CMR-derived extracellular volume fraction (ECV) in asymptomatic heart transplant recipients: correlations with clinical features and myocardial edema

Myocardial interstitial expansion seems to be fundamental to the process of adverse left ventricular remodeling. Recent evidence has shown that the extracellular volume fraction (ECV) derived from cardiovascular magnetic resonance (CMR) can be used as a noninvasive method to quantify myocardial interstitial volume in a range of heart diseases. Our aim was to determine whether ECV is increased in asymptomatic orthotopic heart transplant (HTx) patients and its associations with clinical features and T2 values, the elevation of which usually suggests myocardial edema. A group of asymptomatic cardiac transplant recipients and some healthy volunteers were invited to undergo a comprehensive CMR scan, including cine imaging, late gadolinium enhancement, T1 mapping and T2 mapping, from March to June in 2017. All quantitative measurements were averaged from the basal and mid short-axis slices. Fifty-eight recipients (mean age, 42.7?±?11.5 years; 13 females), at a median of 1.8 years (0.3–6.3 years) after HTx, and 20 healthy volunteers (mean age, 39.5?±?11.3 years; 5 females) underwent the CMR scan. We found that both the ECV and T2 values were higher in the post-HTx group (ECV: 26.7?±?3.3 vs. 24.6?±?2.5%, p?=?0.008; T2: 47.7?±?2.8 vs. 44.5?±?1.6 ms, p?<?0.001) than in the control group. ECV was moderately associated with organ ischemia time at the time of transplantation but not with the hemodynamics parameter or the time since transplantation at CMR. Additionally, a relatively strong correlation was observed between ECV and T2 (r?=?0.7, p?<?0.001). So, our conclusion is that CMR-derived ECV is increased and associated with peri-transplant ischemia time in asymptomatic HTx patients. And the strong correlation of ECV with elevated T2 indicates that myocardial edema may be an important part of the extracellular volume expansion after heart transplantation.     

Correlation between right ventricular T<Subscript>1</Subscript> mapping and right ventricular dysfunction in non-ischemic cardiomyopathy

Right ventricular (RV) fibrosis is increasingly recognized as the underlying pathological substrate in a variety of clinical conditions. We sought to employ cardiac magnetic resonance (CMR) techniques of strain imaging and longitudinal relaxation time (T₁) mapping to better examine the relationship between RV function and structure. Our aim was to initially evaluate the feasibility of these techniques to evaluate the right ventricle. We then sought to explore the relationship between RV function and underlying fibrosis, along with examining the evolution of RV remodeling according to the amount of baseline fibrosis. Echocardiography was performed in 102 subjects with non-ischemic cardiomyopathy. Right ventricular parameters were assessed including: fractional area change (FAC) and longitudinal strain. The same cohort underwent CMR. Post-contrast T₁ mapping was performed as a marker of fibrosis with a Look-Locker technique using inversion recovery imaging. Mid-ventricular post-contrast T₁ values of the RV free wall, RV septum and lateral LV were calculated using prototype analysis software. Biventricular volumetric data including ejection fraction was measured by CMR using a cine short axis stack. CMR strain analysis was also performed to assess 2D RV longitudinal and radial strain. Simultaneous biochemical and anthropometric data were recorded. Subjects were followed over a median time of 29 months (IQR 20–37 months) with echocardiography to evaluate temporal change in RV FAC according to baseline post-contrast T₁ values. Longitudinal data analysis was performed to adjust for patient loss during follow-up. Subjects (62% men, 51?±?15 years) had mild to moderately impaired global RV systolic function (RVEF?=?39?±?15%; RVEDV?=?187?±?69 ml; RVESV?=?119?±?68 ml) and moderate left ventricular dysfunction at baseline (LVEF 30?±?17%). Good correlation was observed between mean LV and RV post-contrast T₁ values (r?=?0.652, p?<?0.001), with similar post-contrast T₁ values maintained in both the RV free wall and septum (r?=?0.761, p?<?0.001). CMR RVEF demonstrated a proportional correlation with echocardiographic measures of RV longitudinal function and CMR RV strain (longitudinal r?=??0.449, p?=?0.001; radial r?=??0.549, p?<?0.001). RVEF was related to RV post-contrast T₁ values, particularly in those with RV dysfunction (free wall T₁ r?=?0.259 p?=?0.027; septal T₁ r?=?0.421 p?<?0.001). RV strain was also related to RV post-contrast T₁ values (r?=??0.417, p?=?0.002). Linear regression analysis demonstrated strain and post-contrast T1 values to be independently associated with RVEF. Subjects with severe RV dysfunction (CMR RVEF <25%) demonstrated lower RV CMR strain (longitudinal p?=?0.018; radial p?<?0.001), RV T₁ values (free wall p?=?0.013; septum <0.001) and RV longitudinal echocardiography parameters despite no difference in afterload. During follow-up, those with RV free wall post-contrast T₁ values?≥?350 ms demonstrated ongoing improvement in FAC (Δ6%), whilst values <350 ms were associated with deterioration in RV function (ΔFAC?=??5%) (p?=?0.026). CMR provides a comprehensive method by which to evaluate right ventricular function. Post-contrast T₁ mapping and CMR strain imaging are technically feasible and provide incremental information regarding global RV function and structure. The proportional relationship between RV function and post-contrast T₁ values supports that myocardial fibrosis is a causative factor of RV dysfunction in NICM, irrespective of RV afterload. This same structural milieu also appears integral to the propensity for both positive and negative RV remodeling long-term, suggestive that this is also determined by the degree of underlying RV fibrosis.     

