Circulation: Cardiovascular Imaging最新文献

Background: Coronary computed tomography angiography (CCTA) could evaluate myocardial fibrosis as well by estimating extracellular volume fraction (ECV). While coronary microvascular dysfunction (CMD) has been increasingly recognized as an important pathophysiological mechanism underlying chest pain, the association between CMD in angina with nonobstructive coronary artery disease (ANOCA) and CCTA-derived ECV remains to be elucidated. We sought to evaluate the association between CCTA-derived ECV and CMD in patients with ANOCA.

Methods: We retrospectively analyzed 57 patients with ANOCA from a single center who underwent CCTA on ECV protocol with subtraction method (including precontrast and 7-minute delayed postcontrast) and invasive functional testing using pressure-temperature sensor-tipped wire. Patients with significant epicardial stenosis (fractional flow reserve ≤0.80 or stenosis on computed tomography ≥50%), prior history of revascularization, known myocardial infarction, or heart failure were excluded. CMD was defined as a coronary flow reserve of <2.5 in any of the vessels evaluated. Standard transthoracic echocardiography assessed diastolic dysfunction (DD).

Results: Among the 57 patients included, 26 (45.6%) were diagnosed with CMD. CMD was significantly associated with age, NT-proBNP (N-terminal pro-B-type natriuretic peptide) level, calcium score, DD, and higher ECV. In a multivariable logistic regression analysis, a CCTA-derived ECV >31.9% (the optimal cutoff value derived from receiver operating characteristic curve analysis) was independently associated with CMD (odds ratio, 10.50 [95% CI, 2.34-47.40]; P=0.002). DD also emerged as an independent predictor (odds ratio, 17.90 [95% CI, 2.53-127.00]; P=0.004). The addition of elevated ECV to a clinical model including DD significantly enhanced the discrimination efficacy for CMD (area under the receiver operating characteristic curve, 0.742 versus 0.854; P=0.019).

Conclusions: In patients with ANOCA with CMD, ECV was significantly elevated, alongside a higher prevalence of DD. These findings suggest that ECV and DD may serve as pivotal markers for personalized management strategies in patients with CMD with ANOCA.

Background: In hypertrophic obstructive cardiomyopathy, left ventricular mass index (LVMi) regresses following septal myectomy, but the specific dynamics, mechanisms (involving cellular and extracellular compartments), and related factors remain unclear.

Methods: This prospective study included patients with hypertrophic obstructive cardiomyopathy who underwent septal myectomy. Cardiac magnetic resonance imaging was performed preoperatively and at 6, 12, and 24 months postoperatively. LVMi, indexed cellular volume, and indexed extracellular volume were analyzed using repeated measures ANOVA. Factors associated with LVMi regression, postoperatively, were identified using linear regression.

Results: The study included 27 patients (53.70±13.85 years; 17 female). LVMi significantly decreased from 105.76±25.22 g/m², preoperatively, to 82.52±25.90 g/m² at 6 months, postoperatively, further declining to 78.86±24.73 g/m² at 12 months and 76.22±23.93 g/m² at 24 months (P<0.05). The average percent decrease in LVMi from baseline was 22.97% at 6 months, 26.26% at 12 months, and 28.58% at 24 months postoperatively. This regression is primarily driven by indexed cellular volume regression (23.70%), with a smaller reduction in the indexed extracellular volume (18.40%) in the first 6 months. Both compartments exhibited sustained reductions through 12 months. But from 12 to 24 months, only indexed extracellular volume continued to decline (from 22.13±6.76 to 20.89±6.25 mL/m²; P<0.001). Greater left ventricular outflow tract pressure gradient reduction (β=0.157; P=0.001) was associated with LVMi regression after septal myectomy.

Conclusions: In patients with hypertrophic obstructive cardiomyopathy postseptal myectomy, early LVMi reduction involves both cellular and extracellular compartments, with slower reduction from 12 to 24 months, mainly driven by the extracellular component. This demonstrates rapid myocardial adaptability to afterload relief, with slower extracellular matrix remodeling. Greater left ventricular outflow tract pressure gradient reduction was associated with greater LVMi regression after surgery.

