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Stem cell therapy has begun as a promising and novel approach for the treatment of various diseases. Stem cell therapy involves the identifi cation of correct cells, area of transplantation. Transplantation of functional and healthy stem cells help to renewal of damaged cells and repair injured tissue. Stem cell isolated from bone marrow were the fi rst cell type used in preclinical and clinical investigations for the have been extended to the use of various populations of stem cells. But there are very few studies which show the roles of stem cells in cardiovascular disease. Cardiovascular Disease (CVD) constitutes the most important cause of mortality and morbidity worldwide. CVD represents a group of disorders connected with the defeat of cardiac function. In spite of signifi cant advances in the understanding of the pathophysiological mechanisms of the disease, the problem of cardiac tissue loss has not yet been addressed. Only few therapeutic approaches suggest through tissue repair and regeneration. The most of treatment options aim to control the 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. This review addresses the present state of research as regards stem cell therapy for CVD.

When a young patient presents with ischemic stroke or recurrent venous thromboembolism of unknown aetiology or “young” myocardial infarction in the absence of traditional risk factors, a detailed thrombophilia workup becomes an imperative. In a setting of arterial and venous occlusive disorders hyperhomocysteinemia is an important risk factor in the absence of traditional contributory aetiologies. Here we present a case of 28-year-old man, never-smoker with no known comorbidities who initially presented to the hospital with acute, retrosternal chest pain, radiating to the left side. His ECG showed ST elevation in V1-V3 in the setting of raised cardiac enzymes, and 2d-echo demonstrating regional wall motion abnormality. He was diagnosed to have acute anteroseptal MI and thrombolysed with streptokinase. Subsequently, his coronary angiogram showed a non-occluded LAD. CT Angio with IVUS done at a staged interval revealed minimal luminal irregularities suggestive of MINOCA. 8 months later the patient presented with headeache, fever, and left focal seizure accompanied by signs of increased intracranial pressure. MRI brain with contrast-MR venogram showed complete thrombosis of superior sagittal sinus. Due to the previous history of MI, and present CVT the patient was subjected to detailed thrombophilic evaluation which was normal except the levels of vitamin B12 (126.9 pg/mL) was low his homocysteine level was abnormally elevated to a level of 38.23 μM/L. The patient was treated with heparin, anti-oedema measures and anti-epileptics followed by oral anticoagulant plus folate, vitamin B6, and vitamin B12. Young patients presenting with arterial or venous thrombosis without any risk factors for atherosclerosis and venous thrombosis which is recurrent, unexplained, or at unusual sites, need screening for thrombophilic states and hyperhomocysteinemia should be ruled out as it can lead to both arterial and venous disease.

Objectives: The present study was designed to know the possible protective and regenerative effects of human Umbilical Cord Blood (UCB) derived MSCs in Myocardia Infarction (MI) in rat model using Isoproterenol administration. Material & methods: Isoproterenol injection was given subcutaneously for 2 days to induce MI in rat model. After development of MI various blood and tissue parameters were assessed sich as urea, creatinine, SGOT, SGPT, troponin I, Lactic Dehydrogenase (LDH) and Creatine Kinase (CK). Treatment was given by single dose of MSCs. After treatment period all the parameters were assessed again and comparison were done before and after treatment. Results: After development of MI all the biochemical parameters were elevated. MSC transplantation, performed when MI have already developed, showed better results. It inhibits the degradation of normal collagen and the formation of poorly cross-linked collagens, resulting in attenuation of MI and improvement of heart function by means of troponin I, Lactic Dehydrogenase (LDH) and Creatine Kinase (CK) level. In addition, this impact is not instantaneous but is persistent for at least 90 days, supporting the role of MSC transplantation. Conclusion: Our data suggested that transplantation of MSCs in MI model has improved the cardiac function. Till now, there is no evidence attributing this improvement to regeneration and other paracrine mechanisms are also believed to contribute in the improvement of cardiac function.

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