Cardiac magnetic resonance imaging in preeclampsia complicated by pulmonary edema shows myocardial edema with normal left ventricular systolic function.

BACKGROUND: Preeclampsia complicates approximately 5% of all pregnancies. When pulmonary edema occurs, it accounts for 50% of preeclampsia-related mortality. Currently, there is no consensus on the degree to which left ventricular systolic dysfunction contributes to the development of pulmonary edema. OBJECTIVE: This study aimed to use cardiac magnetic resonance imaging to detect subtle changes in left ventricular systolic function and evidence of acute left ventricular dysfunction (through tissue characterization) in women with preeclampsia complicated by pulmonary edema compared with both preeclamptic and normotensive controls. STUDY DESIGN: Cases were postpartum women aged ≥18 years presenting with preeclampsia complicated by pulmonary edema. Of note, 2 control groups were recruited: women with preeclampsia without pulmonary edema and women with normotensive pregnancies. All women underwent echocardiography and 1.5T cardiac magnetic resonance imaging with native T1 and T2 mapping. Gadolinium contrast was administered to cases only. Because of small sample sizes, a nonparametric test (Kruskal-Wallis) with pairwise posthoc analysis using Bonferroni correction was used to compare the differences between the groups. Cardiac magnetic resonance images were interpreted by 2 independent reporters. The intraclass correlation coefficient was calculated to assess interobserver reliability. RESULTS: Here, 20 women with preeclampsia complicated by pulmonary edema, 13 women with preeclampsia (5 with severe features and 8 without severe features), and 6 normotensive controls were recruited. There was no difference in the baseline characteristics between groups apart from the expected differences in blood pressure. Left atrial sizes were similar across all groups. Women with preeclampsia complicated by pulmonary edema had increased left ventricular mass (P=.01) but had normal systolic function compared with the normotensive controls. Furthermore, they had elevated native T1 values (P=.025) and a trend toward elevated T2 values (P=.07) in the absence of late gadolinium enhancement consistent with myocardial edema. Moreover, myocardial edema was present in all women with eclampsia or hemolysis, elevated liver enzymes, and low platelet count. Women with preeclampsia without severe features had similar findings to the normotensive controls. All cardiac magnetic resonance imaging measurements showed a very high level of interobserver correlation. CONCLUSION: This study focused on cardiac magnetic resonance imaging in women with preeclampsia complicated by pulmonary edema, eclampsia, and hemolysis, elevated liver enzymes, and low platelet count. We have demonstrated normal systolic function with myocardial edema in women with preeclampsia with these severe features. These findings implicate an acute myocardial process as part of this clinical syndrome. The pathogenesis of myocardial edema and its relationship to pulmonary edema require further elucidation. With normal left atrial sizes, any hemodynamic component must be acute.

Diagnostic performance of T1 and T2 mapping to detect intramyocardial hemorrhage in reperfused ST-segment elevation myocardial infarction (STEMI) patients.

PURPOSE: To investigate the performance of T1 and T2 mapping to detect intramyocardial hemorrhage (IMH) in ST-segment elevation myocardial infarction (STEMI) patients treated by primary percutaneous coronary intervention (PPCI). MATERIALS AND METHODS: Fifty STEMI patients were prospectively recruited between August 2013 and July 2014 following informed consent. Forty-eight patients completed a 1.5T cardiac magnetic resonance imaging (MRI) with native T1 , T2 , and T2* maps at 4 ± 2 days. Receiver operating characteristic (ROC) analyses were performed to assess the performance of T1 and T2 to detect IMH. RESULTS: The mean age was 59 ± 13 years old and 88% (24/48) were male. In all, 39 patients had interpretable T2* maps and 26/39 (67%) of the patients had IMH ( T2* <20 msec on T2* maps). Both T1 and T2 values of the hypointense core within the area-at-risk (AAR) performed equally well to detect IMH (T1 maps AUC 0.86 [95% confidence interval [CI] 0.72-0.99] versus T2 maps AUC 0.86 [95% CI 0.74-0.99]; P = 0.94). Using the binary assessment of presence or absence of a hypointense core on the maps, the diagnostic performance of T1 and T2 remained equally good (T1 AUC 0.87 [95% CI 0.73-1.00] versus T2 AUC 0.85 [95% CI 0.71-0.99]; P = 0.90) with good sensitivity and specificity (T1 : 88% and 85% and T2 : 85% and 85%, respectively). CONCLUSION: The presence of a hypointense core on the T1 and T2 maps can detect IMH equally well and with good sensitivity and specificity in reperfused STEMI patients and could be used as an alternative when T2* images are not acquired or are not interpretable. LEVEL OF EVIDENCE: 2 Technical Efficacy: Stage 2 J. MAGN. RESON. IMAGING 2017;46:877-886.

