**Author details**

*Cardiac Diseases - Novel Aspects of Cardiac Risk, Cardiorenal Pathology and Cardiac Interventions*

deeper myocardial tissue layers [115, 133, 134]. Nonetheless, improved myocardial perfusion with remote conditioning may occur based on findings of higher TIMI (thrombosis in myocardial infarction) scores, myocardial blush grade and coronary reserve in cardiac patients. Restoration of blood flow to the deeper layers of the myocardial wall is a crucial risk factor for ventricular remodeling and major

In the clinical setting, results with this intervention (i.e. repeated arm or leg ischemia-reperfusion) are mixed; studies report either manifest cardioprotection [138, 139], no benefit [18, 140, 141] or exacerbation of injury [112, 142]. Failure to provide protection by remote conditioning in patients may be associated with the use of anesthetics such as propofol that abrogates protection [18]; volatile anesthetics are mostly recommended for at-risk cardiac patients [143, 144]. In proofof-concept studies, other forms of remote conditioning, such as remote ischemic perconditioning (intervention performed during evolving myocardial infarction) have reported protection against tissue injury, ST-segment resolution and bio-

Pathogenesis of lethal reperfusion injury remains to be established; the principle

that reperfusion injury contributes to post-ischemic myocardial dysfunction is generally accepted but definitive evidence for its existence is lacking. While evaluation of the nature of cellular changes produced by ischemia and subsequent reperfusion has produced significant novel insights it is unclear that cardiomyocytes are the only cell types (within the myocardium) that are at risk of further injury. Of principle importance is that interventions to limit myocardial injury be instituted at the time of, or in conjunction with other reperfusion strategies. Pharmacologic compounds currently being used in the clinical setting delay, at best, short-term progression of cellular injury; long-term effects of these treatments in large animal ischemia-reperfusion injury models have not been properly investigated. The concept of a "magic bullet" intervention remains utopic, at present, considering the complexity of physiopathological mechanisms involved in cell death and myocardial remodeling. Utilization of exogenous interventions such as ischemic conditioning in combination with pharmacologic treatments remains a significant challenge. Further investigations into combination therapy, particularly in longer-term studies should be envisaged; consideration should also be paid to the existence of comorbidities within the patient population since overall efficacy of any treatment option

adverse cardiac events [135–137].

**3. Concluding comments**

marker release in animal models and patients [145–147].

**20**

will be affected.

John G. Kingma Faculty of Medicine, Department of Medicine, Université Laval, Québec, Canada

\*Address all correspondence to: john.kingma@fmed.ulaval.ca

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
