CD34+ stem cell therapy in nonischemic dilated cardiomyopathy patients.

Recent trends indicate that patients with nonischemic dilated cardiomyopathy represent the largest subpopulation of heart failure patients with a significant need for alternative treatment modalities. Similar to patients with ischemic cardiomyopathy, patients with nonischemic dilated cardiomyopathy have been found to have myocardial regions with flow abnormalities, which may represent targets for neoangiogenic therapies. CD34(+) stem cells might contribute to the formation of new blood vessels from existing vascular structures in ischemic tissues by the direct incorporation of injected cells into the newly developing vasculature or by the production and secretion of angiogenic cytokines. This review summarizes the long-term clinical effects and potential underlying mechanisms of CD34(+) cell therapy in patients with nonischemic dilated cardiomyopathy.

Neurologic recovery after prolonged circulatory arrest in surgery for aortic dissection.

BACKGROUND: Brain injury manifested by subtle, transient neurologic and neuropsychologic dysfunctions occurs in about a quarter of patients who are subjected to periods of deep hypothermia and circulatory arrest (DHCA). We describe a patient who sustained minimal neurologic damage despite prolonged DHCA. METHODS: The patient was a previously healthy 62-year-old woman with acute type A aortic dissection that involved the ascending aorta. During surgery we established retrograde cerebral perfusion and DHCA to provide cerebral protection, and during the procedure the patient underwent 3 separate DHCA periods with a total circulatory arrest time of 91 minutes. Because of tubing damage, retrograde cerebral perfusion was not used during the final period (59 minutes). The patient's head was packed in ice to facilitate maintenance of brain hypothermia. Her average systemic temperature during the third period of circulatory arrest was 22.5 degrees C. RESULTS: Extensive neuropsychologic testing, which was performed to assess the patient's cognitive functions and abilities at 4-month follow-up, showed an absence of global cognitive decline and only a moderate impairment of attentional capacity. Overall cognitive functioning was within the normal range and did not interfere with everyday activities or quality of life. CONCLUSION: Although the total arrest time vastly exceeded the recommended safe period, our patient survived and sustained minimal neurologic damage. The combination of neuroprotective measures used may have contributed to this beneficial outcome.

The -455G/A polymorphism of the beta fibrinogen gene and the Bgl II polymorphism of the alpha2beta1 integrin gene and myocardial infarction in patients with type 2 diabetes.

Platelets and fibrinogen might be involved in the pathogenesis of thrombus formation and MI. The Bgl II gene polymorphism of the alpha2beta1 integrin, which is a platelet collagen receptor, and the -455G/A polymorphism in the beta fibrinogen gene have been suggested as genetic risk factors for MI. The aim of this study was to look for a relationship between the -455G/A polymorphism in the beta fibrinogen gene and the development of MI in Caucasians with type 2 diabetes. One hundred and forty-two subjects with type 2 diabetes and MI were compared to 234 diabetic subjects with no history of coronary artery disease. There were no significant differences in the frequency of the Bgl II gene polymorphism or of the -455G/A polymorphism in the beta fibrinogen gene in the patients with MI compared to the patients without MI: Bgl II (+/+) genotype was found in 19.7% of patients with MI and 15.4% of controls and -455GG genotype was found in 58.4% of patients with MI and 57.7% of controls. The present study demonstrates that neither the Bgl II gene polymorphism nor -455G/A polymorphism in the beta fibrinogen gene is a genetic marker for MI in Slovene population (Caucasians) with type 2 diabetes.