Effects of caffeine intake prior to stress cardiac magnetic resonance perfusion imaging on regadenoson- versus adenosine-induced hyperemia as measured by T1 mapping

The antagonistic effects of caffeine on adenosine receptors are a possible cause of false-negative stress perfusion imaging. The purpose of this study was to determine the effects of coffee intake <4 h prior to stress perfusion cardiac magnetic resonance imaging (CMR) in regadenoson- versus adenosine-induced hyperemia as measured with T1-mapping. 98 consecutive patients with suspected coronary artery disease referred for either adenosine or regadenoson perfusion CMR were included in this analysis. Twenty-four patients reported coffee consumption <4 h before CMR (15 patients with adenosine, and 9 patients with regadenoson); 74 patients reported no coffee intake (50 patients with adenosine, and 24 patients with regadenoson). T1 mapping was performed using a modified look-locker inversion recovery sequence. T1 reactivity was determined by subtracting T1_rest from T1_stress. T1_rest, T1_stress, and T1 reactivity in patients referred for regadenoson perfusion CMR were not significantly different when comparing patients with <4 h coffee intake and patients who reported no coffee intake (976?±?4 ms, 1019?±?48 ms, and 4.4?±?3.2% vs 971?±?33 ms, 1023?±?43 ms, and 5.4?±?2.4%) (p?=?0.70, 0.79, and 0.40), and similar to values in patients without coffee intake undergoing adenosine CMR. In patients with <4 h coffee intake, T1_stress, and T1 reactivity were significantly lower for adenosine (898?±?51 ms, and ?7.8?±?5.0%) compared to regadenoson perfusion CMR (p?<?0.001). Coffee intake <4 h prior to regadenoson perfusion CMR has no effect on stress-induced hyperemia as measured with T1 mapping.     

Value of three-dimensional strain parameters for predicting left ventricular remodeling after ST-elevation myocardial infarction

This study was to evaluate the value of multi-directional strain parameters derived from three-dimensional (3D) speckle tracking echocardiography (STE) for predicting left ventricular (LV) remodeling after ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI) compared with that of two-dimensional (2D) global longitudinal strain (GLS). A total of 110 patients (mean age, 54?±?9 years) after STEMI treated with primary PCI were enrolled in our study. At baseline (within 24 h after PCI), standard 2D echocardiography, 2D STE and 3D STE were performed to acquire the conventional echocardiographic parameters and strain parameters. At 3-month follow-up, standard 2D echocardiography was repeated to all the patients to determine LV remodeling, which was defined as a 20% increase in LV end-diastolic volume. At 3-month follow-up, LV remodeling occurred in 26 patients (24%). Compared with patients without LV remodeling, patients with remodeling had significantly reduced 2D GLS (?12.5?±?3.2% vs ?15.0?±?3.1%, p?<?0.001), 3D GLS (?9.9?±?2.2% vs ?13.1?±?2.7%, p?<?0.001), 3D global area strain (GAS) (?20.3?±?3.9% vs ?23.3?±?4.8%, p?=?0.005) and 3D global radial strain (GRS) (29.0?±?7.4% vs 34.3?±?8.5%, p?=?0.007) at baseline, but there is no significant difference in 3D global circumferential strain (GCS) (?12.7?±?2.9% vs ?13.0?±?3.2%, p?=?0.822). Separated multivariate analysis shows that 2D GLS, 3D GLS, 3D GAS and 3D GRS all can be independent predictors of LV remodeling. However, receiver-operating characteristic curve analysis showed that the area under the curve of 3D GLS (0.82) for predicting LV remodeling was significantly higher than that of 2D GLS (0.72, p?=?0.034), 3D GAS (0.68, p?<?0.001) and 3D GRS (0.68, p?<?0.001). In patients after STEMI, 2D GLS, 3D GLS, 3D GAS and 3D GRS but not 3D GCS measured after primary PCI are independent predictors of LV remodeling and 3D GLS is the most powerful predictor among them.     