Registration: URL: https://www.chictr.org.cn; Unique identifier: ChiCTR2100043699.

Background: The proposed cause of Takotsubo syndrome (TTS) includes coronary microvascular dysfunction. This study aimed to investigate coronary microvascular dysfunction and its recovery in patients with TTS using serial positron emission tomography myocardial perfusion imaging.

Methods: Patients with TTS who underwent cardiac positron emission tomography within 30 days of admission and at 6-month follow-up (May 2017-June 2023) were analyzed. Changes in positron emission tomography parameters, including extent of myocardial perfusion abnormality, left ventricular function, rest and stress myocardial blood flow (MBF), myocardial flow reserve, and coronary vascular resistance (CVR), were assessed from baseline to follow-up. In apical TTS, segmental analyses (basal, mid, distal segments, and apex) and intersegment differences were evaluated.

Results: Of 130 patients screened, 62 patients (median age, 70 years, 97% women) were included. After a median follow-up of 178 (121-282) days, global rest and stress MBF, myocardial flow reserve, and CVR significantly improved at follow-up (0.81-0.89 mL/min per gram, P=0.004; 1.56-2.61 mL/min per gram, P<0.001; 1.96-2.65, P<0.001; 52.0-36.2 mm Hg·min·g/mL, P<0.001, respectively). Among 53 patients with apical TTS, improvements in stress MBF, myocardial flow reserve, and CVR were noted in all myocardial segments (all P<0.001), including the basal segment; however, persistent MBF and CVR abnormalities were identified in the distal segment and apex, despite full recovery of left ventricular function.

Conclusions: Patients who underwent serial positron emission tomography perfusion imaging for TTS demonstrated reversible reductions in rest and stress MBF, myocardial flow reserve, and increases in CVR, suggestive of TTS-related coronary microvascular dysfunction and subsequent subtotal recovery. Coronary microvascular dysfunction extended beyond regions of wall motion abnormalities, and regional coronary flow abnormalities persisted in the medium term even after recovery of left ventricular function.

Background: Intramyocardial injection of hydrogel into myocardial infarction (MI) areas can reduce left ventricular remodeling and potentially increase angiogenesis post-MI. The radiotracer ^99mTc-Maraciclatide binds to activated alpha-v-beta-3 (αvβ3)-integrin, a key factor in angiogenesis, and can be used to evaluate myocardial angiogenesis. This study used multimodality imaging to assess the effects of imageable intramyocardial hydrogel delivery on left ventricular remodeling and angiogenesis after MI.

Methods: Fourteen pigs (N=14) underwent 90 minutes of balloon occlusion and reperfusion. Five days post-MI, they were randomized to receive either intramyocardial hydrogel (n=8) or control saline injections (n=6). Contrast cine-computed tomography was used to assess biomechanical changes before and after treatment (day 1, day 5, and day 12). ^99mTc-Maraciclatide uptake was measured with gamma well counting. Scar burden and angiogenesis were evaluated through histology.

Results: Both groups initially showed a decrease in ejection fraction and an increase in end-diastolic volume post-MI. Hydrogel delivery on day 5 led to a reduction in end-diastolic volume and improvement in left ventricular ejection fraction by day 12. The hydrogel group also exhibited decreased compensatory radial strain in remote myocardial segments, but decreased strain in the hydrogel myocardial segments. There was increased uptake of ^99mTc-maraciclatide in the infarct segments after hydrogel delivery, associated with increased αvβ3-integrin and factor VIII expression in the hydrogel treatment group on histology. However, there was no difference in regional inflammation or scar size between the groups.

Conclusions: Intramyocardial delivery of hydrogel early post-MI resulted in decreased left ventricular remodeling and increased αvβ3-integrin activation associated with an increase in angiogenesis.