Journal of Cardiovascular Magnetic Resonance最新文献

Background: Dysregulated myocardial calcium handling has been demonstrated in ischemic, non-ischemic and diabetic cardiomyopathy. Manganese-enhanced MRI (MEMRI) provides a unique method to quantify in-vivo myocardial calcium uptake but no studies have so far utilized MEMRI in patients with aortic stenosis (AS). We sought to: 1) determine whether myocardial calcium uptake is perturbed in people with severe AS, and 2) assess change in calcium uptake following aortic valve replacement (AVR).

Methods: In this prospective, pilot, case-control study, adults with severe AS underwent MEMRI before and after AVR. A group of healthy controls were also recruited. The primary outcome was the rate of manganese uptake (Ki) as assessed by Patlak modeling to act as a surrogate of myocardial calcium uptake. Comparison of Ki between groups was adjusted for age, body mass index (BMI) and systolic blood pressure.

Results: Twenty-eight controls and ten subjects with severe AS (age 72 [61-75] years, 8 male, 7 symptomatic, valve area 0.81 [0.74-1.0] cm²) were recruited, with seven returning for repeat scans post-AVR. AS patients had higher BMI and blood pressure, and a greater incidence of hyperlipidemia compared to controls. Baseline left ventricular (LV) volumes were similar between the groups, but the AS patients had higher indexed left ventricular mass. Global longitudinal strain and peak early diastolic strain rate were lower in the AS group. There was no significant difference in Ki between patients with severe AS and controls (7.09 [6.33-8.99] vs. 8.15 [7.54-8.78] mL/100g of tissue/min, P=0.815). Following AVR, there was regression in indexed LV mass (68 [51-79] to 49 [47-65] g/m², P=0.018) and mass-volume ratio (0.94 [0.80-1.13] to 0.74 [0.71-0.82] g/mL, P=0.028) but no change in Ki was seen (7.35 [6.81-8.96] to 7.11 [6.16-8.01] mL/100 g of tissue/min, P=0.499).

Conclusions: Despite clear features of adverse LV remodeling and systolic dysfunction, patients with severe AS demonstrated no alteration in calcium uptake at baseline compared to controls. Moreover, AVR led to reverse LV remodeling but no notable change in calcium uptake was seen. This may suggest that altered myocardial calcium handling does not play a significant pathophysiological role in AS.

Background: Aortic diameter growth in type B aortic dissection (TBAD) is associated with progressive aortic dilation, resulting in increased mortality in patients with both de novo TBAD (dnTBAD) and residual dissection after type A dissection repair (rTAAD). Preemptive thoracic endovascular aortic repair may improve mortality in patients with TBAD, although it is unclear which patients may benefit most from early intervention. In vivo hemodynamic assessment using four-dimensional (4D) flow cardiovascular magnetic resonance (CMR) has been used to characterize TBAD patients with growing aortas. In this longitudinal study, we investigated whether changes over time in 4D flow-derived true and false lumen (TL and FL) hemodynamic parameters correlate with aortic growth rate, which is a marker of increased risk.

Methods: We retrospectively identified TBAD patients with baseline and follow-up 4D flow CMR at least 120 days apart. Patients with TBAD intervention before baseline or between scans were excluded. 4D flow CMR data analysis included segmentation of the TL and FL, followed by voxel-wise calculation of TL and FL total kinetic energy (KE), maximum velocity (MV), mean forward flow (FF), and mean reverse flow (RF). Changes over time (Δ) were calculated for all hemodynamic parameters. Maximal diameter in the descending aorta was measured from magnetic resonance angiogram images acquired at the time of 4D flow. Aortic growth rate was defined as the change in diameter divided by baseline diameter and standardized to scan interval.

Results: Thirty-two patients met inclusion criteria (age: 56.9 ± 14.1 years, female: 13, n = 19 rTAAD, n = 13 dnTBAD). Mean follow-up time was 538 days (range: 135-1689). Baseline aortic diameter did not correlate with growth rate. In the entire cohort, Δ FL MV (Spearman's rho [rho] = 0.37, p = 0.04) and Δ FL RF (rho = 0.45, p = 0.01) correlated with growth rate. In rTAAD only, Δ FL MV (rho = 0.48, p = 0.04) and Δ FL RF (rho = 0.51, p = 0.03) correlated with growth rate, while in dnTBAD only, Δ TL KE (rho = 0.63, p = 0.02) and Δ TL MV (rho = 0.69, p = 0.01) correlated with growth rate.

Conclusion: 4D flow-derived longitudinal hemodynamic changes correlate with aortic growth rate in TBAD and may provide additional prognostic value for risk stratification. 4D flow MRI could be integrated into existing imaging protocols to allow for the identification of TBAD patients who would benefit from preemptive surgical or endovascular intervention.

Background: This study aimed to validate respiratory-resolved five-dimensional (5D) flow cardiovascular magnetic resonance (CMR) against real-time two-dimensional (2D) phase-contrast MRI, assess the impact of number of respiratory states, and measure the impact of respiration on hemodynamics in congenital heart disease (CHD) patients.