Quantification of both the area-at-risk and acute myocardial infarct size in ST-segment elevation myocardial infarction using T1-mapping.

BACKGROUND: A comprehensive cardiovascular magnetic resonance (CMR) in reperfused ST-segment myocardial infarction (STEMI) patients can be challenging to perform and can be time-consuming. We aimed to investigate whether native T1-mapping can accurately delineate the edema-based area-at-risk (AAR) and post-contrast T1-mapping and synthetic late gadolinium (LGE) images can quantify MI size at 1.5 T. Conventional LGE imaging and T2-mapping could then be omitted, thereby shortening the scan duration. METHODS: Twenty-eight STEMI patients underwent a CMR scan at 1.5 T, 3 ± 1 days following primary percutaneous coronary intervention. The AAR was quantified using both native T1 and T2-mapping. MI size was quantified using conventional LGE, post-contrast T1-mapping and synthetic magnitude-reconstructed inversion recovery (MagIR) LGE and synthetic phase-sensitive inversion recovery (PSIR) LGE, derived from the post-contrast T1 maps. RESULTS: Native T1-mapping performed as well as T2-mapping in delineating the AAR (41.6 ± 11.9% of the left ventricle [% LV] versus 41.7 ± 12.2% LV, P = 0.72; R2 0.97; ICC 0.986 (0.969-0.993); bias -0.1 ± 4.2% LV). There were excellent correlation and inter-method agreement with no bias, between MI size by conventional LGE, synthetic MagIR LGE (bias 0.2 ± 2.2%LV, P = 0.35), synthetic PSIR LGE (bias 0.4 ± 2.2% LV, P = 0.060) and post-contrast T1-mapping (bias 0.3 ± 1.8% LV, P = 0.10). The mean scan duration was 58 ± 4 min. Not performing T2 mapping (6 ± 1 min) and conventional LGE (10 ± 1 min) would shorten the CMR study by 15-20 min. CONCLUSIONS: T1-mapping can accurately quantify both the edema-based AAR (using native T1 maps) and acute MI size (using post-contrast T1 maps) in STEMI patients without major cardiovascular risk factors. This approach would shorten the duration of a comprehensive CMR study without significantly compromising on data acquisition and would obviate the need to perform T2 maps and LGE imaging.

Defining left ventricular remodeling following acute ST-segment elevation myocardial infarction using cardiovascular magnetic resonance.

