Background A few recent studies have reported that inflammation is associated with the prognosis of acute aortic dissection （AD）. There is, however, no systemic investigation regarding the role of plasma C-reactive ...Background A few recent studies have reported that inflammation is associated with the prognosis of acute aortic dissection （AD）. There is, however, no systemic investigation regarding the role of plasma C-reactive protein （CRP） and white blood cell （WBC） levels in predicting in-hospital clinical events of acute type AAD. Methods The levels of high-sensitivity CRP and WBC counts were systemically determined after admission in 36 patients with acute type A AD. The variations of plasma CRP and WBC levels in different time windows （admission, 1, 2, 3, 4, 6, 8 days） in patients with acute type AAD were analyzed between patients with events and without events. Results During hospitalization, five patients died, and increased levels of CRP and WBC were found in patients died with acute type A AD compared with patients survived （P 〈0.01, respectively）. Medical treatment may significantly decrease inflammatory response in survived patients with acute type A AD. Additionally, patients with complication of pleural effusion showed higher CRP and WBC levers （P=0.046, P=-0.018, respectively）. Lower WBC levels were found in survived patients treated medically （P=-0.001）. Moreover, mean CRP and WBC levels had positive correlations with aortic diameter （r=0.364, P--0.000; r=0.333, P=0.000, respectively） and age （r=0.270, P=0.000, respectively）, while negative correlations with the time from onset of symptoms to hospital admission （r= -0.229, P=0.000, r= -0.200, P=0.002, respectively）. Univariate analysis showed that age 〉65 years, CRP zl 2.05 rag/L, WBC 〉12.16×10^9/L, aortic diameter 〉48 mm, pleural effusion and diastolic blood pressure 〉105 mmHg were associated with hospital mortality. While CRP 〉12.05 mg/L, WBC ≥12.16×10^9/L, aortic diameter 〉48 mm were strongly associated with hospital mortality in multiple Logistic regression analysis. Conclusions The results suggested that CRP and WBC were preferred markers for predicting the clinical events in patients with acute type A AD, especially death during hospitalization. Therefore, further study enrolling larger cohort, prospective study would be warranted.展开更多
Background Left ventricular hypertrophy （LVH） and geometric abnormality are associated with morbidity and mortality of cardiovascular disease and stroke. Hypertension is the major cause of LVH. Yet the prevalence an...Background Left ventricular hypertrophy （LVH） and geometric abnormality are associated with morbidity and mortality of cardiovascular disease and stroke. Hypertension is the major cause of LVH. Yet the prevalence and other risk factors of LVH and geometric abnormality in Chinese hypertensive population are unknown. The objective of this study was to investigate the prevalence and risk factors of LVH and geometric abnormality in community-based Chinese hypertensive population. Methods The study was a community-based cross-sectional study, and comprised 4270 hypertension patients with integrated clinical and echocardiographic data. Left ventricular mass was measured by transthoracic echocardiography. LVH was diagnosed by using the criteria of over 49.2 g/m^2.7 for men and 46.7 g/m^2.7 for women. LV geometric patterns （normal, concentric remodeling, concentric or eccentric hypertrophy） were calculated according to LVH and relative wall thickness. Logistic regression model was used to determine the odds ratio （OR） and 95% confidence intervals （CI） of the risk factors of LVH. Results The prevalence of LVH was 42.7% in 4270 hypertensive patients, with 37.4% in males and 45.4% in females, respectively. The prevalence of concentric remodeling, concentric or eccentric hypertrophy was 24.7%, 20.2%, and 22.6%, respectively. In Logistic regression model, female （OR 1.3, 95%C/ 1.1-1.5, P 〈0.01）, age （OR 1.02, 95%C/ 1.01-1.03, P 〈0.01）, body mass index （OR 1.2, 95%C/1.15-1.20, P 〈0.01）, systolic blood pressure （OR 1.02, 95%C/ 1.01-1.03, P 〈0.01 ）, and serum triglyceride （OR 1.10, 95% CI 1.00-1.20, P 〈0.01 ） were risk factors of LVH. Female, age, body mass index, systolic blood pressure and serum triglyceride were also risk factors of left ventricular geometric abnormality. Conclusions The echocardiographic LVH is the major complication of patients with hypertension in rural area of China, especially for women. To effectively treat hypertension, weight loss and control of serum triglyceride may help to prevent LVH in hypertensive population.展开更多
