Either your web browser doesn't support Javascript or it is currently turned off. In the latter case, please turn on Javascript support in your web browser and reload this page. End stage heart failure is a major cause of death in the US. At syntheskzed, organ transplant and left-ventricular assist devices remain the only viable treatments for these patients. Cardiac tissue engineering presents the possibility of a new option.
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Nanomaterials such as gold nanorods AuNRs and carbon nanotubes CNTs present unique properties that are beneficial for cardiac tissue engineering approaches. In particular, these nanomaterials can modulate electrical conductivity, hardness, and roughness of bulk materials to improve tissue functionality. Moreover, they can deliver bioactive cargo to affect cell phenotypes. This review covers recent advances in the use of nanomaterials for cardiac tissue engineering. Cardiovascular disease is a leading cause of morbidity and mortality across the United States and the world resulting inand 17, annual deaths, respectively [ 1 ].
Atherosclerotic heart disease AHDin particular, is Gelatin cryogel sheets 5% were synthesized using primary driver of these deaths. AHD refers to the formation of atheromatous plaques within coronary vessels which are prone to rupture, resulting in myocardial infarctions MI. In the last several decades, we have become increasingly adept at treating MIs through approaches such as percutaneous coronary intervention PCI.
Although this progress has improved the direct mortality from MI, the survivors of MI often progress toward heart failure HFwhich has continued to increase in prevalence.
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HF has become the most common diagnosis made in US adults over age 65, and approximately 6. The diagnosis of HF portends a downward cycle of declining quality of life, high healthcare costs, and shortened life expectancy [ 345 ]. HF commonly reaches a familiar endpoint, as overUS patients die annually from the uing [ 36 ]. There is Gelatin cryogel sheets 5% were synthesized using complex pathophysiology between myocardial infarction and heart failure. Ischemic insults result in gradual loss of functional myocardium and reductions in cardiac output.
MI occurs when an atheromatous plaque ruptures within a coronary vessel, leading to occlusion of the vessel and loss of perfusion of the distal myocardium. If not intervened upon, the area of ischemic myocardium will infarct and progress through a series of well-defined healing stages [ 7 ].
This process initially includes acute inflammation and edema of the infarcted area, which then progresses to mononuclear inflammation, and, ultimately, collagen scar formation [ 8 ]. Scar within the myocardium represents areas of myocardial tissue death, translating to a decrease in the overall ability of the ventricles to generate cardiac output.
Incremental declines in cardiac output induce pathologic neurohumoral activation, including upregulation of the renin-angiotensin-aldosterone signaling system, and also causes catecholamine excess [ 910 ]. In response to decreased cardiac contractility, these mechanisms attempt to maintain cardiac output by increasing baseline heart rate, increasing systemic vascular tone, and retaining sodium and water. However, elevated levels of circulating neurohumoral products initiate a process of ventricular chamber Gelatin cryogel sheets 5% were synthesized using, which produces thinning of the ventricular walls and gross chamber enlargement [ 1112 ]. Chamber enlargement begets a dangerous cycle of more neurohumoral activation and more remodeling. Medical therapy for HF centers around blocking this neurohumoral cascade and preventing chamber remodeling [ 13 ].
Advanced heart failure refers to patients with persistent HF symptoms that significantly inhibit their daily lives, despite maximal medical therapy. Of the 6 million HF patients in the US, approximatelymeet the criteria for having advanced heart failure [ 14 ]. Patients with advanced heart failure despite medical therapy have limited options to improve cardiac output [ 15 ].
Myocardial tissue has very limited innate regenerative capacity, and no options are currently available for myocardial tissue regeneration. Current options for end organ intervention include either durable left ventricular assist device LVAD or heart transplant [ 1617 ]. Both of these options require massive financial costs and major investment of time and effort by the patient and by medical care teams. Durable LVADs are implantable devices that sit within the cavity of the left ventricle. They use an inflow cannula and outflow cannula to move blood from the LV, through an external pump system, and then back into the systemic circulation [ 18 ]. While these devices have seen incremental improvements in the last several decades, they still entail major long-term risks and do not regenerate the heart [ 1920 ].]
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