Myocardial infarction (MI) is a term used for an event of heart attack which is due to formation of plaques in the interior walls of the arteries resulting in reduced blood flow to the heart and injuring heart muscles because of lack of oxygen supply. The symptoms of MI include chest pain, which travels from left arm to neck, shortness of breath, sweating, nausea, vomiting, abnormal heart beating, anxiety, fatigue, weakness, stress, depression, and other factors. The immediate treatment of MI include, taking aspirin, which prevents blood from clotting, and nitro-glycerin to treat chest pain and oxygen. The heart attack can be prevented by taking an earlier action to lower those risks by controlling diet, fat, cholesterol, salt, smoking, nicotine, alcohol, drugs, monitoring of blood pressure every week, doing exercise every day, and loosing body weight. The treatment of MI includes, aspirin tablets, and to dissolve arterial blockage injection of thrombolytic or clot dissolving drugs such as tissue plasminogen activator, streptokinase or urokinase in blood within 3 h of the onset of a heart attack. The painkillers such as morphine or meperidine can be administered to relieve pain. Nitroglycerin and antihypertensive drugs such as beta-blockers, ACE inhibitors or calcium channel blockers may also be used to lower blood pressure and to improve the oxygen demand of heart. The ECG, coronary angiography and X-ray of heart and blood vessels can be performed to observe the narrowing of coronary arteries. In this article the causes, symptoms and treatments of MI are described.

The congenital heart disease includes abnormalities in heart structure that occur before birth. Such defects occur in the fetus while it is developing in the uterus during pregnancy. About 500,000 adults have congenital heart disease in USA (WebMD, Congenital heart defects medications, www.WebMD.com/heart-disease/tc/congenital-heart-defects-medications , 2014). 1 in every 100 children has defects in their heart due to genetic or chromosomal abnormalities, such as Down syndrome. The excessive alcohol consumption during pregnancy and use of medications, maternal viral infection, such as Rubella virus, measles (German), in the first trimester of pregnancy, all these are risk factors for congenital heart disease in children, and the risk increases if parent or sibling has a congenital heart defect. These are heart valves defects, atrial and ventricular septa defects, stenosis, the heart muscle abnormalities, and a hole inside wall of the heart which causes defect in blood circulation, heart failure, and eventual death. There are no particular symptoms of congenital heart disease, but shortness of breath and limited ability to do exercise, fatigue, abnormal sound of heart as heart murmur, which is diagnosed by a physician while listening to the heart beats. The echocardiogram or transesophageal echocardiogram, electrocardiogram, chest X-ray, cardiac catheterization, and MRI methods are used to detect congenital heart disease. Several medications are given depending on the severity of this disease, and catheter method and surgery are required for serious cases to repair heart valves or heart transplantation as in endocarditis. For genetic study, first DNA is extracted from blood followed by DNA sequence analysis and any defect in nucleotide sequence of DNA is determined. For congenital heart disease, genes in chromosome 1 show some defects in nucleotide sequence. In this review the causes, diagnosis, symptoms, and treatments of congenital heart disease are described.

Myocardial ischemia-reperfusion is the leading cause for the events of cardiovascular disease, and is considered as a major contributor to the morbidity and mortality associated with coronary occlusion. The myocardial damage caused by ischemia-reperfusion injury constitutes the primary pathological manifestation of coronary artery disease. It results from the interaction between the substances that accumulate during ischemia and those that are delivered on reperfusion. The level of this damage can range from a small insult resulting in limited myocardial damage to a large injury culminating in myocyte death. Importantly, major ischemia-reperfusion injury to the heart can result in permanent disability or death. Given the worldwide prevalence of coronary artery disease, developing a strategy to provide cardioprotection against ischemia-reperfusion-induced damage is of great importance. Currently, the treatment of reperfusion injury following ischemia is primarily supportive, since no specific target-oriented therapy has been validated thus far. Nevertheless, therapeutic approaches to protect against myocardial ischemia-reperfusion injury remain an active area of investigation given the detrimental effects of this phenomenon.

Cardiovascular disease constitutes the primary cause of mortality and morbidity worldwide, and represents a group of disorders associated with the loss of cardiac function. Despite considerable advances in the understanding of the pathologic mechanisms of the disease, the majority of the currently available therapies remain at best palliative, since the problem of cardiac tissue loss has not yet been addressed. Indeed, few therapeutic approaches offer direct tissue repair and regeneration, whereas the majority of treatment options aim to limit scar formation and adverse remodeling, while improving myocardial function. Of all the existing therapeutic approaches, the problem of cardiac tissue loss is addressed uniquely by heart transplantation. Nevertheless, alternative options, particularly stem cell therapy, has emerged as a novel and promising approach. This approach involves the transplantation of healthy and functional cells to promote the renewal of damaged cells and repair injured tissue. Bone marrow precursor cells were the first cell type used in clinical studies, and subsequently, preclinical and clinical investigations have been extended to the use of various populations of stem cells. This review addresses the present state of research as regards stem cell therapy for cardiovascular disease.

