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Objective: To explore illness perception (IP) and its predictors among Chinese patients with myocardial infarction (MI)., Methods: The revised Illness Perception Questionnaire (IPQ-R) was used in the present study. A cross-sectional, descriptive design was employed. The study was conducted in four major hospitals in Guangzhou (China) with a sample of 193 MI patients. Pearson's and Spearman's correlation, t test, one-way ANOVA, factor analysis and multiple linear regression were used., Results: Among the 12 common symptoms of MI, on average only 3.37 were recognized by the subjects. Among the six factors of the cause dimension, "immune factors" received the highest score, followed by "gene and chance", "behavioral factors", "psychological factors", "environmental factors", and "physical factors". Subjects perceived MI as a chronic, cyclic illness with serious consequences that could be controlled through treatment, and believed that they had a negative affective response to MI. Furthermore, the dimensions of patients' IP were correlated, and illness-related factors and socio-demographic factors acted as predictors of IP., Conclusion: The IP of Chinese patients with MI needs to be improved., Practice Implications: Based on our findings, effective interventions can be designed to promote MI patients' IP to facilitate their coping strategies after an episode of MI., (Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.)

Objective: To assess the effects of rhBNP on left ventricular (LV) remodeling in rats with acute myocardial infarction (AMI)., Methods: AMI was induced by ligating coronary artery in male Sprague Dawley rats. Two days after surgery, AMI rats received intravenous infusion of rhBNP (15 microg/kg or 5 microg/kg once daily, n = 15 each) or saline (placebo control, n = 15) through Jugular Vein. Sham-operated rats (n = 15) served as normal control. Four weeks later, hemodynamic measurements were performed, left ventricular weight (LVW), ratio of left ventricular weight to body weight (LVW/BW), left ventricular diameter (LVD) and infarct size were determined. Plasma angiotensin II and myocardial angiotensin II levels were also measured., Results: Compared with sham-operated rats, LVW, LVW/BW, LVD and myocardial angiotensin II level were significantly increased, while the LV systolic pressure (LVSP), +/- dp/dt were significantly reduced in saline treated AMI rats (all P < 0.05). LVW/BW, MI size, LVD and myocardial angiotensin II in rhBNP treated AMI rats were significantly lower [LVW: (492.6 +/- 34.0) mg, (498.8 +/- 47.8) mg, (570.0 +/- 24.2) mg, P < 0.01; LVW/BW: 2.0 +/- 0.2, 2.0 +/- 0.2, 2.3 +/- 0.1, P < 0.01; LVD: (25.3 +/- 2.9)%, (31.4 +/- 3.0)%, (46.4 +/- 3.0)%, P < 0.01; myocardial angiotensin II: (881.3 +/- 62.7) pg/L, (1186.0 +/- 94.5) pg/L, (2436.7 +/- 280.3) pg/L, P < 0.05], while LVSP and +/- dp/dt in rhBNP treatment groups were significantly increased than saline treated AMI rats (P < 0.05 or P < 0.01)., Conclusion: RhBNP is effective in attenuating left ventricular remodeling after AMI in rats.

1. Previously, we showed that long-term treatment of rats after myocardial infarction (MI) with B-type natriuretic peptide (BNP) prevented ventricular remodelling. However, it is unclear whether long-term BNP treatment affects cardiac hypertrophy and, if so, its mechanism of action. In the present study, we investigated the effects of long-term BNP treatment on cardiac hypertrophy and the molecular mechanisms involved. 2. Cardiac hypertrophy was established in rats by ligation of the left anterior descending coronary artery . After treatment with BNP (5 or 15 μg/kg per day) for 8 weeks, indices of cardiac hypertrophy were determined. In separate in vitro experiments, cardiomyocyte hypertrophy was induced by treatment of cardiomyocytes with 10−6 mol/L angiotensin (Ang) II for 48 h and cell surface area and [3H] incorporation were measured. Transforming growth factor (TGF)-β1 and smad7 mRNA and protein expression in vivo and in vitro were detected using reverse transcription–polymerase chain reaction and western blotting. 3. Long-term BNP treatment dose-dependently attenuated cardiac hypertrophy and improved cardiac function in rats after MI. Furthermore, BNP attenuated the upregulation of TGF-β1 and downregulation of smad7 mRNA and protein expression. The in vitro experiments further proved that BNP inhibited cardiac hypertrophy and changes in the TGF-β1/smad7 pathway, which were completely blocked by the cyclic GMP-dependent protein kinase (PKG) inhibitor, KT5823 (cells were treated with 10−6 mol/L KT5823 for 48 h). 4. The results of the present study demonstrate that long-term treatment of rats with BNP dose-dependently attenuates cardiac hypertrophy and that this is associated with downregulation of TGF-β1 and upregulation of smad7 via PKG signalling. Long-term BNP treatment may be a new therapeutic strategy to prevent cardiac hypertrophy and progression to heart failure. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Angiotensin-(1–7) [ANG-(1–7)] has been reported to attenuate neointimal formation after vascular injury and stent implantation in rats, but the mechanism remains mostly unresolved. Interestingly, the levels of circulating transforming growth factor-beta1 (TGF-β1) after myocardial infarction were suppressed by ANG-(1–7), which suggests a possible downstream target for the anti-remodeling action of ANG-(1–7). Our study focused on the effects of ANG-(1–7) on vascular remodeling, including neointimal formation and collagen synthesis, and determining whether or not these effects were dependent upon the TGF-β signaling pathway. Methods: Thirty-two New Zealand white rabbits underwent sham surgery or angioplasty in abdominal aorta. The animals were divided into four groups, which were sham, control, ANG-(1–7), and ANG-(1–7)+A-779. Subsequently, an osmotic minipump was implanted to deliver saline, ANG-(1–7) (576μgkg−1 d−1) or ANG-(1–7)+A-779 (576μgkg−1 d−1) for 4weeks. Results: The ANG-(1–7) group displayed a significant reduction in neointimal thickness (207.51±16.70μm vs. 448.08±15.30μm, P <0.001), neointimal area (0.266±0.009mm2 vs. 0.408±0.002mm2, P <0.001), and restenosis rate (28.13±2.74% vs. 40.13±2.74%, P <0.001) when compared to the control group. ANG-(1–7) also inhibited collagen synthesis by significantly decreasing the mRNA expression of Collagen I and Collagen III (vs. Control group: 0.2190±0.0036 vs. 0.3852±0.0212, P <0.001 and 1.1328±0.0554 vs. 1.7378±0.1164, P <0.001, respectively). Furthermore, the expression of TGF-β1 and phosphor-Smad2 (p-Smad2) were significantly suppressed by ANG-(1–7) (vs. Control group: 1.21±0.07 vs. 1.54±0.08, P <0.001 and 0.31±0.01 vs. 0.43±0.02, P <0.001, respectively), but no effect on p38 phosphorylation was observed. [d-Ala7]-ANG-(1–7) (A-779), showed a tendency to attenuate the anti-remodeling effects of ANG-(1–7). Conclusion: ANG-(1–7) decreases the amount of vascular remodeling, including a reduction in neointimal formation and collagen synthesis, after angioplasty in rabbits. The responsible mechanism may function through the possible down-regulation of TGF-β1 levels and inhibition of the Smad2 pathway. [Copyright &y& Elsevier]