Out-of-hospital cardiac arrest in a young adult survivor with sequelae of childhood Kawasaki disease: A case report.

BACKGROUND: Kawasaki disease (KD) is an acute type of systemic vasculitis involving small to medium-sized muscular arteries and outbreaks during childhood. KD can cause myocardial ischemia, infarction, and sudden cardiac arrest. We present a case of a young adult survivor of out-of-hospital cardiac arrest as late KD sequelae. CASE SUMMARY: A 29-year-old man with presumed acute KD history at the age of 5 suddenly lost consciousness while jogging and was diagnosed a sudden cardiac arrest by an emergency doctor. After about 10 min cardiopulmonary resuscitation, return of spontaneous circulation was achieved, and the patient was transferred to our hospital. A coronary computed tomography angiogram and coronary angiography revealed extensive calcifications of left anterior descending and right coronary artery aneurysms. The patient was an active individual who took exercise regularly and claimed no previous symptoms of chest pain or shortness of breath on exertion. The most possible cause of his sudden cardiac arrest could be presumed as a thrombus within the coronary artery aneurysms. After that, a thromboembolism induced extensive ischemia, and this ischemia-induced arrhythmia led to a cardiac arrest. CONCLUSION: Few patients who suffer a late sequela of KD can survive from out-of-hospital cardiac arrest. Medications, surgical intervention, and active follow-up are extremely important for this patient to prevent occurrence of adverse events in the future.

Farnesyl Pyrophosphate Synthase Blocker Ibandronate Reduces Thoracic Aortic Fibrosis in Diabetic Rats.

BACKGROUND: This study assessed the effect of ibandronate (IBN), a farnesyl pyrophosphate synthase (FPPS) inhibitor, on vascular remodeling in diabetic rats. METHODS: A rat model of diabetes was induced by a high-fat and high-sugar diet combined with a small dose of streptozotocin. The diabetic rats received 5 µg/kg of ibandronate solution or normal saline subcutaneously every morning for 16 weeks. The morphology of the thoracic aorta was assessed by hematoxylin and eosin and Masson's trichrome staining techniques. Gene expression levels of connective tissue growth factor (CTGF) and FPPS were assessed by quantitative real-time polymerase chain reaction (qRT-PCR) analysis. CTGF and FPPS protein levels were determined by Western blotting analysis. RESULTS: Rats with diabetes mellitus showed moderate hyperglycemia, insulin resistance, hyperlipidemia and thoracic aortic fibrosis. FPPS was significantly upregulated in the thoracic aorta from diabetic animals. Interestingly, IBN treatment for 16 weeks alleviated the diabetes-induced histopathologic changes in the thoracic aortic wall and reduced CTGF protein and mRNA levels. CONCLUSIONS: These findings provided evidence that FPPS is involved in thoracic aortic fibrosis in diabetic rats. Meanwhile, IBN could alleviate vascular remodeling in diabetic animals.

Regulation of autophagy by tea polyphenols in diabetic cardiomyopathy.

OBJECTIVE: To investigate the effect of tea polyphenols on cardiac function in rats with diabetic cardiomyopathy, and the mechanism by which tea polyphenols regulate autophagy in diabetic cardiomyopathy. METHODS: Sixty Sprague-Dawley (SD) rats were randomly divided into six groups: a normal control group (NC), an obesity group (OB), a diabetic cardiomyopathy group (DCM), a tea polyphenol group (TP), an obesity tea polyphenol treatment group (OB-TP), and a diabetic cardiomyopathy tea polyphenol treatment group (DCM-TP). After successful modeling, serum glucose, cholesterol, and triglyceride levels were determined; cardiac structure and function were inspected by ultrasonic cardiography; myocardial pathology was examined by staining with hematoxylin-eosin; transmission electron microscopy was used to observe the morphology and quantity of autophagosomes; and expression levels of autophagy-related proteins LC3-II, SQSTM1/p62, and Beclin-1 were determined by Western blotting. RESULTS: Compared to the NC group, the OB group had normal blood glucose and a high level of blood lipids; both blood glucose and lipids were increased in the DCM group; ultrasonic cardiograms showed that the fraction shortening was reduced in the DCM group. However, these were improved significantly in the DCM-TP group. Hematoxylin-eosin staining showed disordered cardiomyocytes and hypertrophy in the DCM group; however, no differences were found among the remaining groups. Transmission electron microscopy revealed that the numbers of autophagosomes in the DCM and OB-TP groups were obviously increased compared to the NC and OB groups; the number of autophagosomes in the DCM-TP group was reduced. Western blotting showed that the expression of LC3-II/I and Beclin-1 increased obviously, whereas the expression of SQSTM1/p62 was decreased in the DCM and OB-TP groups (P<0.05). CONCLUSIONS: Tea polyphenols had an effect on diabetic cardiomyopathy in rat cardiac function and may alter the levels of autophagy to improve glucose and lipid metabolism in diabetes.

