The circadian rhythms of myoglobin concentrations in the blood serum in acute myocardial infarct and unstable stenocardia]

Patients with acute myocardial infarction and unstable angina pectoris do not demonstrate circadian time organization of myoglobin concentration rhythms. The predominance of ultraradian and infraradian neorhthmostasis is typical of such patients. Determination of myoglobin concentration rhythms in the given patients' group may be helpful in the measurement of the size of the focus of necrosis and prediction of the course and outcome of the diseases under consideration.     

The measurement and cotrrol of myocardial infarct size

Direct, chemical, electrocardiographic and radio-isotopic methods are described for the estimation of myocardial infarct size in animals and man. Their relative points and failings are discussed. The effects of interventions, physical, metabolic and pharmacological, upon the size of myocardial infarcts, are examined and work attempting to reduce myocardial infarct size in man reviewed.     

Polymeric gene delivery of ischemia-inducible VEGF significantly attenuates infarct size and apoptosis following myocardial infarct

The development of clinically beneficial myocardial gene therapy has been slowed by reliance on the use of viral carriers and non-physiologic, constitutive gene expression. To specifically address these issues, we have developed a non-viral gene carrier, water-soluble lipopolymer (WSLP), and an ischemia-inducible plasmid construct expressing vascular endothelial growth factor (VEGF), pRTP801-VEGF, to treat myocardial ischemia and infarction. Rabbits underwent ligation of the circumflex artery followed by injection of (a) an ischemia-inducible VEGF gene construct in a WSLP carrier; (b) a constitutively expressed, or unregulated, SV-VEGF gene construct in a WSLP carrier; (c) WSLP carrier alone; or (d) no injection therapy. Following 4 weeks treatment, ligation alone resulted in infarction of 48+/-7% of the left ventricle. With injection of WSLP carrier alone, 49+/-6% of the left ventricle was infarcted (P=NS). The constitutively expressed gene construct, SV-VEGF, reduced the infarct size to 32+/-7% of the left ventricle (P=0.007). The ischemia-inducible gene construct, RTP801-VEGF, further reduced the infarct size to 13+/-4% of the left ventricle (P<0.001). The use of a non-viral carrier to deliver an ischemia-inducible VEGF construct is effective in the treatment of acutely ischemic myocardium.     

C-reactive-protein-associated increase in myocardial infarct size after ischemia/reperfusion

C-Reactive protein (CRP), a marker for acute inflammation, is associated with increased risk of cardiovascular events. The mechanism underlying this association is uncertain. An acute inflammatory response was induced in rabbits by subcutaneous injection of croton oil (CO) 1 to 3 days before 30 min of regional myocardial ischemia/180 min of reperfusion. CO treatment increased plasma CRP from below the limit of detection to 2.5 +/- 0.5 mg/dl and was associated with an increase in infarct size expressed as percentage of risk region [32 +/- 6% vehicle controls (n = 7) to 47 +/- 9% CO-treated rabbits (n = 7; P < 0.05]. After 10 min of ischemia and 180 min reperfusion, no infarct was found in controls; however, an infarct of 7 +/- 1% was found in CO-treated rabbits (P < 0.05; CRP, 2.3 +/- 0.4 mg/dl). The CRP-related increase in infarct size was not observed in croton oil-treated, C6-deficient rabbits (n = 5/group), indicating the involvement of complement. In these rabbits, infarct size was 22 +/- 2% (P < 0.05) despite having plasma CRP of 4.3 +/- 0.4 mg/dl. The CRP-associated increase in infarct size was ameliorated by pretreatment with heparin (n = 7; infarct size 33 +/- 3%; CRP, 2.3 +/- 0.3 mg/dl; P < 0.05) or N-acetylheparin (n = 7; infarct size 23 +/- 4%; CRP, 3.1 +/- 0.5 mg/dl; P < 0.05). These observations may explain why increased serum CRP is associated with an augmented risk for cardiovascular events.     

间歇二次谐波全氟显超声造影评价心肌缺血与坏死的价值

目的 评价间歇二次谐波心肌声学造影（ｍｙｏｃａｒｄｉａｌ ｃｏｎｔｒａｓｔ ｅｃｈｏｃａｒｄｉｏｇｒａｐｈｙ,ＭＣＥ）在梗死心财灌注研究中的价值。方法 用前降支冠状动脉套扎建立开胸犬模型。分两组：缺血再灌注组于血流阻断１ｈ后再灌注２ｈ．;缺血预适应组则在缺血１ｈ前预缺血和再灌注各５ｍｉｎ,反复４次。两组均于再灌注２ｈ后经静脉注射全氟显进行ＭＣＥ,随后取出心脏用Ｅｖａｎ蓝和ＴＴＣ染色,对照两种方法所