Quantitative diffusion-weighted magnetic resonance imaging in the assessment of myocardial fibrosis in hypertrophic cardiomyopathy compared with T1 mapping

To identify myocardial fibrosis in hypertrophic cardiomyopathy (HCM) subjects using quantitative cardiac diffusion-weighted imaging (DWI) and to compare its performance with native T1 mapping and extracellular volume (ECV). Thirty-eight HCM subjects (mean age, 53?±?9 years) and 14 normal controls (mean age, 51?±?8 years) underwent cardiac magnetic resonance imaging (CMRI) on a 3.0T magnetic resonance (MR) machine with DWI, T1 mapping and late gadolinium enhancement (LGE) imaging as the reference standard. The mean apparent diffusion coefficient (ADC), native T1 value and ECV were determined for each subject. Overall, the HCM subjects exhibited an increased native T1 value (1241.04?±?78.50 ms), ECV (0.31?±?0.03) and ADC (2.36?±?0.34 s/mm²) compared with the normal controls (1114.60?±?37.99 ms, 0.24?±?0.04, and 1.62?±?0.38 s/mm², respectively) (p?<?0.05). DWI differentiated healthy and fibrotic myocardia with an area under the curve (AUC) of 0.93, while the AUCs of the native T1 values (0.93), (p?>?0.05) and ECV (0.94), (p?>?0.05) exhibited an equal differentiation ability. Both HCM LGE+ and HCM LGE? subjects had an increased native T1 value, ECV and ADC compared to the normal controls (p?<?0.05). HCM LGE+ subjects exhibited an increased ECV (0.31?±?0.04) and ADC (2.43?±?0.36 s/mm²) compared to HCM LGE? subjects (p?<?0.05). HCM LGE+ and HCM LGE? subjects had similar native T1 values (1250?±?76.36 ms vs. 1213.98?±?92.30 ms, respectively) (p?>?0.05). ADC values were linearly associated with increased ECV (R²?=?0.36) and native T1 values (R²?=?0.40) among all subjects. DWI is a feasible alternative to native T1 mapping and ECV for the identification of myocardial fibrosis in patients with HCM. DWI and ECV can quantitatively characterize the extent of fibrosis in HCM LGE+ and HCM LGE? patients.     

Myocardial salvage after primary percutaneous coronary intervention in patients with ST-elevation myocardial infarction presenting early versus late after symptom onset

Primary percutaneous coronary intervention (PCI) is the treatment of choice in patients with ST-elevation myocardial infarction (STEMI) presenting within 12 h of symptom onset. A benefit in the subacute stage is less clear. The aim of the present analysis was to compare myocardial salvage and infarct size between patients with early and late reperfusion after STEMI. We compared cardiac magnetic resonance (CMR) data from a randomized controlled trial (RCT) in STEMI patients presenting within 12 h (n?=?695) and a RCT of subacute STEMI patients presenting between 12 and 48 h (n?=?93) after symptom onset. CMR imaging was performed 3.9?±?6.3 days after myocardial infarction. Analyses were performed for an unmatched cohort comprising all patients (n?=?788) and a cohort matched for area at risk (n?=?186). In the overall cohort, area at risk was similar in both groups [37.1?±?16.1% of left ventricular mass (%LV) vs. 38.3?±?16.2%LV; p?=?0.50]. Compared to STEMI patients with early reperfusion, patients with late PCI demonstrated larger infarct size (18.0?±?12.5%LV vs. 28.9?±?16.9%LV; p?<?0.01) and higher extent of microvascular obstruction (1.5?±?2.9%LV vs. 2.7?±?4.1%LV; p?=?0.01). Myocardial salvage index was significantly smaller in patients with late reperfusion (52.1?±?25.9 vs. 27.4?±?26.0; p?<?0.01). Analysis of the matched cohorts confirmed the decreased myocardial salvage (p?<?0.01) and increased infarct size (p?<?0.01) in case of late reperfusion. Compared to patients with timely primary PCI, late reperfusion after STEMI results in decreased myocardial salvage and increased infarct size. However, salvageable myocardium was also found in subacute stages of STEMI.     

Caffeine intake inverts the effect of adenosine on myocardial perfusion during stress as measured by T1 mapping

Caffeine intake before adenosine stress myocardial perfusion imaging may cause false negative findings. We hypothesized that the antagonistic effect of caffeine can be measured by T1 relaxation times in rest and adenosine stress cardiac magnetic resonance imaging (CMR), as T1 mapping techniques are sensitive to changes in myocardial blood volume. We prospectively analyzed 105 consecutive patients with adenosine stress perfusion CMR on a 1.5-T MRI system. Rest and stress T1 mapping was performed using Modified Look-Locker Inversion recovery. T1 reactivity was defined as difference in T1_rest and T1_stress (?T1). Fifteen patients drank coffee within 4 h of CMR (<4H caffeine group), and 10 patients had coffee the day before (>8H caffeine group). Comparison was made to patients without self-reported coffee intake: 50 with normal CMR (control group), 18 with myocardial ischemia, and 12 with myocardial infarction. The national review board approved the study; all patients gave written informed consent. The <4H caffeine group showed inverted ?T1 of ?7.8?% (T1_rest 975?±?42 ms, T1_stress 898?±?51 ms, p?<?0.0005). The >8H caffeine group showed reduced T1 reactivity (1.8?%; T1_rest 979 ms, T1_stress 997 ms) compared to the controls (4.3?%; T1_rest 977?±?40 ms, T1_stress 1018?±?40 ms), p?<?0.0005. Ischemic and infarcted myocardium showed minimal T1 reactivity (0.2 and 0.3?%, respectively). Caffeine intake inverts the adenosine effect during stress perfusion CMR as measured by T1 mapping. T1 reactivity can assess the adequacy of adenosine-induced stress in perfusion CMR.     