Effects of total flavones from Dendranthema morifolium on vasocontraction and proliferation of vascular smooth muscle cells.

Pharmacological studies have shown that the active components in Dendranthema morifolium exhibit protective effects against ischemia/reperfusion injury; however, its pharmacological action on blood vessels has not yet been investigated. The purpose of the present study was to assess the effects of the total flavones extracted from D. morifolium (Ramat.) Tzvel. cv. Hangju (FDM) on the vasocontraction and proliferation of vascular smooth muscle cells (VSMCs). The tension of rat thoracic aortic rings was measured using a mechanical force transducer attached to a recording system. FDM induced a dose­dependent relaxation of rings with endothelium pre­contracted by either phenylephrine (PE; 10(­6) mol/l) or a high concentration of potassium chloride (KCl; 60 mmol/l). FDM did not significantly affect the vasorelaxant effects on mechanically removed endothelium. In endothelium­denuded aortic rings depolarized by 60 mmol/l KCl, FDM inhibited the contraction induced by Ca2+. FDM reduced the transient contraction caused by PE in a Ca2+­free solution, but did not affect the contraction induced by phorbol ester. Furthermore, FDM inhibited the proliferation of VSMCs with or without growth stimulation by insulin. In conclusion, that the vasorelaxation induced by FDM in rat aortic rings is not dependent on the endothelium but is mediated via a reduction of the influx of extracellular Ca2+ through the voltage­dependent and receptor­operated channels and via the inhibition of the release of intracellular Ca2+ in VSMCs. The anti­proliferative activity of FDM suggests that it may be beneficial in inhibiting atherosclerosis.

Inhibition of farnesyl pyrophosphate synthase attenuates angiotensin II-induced fibrotic responses in vascular smooth muscle cells.

Through the regulation of the RhoA/Rho kinase (ROCK) pathway, angiotensin II (Ang II)-induced fibrotic responses contribute to vascular remodeling. Farnesyl pyrophosphate synthase (FPPS) plays an important role in cardiovascular remodeling through the modulation of the above-mentioned pathway. However, the role of FPPS in Ang II-induced fibrotic responses and the related molecular mechanisms have not yet been elucidated. In the present study, vascular smooth muscle cells (VSMCs) from Sprague-Dawley (SD) rats were stimulated with Ang II. Cell proliferation was measusred usin the cell counting kit-8 (CCK-8). The levels of connective tissue growth factor (CTGF), FPPS, and those of phosphorylated and total extracellular signal-regulated kinase (ERK)1/2, p38 and c-Jun N-terminal kinase (JNK) were determined by western blot analysis. RhoA activity was determined using a pull-down assay. The results revealed that stimulation with Ang II enhanced cell proliferation, and increased the protein expression levels of FPPS and CTGF in the VSMCs. The inhibition of FPPS with ibandronate sodium attenuated the Ang II-induced increase in cell proliferation, CTGF expresison and RhoA activity; these effects were partially reversed by treatment with geranylgeraniol and were mimicked by GGTI-286. Furthermore, both SB203580 (a specific inhibitor of p38) and SP600125 (JNK1, JNK2 and JNK3 inhibitor) diminished the Ang II-induced production of CTGF; however, the inhibition of FPPS reduced the Ang II-induced activation of p38 mitogen-activated protein kinase (MAPK) and JNK. In conclusion, our data indicate that FPPS may play an important role in Ang II-induced fibrotic responses in VSMCs, and the underlying mechanisms at least partly involve the modulation of RhoA activity, and the p38 and JNK pathways.

[Expression of extracellular matrix metalloproteinase inducer in the unstable plaque of patients with acute coronary syndrome].

