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Angiotensin II type 2 receptor ([AT.sub.2]R) overexpression ([AT.sub.2]TG) attenuates left ventricular remodeling in a mouse model of anterior myocardial infarction (MI). We hypothesized that the beneficial effects of cardiac [AT.sub.2]TG are mediated via the bradykinin subtype 2 receptor ([B.sub.2]R). Fourteen transgenic mice overexpressing the [AT.sub.2]R ([AT.sub.2]TG mice), 10 mice with a [B.sub.2]R deletion ([B.sub.2]KO mice), 13 [AT.sub.2]TG mice with [B.sub.2]R deletion ([AT.sub.2]TG/[B.sub.2]KO mice), and 11 wild-type (WT) mice were studied. All mice were on a C57BL/6 background. Mice were studied by cardiac magnetic resonance imaging at baseline and days 1, 7, and 28 after MI induced by 1 h of occlusion of the left anterior descending artery followed by reperfusion. Short-axis images from apex to base were used to compare ventricular volumes and ejection fraction (EF). At baseline, end-diastolic volume index (EDVI) and end-systolic volume index (ESVI) were lower and EF higher in [AT.sub.2]TG mice compared with the other three strains. Infarct size was similar between groups. No differences were observed in global remodeling parameters at day 28 between [AT.sub.2]TG and [AT.sub.2]TG/[B.sub.2]KO mice; however, EDVI and ESVI were lower and EF higher in both transgenic groups than in WT or [B.sub.2]KO mice. Both strains lacking [B.sub.2]R demonstrated increased collagen content and less hypertrophy in adjacent noninfarcted regions at day 28. Attenuation of postinfarct remodeling by overexpression of [AT.sub.2]R is not directly mediated via a [B.sub.2]R pathway. However, [B.sub.2]R does appear to have a role in the smaller cavity size and hyperdynamic function observed at baseline in [AT.sub.2]TG mice and in limiting collagen deposition during postinfarct remodeling. magnetic resonance imaging; remodeling

A high resolution, noninvasive approach to quantify atherosclerotic plaque in the peripheral vasculature could have significant clinical and research utility. Seventeen patients with peripheral arterial disease (PAD) were studied in a 1.5T CMR scanner. Atherosclerotic plaque volume in the superficial femoral artery was measured and interobserver, intraobserver, and test-retest variability determined. Nineteen vessels were studied with mean acquisition time of 13.1 minutes per vessel. Mean plaque volume was 7.27 ± 3.73 cm3. Intra-observer intraclass correlation was R = 0.997, inter-observer was R = 0.987, and test-retest reproducibility was R = 0.996. Thus, high resolution measurement of plaque volume in PAD is reliable and reproducible. [ABSTRACT FROM AUTHOR]

Angiotensin II type 2 receptor (AT 2 -R) overexpression in the mouse heart preserves left ventricular (LV) size and global LV function during post-MI remodeling. We hypothesized that CMR tagging would localize regional improvements in myocardial function during post-MI remodeling in AT 2 -R cardiac overexpressed transgenic mice (TG), which could explain the preservation of global LV function post-MI. Six male wild-type (WT) C57BL/6 mice and 10 TG mice were studied by CMR at baseline (day 0) and days 1, 7, and 28 post-MI. MI was induced by 1 hour occlusion of the LAD followed by reperfusion. On day 1 post-MI, gadolinium-DTPA was injected to assess infarct size. LV size and function was assessed by cine CMR. Mean % circumferential shortening (%CS) was calculated within infarcted, adjacent, and remote regions at each time point in WT and TG mice. Quantitative interstitial collagen and mean myocyte cross-sectional area was measured postmortem at day 28 post-MI. LV end-systolic volume was lower and ejection fraction higher at baseline in the TG group and these differences were maintained post-MI. Within infarcted and remote zones, although %CS was higher in TG mice at day 0, there was no difference by day 28 between groups. Within adjacent regions, while there was no difference at day 0 or 1 in TG vs. WT, %CS was significantly higher in TG mice by day 7, and these changes persisted out to day 28 post-MI. Regional interstitial collagen and myocyte size were similar between groups. Thus, myocardial tagging can detect regional differences in contractile function post-MI in TG mice, and AT 2 -R overexpression is associated with improved contractile function in adjacent noninfarcted myocardium. [ABSTRACT FROM AUTHOR]

