Stem cell treatments are a desirable therapeutic option to regenerate myocardium and improve cardiac function after myocardial infarction. Several different types of cells have been explored, each with their own benefits and limitations. Induced pluripotent stem cells possess an embryonic-like state and therefore have a high proliferative capacity, but they also pose a risk of teratoma formation. Mesenchymal stem cells have been investigated from both bone marrow and adipose tissue. Their immunomodulatory characteristics may permit the use of allogeneic cells as universal donor cells in the future. Lastly, studies have consistently shown that cardiac stem cells are better able to express markers of cardiogenesis compared to other cell types, as well improve cardiac function. The ideal source of stem cells depends on multiple factors such as the ease of extraction/isolation, effectiveness of engraftment, ability to differentiate into cardiac lineages and effect on cardiac function. Although multiple studies highlight the benefits and limitations of each cell type and reinforce the successful potential use of these cells to regenerate damaged myocardium, more studies are needed to directly compare cells from various sources. It is interesting to note that research using stem cell therapies is also expanding to treat other cardiovascular diseases including non-ischemic cardiomyopathies.

Stem cell transplantation is a potential therapeutic option to regenerate damaged myocardium and restore function after infarct. Current research is focused on the use of allogeneic mesenchymal stem cells (MSCs) due to their unique immunomodulatory characteristics and ability to be harvested from young and healthy donors. Both animal and human studies support the immunoprivileged state of MSCs and even demonstrate improvements in cardiac function after transplantation. This research continues to be a topic of interest, as advances will ultimately enable the clinical use of these universal cells for therapy after a myocardial infarction. Updated in vitro, in vivo, and clinical trial studies are discussed in detail in the following review.

A 35-year-old man with a known history of Emery-Dreifuss muscular dystrophy called emergency medical services (EMS) while at work one morning, reporting palpitations, lightheadedness, fatigue and a rapid heart rate. On arrival by EMS, his pulse was documented at 195-200 beats/min, and his rhythm strips showed ventricular tachycardia ( Figure 1A). He underwent cardioversion and was given a bolus of amiodarone, 150 mg intravenously. In the emergency department and during admission, his symptoms persisted with rhythm strips showing recurrent episodes of sustained ventricular tachycardia (Figure 1B). He was subsequently started on an amiodarone drip and oral metoprolol. Echocardiography performed during admission showed dilated cardiomyopathy with severe systolic dysfunction and an estimated ejection fraction of 23%. Cardiac catheterization was performed to rule out an ischemic cause of the cardiomyopathy and showed normal coronary arteries. The patient received an implantable cardioverter-defibrillator and was discharged with prescriptions for an oral β-blocker and amiodarone. As an out patient, his amiodarone is slowly being weaned because he has had no recurrent episodes of ventricular tachycardia.With respect to the patient's diagnosis of Emery-Dreifuss muscular dystrophy, he first saw a neurologist at age 14 years after multiple operations to lengthen his Achilles tendon owing to persistent "toe walking," which is characteristic of the disease. He was subsequently referred to a muscular dystrophy specialist at age 15, when the diagnosis of Emery-Dreifuss muscular dystrophy was confirmed. Aside from the contractures of his Achilles tendons, he also has substantial difficulty with neck flexion secondary to contractures in his neck extensors. The patient lives in a community with limited access to specialist care and has therefore not followed up with a muscular dystrophy specialist since age 15, because it would require substantial travel to a larger tertiary care centre. The patient's first echocardiogram at age 15 showed a dilated cardiomyopathy with an ejection fraction of 45%-50%. He was subsequently started on an angiotensinconverting enzyme (ACE) inhibitor by a cardiologist. He elected not to start a β-blocker because of potential adverse effects, including fatigue. Subsequently, he had a total of 4 follow-up appointments over the next 20 years with his cardiologist, where he remained completely asymptomatic from a cardiac perspective. He underwent serial echocardiography tests, which ultimately showed progression of his cardiomyopathy. His next echocardiogram almost 10 years later showed a dilated left ventricle with mild global systolic dysfunction (ejection fraction of 45%), which progressed to moderate left ventricular systolic dysfunction (ejection fraction of 35%-40%) over the PRACTICE | CASES