## 1 Introduction  
Myocardial infarction (MI), commonly known as a heart attack, is caused by an interruption of the blood supply to a part of the heart with cardiovascular disorder [1]. If left untreated, the ischemia or resulting restriction in the blood supply may cause damage to the myocardium or cardiomyocyte apoptosis, thus leading to heart failure. According to the latest statistics from the American Heart Association [2], MI and other cardiovascular diseases are the leading causes of death worldwide. The heart is primarily composed of the myocardium and coronary arteries. Supplied with oxygen- and nutrient-rich blood through the coronary arteries, the myocardium continuously contracts and relaxes, to pump blood throughout the body. The myocardium has an extremely limited regeneration potential [3, 4], and so, after MI, the ischemic myocardium ceases to function properly, due to the loss or death of cardiomyocytes, i.e., the cells of which it is comprised. Cardiomyoplasty is a therapy used in MI repair, in which cardiomyocytes or other types of stem cells are directly injected into the injured heart, serving as renewable cellular sources which aid in the repair of the damaged myocardium [5; 6]. To compensate for damaged or dead cardiomyocytes in the MI area, the transplantation of various types of stem cells or exogenous cardiomyocytes has been studied. Among them, cardiomyocytes [7; 8], embryonic stem cells [9; 10], and bone marrow-derived mesenchymal stem cells [11] have been investigated, but the ideal cell type for MI repair is far from certain [12]. Muscle-derived stem cells (MDSCs) are a promising type of cell for MI repair because they have the ability to trans-differentiate into cardiomyocytes when co-cultured with cardiomyocytes [13], resist oxidative stress-induced apoptosis [14], reduce scar formation [14; 15], and improve cardiac function [16; 17] after transplantation. Although cardiomyopathyoplasty is promising for MI repair, low cell viability after transplantation, and then gradually decreasing cell survival after long-term cultivation, are issues that remain to be addressed. Encapsulating the cells to be transplanted into MI hearts in synthesized hydrogels may be an effective way to improve the cell survival rate. Scaffolds or engineered constructs are important for tissue engineering [18], especially those with bioactive growth factors as a delivery system, which are of great importance for cardiovascular tissue engineering [19]. The co-release of growth factors of VEGF (vascular endothelial growth factor), bFGF (basic fibroblast growth factor), and PDGF (platelet derived growth factor) from engineered constructs for cardiac repair after MI is promising [20], but many conditions, such as the release rate, need to be regulated. Hydrogels are cross-linked networks of polymers, such as fibrin and alginate, with a high water content between polymer chains [21; 22]. When used for cell encapsulation, hydrogels provide a hydrated tissue-like environment for cell attachment and protection, thereby improving cell viability. Hydrogels can provide biochemical cues and structural support, along with the possible recruitment of endogenous stem cells [23]. Cellular growth and functions are critically affected by both the cell compatibility of materials [24], and the pore sizes in the hydrogel structure [25], which lead to varying cell viabilities. Combining injectable microspheres with a hydrogel is an alternative approach [26]; however, research into cell therapies integrating microspheres and hydrogels has been limited [27]. Among various injectable hydrogels, alginate cross-linked in the presence of calcium ions has been drawing considerable attention for use in MI repair and can lead to enhanced cell viability and proliferation, as well as an improved contractile function [28; 29]. Alginate, a biodegradable and biocompatible polysaccharide commonly found in algae, was employed in this study, due to its successful use as a hydrogel for tissue engineering [30; 31].