OBJECTIVE: To observe the expression of extracellular matrix metalloproteinase inducer (EMMPRIN) in the unstable plaque of patients with acute coronary syndrome (ACS), and the impact of leukotriene B4 (LTB4) on the EMMPRIN expression in macrophages. METHODS: The EMMPRIN expression was detected by immunohistochemistry in 11 unstable plaques from patients with ACS. Protein expression of EMMPRIN was evaluated by Western blot on macrophages differentiated from THP-1 which were stimulated with LTB4 in the absence or presence of LTB4 antagonist U75302. There are 8 study groups: 1-THP-1, 2-8-the macrophages derived from THP-1, 2-6-macrophages were stimulated by LTB4 (0, 10(-10), 10(-9), 10(-8) and 10(-7) mol/L) for 24 h, 7-8-the macrophages were pretreated by 10(-6) mol/L or 10(-7) mol/L U75302 2 h before the LTB4 (10(-7) mol/L) stimulation. RESULTS: Abundant EMMPRIN expression was detected in macrophages and smooth muscle cells of unstable plaques from ACS patients. As to the THP-1 derived macrophages, EMMPRIN expression was significantly upregulated in a concentration-dependent manner in LTB4 stimulated groups, which was significantly higher in group 3-6 than in the THP-1 group (group 1) and macrophages group (group 2) (all P < 0.05) and pretreatment with U75302 significantly reduced the LTB4 induced upregulation of EMMPRIN in a dose-dependent manner (P < 0.05). CONCLUSION: EMMPRIN expression is enhanced in macrophages and smooth muscle cells on unstable coronary artery plaques from ACS patients. LTB4 could stimulate EMMPRIN expression on THP-1 derived macrophages suggesting that LTB4 and EMMPRIN might be both involved in the formation and progression of unstable plaques, future studies are warranted to explore if LTB4 and EMMPRIN antagonists are effective or not for treating patients with ACS.

[Angiogenesis in chronic ischemic porcine myocardium after transfer of VEGF165 and angiopoietin-1 mediated by recombinant adeno-associated viral vector].

OBJECTIVE: To study the effects of combination of angiopoietin-1 (ANG-1) and vascular endothelial growth factor165 (VEGF165) gene transfer mediated by recombinant adeno-associated viral vector on the neovascularization in chronic ischemic porcine myocardium. METHODS: An ameroid constrictor was implanted around the left circumflex coronary artery (LCX) via endoscopy. Six weeks later, coronary angiography revealed that the myocardial ischemia was established by gradual occlusion of the left circumflex coronary artery (LCX). Sixteen swine with the total occlusion or partial stenosis (> 85 %) of the LCX were divided into 4 groups (4 in each group): group I, group II and group IV (control) received direct myocardium injection of rAAV2 VEGF165, rAAV2 ANG-1 or PBS alone, respectively; group III received rAAV2 VEGF165 and rAAV2 ANG-1. Selective coronary angiography and ultrasonography were performed perioperatively to evaluate the cardiac function and the formation of collateral circulation. The expression of VEGF165 and ANG-1 proteins were assessed using ELISA or Western blot. The degree of angiogenesis was assessed by use of immunohistochemical analysis. RESULT: Angiography showed that the occlusion of all LCX was completed or exceeded 95% 6 weeks after ameroid constrictor implantation, indicating the successful establishment of animal model. The expression levels of VEGF165 in group I and III and ANG-1 in groups II and III began to increase at d7 after transfection and reached the peak at d14; then decreased gradually to the normal level after 3 months. The expression levels of VEGF165 in group II and group IV or that of ANG-1 protein in group I and group IV had no markedly changes at different time after transfection. There were significant increase in capillary density and arteriole density and more side branch vessels formed in group III compared with other groups. Echocardiographic measurements showed that the left ventricular systolic function of animals in groups I, II and III increased significantly after gene transfection, especially in group III; but there was no changes in group IV. CONCLUSION: Myocardial perfusion and the left ventricular systolic function are improved after rAAV2 VEGF165 or rAAV2 ANG-1 transfection, which is associated with the angiogenesis in porcine model of chronic myocardial ischemia.

Relation of uric acid levels to aortic root dilatation in hypertensive patients with and without metabolic syndrome.

