Magnetic resonance imaging detects significant sex differences in human myocardial strain

<p>Abstract</p> <p>Background</p> <p>The pathophysiology responsible for the significant outcome disparities between men and women with cardiac disease is largely unknown. Further investigation into basic cardiac physiological differences between the sexes is needed. This study utilized magnetic resonance imaging (MRI)-based multiparametric strain analysis to search for sex-based differences in regional myocardial contractile function.</p> <p>Methods</p> <p>End-systolic strain (circumferential, longitudinal, and radial) was interpolated from MRI-based radiofrequency tissue tagging grid point displacements in each of 60 normal adult volunteers (32 females).</p> <p>Results</p> <p>The average global left ventricular (LV) strain among normal female volunteers (n = 32) was significantly larger in absolute value (functionally better) than in normal male volunteers (n = 28) in both the circumferential direction (Male/Female = -0.19 ± 0.02 vs. -0.21 ± 0.02; p = 0.025) and longitudinal direction (Male/Female = -0.14 ± 0.03 vs. -0.16 ± 0.02; p = 0.007).</p> <p>Conclusions</p> <p>The finding of significantly larger circumferential and longitudinal LV strain among normal female volunteers suggests that baseline contractile differences between the sexes may contribute to the well-recognized divergence in cardiovascular disease outcomes. Further work is needed in order to determine the pathologic changes that occur in LV strain between women and men with the onset of cardiovascular disease.</p

Ventricular function after coronary artery bypass grafting: Evaluation by magnetic resonance imaging and myocardial strain analysis

AbstractObjectiveMagnetic resonance imaging with radiofrequency tissue tagging permits quantitative assessment of regional systolic myocardial strain. We sought to investigate the utility of this imaging modality to quantitatively determine preoperative impairment and postoperative improvement in ventricular function in patients with ischemic heart disease.MethodsMagnetic resonance imaging with radiofrequency tissue tagging was performed on 6 patients (average age 60.2 ± 13.7 years) with coronary artery disease and 32 control subjects with no known heart disease. Patients with coronary artery disease underwent imaging before and 3 months after coronary artery bypass grafting. The ventricle was divided into 6 segments within a midventricular plane. Regional 2-dimensional left ventricular circumferential strain was calculated from tagged magnetic resonance images throughout systole. Circumferential strain results were compared in patients before and after and 3 months after coronary artery bypass grafting and also in control subjects.ResultsBefore the operation circumferential strain identified 100% (10/10) of all regional wall motion abnormalities seen by preoperative ventriculography. Postoperatively, improvements were demonstrated in 56% (20/36) of the regions, and these improvements agreed with viability testing by single-photon emission computed tomography when available. Additionally, preoperative global circumferential strain for the ischemic group was significantly depressed relative to that in control subjects (0.11 ± 0.05 vs 0.20 ± 0.03, P < .001). Global circumferential strain correlated with ejection fraction by ventriculography (r = 0.84, P < .01) and improved after coronary artery bypass grafting (0.14 ± 0.05 vs 0.11 ± 0.05, P < .01).ConclusionsMagnetic resonance imaging with radiofrequency tissue tagging permitted circumferential strain calculation. This technology quantitatively demonstrated improvements in left ventricular wall motion after coronary artery bypass grafting for both individual regions and the entire ventricle. This noninvasive method may prove useful in preoperative evaluation and postoperative serial assessment of left ventricular wall motion

Improved heart function follows enhanced inflammatory cell recruitment and angiogenesis in 11 beta HSD1-deficient mice post-MI

AIMS: Mice unable to locally regenerate corticosterone due to deficiency of 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) have enhanced angiogenesis during acute myocardial infarct healing. The present study investigates the hypotheses that in these mice (i) inflammation and angiogenic signalling are promoted and (ii) longer-term remodelling and function are improved. METHODS AND RESULTS: Myocardial infarction (MI) was induced by coronary artery ligation in 11βHSD1(−/−) and wild-type (C57BL/6) mice. Studies were terminated 2, 4, 7, and 28 days post-surgery. Increased vessel density (CD31 immunoreactivity) on the infarct border was confirmed 7 days after MI in 11βHSD1(−/−) hearts (P < 0.05) and was accompanied by improved ejection fraction (ultrasound) compared with C57BL/6. During wound healing, recruitment of neutrophils (at 2 days after MI) and macrophages (from 4 days after MI) and expression of monocyte-chemoattractant protein-1 was increased in 11βHSD1(−/−) compared with C57BL/6 hearts (P < 0.05). Recruitment of alternatively activated YM1-positive macrophages was particularly enhanced in the period preceding increased vessel density and was accompanied by increased expression of pro-angiogenic IL-8. By 28 days post-MI, when the infarct scar had matured, higher vessel density was maintained in 11βHSD1(−/−) hearts and vessels were smooth-muscle coated. Infarct scars were thicker (P < 0.001) in 11βHSD1(−/−) compared with C57BL/6 hearts and ejection fraction was higher (P < 0.05). CONCLUSION: Increased vessel density in healing infarcts of mice deficient in 11(−/−)HSD1 follows recruitment of pro-reparative macrophages and increased pro-angiogenic signalling. Mature infarcts show less thinning and cardiac function is improved relative to wild-type mice, suggesting that 11βHSD1 may be a novel therapeutic target after MI