JOURNAL OF TISSUE ENGINEERING AND REGENERATIVE MEDICINE REVIEW ARTICLE J Tissue Eng Regen Med 2007; 1: 327–342. Published online in Wiley InterScience (www.interscience.wiley.com) DOI: 10.1002/term.46 Myocardial tissue engineering: a review H. Jawad, 1 N. N. Ali, 2 A.R. Lyon, 2 Q. Z. Chen, 1 S. E. Harding 2 and A. R. Boccaccini 1 * 1 Department of Materials, Imperial College London, Prince Consort Road, London SW7 2BP, UK 2 National Heart and Lung Institute, Imperial College London, Dovehouse Street, London SW3 6LY, UK Abstract Myocardial tissue engineering, a concept that intends to overcome the obstacles to prolonging patients’ life after myocardial infarction, is continuously improving. It comprises a biomaterial based ‘vehicle’, either a porous scaffold or dense patch, made of either natural or synthetic polymeric materials, to aid transportation of cells into the diseased region in the heart. Many different cell types have been suggested for cell therapy and myocardial tissue engineering. These include both autologous and embryonic stem cells, both having their advantages and disadvantages. Biomaterials suggested for this specific tissue-engineering application need to be biocompatible with the cardiac cells and have particular mechanical properties matching those of native myocardium, so that the delivered donor cells integrate and remain intact in vivo. Although much research is being carried out, many questions still remain unanswered requiring further research efforts. In this review, we discuss the various approaches reported in the field of myocardial tissue engineering, focusing on the achievements of combining biomaterials and cells by various techniques to repair the infarcted region, also providing an insight on clinical trials and possible cell sources in cell therapy. Alternative suggestions to myocardial tissue engineering, in situ engineering and left ventricular devices are also discussed. Copyright  2007 John Wiley & Sons, Ltd. Received 7 June 2007; Accepted 27 August 2007 Keywords myocardial infarction; tissue engineering; biomaterials; scaffolds; cell therapy 1. Introduction Cardiovascular disease (CVD) is a major health problem and the leading cause of death in the Western world. In the UK, CVD accounts for 238 000 annual deaths, comprising 39% of all deaths per annum. Heart attacks are the main cause of death in patients with CVD. Approximately 30% of the 270 000 patients suffering from heart attacks each year die suddenly before reaching the hospital (www.bhf.org.uk). In the remaining patients who survive their initial acute event, the damage sustained by the heart may eventually develop into heart failure. A heart attack, known as a myocardial infarction (MI), occurs when one or more of the blood vessels supplying the heart suddenly occlude. These vessels are the coronary arteries and, when blocked abruptly, there is a sudden decrease in the supply of nutrients and oxygen to the portion of heart muscle supplied by the artery. If blood flow is not restored rapidly, *Correspondence to: A. R. Boccaccini, Department of Materials, Imperial College London, Prince Consort Road, London SW7 2BP, UK. E-mail: a.boccaccini@imperial.ac.uk the result is irreversible cell death within the affected part of the heart muscle. The adult heart cannot repair the damaged tissue, as the mature contracting cardiac cells, the cardiomyocytes, are unable to divide. The result of the myocardial infarction is the formation of scar tissue which does not have contractile, mechanical and electrical properties of normal myocardium (heart muscle). The replacement of contractile myocardium with non- contracting fibrous scar reduces the pumping efficiency of the ventricles, the heart’s main pumping chambers. Various compensatory mechanisms are activated in response to the reduced cardiac output. These initially stabilize the damaged heart and maintain cardiac output at acceptable levels. Ultimately these ‘compensatory systems’ place extra burden on the weakened heart muscle. This leads to a downward spiral of cardiac function and the development of the clinical syndrome of heart failure. The deterioration of heart function accelerates as heart failure progresses. Ultimately at the end-stage of heart failure, mechanical ventricular assist devices (VADs; Birks et al., 2006) or heart transplantation are the only options. However, due to the high cost Copyright  2007 John Wiley & Sons, Ltd.