OBJECTIVE: Uric acid (UA) is considered to be a powerful predictor of cardiovascular risk and hyperuricemia might be involved in the metabolic syndrome (MS). This study aims to investigate the relation between UA levels and aortic root dilatation. METHODS: A total of 348 hypertensive patients [age (67.5+/-9.8) years] with or without MS were included in the study. The aortic root diameters at the aortic annulus, the sinuses of Valsalva, the sinotubular junction, and the proximal part of the ascending aorta were measured using a two-dimensional (2D) echocardiography. Serum UA levels were also measured for all patients. RESULTS: A high UA level is independently associated with aortic root diameters at the sinuses of Valsalva (P=0.001) and the proximal ascending aorta (P<0.0001) in the hypertensive patients without MS. In contrast, aortic root diameters were not significantly related to UA levels in the hypertensive patients with MS. Furthermore, increased UA levels were associated with an increased risk for aortic root dilatation in the patients without MS (sex-adjusted hazard ratio 1.75, 95% confidence intervals (CI) 1.27-2.41), but not in those with MS. CONCLUSIONS: This study demonstrated an independent relationship between the aortic root dimensions and increased levels of serum UA in the hypertensive patients without MS. Further understanding of the mechanisms underlying these associations may allow a clearer interpretation of the potential value of specific urate-lowering treatment on cardiovascular disease.

[Construction of adeno-associated virus vector containing ANG-1 gene and its expression in pig mesenchymal stem cells].

OBJECTIVE: To construct recombinant adeno-associated virus (rAAV) vector containing angiopoietin-1 (ANG-1) gene and to express the ANG-1 in targeting cells. METHODS: ANG-1 cDNA was obtained from human spleen by RT-PCR and was inserted into AAV vectors to form rAAV ANG-1, the virus stocks in high titer were harvested. The rAAVANG-1 and rAAV GFP were transferred into pig mesenchymal stem cells and the expression of ANG-1 was detected by Western blot. RESULTS: The cloned ANG-1 cDNA was 1515bp in length which was in accordance with that reported previously. Titration of rAAVANG-1 stock was 9 X 10(11)v.g/ml. The expression of ANG-1 gene was detected in transfected cells. Forty-eight hours after rAAV GFP was transfected into mesenchymal stem cells, 55% cells expressed GFP. CONCLUSION: The constructed rAAV ANG-1 vector has successfully transfered and expressed in pig mesenchymal stem cells.

Improvement in cardiac function after sarcoplasmic reticulum Ca2+-ATPase gene transfer in a beagle heart failure model.

BACKGROUND: Heart failure (HF) is a major cause of morbidity and mortality worldwide, but current treatment modalities cannot reverse the underlying pathological state of the heart. Gene-based therapies are emerging as promising therapeutic modalities in HF patients. Our previous studies have shown that recombinant adeno-associated viral (rAAV) gene transfer of Sarco-endoplasmic reticulum calcium ATPase (SERCA2a) can be effective in treating rats with chronic heart failure (CHF). The aim of this study was to examine the effects of SERCA2a gene transfer in a large HF animal model. METHODS: HF was induced in beagles by rapid right ventricular pacing (230 beats/min) for 30 days. A reduced rate ventricular pacing (180 beats/min) was continued for another 30 days. The beagles were assigned to four groups: (a) control group (n = 4); (b) HF group (n = 4); (c) enhanced green fluorescent protein group (n = 4); and (d) SERCA2a group (n = 4). rAAV1-EGFP (1 x 10(12) microg) and rAAV1-SERCA2a (1 x 10(12) microg) were delivered intramyocardially. SERCA2a expression was assessed by Western blotting and immunohistochemistry. RESULTS: Following 30 days of SERCA2a gene transfer in HF beagles its protein expression was significantly higher than in the HF group than in the control group (P < 0.05). Heart function improved along with the increase in SERCA2a expression. Left ventricular systolic function significantly improved, including the ejection fraction, left ventricular systolic pressure, maximal rate of rise of left ventricular pressure (+dp/dt(max)), and the maximal rate of decline of left ventricular pressure (-dp/dt(max)) (P < 0.05). Left ventricular end-diastole pressure significantly decreased (P < 0.05). The expression of SERCA2a in the myocardial tissue was higher in the SERCA2a group than in the HF group (P < 0.05). CONCLUSIONS: Intramyocardial injection of rAAV1-SERCA2a can improve the cardiac function in beagles induced with HF. We expect further studies on SERCA2a's long-term safety, efficacy, dosage and the optimization before using it in humans with HF.

