller targets. Borderline LIMA flow should be considered as potentially dangerous, if satisfactory explanations are missing, e.g. in the absence of a large coronary target without flow competition