Comparison of quantitative imaging parameters using cardiovascular magnetic resonance between cardiac amyloidosis and hypertrophic cardiomyopathy: inversion time scout versus T1 mapping

To compare inversion time (TI) parameters, native T1, and extracellular volume (ECV) on cardiac magnetic resonance (CMR) imaging between patients with cardiac amyloidosis (CA) or hypertrophic cardiomyopathy (HCMP). Forty six patients with biopsy-confirmed CA and 30 patients with HCMP who underwent CMR were included. T1 and TI values were measured in the septum and cavity of the left ventricle on T1 mapping and TI scout images. TI values were selected at nulling point for each myocardium and blood pool. Native T1, ECV, and TI interval values were significantly different between the CA (1170.5?±?86.4 ms, 56.7?±?12.2, ? 11.5?±?28.4 ms) and HCMP (1059.5?±?63.4 ms, 28.5?±?5.8, 66.2?±?25.4 ms) (all p?<?0.001). The diagnostic performance of the TI interval (area under the ROC curve, 0.975) was not inferior to that of the ECV (0.980, p?=?0.776), and it was superior to that of the native T1 (0.845, p?=?0.004). The diagnostic performance of TI interval was comparable to that of ECV for differential diagnosis between CA and HCMP. TI interval showed the feasibility as quantitative CMR parameter when T1 mapping images are not available.     

The ventricular residence time distribution derived from 4D flow particle tracing: a novel marker of myocardial dysfunction

4D flow cardiac magnetic resonance (CMR) imaging allows visualisation of blood flow in the cardiac chambers and great vessels. Post processing of the flow data allows determination of the residence time distribution (RTD), a novel means of assessing ventricular function, potentially providing additional information beyond ejection fraction. We evaluated the RTD measurement of efficiency of left and right ventricular (LV and RV) blood flow. 16 volunteers and 16 patients with systolic dysfunction (LVEF?<?50%) underwent CMR studies including 4D flow. The RTDs were created computationally by seeding virtual ‘particles’ at the inlet plane in customised post-processing software, moving these particles with the measured blood velocity, recording and counting how many exited per unit of time. The efficiency of ventricular flow was determined from the RTDs based on the time constant (RTDc?=???1/B) of the exponential decay. The RTDc was compared to ejection fraction, T1 mapping and global longitudinal strain (GLS). There was a significant difference between groups in LV RTDc (healthy volunteers 1.2?±?0.13 vs systolic dysfunction 2.2?±?0.80, p?<?0.001, C-statistic?=?1.0) and RV RTDc (1.5?±?0.15 vs 2.0?±?0.57, p?=?0.013, C-statistic?=?0.799). The LV RTDc correlated significantly with LVEF (R?=???0.84, P?<?0.001) and the RV RTDc had significant correlation with RVEF (R?=???0.402, p?=?0.008). The correlation between LV RTDc and LVEF was similar to GLS and LVEF (0.926, p?<?0.001). The ventricular residence time correlates with ejection fraction and can distinguish normal from abnormal systolic function. Further assessment of this method of assessment of chamber function is warranted.     

Prognostic value of real-time three-dimensional echocardiography compared to two-dimensional echocardiography in patients with systolic heart failure

Heart failure (HF) is associated with morbidity and mortality. Real-time three-dimensional echocardiography (RT3DE) may offer additional prognostic data in patients with HF. The study aimed to evaluate the prognostic value of real-time three-dimensional echocardiography (RT3DE). This is a prospective study that included 89 patients with HF and left ventricular ejection fraction (LVEF)?<?0.50 who were followed for 48 months. Left atrium and ventricular volumes and functions were evaluated by RT3DE. TDI and two-dimensional echocardiography parameters were also obtained. The endpoint was a composite of death, heart transplantation and hospitalization for acute decompensated HF. The mean age was 55?±?11 years, and the LVEF was 0.32?±?0.10. The composite endpoint occurred in 49 patients (18 deaths, 30 hospitalizations, one heart transplant). Patients with outcomes had greater left atrial volume (40?±?16 vs. 32?±?12 mL/m²; p?<?0.01) and right ventricle diameter (41?±?9 vs. 37?±?8 mm, p?=?0.01), worse total emptying fraction of the left atrium (36?±?13% vs. 41?±?11%; p?=?0.03), LVEF (0.30?±?0.09 vs. 0.34?±?0.11; p?=?0.02), right ventricle fractional area change (34.8?±?12.1% vs. 39.2?±?11.3%; p?=?0.04), and greater E/e′ ratio (19?±?9 vs. 16?±?8; p?=?0.04) and systolic pulmonary artery pressure (SPAP) (50?±?15 vs. 36?±?11 mmHg; p?<?0.01). In multivariate analysis, LVEF (OR 4.6; CI 95% 1.2–17.6; p?<?0.01) and SPAP (OR 12.5; CI 95% 1.8–86.9; p?<?0.01) were independent predictors of patient outcomes. LVEF and the SPAP were independent predictors of outcomes in patients with HF.     