Delayed contrast-enhanced cardiac magnetic resonance imaging (ceCMR) delineates infarct size. The presence of hypoenhancement consistent with microvascular obstruction (MO) signifies larger infarcts with a worse prognosis. We hypothesized that the size of the contrast defect (CD) on ceCMR in acutely infarcted myocardium may change during infarct healing and depend upon the presence of MO. Twenty-five patients underwent CMR on weeks 1 and 8 after reperfused myocardial infarction. After short-axis cine CMR was performed, gadolinium was infused and ceCMR images and matched tagged cine MR images were obtained in the three most dysfunctional short-axis slices on cine CMR. The area and transmural extent of hyperenhancement (HE) with or without MO representing total CD size were planimetered. Between week I and week 8, the CD area fell from 1729 ± 970 mm2 at week 1 to 1270±706 mm2 (p<0.001), as did the transmural extent of infarction (7 1±22% to 63±24%, p<0.001). The decline in CD trended to be higher in patients with MO (840± 807 mm2) than in HE (3 12±485 mm2, p<0.07). In the patient group as a whole, ejection fraction (Eli improved (56±9% to 60± 10%, p=0.002) between weeks I and 8, but patients with MO showed no increase in EF. Segments with some HE demonstrated partial functional improvement whereas no improvement was seen in HE+MO segments. In patients 8 weeks after reperfused myocardial infarction (MI), the size of infarction by ceCMR decreases compared to week 1 post-MI, especially in those with microvascular obstruction in whom there is little improvement in regional or global function. [ABSTRACT FROM AUTHOR]

Background: Obesity is a known risk factor for heart failure with preserved ejection fraction (HFpEF) and is considered a distinct phenotype with more concentric remodeling. Epicardial adipose tissue (EAT) is also increased in obesity-related HFpEF and is associated with adverse events., Objective: The Cardiac Magnetic Resonance (CMR) Substudy of the SUMMIT trial was aimed to examine the effects of tirzepatide on cardiac structure and function with the underlying hypothesis that it would reduce left ventricular (LV) mass and EAT in obesity-related HFpEF., Methods: One hundred seventy-five patients with obesity-related HFpEF from the parent study of tirzepatide (2.5mg SQ weekly, increasing to a maximum of 15mg weekly) or matching placebo underwent CMR at baseline, which consisted of multiplanar cine imaging. One hundred six patients completed the CMR and had adequate image quality for analysis of LV and LA structure and function and paracardiac (epicardial plus pericardial) adipose tissue at both baseline and 52 weeks. The prespecified primary endpoint of this substudy was between-group changes in LV mass., Results: LV mass decreased by 11 g (95% C.I. -19 to -4) in the treated group (n = 50) when corrected for placebo (n =56) (p=0.004). Paracardiac adipose tissue decreased in the treated group by 45 ml (95% C.I. -69 to -22) when corrected for placebo (p<0.001). The change in LV mass in the treated group correlated with changes in body weight (p<0.02) and, tended to correlate with changes in waist circumference and blood pressure (p=0.06 for both). The LV mass change also correlated with changes in LV end diastolic volume and LA end diastolic and end systolic volumes (p<0.03 for all)., Conclusion: The CMR substudy of the SUMMIT trial demonstrated that tirzepatide therapy in obesity-related HFpEF led to reduced LV mass and paracardiac adipose tissue as compared to placebo and the change in LV mass paralleled weight loss. These physiologic changes may contribute to the reduction in heart failure events seen in the main SUMMIT trial., (Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)