BACKGROUND: The assessment of post-myocardial infarction (MI) left ventricular (LV) remodeling by cardiovascular magnetic resonance (CMR) currently uses criteria defined by echocardiography. Our aim was to provide CMR criteria for assessing LV remodeling following acute MI. METHODS: Firstly, 40 reperfused ST-segment elevation myocardial infarction (STEMI) patients with paired acute (4 ± 2 days) and follow-up (5 ± 2 months) CMR scans were analyzed by 2 independent reviewers and the minimal detectable changes (MDCs) for percentage change in LV end-diastolic volume (%ΔLVEDV), LV end-systolic volume (%ΔLVESV), and LV ejection fraction (%ΔLVEF) between the acute and follow-up scans were determined. Secondly, in 146 reperfused STEMI patients, receiver operator characteristic curve analyses for predicting LVEF <50% at follow-up (as a surrogate for clinical poor clinical outcome) were undertaken to obtain cut-off values for %ΔLVEDV and %ΔLVESV. RESULTS: The MDCs for %ΔLVEDV, %ΔLVESV, and %ΔLVEF were similar at 12%, 12%, 13%, respectively. The cut-off values for predicting LVEF < 50% at follow-up were 11% for %ΔLVEDV on receiver operating characteristic curve analysis (area under the curve (AUC) 0.75, 95% CI 0.6 to 0.83, sensitivity 72% specificity 70%), and 5% for %ΔLVESV (AUC 0.83, 95% CI 0.77 to 0.90, sensitivity and specificity 78%). Using cut-off MDC values (higher than the clinically important cut-off values) of 12% for both %ΔLVEDV and %ΔLVESV, 4 main patterns of LV remodeling were identified in our cohort: reverse LV remodeling (LVEF predominantly improved); no LV remodeling (LVEF predominantly unchanged); adverse LV remodeling with compensation (LVEF predominantly improved); and adverse LV remodeling (LVEF unchanged or worsened). CONCLUSIONS: The MDCs for %ΔLVEDV and %ΔLVESV between the acute and follow-up CMR scans of 12% each may be used to define adverse or reverse LV remodeling post-STEMI. The MDC for %ΔLVEF of 13%, relative to baseline, provides the minimal effect size required for investigating treatments aimed at improving LVEF following acute STEMI.

Provision of magnetic resonance imaging for patients with 'MR-conditional' cardiac implantable electronic devices: an unmet clinical need.

AIMS: Increasing need for magnetic resonance imaging (MRI) has driven the development of MR-conditional cardiac implantable electronic devices (CIEDs; pacemakers and defibrillators); however, patients still report difficulties obtaining scans. We sought to establish current provision for MRI scanning of patients with CIEDs in England. METHODS AND RESULTS: A survey was distributed to all hospitals in England with MRI, to assess current practice. Information requested included whether hospitals currently offer MRI to this patient group, the number and type of scans acquired, local safety considerations, complications experienced and perceived obstacles to service provision in those departments not currently offering it. Responses were received from 195 of 227 (86%) of hospitals surveyed. Although 98% of departments were aware of MR-conditional devices, only 46% (n = 89) currently offer MRI scans to patients with CIED's; of these, 85% of departments perform ≤10 scans per year. No major complications were reported from MRI scanning in patients with MR-conditional devices. Current barriers to service expansion include perceived concerns regarding potential risk, lack of training, logistical difficulties, and lack of cardiology support. CONCLUSION: Provision of MRI for patients with CIEDs is currently poor, despite increasing numbers of patients with MR-conditional devices and extremely low reported complication rates.

Prognostic Value of Late Gadolinium Enhancement Cardiovascular Magnetic Resonance in Cardiac Amyloidosis.

BACKGROUND: The prognosis and treatment of the 2 main types of cardiac amyloidosis, immunoglobulin light chain (AL) and transthyretin (ATTR) amyloidosis, are substantially influenced by cardiac involvement. Cardiovascular magnetic resonance with late gadolinium enhancement (LGE) is a reference standard for the diagnosis of cardiac amyloidosis, but its potential for stratifying risk is unknown. METHODS AND RESULTS: Two hundred fifty prospectively recruited subjects, 122 patients with ATTR amyloid, 9 asymptomatic mutation carriers, and 119 patients with AL amyloidosis, underwent LGE cardiovascular magnetic resonance. Subjects were followed up for a mean of 24±13 months. LGE was performed with phase-sensitive inversion recovery (PSIR) and without (magnitude only). These were compared with extracellular volume measured with T1 mapping. PSIR was superior to magnitude-only inversion recovery LGE because PSIR always nulled the tissue (blood or myocardium) with the longest T1 (least gadolinium). LGE was classified into 3 patterns: none, subendocardial, and transmural, which were associated with increasing amyloid burden as defined by extracellular volume (P<0.0001), with transitions from none to subendocardial LGE at an extracellular volume of 0.40 to 0.43 (AL) and 0.39 to 0.40 (ATTR) and to transmural at 0.48 to 0.55 (AL) and 0.47 to 0.59 (ATTR). Sixty-seven patients (27%) died. Transmural LGE predicted death (hazard ratio, 5.4; 95% confidence interval, 2.1-13.7; P<0.0001) and remained independent after adjustment for N-terminal pro-brain natriuretic peptide, ejection fraction, stroke volume index, E/E', and left ventricular mass index (hazard ratio, 4.1; 95% confidence interval, 1.3-13.1; P<0.05). CONCLUSIONS: There is a continuum of cardiac involvement in systemic AL and ATTR amyloidosis. Transmural LGE is determined reliably by PSIR and represents advanced cardiac amyloidosis. The PSIR technique provides incremental information on outcome even after adjustment for known prognostic factors.