Prognostic value of T1-mapping in TAVR patients: extra-cellular volume as a possible predictor for peri- and post-TAVR adverse events

The benefit of a transcatheter aortic valve replacement (TAVR) can differ in patients, and therapy bears severe risks. High-degree aortic stenosis can lead to cardiac damage such as diffuse myocardial fibrosis, evaluable by extra-cellular volume (ECV) in CMR. Therefore, fibrosis might be a possible risk factor for unfavorable outcome after TAVR. We sought to assess the prognostic value of T1-mapping and ECV to predict adverse events during and after TAVR. The study population consisted of patients undergoing clinically indicated TAVR by performing additional CMR with native and contrast-enhanced T1-mapping sequences for additional evaluation of ECV. Study endpoints were congestive heart failure (CHF) and TAVR-associated conduction abnormalities defined as new onset of left bundle branch block (LBBB), AV-Block or implantation of a pacemaker. 94 patients were examined and followed. Median follow up time was 187 days (IQR 79–357 days). ECV was increased (>30?%) in 38 patients (40?%). There was no significant correlation between ECV and death, Hazard ratio (HR) 0.847 (95?% CI 0.335; 2.14), p?=?0.72. ECV in patients with subsequent CHF was higher than in those without an event (33.5?±?4.6 and 29.1?±?4.1?%, respectively), but the difference just did not reach the level of significance HR 2.16 (95?% CI 0.969; 4.84), p?=?0.06. Patients with post-TAVR conduction abnormality (LBBB, AV-block or pacemaker implantation) had statistically relevant lower ECV values compared to those without an event. Patients with an event had a mean ECV of 28.1?±?3.16?%; patients without an event had a mean ECV of 29.8?±?4.53, HR 0.56 (95?% CI 0.32; 0.96), p?=?0.036. In this study, elevated myocardial ECV is a predictor of CHF by trend; CMR may be helpful in identifying patients with a high risk for post-TAVR cardiac decompensation benefitting from an intensified post-interventional surveillance. Patients with post-TAVR conductions abnormalities have a significantly decreased ECV. Nevertheless, it remains unclear which precise molecular tissue alteration is the protective factor or risk factor in this case.     

Acute recoordination rather than functional hemodynamic improvement determines reverse remodelling by cardiac resynchronisation therapy

Purpose: Cardiac resynchronisation therapy (CRT) improves left ventricular (LV) function acutely, with further improvements and reverse remodelling during chronic CRT. The current study investigated the relation between acute improvement of LV systolic function, acute mechanical recoordination, and long-term reverse remodelling after CRT. Methods: In 35 patients, LV speckle tracking longitudinal strain, LV volumes & ejection fraction (LVEF) were assessed by echocardiography before, acutely within three days, and 6 months after CRT. A subgroup of 25 patients underwent invasive assessment of the maximal rate of LV pressure rise (dP/dt_max,) during CRT-implantation. The acute change in dP/dt_max, LVEF, systolic discoordination (internal stretch fraction [ISF] and LV systolic rebound stretch [SRSlv]) and systolic dyssynchrony (standard deviation of peak strain times [2DS-SD18]) was studied, and their association with long-term reverse remodelling were determined. Results: CRT induced acute and ongoing recoordination (ISF from 45?±?18 to 27?±?11 and 23?±?12%, p?<?0.001; SRS from 2.27?±?1.33 to 0.74?±?0.50 and 0.71?±?0.43%, p?<?0.001) and improved LV function (dP/dt_max 668?±?185 vs. 817?±?198 mmHg/s, p?<?0.001; stroke volume 46?±?15 vs. 54?±?20 and 52?±?16 ml; LVEF 19?±?7 vs. 23?±?8 and 27?±?10%, p?<?0.001). Acute recoordination related to reverse remodelling (r?=?0.601 and r?=?0.765 for ISF & SRSlv, respectively, p?<?0.001). Acute functional improvements of LV systolic function however, neither related to reverse remodelling nor to the extent of acute recoordination. Conclusion: Long-term reverse remodelling after CRT is likely determined by (acute) recoordination rather than by acute hemodynamic improvements. Discoordination may therefore be a more important CRT-substrate that can be assessed and, acutely restored.

