The heart is a muscle and, as such, can suffer injuries. Cardioprotection is the ability of the heart to protect itself from injury.

The defense passes through chemical and phytochemical remedies (plants that have cardioprotective properties).

Some examples of phytochemicals:

• Astragalus polysaccharide
• Astragalus membraneaceus
• Alpinia zerumbet
• Sativum Coriandrum
• Aronia melanocarpa
• Turcuin
• Plinia cauliflora
• Rheum turkestanicum Janisch
• Paeoniflorin
• Danshen
• Mangiferin

Some examples of hormone:

• Erythropoietin
• Irisin

A few examples of amino acids:

• Homoarginine

Some examples of flavonoids

• Icariin
• Hesperidin

Other components

• Diallyl trisulfide

Studies

Rodionov RN, Begmatov H, Jarzebska N, Patel K, Mills MT, Ghani Z, Khakshour D, Tamboli P, Patel MN, Abdalla M, Assaf M, Bornstein SR, Millan JL, Bode-Böger SM, Martens-Lobenhoffer J, Weiss N, Savinova OV. Homoarginine Supplementation Prevents Left Ventricular Dilatation and Preserves Systolic Function in a Model of Coronary Artery Disease. J Am Heart Assoc. 2019 Jul 16;8(14):e012486. doi: 10.1161/JAHA.119.012486. 

Abstract. Background Homoarginine ( hA rg) has been shown to be cardioprotective in a model of ischemic heart failure; however, the mechanism remains unknown. hA rg can inhibit tissue-nonspecific alkaline phosphatase ( TNAP ), an enzyme that promotes vascular calcification. We hypothesized that hA rg will exert beneficial effects by reducing calcification in a mouse model of coronary artery disease associated with TNAP overexpression and hypercholesterolemia. Methods and Results TNAP was overexpressed in the endothelium in mice homozygous for a low-density lipoprotein receptor mutation (wicked high cholesterol [ WHC ] allele). WHC and WHC -endothelial TNAP mice received placebo or hA rg supplementation (14 mg/L in drinking water) starting at 6 weeks of age simultaneously with an atherogenic diet. Outcomes were compared between the groups after 4 to 5 weeks on treatment. Experiments were performed in males, which presented a study limitation. As expected, WHC -endothelial TNAP mice on the placebo had increased mortality (median survival 27 days, P<0.0001), increased coronary calcium and lipids ( P<0.01), increased left ventricular end-diastolic diameter ( P<0.0001), reduced ejection fraction ( P<0.05), and increased myocardial fibrosis ( P<0.0001) compared with WHC mice. Contrary to our hypothesis, hA rg neither inhibited TNAP activity in vivo nor reduced coronary artery calcification and atherosclerosis in WHC -endothelial TNAP mice; however, compared with the placebo, hA rg prevented left ventricular dilatation ( P<0.01), preserved ejection fraction ( P<0.05), and reduced myocardial fibrosis ( P<0.001). Conclusions The beneficial effect of hA rg supplementation in the setting of calcified coronary artery disease is likely due to its direct protective actions on the myocardial response to the ischemic injury and not to the inhibition of TNAP activity and calcification.

Chen X, Li HY, Hu XM, Zhang Y, Zhang SY. Current understanding of gut microbiota alterations and related therapeutic intervention strategies in heart failure. Chin Med J (Engl). 2019 Aug 5;132(15):1843-1855. doi: 10.1097/CM9.0000000000000330.

Abstract. Objective: The purpose of this review is to stress the complicated interactions between the microbiota and the development of heart failure. Moreover, the feasibility of modulating intestinal microbes and metabolites as novel therapeutic strategies is discussed....Conclusions: The composition of the gut microbiota in people with heart failure is different from those with healthy status. A reduction in SCFA-producing bacteria in patients with heart failure might be a notable characteristic for patients with heart failure. Moreover, an increase in the microbial potential to produce TMAO and lipopolysaccharides is prominent. More researches focused on the mechanisms of microbial metabolites and the clinical application of multiple therapeutic interventions is necessarily required.

Schanze N, Bode C, Duerschmied D. Platelet Contributions to Myocardial Ischemia/Reperfusion Injury. Front Immunol. 2019 Jun 6;10:1260. doi: 10.3389/fimmu.2019.01260. 

Abstract. Obstruction of a coronary artery causes ischemia of heart tissue leading to myocardial infarction. Prolonged oxygen deficiency provokes tissue necrosis, which can result in heart failure and death of the patient. Therefore, restoration of coronary blood flow (reperfusion of the ischemic area) by re-canalizing the affected vessel is essential for a better patient outcome. Paradoxically, sudden reperfusion also causes tissue injury, thereby increasing the initial ischemic damage despite restoration of blood flow (=ischemia/reperfusion injury, IRI). Myocardial IRI is a complex event that involves various harmful mechanisms (e.g., production of reactive oxygen species and local increase in calcium ions) as well as inflammatory cells and signals like chemokines and cytokines. An involvement of platelets in the inflammatory reaction associated with IRI was discovered several years ago, but the underlying mechanisms are not yet fully understood. This mini review focusses on platelet contributions to the intricate picture of myocardial IRI. We summarize how upregulation of platelet surface receptors and release of immunomodulatory mediators lead to aggravation of myocardial IRI and subsequent cardiac damage by different mechanisms such as recruitment and activation of immune cells or modification of the cardiac vascular endothelium. In addition, evidence for cardioprotective roles of distinct platelet factors during IRI will be discussed.

Ren GD, -Y Cui Y, Li WL, Li FF, Han XY. Research on cardioprotective effect of irbesartan in rats with myocardial ischemia-reperfusion injury through MAPK-ERK signaling pathway. Eur Rev Med Pharmacol Sci. 2019 Jun;23(12):5487-5494. doi: 10.26355/eurrev_201906_18218. 

Abstract. Objective: The aim of this study was to explore whether the mechanism of Irbesartan (IRB) in the treatment of rats with myocardial ischemia-reperfusion injury (MIRI) was related to the mitogen-activated protein kinase (MAPK)-extracellular signal-regulated kinase (ERK) signaling pathway....Conclusions: The cardioprotective mechanism of IRB in MIRI rats may be related to the inhibition of the activation of the MAPK-ERK signaling pathway.

Liu K, Wang F, Wang S, Li WN, Ye Q. Mangiferin Attenuates Myocardial Ischemia-Reperfusion Injury via MAPK/Nrf-2/HO-1/NF-κB In Vitro and In Vivo. Oxid Med Cell Longev. 2019 May 13;2019:7285434. doi: 10.1155/2019/7285434. 

Abstract. The aim of this study was to investigate the cardioprotective effect of mangiferin (MAF) in vitro and in vivo. Oxidative stress and inflammatory injury were detected in coronary artery ligation in rats and also in hypoxia-reoxygenation- (H/R-) induced H9c2 cells. MAF inhibited myocardial oxidative stress and proinflammatory cytokines in rats with coronary artery occlusion. The ST segment of MAF treatment groups also resumed. Triphenyltetrazolium chloride (TTC) staining and pathological analysis showed that MAF could significantly reduce myocardial injury. In vitro data showed that MAF could improve hypoxia/reoxygenation- (H/R-) induced H9c2 cell activity. In addition, MAF could significantly reduce oxidative stress and inflammatory pathway protein expression in H/R-induced H9c2 cells. This study has clarified the protective effects of MAF on myocardial injury and also confirmed that oxidative stress and inflammation were involved in the myocardial ischemia-reperfusion injury (I/R) model.