T1 mapping and survival in systemic light-chain amyloidosis.

AIMS: To assess the prognostic value of myocardial pre-contrast T1 and extracellular volume (ECV) in systemic amyloid light-chain (AL) amyloidosis using cardiovascular magnetic resonance (CMR) T1 mapping. METHODS AND RESULTS: One hundred patients underwent CMR and T1 mapping pre- and post-contrast. Myocardial ECV was calculated at contrast equilibrium (ECV(i)) and 15 min post-bolus (ECVb). Fifty-four healthy volunteers served as controls. Patients were followed up for a median duration of 23 months and survival analyses were performed. Mean ECV(i) was raised in amyloid (0.44 ± 0.12) as was ECV(b) (mean 0.44 ± 0.12) compared with healthy volunteers (0.25 ± 0.02), P < 0.001. Native pre-contrast T1 was raised in amyloid (mean 1080 ± 87 ms vs. 954 ± 34 ms, P < 0.001). All three correlated with pre-test probability of cardiac involvement, cardiac biomarkers, and systolic and diastolic dysfunction. During follow-up, 25 deaths occurred. An ECV(i) of >0.45 carried a hazard ratio (HR) for death of 3.84 [95% confidence interval (CI): 1.53-9.61], P = 0.004 and pre-contrast T1 of >1044 ms = HR 5.39 (95% CI: 1.24-23.4), P = 0.02. Extracellular volume after primed infusion and ECVb performed similarly. Isolated post-contrast T1 was non-predictive. In Cox regression models, ECV(i) was independently predictive of mortality (HR = 4.41, 95% CI: 1.35-14.4) after adjusting for E:E', ejection fraction, diastolic dysfunction grade, and NT-proBNP. CONCLUSION: Myocardial ECV (bolus or infusion technique) and pre-contrast T1 are biomarkers for cardiac AL amyloid and they predict mortality in systemic amyloidosis.

Splenic Switch-off: A Tool to Assess Stress Adequacy in Adenosine Perfusion Cardiac MR Imaging.