     

Serial assessment of left ventricular morphology and function in a rodent model of ischemic cardiomyopathy

Left ventricular remodelling (LVr) occurs post myocardial infarction (MI), predisposing people to heart failure (HF). LV mechanics and morphology are important in this process. We hence sort to characterize LV mechanics and geometry in a post-MI rodent model. Thirty-two male Sprague–Dawley rats (150–200 g) sustained MI (n?=?24) or sham (Sham; n?=?8) surgery. In another six sham rats invasive blood pressure measurements were performed. Ultrasound imaging was done at baseline, and 1, 3, 7, 14, 30 and 60 days following surgery, and LV mechanics and morphology assessed. LV volumes increased with time (p?<?0.01), at a greater rate in the MI group than the Sham group (p?<?0.01). Strain was impaired in MI rats at day 1 (13.50?±?6.64 vs. 25.71?±?4.94%, p?<?0.01) and remained impaired at day 60 (14.07?±?5.37 vs. 22.98?±?5.87%, p?<?0.01). Strain rate was lower at day 1 (4.11?±?1.29 vs. 8.10?±?2.18%/s, p?<?0.01), remained lower throughout follow-up (p?<?0.01), and decreased at a greater rate in MI rats (p?<?0.01). Mean systolic (204?±?43 vs. 322?±?75 1/m, p?<?0.01) and diastolic (167?±?21 vs. 192?±?11 1/m, p?<?0.01) curvature was lower in the MI rats at day 1 post surgery and throughout follow-up (p?<?0.01). Maximum principal curvature decreased throughout time (p?<?0.01), while minimum principal curvature did not (p?=?0.86). Wall stress increased significantly after infarction in MI rats (p?<?0.01). ST-elevation myocardial infarction (STEMI) changed LV shape and contractile function. The assessment of these indices may prove useful in understanding LVr and the development of HF.     

Diagnostic value of myocardial deformation pattern in children with noncompaction cardiomyopathy

The current echocardiographic diagnostic criteria for noncompaction cardiomyopathy (NCC) have variable sensitivity and low specificity. Moreover, there are limited data on the use of myocardial deformation imaging for early detection of myocardial dysfunction in children with NCC. We describe left ventricular (LV) deformation patterns in children with NCC, with the goal of identifying a potential diagnostic pattern. We prospectively enrolled 30 children with NCC (47% male; mean age 7.2 years) and 30 age- and gender-matched controls. Extent and severity of non compaction in each segment were evaluated in LV 16-segment model. Regional (base, mid and apex) and segmental (16 segments) longitudinal strain (LS), circumferential strain (CS) and radial strain (RS) were measured using speckle tracking echocardiography. In all patients with NCC, regional and segmental CS and RS at the apex were significantly decreased compared to controls (CS apex: ??19.2?±?5.4% vs. ??30.2?±?6.9%, p?<?0.001/RS apex: 23.5?±?8.6% vs. 44.1?±?14.5%, p?<?0.001). Thirty percent (9/30) of patients had an EF?<?50%. In these patients, there was additional decrease in CS in basal segments and in LS in basal, mid-cavity and apical segments (CS base: ??16.4?±?4.7% vs. ??24.6?±?3.9%, p?<?0.001/LS (average all LV segments): ??13.9?±?3.1% vs. ??20.7?±?4.7%, p?<?0.001). A cut-off value of CS at the apex of ??24.5% was a strong differentiating feature between patients with NCC and EF?>?50% and controls (sensitivity: 87%, specificity 79%, AUC 0.88, p?<?0.001). Children with NCC exhibit a deformation pattern characterized by decreased apical circumferential strain, which may serve as a potential diagnostic tool for NCC. The role of decreased global LV longitudinal and basal circumferential strain should be further evaluated as a potential prognostic tool.     

Myocardial perfusion reserve and global longitudinal strain as potential markers of coronary allograft vasculopathy in late-stage orthotopic heart transplantation

Coronary allograft vasculopathy (CAV) is a major cause of mortality in late-stage orthotopic heart transplantation (OHT) patients. Recent evidence has shown that myocardial perfusion reserve (MPR) derived from vasodilator cardiovascular magnetic resonance imaging (vCMR) and global longitudinal strain (GLS) from transthoracic echocardiography (TTE) are useful to detect CAV. However, previous studies have not comprehensively addressed whether these parameters are confounded by allograft rejection, myocardial scar/fibrosis, or allograft dysfunction. Our aim was to determine whether changes in late post-OHT MPR and GLS are due to CAV or other confounding factors. Twenty OHT patients (time from transplant to vCMR was 8.1?±?4.1 years) and 30 controls (10 healthy volunteers and 20 with prior myocardial infarction to provide perspective with regards to the severity of any abnormalities seen in post-OHT patients) underwent vasodilator vCMR from which MPR index (MPRi), left ventricular ejection fraction (LVEF), and burden of late gadolinium enhancement (LGE) were quantified. TTE was used to measure GLS. The presence of CAV was determined from invasive coronary angiograms using thrombolysis in myocardial infarction (TIMI) frame counts and grading severity per guidelines. Previous endomyocardial biopsies were reviewed to assess association with episodes of rejection. We examined the correlations between MPRi and GLS with markers of CAV, allograft function, scar/fibrosis, and rejection. MPRi was abnormal in post-OHT patients compared to both healthy volunteers and MI controls. While there was no relationship between MPRi or GLS and LVEF, episodes of rejection, or LGE burden, both MPRi and GLS were associated with TIMI frame counts and presence and severity of CAV. Additionally, MPRi correlated with GLS (R?=?0.68, P?=?0.0002). In conclusion, MPRi and GLS are abnormal in late-stage OHT and associated with CAV, but not related to allograft rejection, myocardial scar/fibrosis, or allograft dysfunction. Non-invasive monitoring of MPRi and GLS may be a useful strategy to detect CAV.     