Valvular heart disease (VHD) is caused by either damage or defect in one of the four heart valves, aortic, mitral, tricuspid or pulmonary. Defects in these valves can be congenital or acquired. Age, gender, tobacco use, hypercholesterolemia, hypertension, and type II diabetes contribute to the risk of disease. VHD is an escalating health issue with a prevalence of 2.5% in the United States alone. Considering the likely increase of the aging population worldwide, the incidence of acquired VHD is expected to increase. Technological advances are instrumental in identifying congenital heart defects in infants, thereby adding to the growing VHD population. Almost one-third of elderly individuals have echocardiographic or radiological evidence of calcific aortic valve (CAV) sclerosis, an early and subclinical form of CAV disease (CAVD). Of individuals ages >60, ~2% suffer from disease progression to its most severe form, calcific aortic stenosis. Surgical intervention is therefore required in these patients as no effective pharmacotherapies exist. Valvular calcium load and valve biomineralization are orchestrated by the concerted action of diverse cell-dependent mechanisms. Signaling pathways important in skeletal morphogenesis are also involved in the regulation of cardiac valve morphogenesis, CAVD and the pathobiology of cardiovascular calcification. CAVD usually occurs without any obvious symptoms in early stages over a long period of time and symptoms are identified at advanced stages of the disease, leading to a high rate of mortality. Aortic valve replacement is the only primary treatment of choice. Biomarkers such as asymmetric dimethylarginine, fetuin-A, calcium phosphate product, natriuretic peptides and osteopontin have been useful in improving outcomes among various disease states. This review, highlights the current understanding of the biology of VHD, with particular reference to molecular and cellular aspects of its regulation. Current clinical questions and the development of new strategies to treat various forms of VHD medically were addressed.

The prevalence of cardiovascular disease (CVD) is increasing dramatically especially in developing countries like India. CVD is a leading cause of morbidity and mortality. There has been a growing awareness of the role of nutrients in the prevention of CVD. One specific recommendation in the battle against CVD is the increased intake of omega-3 fatty acids, which are polyunsaturated fatty acids. Studies have reported inverse associations of CVD with dietary intake of omega-3 fatty acids, suggesting that omega-3 fatty acids supplementation might exert protective effects on CVD. They exert their cardioprotective effect through multiple mechanisms. Omega-3 fatty acid therapy has shown promise as a useful tool in the primary and secondary prevention of CVD. This review briefly summarizes the effects of omega-3 fatty acids in primary and secondary prevention of CVD.

The inflammation of the heart muscles, such as myocarditis, the membrane sac which surrounds the heart called as pericarditis, and the inner lining of the heart or the myocardium, heart muscle as endocarditis are known as the inflammatory heart diseases. Inflammation of heart is caused by known infectious agents, viruses, bacteria, fungi or parasites, and by toxic materials from the environment, water, food, air, toxic gases, smoke, and pollution, or by an unknown origin. Myocarditis is induced by infection of heart muscle by virus like sarcoidosis and immune diseases. The symptoms include chest pain, angina, pain in heart muscle, and shortness of breath, edema, swelling of feet or ankles, and fatigue. The ECG, X-ray, and MRI can diagnose the disease; blood test and rise in enzymes levels provide abnormality in heart function. The treatment includes use of antibiotics for inflammation of heart muscle and medications. The ultrasound imaging indicates further damage to the heart muscle. In severe cases of infection heart failure can occur so long-term medications are necessary to control inflammation. The various biomarkers are reported for the inflammatory heart diseases. The causes, symptoms and treatments of inflammatory heart diseases are described.

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality. CVD has a significant impact on health care systems worldwide and over 23 million individuals are expected to succumb to the disease by 2030. Early onset of atherosclerosis in childhood along with other risk factors of CVD, including elevated circulating lipids, have been shown to persist in adulthood and lead to CVD. Vitamin D deficiency is considered a risk factor for the pathogenesis of CVD, with childhood nutritional status of vitamin D being an important determinant of the development of CVD. Low levels of 25-hydroxyvitamin D can arise due to reduced intake as well as geographical location, and other diseases/conditions such as chronic kidney disease and obesity. Childhood vitamin D deficiency can progress and lead to atherosclerosis and other CVDs in adulthood. Early intervention with vitamin D supplementation is an ideal approach towards preventive therapy. However, there is no clear consensus regarding the role of vitamin D in childhood CVD. In the present study, we reviewed the available evidence in favor of and against such a role for this vitamin.