Objective: To compare the extent and distribution of focal fibrosis by gadolinium contrast-enhanced magnetic resonance imaging (MRI; delayed hyperenhancement) in severe left ventricular (LV) hypertrophy in patients with pressure overload caused by aortic stenosis (AS) and with genetically determined hypertrophic cardiomyopathy (HCM). Methods: 44 patients with symptomatic valvular AS (n = 22) and HCM (n = 22) were studied. Cine images were acquired with fast imaging with steady-state precession (trueFISP) on a 1.5 T scanner (Sonata, Siemens Medical Solutions). Gadolinium contrast-enhanced MRI was performed with a segmented inversion-recovery sequence. The location, extent and enhancement pattern of hyperenhanced myocardium was analysed in a 12-segment model. Results: Mean LV mass was 238.6 (SD 75.3) g in AS and 205.4 (SD 80.5) g in HCM (p = 0.17). Hyperenhancement was observed in 27% of patients with AS and in 73% of patients with HCM (p , 0.01). In AS, hyperenhancement was observed in 60% of patients with a maximum diastolic wall thickness > 18 mm, whereas no patient with a maximum diastolic wall thickness , 18 mm had hyperenhancement (p , 0.05). Patients with hyperenhancement had more severe AS than patients without hyperenhancement (aortic valve area 0.80 (0.09) cm 2 v 0.99 (0.3) cm 2 , p , 0.05; maximum gradient 98 (22) mm Hg v 74 (24) mm Hg, p , 0.05). In HCM, hyperenhancement was predominant in the anteroseptal regions and patients with hyperenhancement had higher end diastolic (125.4 (36.9) ml v 98.8 (16.9) ml, p , 0.05) and end systolic volumes (38.9 (18.2) ml v 25.2 (1.7) ml, p , 0.05). The volume of hyperenhancement (percentage of total LV myocardium), where present, was lower in AS than in HCM (4.3 (1.9)% v 8.6 (7.4)%, p, 0.05). Hyperenhancement was observed in 4.5 (3.1) and 4.6 (2.7) segments in AS and HCM, respectively (p = 0.93), and the enhancement pattern was mostly patchy with multiple foci. Conclusions: Focal scarring can be observed in severe LV hypertrophy caused by AS and HCM, and correlates with the severity of LV remodelling. However, focal scarring is significantly less prevalent in adaptive LV hypertrophy caused by AS than in genetically determined HCM. R emodelling in left ventricular (LV) hypertrophy is accompanied by several structural changes. Interstitial and replacement fibrosis are among the morphological alterations that have been observed in LV hypertrophy caused by pressure overload and in genetically determined hypertrophic cardiomyopathy (HCM).

A transgenic rat line, TGR(mREN2)27, was established by introducing the murine Ren-2 gene into the genome of rats by microinjection techniques. These rats exhibit severe hypertension, making them an interesting model in which to study the role of renin in the pathophysiology of hypertension. However, although the additional renin gene is the only genetic difference compared with control rats, the exact mechanism of hypertension in TGR(mREN2)27 rats is still unclear. It cannot be attributed to a stimulation of the endocrine renin-angiotensin system or to an overexpression of renin in the kidney, since plasma and kidney renin and renin gene expression in the kidney are low in these animals. Here we describe recent progress made toward elucidating mechanisms of hypertension in TGR(mREN2)27 rats. 1) TGR(mREN2)27 rats were bred to homozygosity. The development of high blood pressure in homozygous rats is accelerated compared with that of heterozygous rats. This is paralleled by a higher mortality rate in homozygous TGR(mREN2)27 rats. Blood pressure and mortality rate of homozygous transgenic rats were effectively reduced by 10 mg captopril per kilogram body weight. 2) Treatment of 8-week-old heterozygous TGR(mREN2)27 rats with 10 mg/kg body wt per day of the angiotensin II receptor antagonist DuP 753 for 4.5 weeks normalized blood pressure. After withdrawal of the drug, blood pressure increased rapidly, reaching control levels after 3 weeks. In another group of TGR(mREN2)27 rats treated with 0.5 mg/kg per day, there was no change in blood pressure. Plasma renin and plasma angiotensin II were significantly higher in the high-dose group compared with the low-dose group. These data indicate that angiotensin II plays a major role in hypertension of TGR(mREN2)27 rats. 3) Because the activity of the plasma renin-angiotensin system is reduced in TGR(mREN2)27 rats but the pharmacological interventions with captopril and DuP 753 suggest an important role of angiotensin II for hypertension, our interest focused on tissue renin-angiotensin systems. By Northern hybridization, highest transgene expression was detected in the adrenal gland followed by thymus, tissues of the gastrointestinal and genital tracts, kidney, brain, and lung. No expression was found in the liver and submandibular gland. 4) Compared with Sprague-Dawley rats, urinary glucocorticoid and mineralocorticoid excretion was significantly enhanced in TGR(mREN2)27 rats up to an age of 18 weeks, suggesting that corticoids may be involved in the pathogenesis of hypertension in TGR(mREN2)27 rats. Treatment of 4-and 18-week-old TGR(mREN2)27 rats with the mineralocorticoid receptor antagonist spironolactone, however, did not influence blood pressure. The high expression of Ren-2 in the adrenal glands and the corticosteroid excretion analyses point to an important role of a local adrenal renin-angiotensin system in the pathophysiology of hypertension in TGR (mREN2) or more than two decades, hypertensive rat strains like spontaneously hypertensive rats (SHR) have been use...