Improved border sharpness of post-infarct scar by a novel self-navigated free-breathing high-resolution 3D whole-heart inversion recovery magnetic resonance approach

The border zone of post-infarction myocardial scar as identified by late gadolinium enhancement (LGE) has been identified as a substrate for arrhythmias and consequently, high-resolution 3D scar information is potentially useful for planning of electrophysiological interventions. This study evaluates the performance of a novel high-resolution 3D self-navigated free-breathing inversion recovery magnetic resonance pulse sequence (3D-SN-LGE) vs. conventional 2D breath-hold LGE (2D-LGE) with regard to sharpness of borders (S_Border) of post-infarction scar. Patients with post-infarction scar underwent two magnetic resonance examinations for conventional 2D-LGE and high-resolution 3D-SN-LGE acquisitions (both 15 min after 0.2 mmol/kg Gadobutrol IV) at 1.5T. In the prototype 3D-SN-LGE sequence, each ECG-triggered radial steady-state-free-precession read-out segment is preceded by a non-slice-selective inversion pulse. Scar volume and S_Border were assessed on 2D-LGE and matching reconstructed high-resolution 3D-SN-LGE short-axis slices. In 16 patients (four females, 58?±?10y) all scars visualized by 2D-LGE could be identified on 3D-SN-LGE (time between 2D-LGE and 3D-SN-LGE 48?±?53 days). A good agreement of scar volume by 3D-SN-LGE vs. 2D-LGE was found (Bland–Altman: ?3.7?±?3.4 ml, correlation: r?=?0.987, p?<?0.001) with a small difference in scar volume (20.5 (15.8, 35.2) ml vs. 24.5 (20.0, 41.9)) ml, respectively, p?=?0.002] and a good intra- and interobserver variability (1.1?±?4.1 and ?1.1?±?11.9 ml, respectively). S_Border of border “scar to non-infarcted myocardium” was superior on 3D-SN-LGE vs. 2D-LGE: 0.180?±?0.044 vs. 0.083?±?0.038, p?<?0.001. Detection and quantification of myocardial scar by 3D-SN-LGE is feasible and accurate in comparison to 2D-LGE. The high spatial resolution of the 3D sequence improves delineation of scar borders.     

Evaluation of radiological risk during coronary angioplasty procedures: comparison of transradial and transfemoral approaches

Increasing operator experience and newer available interventional cardiology devices require reassessment of radiological risk related to percutaneous coronary interventions (PCI). We aimed at comparison of radiological risk and procedural data of PCIs performed by radial (RA) and femoral (FA) approach in real life patients. Detailed retrospective analysis of 1500 consecutive PCIs with the use of radial or femoral access was performed. Comparison between RA and FA groups included procedural time (PT), fluoroscopy time (FT), radiation dose and contrast volume usage. There was no significant differences between RA and FA procedures in FT (12.6?±?13.5 vs. 11.7?±?9.5 min), X-ray dose generated during PCI (805.9?±?615.9 vs. 792.2?±?633.9 mGy) and use of contrast medium (145.2?±?62.2 vs. 152.5?±?64.2 ml). Mean total PT was shorter in RA (43.7?±?24.5 min) than in FA group (47.2?±?30.13 min, p?<?0.02). Patients’ age positively correlated with FT (r?=?0.14, p?<?0.05) and PT (r?=?0.07, p?<?0.05) in RA but not in FA group (r?=?0.05; r?=??0.06, respectively). Despite younger age, PCIs in males needed higher usage of contrast medium (151.7?±?69.2 vs. 139.1?±?49.3 ml; p?<?0.001), and higher X-ray dose (887.0?±?660.4 vs. 657.8?±?515.2 mGy; p?<?0.001). Age significantly correlated with PT only in female (r?=?0.093, p?<?0.05) but not in male patients (r?=?0.015). We conclude that fluoroscopy times, X-ray dose and use of contrast medium were similar in RA and FA, but mean total procedural time was significantly shorter in RA than in FA group. However, older patients in RA group needed longer fluoroscopy and procedural times to complete PCI and this was not seen in FA.     