PURPOSE: To investigate the pharmacology and potential clinical utility of splenic switch-off to identify understress in adenosine perfusion cardiac magnetic resonance (MR) imaging. MATERIALS AND METHODS: Splenic switch-off was assessed in perfusion cardiac MR examinations from 100 patients (mean age, 62 years [age range, 18-87 years]) by using three stress agents (adenosine, dobutamine, and regadenoson) in three different institutions, with appropriate ethical permissions. In addition, 100 negative adenosine images from the Clinical Evaluation of MR Imaging in Coronary Heart Disease (CE-MARC) trial (35 false and 65 true negative; mean age, 59 years [age range, 40-73 years]) were assessed to ascertain the clinical utility of the sign to detect likely pharmacologic understress. Differences in splenic perfusion were compared by using Wilcoxon signed rank or Wilcoxon rank sum tests, and true-negative and false-negative findings in CE-MARC groups were compared by using the Fisher exact test. RESULTS: The spleen was visible in 99% (198 of 200) of examinations and interobserver agreement in the visual grading of splenic switch-off was excellent (κ = 0.92). Visually, splenic switch-off occurred in 90% of adenosine studies, but never in dobutamine or regadenoson studies. Semiquantitative assessments supported these observations: peak signal intensity was 78% less with adenosine than at rest (P < .001), but unchanged with regadenoson (4% reduction; P = .08). Calculated peak splenic divided by myocardial signal intensity (peak splenic/myocardial signal intensity) differed between stress agents (adenosine median, 0.34; dobutamine median, 1.34; regadenoson median, 1.13; P < .001). Failed splenic switch-off was significantly more common in CE-MARC patients with false-negative findings than with true-negative findings (34% vs 9%, P < .005). CONCLUSION: Failed splenic switch-off with adenosine is a new, simple observation that identifies understressed patients who are at risk for false-negative findings on perfusion MR images. These data suggest that almost 10% of all patients may be understressed, and that repeat examination of individuals with failed splenic switch-off may significantly improve test sensitivity.

Differential Myocyte Responses in Patients with Cardiac Transthyretin Amyloidosis and Light-Chain Amyloidosis: A Cardiac MR Imaging Study.

PURPOSE: To investigate cardiac magnetic resonance (MR) imaging measurements of extracellular volume (ECV) and total cell volume in immunoglobulin light-chain amyloidosis (AL) and transthyretin amyloidosis (ATTR) in order to evaluate the amyloid and myocyte volumes. MATERIALS AND METHODS: All ethics were approved, and participants provided written informed consent. Of the 257 subjects who were recruited, 92 had AL (mean age, 62 years ± 10), 44 had mutant ATTR (mean age, 68 years ± 10), and 66 had wild-type ATTR (mean age, 75 years ± 7). In addition, eight healthy subjects with ATTR mutations (mean age, 47 years ± 6) and 47 healthy volunteers (mean age, 45 years ± 15) participated. All participants underwent equilibrium contrast material-enhanced cardiac MR imaging. ECV and total cell volume were measured in the heart. T test, χ(2), and one-way analysis of variance with posthoc Bonferroni correction were used. RESULTS: Both the left ventricular indexed mass and ECV were elevated in patients with amyloidosis. For left ventricular indexed mass, mean AL was 107 g/m(2) ± 30; mean mutant ATTR was 137 g/m(2) ± 29; and mean wild-type ATTR was 133 g/m(2) ± 27 versus 65 g/m(2) ± 15 in healthy subjects (P < .0001 for all measures). For ECV, mean AL was 0.54 ± 0.07, mean mutant ATTR was 0.60 ± 0.07, and mean wild-type ATTR was 0.57 ± 0.06 versus 0.27 ± 0.03 in healthy subjects (P < .0001 for all measures). Patients with ATTR had a higher total cell volume than did healthy subjects (mean, 53 mL/m(2) ± 12 vs 45 mL/m(2) ± 11; P = .001), but in patients with AL, total cell volume was normal (mean, 47 mL/m(2) ± 17 vs 45 mL/m(2) ± 11; P > .99). The result is that, in patients with AL, all of the increase in left ventricular indexed mass is extracellular volume, whereas in patients with ATTR, the increase is extracellular, with an additional 18% increase in the intracellular space. CONCLUSION: Quantification of ECV measures cardiac amyloid deposition in both types of amyloidosis and shows that amyloid deposition is more extensive in patients with ATTR than in those with AL; however, ATTR is associated with higher cell volume, which suggests concomitant cell hypertrophy.

Extracellular volume quantification in isolated hypertension - changes at the detectable limits?

