[Correlation between resting heart rate and blood glucose level in elderly patients with coronary heart disease and diabetes mellitus].

OBJECTIVE: To explore the correlation between resting heart rate (RHR) and blood glucose level in elderly patients with coronary heart disease (CHD) complicated by diabetes mellitus. METHODS: Between April and July, 2011, a total of 1336 outpatients over 60 years of age recruited from 165 hospitals were asked to complete a questionnaire and received blood glucose and RHR examination. According to baseline RHR, the patients were divided into 3 groups with HRH <70 min-1 (group I, 372 cases), between 70 and 79 min(-1) (group II, 533 cases), and ≥80 min(-1) (group III, 431cases) for analysis of the relationships of RHR with blood glucose control rate. RESULTS: HbA1c levels in the total, male and female patients differed significantly among the 3 groups (F=15.436, 15.436, and 24.270, respectively, P<0.05), and increased in the order from group I to group III. Blood glucose control rate in the total, male and female patients also differed significantly among the 3 groups (χ(2)=13.471, 6.752, and 6.522, respectively, P<0.05), and was significantly lower in group III than in group I (P<0.05). RHR was found to positively correlate with FPG, 2 hPG and HbA1c by Pearson correlation analysis (r=0.058, 0.085, and 0.058, respectively; P<0.05) and multiple linear regression analysis (ß=0.075, 0.075, and 0.018, respectively; P<0.05). Multivariable logistic regression equation showed that compared with patients with RHR <70 min-1, the total, male and female patients with RHR ≥80 min(-1) had OR values of blood glucose control failure of 1.99 (95% CI: 1.23-2.37, P<0.05), 1.81 (95% CI: 1.17-2.77, P<0.05), and 2.18 (95% CI: 1.12-3.74, P<0.05), respectively. CONCLUSION: RHR in elderly CHD patients with MD is positively correlated with their blood glucose level, and an increased RHR is associated with an increased risk of poor blood glucose control. Rigorous RHR control in such high-risk patients may prove beneficial for both blood glucose control and secondary prevention of CHD.

Prevalence of pulmonary embolism at autopsy among elderly patients in a Chinese general hospital.

OBJECTIVES: To investigate the prevalence and characteristics of pulmonary embolism (PE) at autopsy in a Chinese general hospital over a period of 10 years, and to evaluate the antemortem achievement of the prophylaxis, diagnosis, and treatment of PE. METHODS: All medical records of deaths from the West Branch of the Chinese People's Liberation Army (PLA) General Hospital were retrospectively reviewed, for the period of January 1, 2006 to December 31, 2015. Cases in which autopsies had been performed were identified and further analyzed. The numbers and detailed characteristics of patients who had PEs were noted. Prophylactic measures, along with diagnosis and treatment of PE, were recorded, if performed. RESULTS: During the 10-year period, 1057 patients died in the study hospital and 278 necropsies were performed (autopsy rate: 26.3%). Nine patients were found to have PE (3.2%), and in seven of these patients (2.5%), the PE was considered to be fatal. Embolisms were found in the trunk and bilateral main branches of the pulmonary artery tree in all seven of the fatal PE cases. Right intracardiac thrombosis was detected in five of the nine PE patients (55.6%). All patients with PE had been hospitalized in medical departments, and only one had undergone surgery during hospitalization. Antemortem prophylaxis was performed in two of the nine PE cases (22.2%). None of the 9 patients had received a clinical diagnosis of PE before death. CONCLUSIONS: The incidence of and death rate associated with PE may vary among different races and regions. Continuous monitoring of PE by means of necropsy in certain representative medical institutions is necessary.

Postinfarction healing dynamics in the mechanically unloaded rat left ventricle.