T1 mapping in children and young adults with hypertrophic cardiomyopathy

To assess the global and segmental left ventricular (LV) native T1 and extracellular volume fraction (ECV) in children and young adults with hypertrophic cardiomyopathy (HCM) compared to a control cohort. The study population included 21 HCM patients (mean 14.1?±?4.6 years) and 21 controls (mean 15.7?±?1.5 years). Native modified Look-Locker inversion recovery sequence was performed before and after contrast injection in 3 short axis planes. Global and segmental LV native T1 and ECV were quantified and compared between HCM patients and controls. Mean native T1 in HCM patients and controls was 1020.4?±?41.2 and 965.6?±?30.2 ms respectively (p?<?0.0001). Hypertrophied myocardium had significantly higher native global T1 and global ECV compared to non-hypertrophied myocardium in HCM (p?<?0.0001,?=?0.14 and 0.048,?=?0.01 respectively). In a subset of patients, ECV was higher in LV segments with LGE compared to no LGE (p?<?0.0001). No significant correlation was identified between global native T1 and ECV and parameters of LV structure and function. Native T1 cut-off of 987 ms provided the highest sensitivity (95?%) and specificity (91?%) to separate HCM patients from controls. Global and segmental native T1 are elevated in HCM patients. LV segments with hypertrophy and/or LGE had higher ECV in a subset of HCM patients. LV native T1 and ECV do not correlate with parameters of LV structure and function. T1 in children and young adults may be used as a non-invasive tool to assess for HCM and related fibrosis.     

Magnetic resonance evaluation of cardiac thrombi and masses by T1 and T2 mapping: an observational study

The purpose of this work was to evaluate CMR T1 and T2 mapping sequences in patients with intracardiac thrombi and masses in order to assess T1 and T2 relaxometry usefulness and to allow better etiological diagnosis. This observational study of patients scheduled for routine CMR was performed from September 2014 to August 2015. All patients referred to our department for a 1.5 T CMR were screened to participate. T1 mapping were acquired before and after Gadolinium injection; T2 mapping images were obtained before injection. 41 patients were included. 22 presented with cardiac thrombi and 19 with cardiac masses. The native T1 of thrombi was 1037?±?152 ms (vs 1032?±?39 ms for myocardium, p?=?0.88; vs 1565?±?88 ms for blood pool, p?<?0.0001). T2 were 74?±?13 ms (vs 51?±?3 ms for myocardium, p?<?0.0001; vs 170?±?32 ms for blood pool, p?<?0.0001). Recent thrombi had a native T1 shorter than old thrombi (911?±?177 vs 1169?±?107 ms, p?=?0.01). The masses having a shorter T1 than the myocardium were lipomas (278?±?29 ms), calcifications (621?±?218 ms), and melanoma (736 ms). All other masses showed T1 values higher than myocardial T1, with T2 consistently >70 ms. T1 and T2 mapping CMR sequences can be useful and represent a new approach for the evaluation of cardiac thrombi and masses.     

The interplay between renin-angiotensin system activation,abnormal myocardial deformation and neurohumoral activation in hypertensive heart disease: a speckle tracking echocardiography study

Angiotensin converting enzyme (ACE) promotes cardiac fibrosis. LV myocardial deformation and torsion are markers of subclinical myocardial dysfunction. We investigated the association of serum ACE levels with LV deformation markers in untreated hypertensives. In 120 untreated patients (age: 53.5?±?11.2 years) with essential hypertension and 60 healthy controls, we measured (a) LV longitudinal, circumferential and radial strain (S), peak torsion and the percentage changes between peak twisting and untwisting at the end of early diastolic filling (%dpTw-Utw_EDF) using speckle tracking echocardiography and (b) serum levels of ACE and NTproBNP. Compared to controls, patients had decreased longitudinal strain (?19.1?±?2.9 vs. ?21.7?±?1.8%), increased peak twisting (19.1?±?4.6 vs.14.0?±?3.7 deg) but decreased %dpTw-Utw_EDF (78?±?8 vs. 86?±?8%) and higher serum ACE levels (27.6?±?8.0 vs 20.9?±?7.1 U/ml) (p?<?0.05 for all comparisons). Increasing serum ACE levels were related to impaired radial strain and longitudinal systolic SR (b?=??0.41 and b?=?0.31 respectively, p?<?0.01), as well as to reduced %dpTw-Utw_EDF (b?=??0.37, p?<?0.05). Furthermore, increasing serum ACE levels were related to increasing NTproBNP levels (b?=?0.41, p?<?0.01). In multivariate analysis, the above relations of serum ACE levels and LV function parameters remained significant after adjustment for other confounding factors (p?<?0.01). The close link between serum ACE levels and impaired LV deformation suggests that activation of renin-angiotensin system is involved in the impairment of LV function resulting in elevated LV filling pressures causing the concomitant elevation of BNP levels in untreated hypertensive patients.