The liver possesses impressive regenerative capacities. Grafts of embryonic liver explants and liver explant-conditioned media have been shown to enhance the mitotic activity of hepatocytes. Hepatocyte growth factor (HGF), also named scatter factor (SF), has been identified as a primary candidate in promoting and regulating liver regeneration. Although initially thought to be a liver-specific mitogen, HGF was later reported to have mitogenic, motogenic, morphogenic, and anti-apoptotic activities in various cell types. By promoting angiogenesis and inhibiting apoptosis, endogenous HGF may play an important role in cardioprotection as well as in the regeneration of endothelial cells and cardiomyocytes after myocardial infarction. Since serum concentration of HGF increases in the early phase of myocardial infarction and in heart failure, HGF may also play a key role as a prognostic and diagnostic biomarker of cardiovascular disease. Here we discuss the role of HGF as a biomarker and mediator in cardioprotection and cardiovascular regeneration.

The concept of electrical protection of the ischemic myocardium is in constant evolution and has recently been supported by experimental and clinical studies. Historically, antiplatelet agents, angiotensin‐converting enzyme inhibitors, β‐blockers, and statins have been all proposed as drugs conferring anti‐ischemic cardioprotection. This was supported by the evidence consistently indicating that all these drugs were capable of reducing mortality and the risk of repeat myocardial infarction. The electrical plasticity paradigm is, however, a novel concept that depicts the benefits of improved sodium channel blockade with drugs such as ranolazine and cariporide. Although it has been hypothesized that the protective role of ranolazine depends on decreased fatty acid β‐oxidation affecting preconditioning, we speculate against such a hypothesis, because inhibition of β‐oxidation requires higher concentrations of the drug, above the therapeutic range. Rather, we discuss the key role of calcium overload reduction through inhibition of the late sodium current (INa). Mechanisms driving cardioprotection involve the block of a cascade of complex ionic exchanges that can result in intracellular acidosis, excess cytosolic calcium, myocardial cellular dysfunction, and eventually cell injury and death. In this review we discuss the studies that demonstrate how electrical plasticity through sodium channel blockers can promote cardioprotection against ischemia in coronary heart disease.

A delay in confirming a diagnosis of AMI may increase the risk of complication and a delay in ruling out the diagnosiscontributes to overcrowding in the emergency department. A crucial step in confirming or ruling out the diagnosis of AMI is themeasurement of myocardial enzymes in the serum. Early administration of thrombolytic therapy results in improved survival after AMI. Sothis study was planned to find out the serum marker with a better predictive value for the identification of acute myocardial infarction at thetime of admission. Design: Cross-sectional study. Setting: Emergency department of Punjab Institute of Cardiology, Lahore. Period:15th May, 2008 to 15th July, 2008. Methods: The study population consisted of 70 patients. Patients from both sexes, with clinicalhistory of typical chest pain for more than 30 minutes in duration with evidence of acute changes of myocardial infarction on ECG wereincluded in the study. This study was conducted to compare the positive predictive value and negative predictive value of creatine kinase-MB (CK-MB), cardiac troponin T (CTnT) and cardiac troponin I (CTnI) for detection of AMI. Data analysis was performed with StatisticalPackage for Social Sciences 11.5 (SPSS 11.5). Results: 88.6% cases had CTnI concentration more than the limit value while 11.4%cases had CTnI less than the limit value. The concentration of CTnT was more than the limit value in 70% cases and below the limit value in30% cases. The concentration of CK-MB was more than the limit value in 35.7% cases and 64.3% cases had CK-MB value less than thelimit value. The positive predictive value (PPV) of CtnI is 100% and negative predictive value (NPV) of CTnT is 100% in this study.Conclusions: It is concluded that CTnl is the better marker for the identification of acute myocardial infarction and CTnT is the bettermarker to exclude AMI as compared to CK-MB.