Lipoprotein(a) level and its association with tumor stage in male patients with primary lung cancer.

BACKGROUND: Recently, attention has been focused on the effect of lipoprotein(a) [Lp(a)] on tumors because of its possible role in development of tumor angiogenesis. The aim of this study was to investigate Lp(a) serum levels in patients with lung cancer and its association with the stages of disease. METHODS: Fasting venous blood samples were collected from 418 untreated male patients with stages I-IV lung carcinoma and were analyzed for Lp(a). The results were compared with the data from 65 healthy male controls. RESULTS: Lp(a) levels were elevated (median 157 mg/L, range 16-1497 mg/L) in patients with lung carcinoma compared to control subjects (median 110 mg/L, range 35-706 mg/L) (p=0.004). Subgroup analysis showed that patients with stages II-IV disease had significantly higher Lp(a) concentrations than did healthy controls (p-0.05). There was an independently positive correlation between tumor stage and Lp(a) levels among patients with stages I-III (r=0.162, p=0.006). However, there was a decrease in Lp(a) in stage IV compared to stage III patients (p=0.03). CONCLUSIONS: There is a significant association between Lp(a) and the presence and stage of lung cancer. Additional investigations with a larger number of lung cancer patients are needed to confirm these findings.

Aortic root dilatation is associated with carotid intima-media thickness but not with carotid plaque in hypertensive men.

BACKGROUND: The role of atherosclerosis-related processes in aortic root dilatation (ARD) has not been fully determined. The present study was to assess the relationship between carotid IMT, carotid plaque, and ARD. METHODS: Hypertensive men with ARD (n = 30) were compared with hypertensive men without ARD (n = 52) and normal control subjects (n = 29). Two-dimensional echocardiography was used to measure the aortic root at the aortic annulus, the sinus of Valsalva, the sinotubular junction and the proximal part of the ascending aorta. Carotid IMT and carotid plaque were also assessed by ultrasound. RESULTS: The measured mean carotid IMT was significantly increased in patients with ARD (1.37 +/- 0.80 mm) compared to the subjects without ARD (1.06 +/- 0.54 mm) and healthy control subjects (0.84 +/- 0.44 mm) (P < 0.05). However, no significant differences of the prevalence of carotid plaque were found in the three groups (P > 0.05). Aortic diameters at all levels except for the diameter of the supra-aortic ridge were significantly related to carotid IMT when the hypertensive population was considered (P < 0.05). No significant correlation was found between carotid plaque and aortic root dimension (P > 0.05). CONCLUSION: This study shows that carotid intima-media thickening, but not carotid atherosclerotic plaque, is positively associated with ARD. Further studies to explore the underlying mechanism are awaited.

Extracellular matrix metalloproteinase inducer (EMMPRIN) is present in smooth muscle cells of human aneurysmal aorta and is induced by angiotensin II in vitro.

The aim of the present study was to determine whether EMMPRIN (extracellular matrix metalloproteinase inducer) is present and is up-regulated in human aneurysmal aortas, and to assess a possible association with AngII (angiotensin II)-induced aneurysm formation. The presence of EMMPRIN was assessed in 41 surgical specimens from patients with a TAA (thoracic aortic aneurysm) (Type A aortic dissection, n=12; Type B aortic dissection, n=7; and TAA without dissection, n=7) or an AAA (abdominal aortic aneurysm, n=15) by immunohistochemistry. EMMPRIN expression in aortic aneurysm tissues was compared with 12 aortas obtained during autopsy (free of any vascular diseases), and scored for both staining intensity and the percentage of vascular cells stained. EMMPRIN protein levels in cultured human aortic SMCs (smooth muscle cells) following stimulation of AngII were analysed by Western blotting. Significant EMMPRIN immunoreactivity was detected in aortic aneurysm lesions from patients with TAAs and AAAs. In the aneurysmal wall, alpha-actin-positive SMCs were the main source of EMMPRIN. The frequency of EMMPRIN overexpression was significantly higher (P=0.026) in TAAs with dissection (68.4%) than TAAs without dissection (14.3%). AngII stimulation up-regulated the expression of EMMPIRN in cultured human aortic SMCs, which was suppressed by the addition of the AT1R (AngII type 1 receptor) antagonist losartan. In conclusion, the present study is the first to report the expression of EMMPRIN in aortic aneurysmal diseases, and we speculate that EMMPRIN may be important in the pathogenesis of these diseases. Whether these abnormalities are potential therapeutic targets deserve further investigation.