BACKGROUND: Diffuse myocardial fibrosis (DMF) is important in cardiovascular disease, however until recently could only be assessed by invasive biopsy. We hypothesised that DMF measured by T1 mapping is elevated in isolated systemic hypertension. METHODS: In a study of well-controlled hypertensive patients from a specialist tertiary centre, 46 hypertensive patients (median age 56, range 21 to 78, 52 % male) and 50 healthy volunteers (median age 45, range 28 to 69, 52 % male) underwent clinical CMR at 1.5 T with T1 mapping (ShMOLLI) using the equilibrium contrast technique for extracellular volume (ECV) quantification. Patients underwent 24-hours Automated Blood Pressure Monitoring (ABPM), echocardiographic assessment of diastolic function, aortic stiffness assessment and measurement of NT-pro-BNP and collagen biomarkers. RESULTS: Late gadolinium enhancement (LGE) revealed significant unexpected underlying pathology in 6 out of 46 patients (13 %; myocardial infarction n = 3; hypertrophic cardiomyopathy (HCM) n = 3); these were subsequently excluded. Limited, non-ischaemic LGE patterns were seen in 11 out of the remaining 40 (28 %) patients. Hypertensives on therapy (mean 2.2 agents) had a mean ABPM of 152/88 mmHg, but only 35 % (14/40) had left ventricular hypertrophy (LVH; LV mass male > 90 g/m(2); female > 78 g/m(2)). Native myocardial T1 was similar in hypertensives and controls (955 ± 30 ms versus 965 ± 38 ms, p = 0.16). The difference in ECV did not reach significance (0.26 ± 0.02 versus 0.27 ± 0.03, p = 0.06). In the subset with LVH, the ECV was significantly higher (0.28 ± 0.03 versus 0.26 ± 0.02, p < 0.001). CONCLUSION: In well-controlled hypertensive patients, conventional CMR discovered significant underlying diseases (chronic infarction, HCM) not detected by echocardiography previously or even during this study. T1 mapping revealed increased diffuse myocardial fibrosis, but the increases were small and only occurred with LVH.

Abnormal septal convexity into the left ventricle occurs in subclinical hypertrophic cardiomyopathy.

BACKGROUND: Sarcomeric gene mutations cause hypertrophic cardiomyopathy (HCM). In gene mutation carriers without left ventricular (LV) hypertrophy (G + LVH-), subclinical imaging biomarkers are recognized as predictors of overt HCM, consisting of anterior mitral valve leaflet elongation, myocardial crypts, hyperdynamic LV ejection fraction, and abnormal apical trabeculation. Reverse curvature of the interventricular septum (into the LV) is characteristic of overt HCM. We aimed to assess LV septal convexity in subclinical HCM. METHODS: Cardiovascular magnetic resonance was performed on 36 G + LVH- individuals (31 ± 14 years, 33 % males) with a pathogenic sarcomere mutation, and 36 sex and age-matched healthy controls (33 ± 12 years, 33 % males). Septal convexity (SCx) was measured in the apical four chamber view perpendicular to a reference line connecting the mid-septal wall at tricuspid valve insertion level and the apical right ventricular insertion point. RESULTS: Septal convexity was increased in G + LVH- compared to controls (maximal distance of endocardium to reference line: 5.0 ± 2.5 mm vs. 1.6 ± 2.4 mm, p ≤ 0.0001). Expected findings occurred in G + LVH- individuals: longer anterior mitral valve leaflet (23.5 ± 3.0 mm vs. 19.9 ± 3.1 mm, p ≤ 0.0001), higher relative wall thickness (0.31 ± 0.05 vs. 0.29 ± 0.04, p ≤ 0.05), higher LV ejection fraction (70.8 ± 4.3 % vs. 68.3 ± 4.4 %, p ≤ 0.05), and smaller LV end-systolic volume index (21.4 ± 4.4 ml/m(2) vs. 23.7 ± 5.8 ml/m(2), p ≤ 0.05). Other morphologic measurements (LV angles, sphericity index, and eccentricity index) were not different between G + LVH- and controls. CONCLUSIONS: Septal convexity is an additional previously undescribed feature of subclinical HCM.

Reproducibility of native myocardial T1 mapping in the assessment of Fabry disease and its role in early detection of cardiac involvement by cardiovascular magnetic resonance.

