[Effects of simvastatin on DNA synthesis in rat cardiac fibroblasts].

OBJECTIVE: To investigate the effects of simvastatin (Sim) and the interference by mevalonate (MVA) against its effect on DNA synthesis in rat cardiac fibroblasts (CFs). METHODS: CFs were isolated from neonatal SD rats by trypsin digestion and growth-arrested CFs were stimulated with Sim and/or MVA at varied concentrations for different time lengths, and the DNA synthesis in the cells was measured by (3)H-thymidine ((3)H-TdR) incorporation assay. RESULTS: Sim decreased (3)H-TdR incorporation in the CFs in a concentration-dependent manner, and (3)H-TdR incorporation was significantly lower in cells treated with 1 x 10(-6) and 1 x 10(-5) mol/L Sim (1,175+/-202.66 and 771+/-164.86 cpm/2000 cells, respectively) than in the control cells (1,608+/-204.32 cpm/2000 cells, P<0.01). As the treatment time with 1 x 10(-5) mol/L Sim prolonged (for 6, 12, 18, 24, 36, 42, and 48 h), (3)H-TdR incorporation in CFs decreased gradually, showing an obvious inverse correlation with the treatment time (r=-919, P<0.01). (3)H-TdR incorporation in cells treated with 1 x 10(-6) to 1 x 10(-3) mol/L MVA and 1 x 10(-5) mol/L Sim rose steadily as MVA concentration increased. A significant difference in the incorporation was found between cells treated with both 1 x 10(-4)/1 x 10(-3) mol/L MVA and 1 x 10(-5) mol/L Sim (1,612+/-308.57 and 1,995+/-353.83 cpm/2000 cells, respectively) and the cells with 1 x 10(-5) mol/L Sim treatment alone (P<0.01); difference was also noted between cells treated with 1 x 10(-5) mol/L MVA and the control cells (P<0.05), but treatment with 1 x 10(-6) mol/L MVA did not produce much difference in comparison with the control cells (P>0.05) With the increase of treatment time (for 6, 12, 18, 24, 36, 42, 48 h), 1 x 10(-3) mol/L MVA caused steady increase in (3)H-TdR incorporation in the CFs, showing a significant positive correlation with the treatment time (r=0.968, P<0.01). CONCLUSION: Sim can decrease DNA synthesis in rat CFs and postpone the occurrence of myocardial fibrosis, which can be reversed by MVA.

[Relation of the ST-segment elevation pattern in acute phase of anterior wall acute myocardial infarction to short-term prognosis].

OBJECTIVE: To observe the relation of ST-segment elevation pattern of electrocardiogram (ECG) recorded in acute phase of anterior wall acute myocardial infarction (AMI) to short-term prognosis. METHODS: Sixty-two patients with first anterior wall AMI were divided into 3 groups according to ST-segment elevation pattern in lead V3 of a 12-lead ECG at admission. Patients in group A (n=18) were characterized by concave type of ST-segment elevation, group B (n=27) by straight type and group C (n=17) by convex type. The peak value of serum creatine phosphate kinase (CPK) and left ventricular ejection fraction (LVEF) were measured. The incidence of serious complications (including malignant arrhythmia, left ventricular dysfunction and cardiogenic shock) and mortality within the initial 4 weeks of hospitalization were recorded. RESULTS: The median value of peak CPK of the 3 groups was 2 014.4, 4 486.8 and 5 826.9 IU/L respectively, and the peak value of CPK in group A was much lower than that in groups B and C ( D<0.05 and P<0.01, respectively). LVEF measured by echocardiogram within 14 d after myocardial infarction were 61.2%, 48.6% and 38.7% respectively, showing significant difference between groups A and B and between groups B and C (P<0.05) as well as between group A and C (P<0.01). The incidences of serious complications and mortality within 4 weeks after AMI in group A were much lower than those in groups B and C (P<0.05), but there was no significant difference between groups B and C ( D>0.05). CONCLUSION: The shape of ST-segment elevation in lead V3 of a 12-lead ECG in acute phase of anterior wall AMI may reflect the severity of myocardial ischemic injury, and convex type of ST-segment elevation in lead V3 in acute phase often indicate poor short-term prognosis.

Pump models assessed by transesophageal echocardiography during cardiopulmonary resuscitation.

OBJECTIVE: Transesophageal echocardiography was performed during closed-chest cardiopulmonary resuscitation (CPR) in in-hospital cardiac arrest to further explore the hemodynamic mechanism of CPR. METHODS: CPR attempts were performed according to advanced cardiovascular life support guidelines in 6 cases of in-hospital cardiac arrest. Multi-plane transesophageal echocardiography was carried out within 15 min of initiation of CPR. Throughout CPR, the motion of the mitral, tricuspid and aortic valves, the changes in the left ventricular cavity size and the thoracic aortic diameter were observed. Trans-mitral and trans-aortic Doppler files of blood flow were also documented. RESULTS: A closure of the mitral and tricuspid valves with simultaneous opening of the aortic valve occurred exclusively during chest compression, resulting in forward blood flow in the pulmonary and systemic circulation. Peak forward aortic flow at a velocity of 58.8 +/- 11.6 cm/s was recorded during the compression phase. Whereas, a closure of the aortic valve and rapid opening of the atrioventricular valves associated with ventricular filling during relaxation of chest compression was noted in all 6 patients. Peak forward mitral flow at a velocity of 60.6 +/- 20.0 cm/s was recorded during the release phase. Mitral regurgitation during the chest compression period was detected in 5 patients, reflecting a positive ventricular-to-atrial pressure gradient. A reduction in the left ventricular chamber and an increase in the thoracic aortic diameter during the compression phase was found in all patients, indicating that direct cardiac compression contributed to forward blood flow. CONCLUSION: These observations favor the cardiac pump theory as the predominant hemodynamic mechanism of forward blood flow during CPR in human beings.