Diabetes mellitus: is it protective against aortic root dilatation?

OBJECTIVES: There is evidence of a negative association between diabetes and both abdominal aortic aneurysm and aortic diameter. However, little information is available on the relation between diabetes and aortic root diameter. METHODS: We studied 109 patients with type 2 diabetes. Two-dimensional echocardiography was used to measure the aortic root at the aortic annulus, the sinus of Valsalva, the sinotubular junction and the proximal part of the ascending aorta. Measured mean values were compared with 218 age- and sex-matched patients without diabetes. A comparison of the prevalence of aortic regurgitation between the 2 groups was also performed. RESULTS: In patients with diabetes, the mean aortic root dimensions were significantly smaller than in nondiabetic patients (p < 0.05). The prevalence of aortic root dilatation was significantly higher in nondiabetic subjects than in patients with diabetes (9.63 vs. 2.75%; p = 0.025). In the multivariable regression model, diabetes was a significant negative determinant of aortic root size at all measured sites. The prevalence of aortic regurgitation tended to be higher in nondiabetic subjects than in diabetic participants (11 vs. 18.8%); however, the difference did not achieve statistical significance (p = 0.071). CONCLUSIONS: In patients with diabetes, the aortic root dimension is significantly smaller than in patients without diabetes.

[Create a standard mini-swine model of chronic ischemic myocardium by thoracoscopy].

OBJECTIVE: To create a standard mini-swine model of chronic ischemic myocardium by endoscopy for the research of gene transfer and stem cell. METHODS: Twenty-three male China experimental minipigs were used, aged from 8 to 11 months with a mean of (9.3 +/- 1.8) months and weighed from 20 to 30 kg with a mean of (29.3 +/- 4.3) kg. The myocardial ischemia was established by gradual occlusion of the left circumflex coronary artery (LCX) with an Ameroid constrictor. The Ameroid constrictor was implanted around LCX by endoscopy. Selective coronary angiography, electrocardiogram and Echo-Doppler study were performed perioperatively to evaluate the degree of stenosis. RESULTS: Chronic ischemic myocardial models were successfully generated in 20 of 23 swine by full-endoscopy. Ameroid constrictors were placed at the LCX accurately. Three swine died of anesthetic accident, cardiac arrhythmia at secondary coronary angiography, and pulmonary infection within 6 weeks after operation respectively. Operation time was 25 to 65 min with a mean of (46 +/- 9) min. The blood loss was 30 to 60 ml with a mean of (55 +/- 12) ml. Six weeks later, coronary angiography revealed the total occlusion and partial stenosis (> 85%) of the LCX occurred in 7 and 13 swine respectively. Cardiac systolic and diastolic dysfunction were found in all swine. The ejection fraction value was (65.0 +/- 6.3)% before operation and (41.0 +/- 9.3)% after operation (P = 0.008). The fractional shortening value was (36.2 +/- 4.3)% before operation and (34.2 +/- 2.3)% after operation (P = 0.027). CONCLUSION: The endoscopic surgery is a less invasive way to create a standard mini-swine model of chronic ischemic myocardium with effective results.

Value of BNP and tumour marker CA125 in patients with heart failure.

OBJECTIVE: The objective was to study the association between B-type natriuretic peptide (BNP) and tumour markers and heart failure (HF) to evaluate the value of BNP and carbohydrate antigen 125 (CA125) in HF patients. DESIGN AND SETTING: A university hospital-based cross-over study of 285 subjects (157 men and 128 women) in HF, chronic obstructive pulmonary disease (COPD), mild-mid pulmonary hypertension patients and control subjects. RESULTS: CA125 and BNP were significantly higher in the HF group than in the non-HF group and in severe HF than in mild HF (P < 0.01). No changes were observed in other tumour markers. CA125 and BNP decreased obviously after clinical improvement by aggressive treatment (P < 0.01). Left ventricular ejection fraction correlated positively with CA125 (r = 0.789, P < 0.01) and BNP (r = 0.730, P < 0.01) in left heart failure patients, but not in other patients. BNP and CA125 had better accuracy and positive predictive value in diagnosing HF from the characteristic receiver-operator curve. CONCLUSIONS: CA125 and BNP are markedly elevated in heart failure and closely reflect heart function. They are better markers in evaluating the efficiency of short-term therapy. Detecting BNP combined with CA125 may be more valuable than only detecting BNP or CA125 for diagnosing HF and evaluating the efficiency of treatment.

