[show abstract][hide abstract] ABSTRACT: Myocardial edema can arise in several disease states. MRI contrast agent can accumulate in edematous tissue, which complicates differential diagnosis with contrast-enhanced (CE)-MRI and might lead to overestimation of infarct size. Sodium Chemical Shift Imaging ((23)Na-CSI) may provide an alternative for edema imaging. We have developed a non-infarct, isolated rat heart model with two levels of edema, which was studied with (23)Na-CSI and CE-MRI. In edematous, but viable tissue the extracellular sodium (Na (e) (+) ) signal is hypothesized to increase, but not the intracellular sodium (Na (i) (+) ) signal. Isolated hearts were perfused at 60 (n = 6) and 140 mmHg (n = 5). Dimethyl methylphosphonate (DMMP) and phenylphosphonate (PPA) were used to follow edema formation by (31)P-MR Spectroscopy. In separate groups, Thulium(III)1,4,7,10 tetraazacyclododecane-N,N',N″,N'''-tetra(methylenephosphonate) (TmDOTP(5-)) and Gadovist were used for (23)Na-CSI (n = 8) and CE-MRI (n = 6), respectively. PPA normalized signal intensity (SI) was higher at 140 versus 60 mmHg, with a ratio of 1.27 ± 0.12 (p < 0.05). The (DMMP-PPA)/dry weight ratio, as a marker of intracellular volume, remained unchanged. The mid-heart cross sectional area (CSA) of the left ventricle (LV) was significantly increased at 140 mmHg. In addition, at 140 mmHg, the LV Na (e) (+) SI increased with a 140 mmHg/60 mmHg ratio of 1.24 ± 0.18 (p < 0.05). Na (i) (+) SI remained essentially unchanged. With CE-MRI, a subendocardially enhanced CSA was identified, increasing from 0.20 ± 0.02 cm(2) at 60 mmHg to 0.31 ± 0.02 cm(2) at 140 mmHg (p < 0.05). Edema shows up in both CE-MRI and Na (e) (+) . High perfusion pressure causes more edema subendocardially than subepicardially. (23)Na-CSI is an attractive alternative for imaging of edema and is a promising tool to discriminate between edema, acute and chronic MI.
The international journal of cardiovascular imaging 07/2012; · 2.15 Impact Factor
[show abstract][hide abstract] ABSTRACT: Imaging of myocardial infarct composition is essential to assess efficacy of emerging therapeutics. T (2) (*) mapping has the potential to image myocardial hemorrhage and fibrosis by virtue of its short T (2) (*) . We aimed to quantify T (2) (*) in acute and chronic myocardial ischemia/reperfusion (I/R) injury in mice.
I/R-injury was induced in C57BL/6 mice (n = 9). Sham-operated mice (n = 8) served as controls. MRI was performed at baseline, and 1, 7 and 28 days after surgery. MRI at 9.4 T consisted of Cine, T (2) (*) mapping and late-gadolinium-enhancement (LGE). Mice (n = 6) were histologically assessed for hemorrhage and collagen in the fibrotic scar.
Baseline T (2) (*) values were 17.1 ± 2.0 ms. At day 1, LGE displayed a homogeneous infarct enhancement. T (2) (*) in infarct (12.0 ± 1.1 ms) and remote myocardium (13.9 ± 0.8 ms) was lower than at baseline. On days 7 and 28, LGE was heterogeneous. T (2) (*) in the infarct decreased to 7.9 ± 0.7 and 6.4 ± 0.7 ms, whereas T (2) (*) values in the remote myocardium were 14.2 ± 1.1 and 15.6 ± 1.0 ms. Histology revealed deposition of iron and collagen in parallel with decreased T (2) (*) .
T (2) (*) values are dynamic during infarct development and decrease significantly during scar maturation. In the acute phase, T (2) (*) values in infarcted myocardium differ significantly from those in the chronic phase. T (2) (*) mapping was able to confirm the presence of a chronic infarction in cases where LGE was inconclusive. Hence, T (2) (*) may be used to discriminate between acute and chronic infarctions.
MAGMA Magnetic Resonance Materials in Physics Biology and Medicine 02/2012; 25(5):369-79. · 1.86 Impact Factor
[show abstract][hide abstract] ABSTRACT: ROS have been implicated in the development of pathological ventricular hypertrophy and the ensuing contractile dysfunction. Using the rat monocrotaline (MCT) model of pulmonary arterial hypertension (PAH), we recently reported oxidative stress in the failing right ventricle (RV) with no such stress in the left ventricle of the same hearts. We used the antioxidant EUK-134 to assess the role of ROS in the pathological remodeling and dysfunction of the RV. PAH was induced by an injection of MCT (80 mg/kg, day 0), treatment with EUK-134 (25 mg/kg, once every 2 days) of control and MCT-injected animals [congestive heart failure (CHF) group] was started on day 10, and animals were analyzed on day 22. EUK-134 treatment of the CHF group attenuated cardiomyocyte hypertrophy and associated changes in mRNA expression (myosin heavy chain-beta and deiodinase type 3). It also reduced RV oxidative stress and proapoptotic signaling and prevented interstitial fibrosis. Cardiac MRI showed that ROS scavenging did not affect the 37% increase in end-diastolic volume of the RV in the CHF relative to the control group, but the threefold increase in end-systolic volume was reduced by 42% in the EUK-134-treated CHF group. The improved systolic function was confirmed using echocardiography by an assessment of tricuspid annular plane systolic excursion. These data indicate an important role of ROS in RV cardiomyocyte hypertrophy and contractile dysfunction due to PAH and show the potential of EUK-class antioxidants as complementary therapeutics in the treatment of RV dysfunction in PAH.