Role of myocardial viability in the improvement of cardiac function after revascularization

Coronary artery disease, associated with a large myocardial infarction, is the cause of heart failure in approximately 50% of current clinical series. The possibility of revascularization, using either coronary bypass surgery or angioplasty, in these patients increases the importance of the determination of viable, but hibernating, myocardium. Positron emission tomography, thallium reinjection, and dobutamine stress echocardiography are the current techniques available for the determination of hibernating myocardium. Thallium reinjection has the greatest sensitivity, but echo dobutamine has greater specificity. Improvement can be expected in patients who have more than 30% of their myocardium demonstrated to be viable by any of these techniques. Improvement in function occurs early after revascularization. It is suggested that 20-40% of patients with congestive heart failure due to previous myocardial infarction, may achieve a clinical improvement by revascularization. There is also evidence to suggest that the recurrent morbidity and mortality events are affected by revascularization. © Kluwer Academic Publishers

Thyroid hormones and their action on the myocardium [Les hormones thyroïdiennes, action sur le myocarde]

Thyroid hormones are closely related to cardiac structure and function. We have been studying their effects for over 15 years in various experimental models: - Daily triidothyronin (T3) administration to rats for 14 days improves the ability of the isolated heart to tolerate ischemia, without abolishing the capacity for ischemic preconditioning (IP). - When hypothyroidism is induced in rats by administering propylthiouracil for 21 days, the isolated heart is markedly more tolerant of 30 min of global ischemia but can no longer undergo IP. - After myocardial infarction induced in rats by left coronary artery ligation, the post - infarct heart is protected against global ischemia but its contractility is reduced. T3 administration for 2 and 13 weeks significantly improves contractility and reduces both remodeling and the sphericity index. - TNF exposure delays cultured neonatal rat myocyte elongation (maturation), and this effect is prevented by concomitant T3 administration. - Thus, thyroid hormones offer valuable insights into cardiac structure and function and may have therapeutic potential in patients with cardiovascular disease

Myocardial protection in man - From research concept to clinical practice

Myocardial protection aims at preventing myocardial tissue loss: (a) In the acute stage, i.e., during primary angioplasty in acute myocardial infarction. In this setup, the attenuation of reperfusion injury is the main target. As a "mechanical" means, post-conditioning has already been tried in man with encouraging results. Pharmacologic interventions that could be of promise are statins, insulin, peptide hormones, including erythropoietin, fibroblast growth factor, and many others. (b) The patient with chronic coronary artery disease offers another paradigm, with the target of avoidance of further myocyte loss through apoptosis and inflammation. Various pharmacologic agents may prove useful in this context, together with exercise and "mechanical" improvement of cardiac function with attenuation of myocardial stretch, which by itself is a noxious influence. A continuous effort toward acute and chronically preserving myocardial integrity is a concept concerning both the researcher and the clinician. © Springer Science+Business Media, LLC 2007

Type 1 diabetes impairs compensatory response after myocardial infarction; role of tissue hypothyroidism and effects of thyroid hormone administration [Le diabète de type 1 diminue la réponse compensatrice après un infarctus du myocarde. Rôle de I'hypothyroïdie tissulaire et effets de I'administration d'hormones thyroïdiennes]

Type I diabetes (TOD) increases the risk of coronary artery disease and myocardial infarction and is characterized by baseline cardiac dysfunction. We investigated the influence of TOD in post-infarct remodeling (REM) and the role of thyroid hormone (TH) signaling in this response. A cute myocardial infarction (A MI) was induced in rats with type I diabetes ( TOD) and in non diabetic rats (NTOD-A MI), sham-operated rats serving as controls (SHAM). AMI resulted in tissue hypothyroidism due to significant downregulation of the TH receptors TRα1 and TRβ1 in the TOD myocardium, while no change in plasma T3 or T4 was observed. This response was associated with increased expression of β-MHC and distinct changes in cardiac function and geometry: EF% was decreased in TOD-AM I as compared to NTOD-A MI. Systolic and diastolic chamber dimensions were increased, with no concomitant increase in wall thickness. Thus, WTI (the ratio of LVIDd12 × posterior wall thickness), an index of wall stress, was significantly increased in TODAMI. The absence of wall thickening in TOD-AMI hearts was associated with changes in stretch-induced kinase hypertrophic signaling: phosporylated (p)ERK andp-p38 MAPK levels were not changed In TOD-AMI in comparison with non infarcted hearts (TODSHA M) and NTOD-A MI hearts. TH administration after A MI prevented tissue hypothyroidism and resulted in decreased β-MHC expression, increased wall thickening and normalized wall stress, while stretch-induced p38 MAPK activation was increased. We conclude that diabetes exacerbates post-ischemic cardiac remodeling and that tissue hypothyroidism may be involved in this response

Protection of the abnormal heart

Myocardial ischemia and reperfusion injury have been extensively investigated in the laboratory mainly in healthy tissues. However, in clinical settings, ischemic heart disease coexists with certain illnesses, which could potentially influence the response of the myocardium to ischemia and reperfusion. Recent research has revealed that the abnormal heart may not be always vulnerable to ischemic injury. Furthermore, the effect of powerful means of protection, such as ischemic preconditioning, may not be in operation under certain pathological conditions. With this evidence in mind, the present review will focus on the response of the abnormal heart to ischemia and reperfusion, the possible underlying mechanisms, and potential cardioprotective strategies. © Springer Science+Business Media, LLC 2007