Increased levels of lipoprotein(a) in non-smoking aortic dissection patients.

OBJECTIVES: To investigate lipoprotein(a) (Lp(a)) serum levels in patients with aortic dissection and the influence of smoking on the level of Lp(a) in aortic dissection patients. METHODS: An age-and sex-matched case-control study was conducted. Lp(a) levels in patients with aortic dissection (n = 52) and healthy subjects (n = 104) were studied. The strength of associations between Lp(a) serum levels and aortic dissection was assessed by means of multivariate logistic regression analysis. RESULTS: Patients with aortic dissection had significantly higher Lp(a) serum levels (median, 17.6 mg/dl; range, 6.4-88.7 mg/dl) compared to healthy individuals (median, 12.4 mg/dl; range, 4.9-26.4 mg/dl) (p = 0.005). The Lp(a) concentration in non-smoking patients with aortic dissection (median, 19.1 mg/dl, range, 10.5-88.7 mg/dl) significantly surpassed that of the smoking patients with aortic dissection of comparable age (median, 10.7 mg/dl; range, 6.4-22.1 mg/dl) (p < 0.0001). Multivariate analysis confirmed an independent association between Lp(a) and aortic dissection in the non-smoking population (p = 0.001). CONCLUSIONS: Serum Lp(a) level is significantly elevated in non-smoking patients with aortic dissection independently of other cardiovascular risk factors. Therefore, determination of Lp(a) levels may be important in identifying subjects at risk of aortic dissection among nonsmokers.

Matrix metalloproteinase-1, -3, and -9 gene polymorphisms and the risk of idiopathic dilated cardiomyopathy in a Chinese Han population.

OBJECTIVES: To investigate the association between matrix metalloproteinase (MMP)-1(-1607 1G/2G), MMP-3(-1171 5A/6A), and MMP-9(-1562 C/T) polymorphism and susceptibility to idiopathic dilated cardiomyopathy (IDCM). DESIGN AND METHODS: MMP-1, -3, -9 genotypes were determined by PCR-RFLP analysis. RESULTS: Genotype frequency of MMP-3, but not MMP-1 and MMP-9 in IDCM patients, was significantly different from that in healthy controls. CONCLUSIONS: Our data suggested that MMP-3 5A/6A polymorphism could be a risk factor for the susceptibility to IDCM.

[Study of relations between matrix metalloproteinase-9 polymorphism (C-1562T) and acute coronary syndrome in Han population of China].

OBJECTIVE: To investigate the association between acute coronary syndrome (ACS) and functional matrix metalloproteinase-9 polymorphism (C-1562-T). METHODS: This study was conducted with a case-control design including 101 patients with angiographically documented ACS and 105 control subjects who were free from coronary artery disease and had normal angiograms. Genotype was determined by polymerase chain reaction-restriction fragment length polymorphism for the common C-1562-T functional promoter polymorphism of the MMP-9 gene.The relationship between the polymorphism in the MMP-9 gene and the severity of coronary arterial stenosis was analyzed. RESULTS: The results of individual polymorphisms analysis showed that the frequency of C/T and T/T genotypes of the C-1562-T polymorphism (27.2%) in patients with ACS was significantly higher than that in those with a normal angiogram (13.34%).The frequencies of -1562T allele were 14.9% and 7.2% in ACS group and control group respectively (Chi2 = 5.617, P = 0.018). The frequencies of C/T and T/T genotypes of the C-1562-T polymorphism were not statistically different among ACS patients with normal and one,two,three or more significantly diseased vessels (Chi2 = 0.601, P = 0.896). CONCLUSION: The present findings suggest that the genetic polymorphism in MMP-9 promoter (C-1562-T) is associated with the susceptibility to ACS in the Han population of China. And the C-1562-T polymorphism may not be useful as a predictor of the severity of coronary atherosclerosis.