Already during the last century, the importance of structurally remodeled tissue has been recognized. In recent animal studies, it has convincingly been shown that large myocardial infarction which causes left ventricular dysfunction is followed by a remodeling process of the left ventricle. In large clinical trials these findings were confirmed and the remodeling process of the left ventricle after myocardial infarction has been recognized as a reparative but finally pathologic process which leads to a further deterioration of the already depressed left ventricular function, to the development of heart failure and finally to death. In view of the increasing number of patients with heart failure due to coronary artery disease the assessment of the remodeling process by a highly accurate and non-invasive method is mandatory. Furthermore, monitoring of preventive and therapeutic strategies has to be monitored by this method. MRI is ideally suited for the assessment of ventricular remodeling because it represents the gold standard for the measurement of cardiac chamber volumes and myocardial mass. Regional myocardial wall motion, regional systolic wall thickening and global ventricular function can be assessed with high accuracy and reproducibility. It is absolutely non-invasive and safe for patients and investigators. Remodeling of the cardiovascular system has been defined as an alteration of the homogeneity of cellular and structural elements of the heart and circulation by disease. This definition includes events on the cellular level such as transcription and translation within resident cells and the extracellular space. Furthermore, a variety of molecular mechanisms, e.g. intracellular high energy phosphate compounds are involved. Alterations of these compounds during myocardial ischemia and in regions of ischemically jeopardized myocardium can be measured, e.g. by 3~p-MR spectroscopy and their changes may have an early impact on the remodeling process and finally the geometrical, morphological and functional alteration of the heart. The remodeling process [1] in left ventricular pressure overload leads to concentric hypertrophy with lateral expansion of the myocytes and myofibrillar proliferation, but the number and average myocyte length remains unchanged. During volume overload excentric left ventricular hypertrophy with lengthening of myocytes, replication of sarcomeres in series, but unchanged sarcomere length and cell surface area of myocytes is observed. After diffuse or focal loss of myocytes e.g. following a myocardial infarction, the remodeling process is twofold. In the zone of myocyte loss stretching and slippage of myocytes, a reduction of the intracellular space and the disruption of the collagene matrix occurs. Consequently wall thinning and chamber dilation is observed. In the normal zone without myocyte loss regional compensatory hypertrophy occurs. However, depletion of energy substrate in the hypertrophied myocardium leads finally to failure, wall thinning and dilation. Thus, the main parameters for the assessment of left ventricular remodeling are left ventricular geometry, left ventricular function and myocardial bioenergetics. Left ventricular dimensions, volumes and the extension of the infarcted myocardium can be assessed most accurately using spin echo or a gradient echo MR sequences. Most of the sequences can be performed during a single breathhold and thus allow a very rapid acquisition. Regional and global left ventricular function can also be assessed with use of breathhold cine gradient echo MR sequences with simultaneous acquisition of a cine loop within two to three imaging planes.