Are we Under Utilizing the Medical Therapies in Preventing the Complications in Peripheral Arterial Disease?

Lower limb Peripheral Artery Disease (PAD) is the third most common cause of atherosclerotic cardiovascular morbidity aіerischemic heart disease and stroke. Lower limb arterial disease is known to affect the quality of life of elderly people and it is associated increased cardiovascular complications and mortality. 
 

Peripheral Arterial Disease

Smoking, Diabetes, Hypertension and hyper-lipidemic are the risk factors for peripheral vascular disease and the associated complications. Нe first global analysis of the lower limb arterial disease found that more than a quarter of a billion people in the world have the disease and poorer countries are disproportionately affected. Like many other life style diseases PAD incidence is also increasing during the past few decades. Read More>>>>>>>>

The Role of FoxO4 in Post-Myocardial Infarction Left Ventricular Remodeling.

Myocardial infarction (MI), commonly known as heart attack, is a major public health problem. MI can result in a maladaptive remodeling of left ventricles (LV) that leads to LV dysfunction and eventual heart failure. The acute mortality of MI is decreasing due to improved managements and treatment strategies including early coronary reperfusion therapy. However, the prevalence of heart failure as a result of a maladaptive post-MI LV remodeling is still steadily increasing. The cardiovascular risk for patients with MI is still 10-fold higher thanhealthy human. Consequently, the morbidity, mortality, and economic cost related to ischemic heart disease are rising worldwide.

Because the heart has limited regenerative capacity, it responds to MI injury by a spontaneous wound repair process which ultimately results in replacement of dead cardiomyocytes with a collagen-based scar. Wound healing is closely intertwined with ventricular remodeling, a complex process that involves both the infarcted and non-infarcted myocardium, and leads to alteration in the size, shape, and physiology of the heart. The extent of post-MI remodeling is an important predictor for mortality of heart failure after infarction, and depends on the size of the infarct and on the mechanical and structural characteristics of the healing wound. Read more......

Novel Cell Replacement Strategies for Heart Failure Treatment

Myocardial infarction (MI), or heart attack, is caused by the blockage of blood flow in the heart, which reduces oxygen levels, damages tissues (ischemia) and kills close to one billion cardiomyocytes (infarction). Fibroblasts then migrate into the infarctedarea where they proliferate to create a cardiomyocytedepleted scar that cannotcontribute to the electrophysiologicallydriven contractions of the heart. This often causes HF leading to fatigue, peripheral edema, or even death. To find more effective therapies for HF, we need to improve our understanding of its pathophysiology and develop new approaches to treating it.

Cell-replacement therapy has emerged as a novel approach to treat HF. This approach relies on the theory that after MI or in HF, lost cardiomyocytes can be replaced by adding either new cardiomyocytes or a potential source of cardiomyocytes such as stem cells. To find the most effective approach, researchers have tested several types of stem cells including skeletal myoblasts, cardiac progenitor cells, and mesenchymal stem cells from bone marrow. However, they have only been modestly successful because the beneficial effects are mainly mediated by indirect paracrine mechanisms: stem cells do not transdifferentiate into cardiomyocytes in-vivo and the number of stem cells retained in the heart after delivery is disappointingly low. 

Fortunately, cell-replacement therapy for HF using pluripotent stemcell- derived cardiomyocytes showed more promising results in rodents and non-human primates because they integrate and electrically couple with the healthy myocardium. However, technologies involving stem-cell-derived cardiomyocytes must be further optimized before they can effectively treat HF. Specifically, we need to find methods that improve the efficiency and consistency of cardiomyocyte differentiation in large scale, their survival in disease conditions, their integration into cardiac tissue, and their resistance to autoimmune rejection.

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