The segmented inversion-recovery turboFLASH sequence produced the greatest differences in regional myocardial signal intensity in animals. Application of this technique in patients with infarction substantially improved differentiation between injured and normal regions.

BACKGROUND The purpose of this work was to further define the value of cardiac 31P magnetic resonance (MR) spectroscopy for patients with coronary artery disease and dilated cardiomyopathy. METHODS AND RESULTS Blood-corrected and T1-corrected 31P MR spectra of anteroseptal myocardium were obtained at rest using image-selected in vivo spectroscopy localization, a selected volume of 85 +/- 12 cm3, and a field strength of 1.5 T. Nineteen volunteers had a creatine phosphate (CP)/ATP ratio of 1.95 +/- 0.45 (mean +/- SD) and a PDE/ATP ratio of 1.06 +/- 0.53; in four patients with left anterior descending coronary artery (LAD) stenosis, six patients with chronic anterior wall infarction, and four patients with chronic posterior wall infarction, CP/ATP and phosphodiester (PDE)/ATP ratios did not differ from those in volunteers. Twenty-five measurements of 19 patients with dilated cardiomyopathy yielded a CP/ATP of 1.78 +/- 0.51 and a PDE/ATP of 0.98 +/- 0.56 (p = NS versus volunteers). When these patients were grouped according to the severity of heart failure, however, CP/ATP was 1.94 +/- 0.43 in mild (p = NS versus volunteers) and 1.44 +/- 0.52 in severe DCM (p < 0.05), respectively. No correlation was found between CP/ATP and left ventricular ejection fraction or fractional shortening, but correlation of CP/ATP with the New York Heart Association (NYHA) class was significant (r = 0.60, p < 0.005). Six patients with dilated cardiomyopathy were studied repeatedly before and after 12 +/- 6 weeks of drug treatment leading to clinical recompensation with improvement of the NYHA status by 0.8 +/- 0.3 classes. Concomitantly, CP/ATP increased from 1.51 +/- 0.32 to 2.15 +/- 0.27 (p < 0.01), whereas PDE/ATP did not change significantly. CONCLUSIONS Cardiac high-energy phosphate metabolism at rest is normal in LAD stenosis and chronic myocardial infarction in the absence of heart failure. The CP/ATP ratio has low specificity for the diagnosis of dilated cardiomyopathy. However, CP/ATP correlated with the clinical severity of heart failure and may improve during clinical recompensation.

A reduction in the transmural extent of hyperenhancement by contrast-enhanced MRI early after myocardial infarction is associated with an early restoration of flow and future improvement in contractile function.

Concurrent directionally opposite changes in infarcted and noninfarcted myocardium can be defined serially, noninvasively, and with high spatial resolution and full ventricular coverage following myocardial infarction.

Experimental studies demonstrated persistently increased 23 Na content in nonviable myocardium post-myocardial infarction (MI). We hypothesized that nonviable myocardium in humans would show elevated 23 Na content at all stages of infarct development, and therefore could be imaged with 23 Na MRI. Ten patients were examined on days 4, 14, and 90 after infarction, and five of these patients participated in a 12-month follow-up. Physicians frequently require a diagnosis of myocardial viability in patients with large akinetic myocardial regions when they attempt to determine whether such patients should receive revascularization therapy. While nonviable myocardium cannot recover regional function, viable but stunned or hibernating myocardium will eventually resume contractile function following revascularization by percutaneous coronary intervention or bypass grafting (1). Current methods used to diagnose viability, such as positron emission tomography (PET), single photon emission tomography, or stress echocardiography, all have intrinsic limitations related to the use of ionizing radiation, limited access, patient discomfort, or limited acoustic windows. Recently, it was proposed that contrast-enhanced MRI is able to discriminate viable from nonviable myocardium (2).23 Na MRI is another promising approach for the detection of myocardial viability in human cardiac imaging without the need for an intravenous contrast agent (3,4). It has the potential to quantify infarct size, as well as to identify myocardial scars (5-8). In a recent experimental study employing 23 Na MR spectroscopy (MRS) and ion chromatography in the rat post-myocardial infarction (MI) model, we showed that the regional 23 Na concentration is significantly elevated in irreversibly injured myocardium following coronary ligation, both acutely and during the process of chronic scar formation (9). In the same study, we also showed that the Na signal was unchanged in stunned or hibernating myocardium. Thus, 23 Na MRI may allow physicians to diagnose myocardial viability in patients with akinetic areas, using Na content as an intrinsic contrast marker. In human studies, we were able to show that 1) cardiac 23 Na MRI can be applied in humans, 2) the myocardium/blood 23 Na signal intensity (SI) ratio represents the ratio of the 23 Na concentrations in myocardium and blood, and 3) 23 Na SI is elevated in MI (10,11). A comparison of 23 Na MRI with 1 H MRI techniques in patients with subacute or chronic MI, respectively, revealed an area of elevated 23 Na SI that significantly correlated with wall motion abnormalities, as detected by cine MRI, in all patients after subacute MI and 80% of patients with chronic MI (12). Myocardial edema in subacute MI also correlated with the areas of elevated 23 Na SI, but it was extensively larger, whereas a significant correlation of late enhancement with 23 Na MRI was found only in the subacute group. In the present clinical study, we hypothesized that total myocardial Na content would be elevated in patients with nonviabl...