MR imaging-guided stent placement in iliac arteries is feasible in select patients. The presented technique has limitations-that is, long procedure times, lack of real-time monitoring, and stent artifacts-that necessitate further modifications before it can be recommended for clinical use.

We report the diagnostic potential of cardiovascular magnetic resonance (CMR) to visualize the time course of eosinophilic myocarditis upon successful treatment. A 50-year-old man was admitted with a progressive heart failure. Endomyocardial biopsies were taken from the left ventricle because of a white blood cell count of 17000/mm 3 with 41% eosinophils. Histological evaluation revealed endomyocardial eosinophilic infiltration and areas of myocyte necrosis. The patient was diagnosed with hypereosinophilic myocarditis due to idiopathic hypereosinophilic syndrome. CMR-studies at presentation and a follow-up study 3 weeks later showed diffuse subendocardial LGE in the whole left ventricle. Upon treatment with steroids, CMR-studies revealed marked reduction of subendocardial LGE after 3 months in parallel with further clinical improvement. This case therefore highlights the clinical importance of CMR to visualize the extent of endomyocardial involvement in the diagnosis and treatment of eosinophilic myocarditis. Case reportA 50-year-old man was admitted with a suspicion of an acute coronary syndrome because of progressive dyspnea and positive Troponin I (9.5 ng/ml). A two-dimensional echocardiogram revealed severe left ventricular hypokinesis with an ejection fraction of 27%. Upon coronary angiography, coronary artery disease was excluded. Because of a white blood cell count of 17000/mm 3 with 41% eosinophils, endomyocardial biopsies were taken from the left ventricle. Histological evaluation showed marked endomyocardial eosinophilic infiltration and areas of myocyte necrosis ( Figure 1A). Further evaluation revealed no evidence of secondary hypereosinophilia (malignant diseases, allergy, vasculitis, parasitic infection). The patient was diagnosed with hypereosinophilic myocarditis due to idiopathic hypereosinophilic syndrome. Medication with steroids and heart failure was initiated promptly and the patient improved rapidly.CMR-studies at presentation and a follow-up study 3 weeks later showed diffuse subendocardial LGE in the whole left ventricle with involvement of the papillary muscles. Upon 3 months follow up, however, subendocardial LGE has markedly decreased in parallel with further clinical improvement ( Figures 1B,C,D). Ejection fraction has improved from 27% at baseline to 35% after

Planimetry of aortic valve area by MRI can be performed with better image quality as compared with TEE. In the clinical management of patients with aortic stenosis, it has to be considered that MRI slightly overestimates aortic valve area as compared with catheterization despite an excellent correlation.

Magnetic resonance planimetry of the mitral valve orifice in mitral stenosis offers a reliable and safe method for noninvasive quantification of mitral stenosis. In the clinical management of patients with mitral stenosis, it has to be considered that planimetry by MRI slightly overestimates MVA, as compared with MVA calculated echocardiographically and at catheterization.

Atrial septum defects (ASDs), ventricular septum defects (VSDs) and patent ductus arteriosus (PDA) are the most common adult congenital heart defects. The degree of left-to-right shunting as assessed by the ratio of flow in the pulmonary (Qp) and systemic circulation (Qs) is crucial in the management of these conditions. This study compared phase-contrast cine magnetic resonance imaging (PC-MRI), a non-invasive imaging technique, with invasive oximetry for the measurement of shunt volumes during cardiac catheterisation in adults with left-to-right shunting. Both invasive oximetry and shunt quantification by PC-MRI (1.5 T scanner; Sonata, Siemens Medical Solutions) were performed on 21 patients with left-to-right shunting (14 ASD, 5 VSD, 2 PDA) and data on Qp/Qs ratios and left-to-right shunt fraction compared. Mean Qp/Qs ratios assessed by PC-MRI and oximetry were 2.10+/-0.76 and 1.96+/-0.77, respectively (p = 0.37). Mean shunt fraction was 46.3+/-19.6% when calculated by PC-MRI and 42.3+/-20.1% when obtained by oximetry (p = 0.12). There was a strong correlation of Qp/Qs ratios and shunt fraction between both methods (r = 0.61, p < 0.01 and r = 0.84, p < 0.0001, respectively). The two methods had a good agreement according to Bland and Altman plots with a small but non-significant overestimation of Qp/Qs-ratios and shunt fraction by PC-MRI. On receiver operating characteristic analysis, the sensitivity and specificity of PC-MRI to detect an oximetry-derived Qp/Qs ratio of > or =1.5:1 were 93% and 100% at a PC-MRI threshold of a Qp/Qs ratio > or =1.75:1 (area under curve (AUC) = 0.99). Quantification of left-to-right shunting can be performed reliably and accurately by PC-MRI and the data obtained by this method correlate closely to those from invasive oximetry.

CMR allows excellent characterisation of valve phenotype in patients with BAV. The present data demonstrate that a raphe is present in the vast majority of cases and RL fusion is the predominant phenotype of BAV. No significant differences in the aortic dimensions were observed.