Methods: Respiratory-resolved 5D flow MRI-derived net and peak flow measurements were compared to real-time 2D phase-contrast MRI-derived measurements in 10 healthy volunteers. Pulmonary-to-systemic flow ratios (Qp:Qs) were measured in 19 CHD patients and aortopulmonary collateral burden was measured in 5 Fontan patients. Additionally, the impact of number of respiratory states on measured respiratory-driven net flow changes was investigated in 10 healthy volunteers and 19 CHD patients (shunt physiology, n = 11, single ventricle disease [SVD], n = 8).

Results: There was good agreement between 5D flow MRI and real-time 2D phase-contrast-derived net and peak flow. Respiratory-driven changes had a good correlation (rho = 0.64, p < 0.001). In healthy volunteers, fewer than four respiratory states reduced measured respiratory-driven flow changes in veins (5.2 mL/cycle, p < 0.001) and arteries (1.7 mL/cycle, p = 0.05). Respiration drove substantial venous net flow changes in SVD (64% change) and shunt patients (57% change). Respiration had significantly greater impact in SVD patients compared to shunt patients in the right and left pulmonary arteries (46% vs 15%, p = 0.003 and 59% vs 20%, p = 0.002). Qp:Qs varied by 37 ± 24% over respiration in SVD patients and 12 ± 20% in shunt patients. Aortopulmonary collateral burden varied by 118 ± 84% over respiration in Fontan patients. The smallest collateral burden was measured during active inspiration in all patients and the greatest burden was during active expiration in four of five patients. Reduced respiratory resolution blunted measured flow changes in the caval veins of shunt and SVD patients (p < 0.005).

Conclusions: Respiratory-resolved 5D flow MRI measurements agree with real-time 2D phase contrast. Venous measurements are sensitive to number of respiratory states, whereas arterial measurements are more robust. Respiration has a substantial impact on caval vein flow, Qp:Qs, and collateral burden in CHD patients.

Background: The extent of late gadolinium enhancement (LGE) on cardiovascular magnetic resonance (CMR) in patients with hypertrophic cardiomyopathy (HCM) is associated with an increased risk of sudden cardiac death events. However, the clinical significance of age-specific longitudinal changes in LGE is not well characterized in HCM. We sought to assess whether the risk of LGE progression diverges between young to middle-aged (ages 20-59 years) and older (≥ 60) adults with HCM.

Methods: A total of 102 HCM patients (age <60 years; n=75, age ≥60 years; n=27) undergoing serial CMR studies from two tertiary medical centers were evaluated. The median time interval between initial and follow-up CMR scans was 3.7 years. LGE was semiautomatically quantified by measuring regions with signal intensity >6 SD above the nulled remote myocardium and manually adjusting a grayscale threshold.

Results: LGE was identified at baseline in 61 of the 102 HCM patients (60%), occupying 4.8 ± 3.9% of the left ventricular (LV) mass. At the end of the follow-up period, 53 of the 61 patients (87%) demonstrated an increase in the extent of LGE to 7.7 ± 5.4%, and 8 patients had no change. In 5 patients (5%), LGE increased to extensive with >15% of the LV mass. The rate of LGE progression was 0.7 ± 1.0%/year, including 21 patients (21%) with particularly accelerated progression of ≥1%/year. The risk of LGE progression ≥1%/year was significantly higher in patients <60 years than those ≥ 60 years (25% vs. 7%, p=0.03). The odds of LGE progression ≥1%/year was almost 4 times greater for patients <60 years compared with those ≥ 60 years (odds ratio, 4.2; 95%CI, 1.1-27.9). Age <60 years and LGE extent ≥ 10% were significant baseline predictors for future LGE progression ≥1%/year, even after adjustment for other potential risk factors.

Conclusion: In HCM, progressive fibrosis occurs more frequently in young to middle-aged patients, underscoring the importance of repeating CMR to re-evaluate for potential LGE progression in this age group.

Background: There is conflicting evidence regarding the response to a fixed dose of regadenoson in patients with high body weight. The aim of this study was to evaluate the effectiveness of regadenoson in patients with varying body weights using novel quantitative cardiovascular magnetic resonance (CMR) perfusion parameters in addition to standard clinical markers.

Methods: Consecutive patients with typical angina and/or risk factors for coronary artery disease (N = 217) underwent regadenoson stress CMR perfusion imaging using a dual-sequence quantitative protocol with perfusion parameters generated from an artificial intelligence (AI)-based algorithm. CMR was performed on 1.5T scanners using a standard 0.4 mg injection of regadenoson. A cohort of consecutive patients undergoing adenosine stress perfusion (N = 218) was used as a control group.