BACKGROUND: Cardiovascular magnetic resonance (CMR) derived native myocardial T1 is decreased in patients with Fabry disease even before left ventricular hypertrophy (LVH) occurs and may be the first non-invasive measure of myocyte sphingolipid storage. The relationship of native T1 lowering prior to hypertrophy and other candidate early phenotype markers are unknown. Furthermore, the reproducibility of T1 mapping has never been assessed in Fabry disease. METHODS: Sixty-three patients, 34 (54%) female, mean age 48±15 years with confirmed (genotyped) Fabry disease underwent CMR, ECG and echocardiographic assessment. LVH was absent in 25 (40%) patients. Native T1 mapping was performed with both Modified Look-Locker Inversion recovery (MOLLI) sequences and a shortened version (ShMOLLI) at 1.5 Tesla. Twenty-one patients underwent a second scan within 24 hours to assess inter-study reproducibility. Results were compared with 63 healthy age and gender-matched volunteers. RESULTS: Mean native T1 in Fabry disease (LVH positive), (LVH negative) and healthy volunteers was 853±50 ms, 904±46 ms and 968±32 ms (for all p<0.0001) by ShMOLLI sequences. Native T1 showed high inter-study, intra-observer and inter-observer agreement with intra-class correlation coefficients (ICC) of 0.99, 0.98, 0.97 (ShMOLLI) and 0.98, 0.98, 0.98 (MOLLI). In Fabry disease LVH negative individuals, low native T1 was associated with reduced echocardiographic-based global longitudinal speckle tracking strain (-18±2% vs -22±2%, p=0.001) and early diastolic function impairment (E/E'=7 [6-8] vs 5 [5-6], p=0.028). CONCLUSION: Native T1 mapping in Fabry disease is a reproducible technique. T1 reduction prior to the onset of LVH is associated with early diastolic and systolic changes measured by echocardiography.

Severe Aortic Stenosis in a Pregnant Patient Displaced by the Ukrainian-Russian War.

We describe the complex case of a 32-year-old pregnant woman with known severe aortic stenosis, who was displaced by the Ukrainian-Russian War. She arrived in the United Kingdom at 32 weeks' gestation speaking minimal English, but requiring urgent multidisciplinary care to facilitate appropriate antenatal, peripartum, and postpartum care.

Therapeutic Dilemmas Faced When Managing a Life-Threatening Presentation of a Myocardial Bridge.

Background. Myocardial bridges are congenital abnormalities, where a segment of coronary artery travels intramyocardially, rather than the typical epicardial course. The overlying muscle segment is termed "the bridge". Most myocardial bridges are asymptomatic, but some can result in myocardial ischaemia, arrhythmias, and sudden cardiac death. Case Presentation. A 31-year-old male with no past medical history presented to our tertiary cardiac centre following an out-of-hospital ventricular fibrillation arrest. Coronary angiography and computed tomography of the coronary arteries revealed a 2 cm myocardial bridge overlying the left anterior descending (LAD) artery. An exercise echocardiogram demonstrated severe apical ballooning and hypokinesis during peak exercise, with corresponding ST-segment elevation, resolving on rest. Options for medical therapy of a symptomatic myocardial bridge include beta blockers, calcium channel blockers, ivabradine, or a combination thereof. Surgical interventions include deroofing the bridge and revascularisation of the affected region with bypass grafting. However, a lack of trial data comparing medical regimens and surgical interventions makes it difficult to ascertain the most effective management strategy for each patient. There was disagreement between experts at different tertiary centres over the optimal management of this patient. He was treated with multiple regimes of medical therapy with ongoing ischaemia on stress testing, before undergoing a negative stress test on amlodipine, diltiazem, and isosorbide mononitrate. It was felt that no further intervention was necessary at this time given his exercise test was now negative for ischaemia. However, after seeking a second opinion, he underwent surgical intervention with bypass grafting of his left anterior descending artery, followed by implantation of an implantable cardiac defibrillator. Subsequently, an angiogram postsurgery demonstrated concomitant spasm of the LAD and he was resumed on medical therapy with calcium channel blockers and nitrates. Discussion. Without randomised trials, it is impossible to determine the optimal management strategy for each patient. It is possible that some patients with myocardial bridges are not being trialled on optimal medical therapy prior to undergoing invasive and irreversible interventions.