The healing process is a key determinant for postinfarction left ventricular (LV) remodeling and the development of heart failure, which could be influenced by mechanical (pressure and/or volume) load. So far, limited information exists regarding an indepth characterization of the postinfarct healing process in the mechanically unloaded state. In the present work, we performed isogenic Lewis-to-Lewis rat abdominal heterotopic heart transplantation, which is characterized by hemodynamic unloading in the left ventricle, and simultaneously ligated the left anterior descending coronary artery (T-infarct group). Pathological evolution was dynamically compared with that of in situ infarcted Lewis hearts (I-infarct group) on days 3, 7, 14, and 35. There was a remarkable myocardial salvage in the unloaded heart, as shown by the improvement in infarct size (T-infarct group: 25.47% ± 4.31% vs. I-infarct group: 38.46% ± 4.82%, P < 0.01) and the smaller fraction of fibrosis in infarct segments (T-infarct group: 42.12% ± 8.40% vs. I-infarct group: 75.65% ± 10.51%, P < 0.01). In addition, there was a progressive disorganization of the two-dimensional collagen fiber alignment as well as retarded collagen fiber maturation in the T-infarct group. We also observed enhanced angiogenesis, lymphangiogenesis, and inflammatory cell retention in the infarct region during mechanical unloading. Moreover, capillary density and collagen deposition were significantly increased in the noninfarcted area of the unloaded heart compared with the same region in the in situ infarcted heart. In conclusion, ischemic insult in the mechanically unloaded heart elicits an altered inflammatory and healing response, which is characterized by myocardial salvage, delayed resolution of inflammation, and disorganization of the collagen orientation in the infarcted region. These findings could provide novel insights into the contribution of hemodynamic load in the postinfarction healing process. Further studies are warranted to elucidate its potential mechanism.

[Extracellular matrix accumulation and expression of gelatinases and their tissue inhibitors in a mechanically unloaded heart model].

AIM: To investigate the relationship between the expression of MMP-2, MMP-9, TIMP-1 and TIMP-2 and ECM accumulation in rat left ventricle in a mechanical unloaded heart model. METHODS: 12-week-old male Lewis rats were subjected to abdominal heterotopic heart transplantation to achieve pressure and volume unloading(mechanical unloading). Age and sex matched in situ heart of Lewis rats were used as control. Collagen volume fraction(CVF) was analyzed by picrosiris-red staining plus polarized microscopy. MMP-2 and -9 gelatinolytic activity were measured by gelatin-zymography. mRNA level of MMP-2, MMP-9, TIMP-1 and TIMP-2 were measured by real-time quantitative PCR. TIMP-1 and TIMP-2 protein level were measured by immunoblotting. RESULTS: Myocardial cross-sectional area of transplanted heart was significantly reduced, and accompanied by excessive ECM deposition (CVF 5.22% +/- 1.6% vs. 2.21% +/- 0.9%, P < 0.05) compared to in situ heart. MMP-2 and MMP-9 activity were significantly increased, as well as mRNA level of MMP-2, MMP-9, TIMP-1 and TIMP-2 compared to in situ heart. TIMP-1 and TIMP-2 protein level in mechanically unloaded heart were significantly upregulated compared to in situ heart, especially for TIMP-1. CONCLUSION: Mechanical unloading of left ventricle may lead to excessive ECM deposition, accompanied by imbalance between MMPs and TIMPs system, especially the upregulation of TIMPs.

Effects of intramyocardial injection of platelet-rich plasma on the healing process after myocardial infarction.

OBJECTIVE: Platelet activation and subsequent release of granules containing a variety of growth factors, at the site of injury, is crucial for the wound healing process. We postulated that a platelet-mediated paracrine effect may accelerate the healing process after myocardial infarction. METHODS: Allogenic platelet-rich and platelet-poor plasma (PRP and PPP) were collected from 15 healthy male Wistar rats. After thrombin activation, the level of vascular endothelial growth factor (VEGF) in PRP and PPP was measured by enzyme-linked immunosorbent assay. A rat model of myocardial infarction was induced by permanent ligation of the left anterior descending artery, and thrombin-activated PRP and PPP, respectively, were injected into the ischemic region. Seven days and 28 days after operation, surviving rats were killed. Ex-vivo left ventricular pressure-volume relationship was performed to evaluate passive diastolic function. Collagen analysis was performed by picrosirius red staining plus polarized microscopy. Angiogenesis and arteriogenesis were evaluated by immunofluorescent staining. RESULTS: After thrombin activation, VEGF level in PRP was significantly higher than that in PPP (187.5+/-45.5 vs. 30.1+/-7.8 pg/ml, P<0.01). Injection of thrombin-activated PRP into the infarcted area resulted in improvement of ventricular remodeling and accelerated healing, as demonstrated by limitation of ventricular expansion, attenuation of myocardial hypertrophy in the noninfarct region, facilitation of angiogenesis and arteriogenesis in the infarct. CONCLUSION: Injection of thrombin-activated PRP could modulate favorably the postinfarction remodeling process. Platelet-released VEGF may participate in this protective effect.