Results: An inverse association of myocardial perfusion reserve and weight (mean decrease -0.05 per 10 kg increase, 95% confidence interval [CI] -0.009/-0.0001, P = 0.045) was noted in the regadenoson group but not in patients stressed with adenosine (P = 0.77). Adjusted logistic regression analysis revealed a 10 kg increase resulted in 36% increased odds for inadequate stress response (odds ratio [OR] = 1.36, 95% CI 1.10-1.69, P = 0.005). Moreover, a significant interaction (OR = 1.09, 95% CI 1.02-1.16, P = 0.012) between stressor type (regadenoson vs adenosine) and weight was noted. This was also confirmed in the propensity-matched subgroup (P = 0.024) and was not attenuated after adjustment (P = 0.041). Body surface area (BSA) (P = 0.006) but not body mass index (P = 0.055) was differentially associated with inadequate response conditional to the stressor used, and this association remained significant after adjustment for confounders (P = 0.025). Patients in the highest quartile of weight (>93 kg) or BSA (>2.06 m²) had substantially increased odds for inadequate response with regadenoson (OR = 8.19, 95% CI 2.04-32.97, P = 0.003 for increased weight and OR = 7.75, 95% CI 1.93-31.13, P = 0.004 for increased BSA). Both weight and BSA had excellent discriminative ability for inadequate regadenoson response (receiver operating characteristic area under curves 0.84 and 0.83, respectively).

Conclusion: Using quantitative perfusion CMR in patients undergoing pharmacological stress with regadenoson, we found an inverse relationship between patient weight and both clinical response and myocardial perfusion parameters. A fixed-dose bolus approach may not be adequate to induce maximal hyperemia in patients with increased weight. Weight-adjusted stressors, such as adenosine, may be considered instead in patients with body weight >93 kg and BSA >2.06 m².

Background: Quantitative myocardial tissue characterization with T₁ and T₂ parametric mapping can provide an accurate and complete assessment of tissue abnormalities across a broad range of cardiomyopathies. However, current clinical T₁ and T₂ mapping tools rely predominantly on two-dimensional (2D) breath-hold sequences. Clinical adoption of three-dimensional (3D) techniques is limited by long scan duration. The aim of this study is to develop and validate a time-efficient 3D free-breathing simultaneous T₁ and T₂ mapping sequence using multi-parametric SAturation-recovery and Variable-flip-Angle (mSAVA).

Methods: mSAVA acquires four volumes for simultaneous whole-heart T₁ and T₂ mapping. We validated mSAVA using simulations, phantoms, and in-vivo experiments at 3T in 11 healthy subjects and 11 patients with diverse cardiomyopathies. T₁ and T₂ values by mSAVA were compared with modified Look-Locker inversion recovery (MOLLI) and gradient and spin echo (GraSE), respectively. The clinical performance of mSAVA was evaluated against late gadolinium enhancement (LGE) imaging in patients.

Results: Phantom T₁ and T₂ by mSAVA showed a strong correlation to reference sequences (R² = 0.98 and 0.99). In-vivo imaging with an imaging resolution of 1.5 × 1.5 × 8 mm³ could be achieved. Myocardial T₁ and T₂ of healthy subjects by mSAVA were 1310 ± 46 and 44.6 ± 2.0 ms, respectively, with T₁ standard deviation higher than MOLLI (105 ± 12 vs 60 ± 16 ms) and T₂ standard deviation lower than GraSE (4.5 ± 0.8 vs 5.5 ± 1.0 ms). mSAVA T₁ and T₂ maps presented consistent findings in patients undergoing LGE. Myocardial T₁ and T₂ of all patients by mSAVA were 1421 ± 79 and 47.2 ± 3.3 ms, respectively.

Conclusion: mSAVA is a fast 3D technique promising for clinical whole-heart T₁ and T₂ mapping.

Background: Heart failure (HF) most commonly occurs in patients who have had a myocardial infarction (MI), but factors other than MI size may be deterministic. Fibrosis of myocardium remote from the MI is associated with adverse remodeling. We aimed to 1) investigate the association between remote myocardial fibrosis, measured using cardiovascular magnetic resonance (CMR) extracellular volume fraction (ECV), and HF and death following MI, 2) identify predictors of remote myocardial fibrosis in patients with evidence of MI and determine the relationship with infarct size.

Methods: Multicenter prospective cohort study of 1199 consecutive patients undergoing CMR with evidence of MI on late gadolinium enhancement. Median follow-up was 1133 (895-1442) days. Cox proportional hazards modeling was used to identify factors predictive of the primary outcome, a composite of first hospitalization for HF (HHF) or all-cause mortality, post-CMR. Linear regression modeling was used to identify determinants of remote ECV.

Results: Remote myocardial fibrosis was a strong predictor of primary outcome (χ²: 15.6, hazard ratio [HR]: 1.07 per 1% increase in ECV, 95% confidence interval [CI]: 1.04-1.11, p < 0.001) and was separately predictive of both HHF and death. The strongest predictors of remote ECV were diabetes, sex, natriuretic peptides, and body mass index, but, despite extensive phenotyping, the adjusted model R² was only 0.283. The relationship between infarct size and remote fibrosis was very weak.

Conclusion: Myocardial fibrosis, measured using CMR ECV, is a strong predictor of HHF and death in patients with evidence of MI. The mechanisms underlying remote myocardial fibrosis formation post-MI remain poorly understood, but factors other than infarct size appear to be important.