Cardiac Computed Tomography: Application in Valvular Heart Disease.

The incidence and prevalence of valvular heart disease (VHD) is increasing and has been described as the next cardiac epidemic. Advances in imaging and therapeutics have revolutionized how we assess and treat patients with VHD. Although echocardiography continues to be the first-line imaging modality to assess the severity and the effects of VHD, advances in cardiac computed tomography (CT) now provide novel insights into VHD. Transcatheter valvular interventions rely heavily on CT guidance for procedural planning, predicting and detecting complications, and monitoring prosthesis. This review focuses on the current role and future prospects of CT in the assessment of aortic and mitral valves for transcatheter interventions, prosthetic valve complications such as thrombosis and endocarditis, and assessment of the myocardium.

Apical hypertrophic cardiomyopathy associated with circumflex to left ventricular fistulae: a case report of two rare subtypes of rare conditions occurring together.

BACKGROUND: Coronary arterial fistulae are rare yet have been associated with hypertrophic cardiomyopathy (HCM). We present a patient who was found to have a left circumflex (LCx) to left ventricular (LV) fistula in combination with apical HCM. CASE SUMMARY: A 72-year-old female presented with syncope after exercise. She sustained facial injuries including fracture of her nasal bones. There were no previous episodes, no cardiac history, and she denied chest pain or anginal symptoms. Electrocardiogram showed sinus rhythm with T-wave inversion throughout the chest leads. Echocardiography suggested apical HCM with hypertrophy of the LV apex but good systolic function. This was confirmed on cardiac magnetic resonance imaging with a characteristically spade-shaped LV cavity. Coronary angiography demonstrated a distal LCx to LV fistula from the apical hypertrophy but no coronary artery disease. She was started on beta-blockers and has had no further episodes, remaining well. DISCUSSION: Coronary fistulae are present in 0.002% of the population but clinical outcomes are poorly understood. The majority are asymptomatic but anginal chest pains can occur through the 'coronary steal' phenomenon. Apical HCM is a subtype of HCM characterized by spade-shaped LV cavity obliteration. It is unclear whether the association between fistulae and HCM occur because of the increased vascularization and fibrosis associated with HCM or whether congenital malformation leads to hypertrophy. Both can produce a constellation of cardiac symptoms. Our patient has the previously unreported combination of apical HCM and an LCx fistula; two rarer subtypes of rare conditions appearing together.

Noninvasive rapid cardiac magnetic resonance for the assessment of cardiomyopathies in low-middle income countries.

Introduction: Cardiac Magnetic Resonance (CMR) is a crucial diagnostic imaging test that redefines diagnosis and enables targeted therapies, but the access to CMR is limited in low-middle Income Countries (LMICs) even though cardiovascular disease is an emergent primary cause of mortality in LMICs. New abbreviated CMR protocols can be less expensive, faster, whilst maintaining accuracy, potentially leading to a higher utilization in LMICs.Areas covered: This article will review cardiovascular disease in LMICs and the current role of CMR in cardiac diagnosis and enable targeted therapy, discussing the main obstacles to prevent the adoption of CMR in LMICs. We will then review the potential utility of abbreviated, cost-effective CMR protocols to improve cardiac diagnosis and care, the clinical indications of the exam, current evidence and future directions.Expert opinion: Rapid CMR protocols, provided that they are utilized in potentially high yield cases, could reduce cost and increase effectiveness. The adoption of these protocols, their integration into care pathways, and prioritizing key treatable diagnoses can potentially improve patient care. Several LMIC countries are now pioneering these approaches and the application of rapid CMR protocols appears to have a bright future if delivered effectively.