Background Even carrying an identical gene mutation, inter- and intra-family variations have been noticed worldwide in the presence and the severity of left ventricular hypertrophy and sudden death in patients with hy...Background Even carrying an identical gene mutation, inter- and intra-family variations have been noticed worldwide in the presence and the severity of left ventricular hypertrophy and sudden death in patients with hypertrophic cardiomyopathy （HCM）. Modifier genes may contribute to the diversity. Angiotensin-converting enzyme 2 （ACE2） gene has been established to be associated with parameters of left ventricular hypertrophy in community based male subjects. The objective of the present study was to investigate the association of ACE2 gene polymorphisms with the phenotype of HCM. Methods A total of 261 consecutive HCM patients and 609 healthy controls were enrolled into this study. The polymorphism of rs2106809 and rs6632677 were genotyped by polymerase chain reaction-restriction fragment length polymorphism （PCR-RFLP） and confirmed by sequencing. Logistic regression model and multivariate analysis were used to determine the odds ratio （OR） and 95% confidence intervals （CO of variations of ACE2 for HCM. Results The T allele of rs2106809 and C allele of rs6632677 conferred increasing risk for HCM （OR 1.34, 95%C/ 1.01-1.77, P=0.04; OR 1.11, 95%C/ 1.03-1.21, P=0.002, respectively）, and the 2 single nucleotide polymorphisms （SNPs） were in strong linkage disequilibrium （LD）, the TC haplotype was independently associated with a higher OR for HCM （OR=1.59, 95%C/1.21-1.87） after adjusted for conventional risk factors. And the risk alleles were associated with thicker interventricular septal thickness of HCM （（20.0±6.3） mm vs （17.9±5.5） mm, P=0.03 and （21.3±5.9） mm vs （17.9±5.8） mm, P=0.04, respectively）. No association was found between the two polymorphisms with female patients with HCM. Conclusion Minor alleles of ACE2 gene might be the genetic modifier for the magnitude of left ventricular hypertrophy in male patients with HCM.展开更多
Background Severe bilateral carotid stenosis caused by atherosclerosis has not been unusual in the elderly. Such patients have high stroke risk. Many studies show that carotid artery stenting （CAS） is an alternative...Background Severe bilateral carotid stenosis caused by atherosclerosis has not been unusual in the elderly. Such patients have high stroke risk. Many studies show that carotid artery stenting （CAS） is an alternative to treat unilateral carotid stenosis. However, the optimal procedural strategy of bilateral carotid stenosis remains unclear. The purpose of our study was to evaluate the safety of simultaneous bilateral carotid artery stenting （SBCAS） compared with unilateral carotid artery stenting （UCAS）. Methods In this single-center retrospective study, we analyzed 234 consecutive patients who underwent carotid stenting from January 2005 to December 2009. Thirty-nine patients （16.7%） of them underwent SBCAS, and the others （n=195） underwent UCAS. Indication for CAS was defined as carotid artery diameter reduction 〉60% （symptomatic） or 〉80% （asymptomatic）. Six-month and 30-day hemodynamic depression （HD）, hyperperfusion syndrome （HPS）, stroke, death and myocardial infarction （MI） after carotid stenting were assessed. Results SBCAS group had no more HD and HPS compared with UCAS group at 30 days （HD： 28.2% vs. 20.0%, P=0.396; HPS： 2.6% vs. 2.1%, P=0.262）. Moreover, there was no statistically significant difference between SBCAS group and UCAS group in major stroke, death, MI and their combinations within 30 days （major stroke： 0 vs. 3.6%, P=0.604; death： 2.6% vs. 1.5%, P=0.520; MI： 2.6% vs. 0.5%, P=0.306; and their combinations： 5.1% vs. 4.6%, P=1.000） and 6 months （major stroke： 0 vs. 3.6%, P=0.604; death： 5.1% vs. 2.1%, P=0.262; MI： 5.1% vs.1.0%, P=0.130 and their combinations： 7.7% vs. 5.1%, P=0.459）. Conclusions The patients undergoing SBCAS had no more events than those undergoing UCAS in 30-day and 6-month follow-up. Our finding suggests that SBCAS appears to be as safe as UCAS.展开更多
Background Tumor necrosis factor-induced protein 3 （TNFAIP3） gene has been shown important in cardiac remodeling. The aim of the present study was to investigate whether the variants of TNFAIP3 gene are associated w...Background Tumor necrosis factor-induced protein 3 （TNFAIP3） gene has been shown important in cardiac remodeling. The aim of the present study was to investigate whether the variants of TNFAIP3 gene are associated with left ventricular hypertrophy （LVH） in hypertensive patients.Methods Four representatives of all the other single nucleotide polymorphisms （SNPs） in TNFAIP3 gene were tested for association with hypertrophy in two independent hypertensive populations （n=2120 and n=324）.Results We found that only the tag SNP （rs5029939） was consistently lower in the hypertensives with cardiac hypertrophy than in those without cardiac hypertrophy in the two study populations, indicating a protective effect on LVH （odds ratio （OR） （95% confidence interval （CI））0.58 （0.358-0.863）, P=0.035; OR （95% CI）=0.477 （0.225-0.815）, P〈0.05,respectively）. Multiple regression analyses confirmed that the patients with G allele of rs5029939 had less thickness in inter-ventricular septum, left ventricular posterior wall, relative wall thickness and left ventricular mass index than did those with CC allele in the hypertensive patients in both study populations （all P〈0.01）.Conclusion These findings indicate that the SNP （rs5029939） in the TNFAIP3 gene may serve as a novel protective genetic marker for the development of LVH in patients with hypertension展开更多
Background The association between fish consumption and heart failure （HF） incidence is inconsistent. Methods We performed a systematic search of Pubmed and Embase （from 1953 to June 2012） using key words related ...Background The association between fish consumption and heart failure （HF） incidence is inconsistent. Methods We performed a systematic search of Pubmed and Embase （from 1953 to June 2012） using key words related to fish and HF. Studies with at least three categories of fish consumption reporting both relative risk （RR） and corresponding 95% confidence interval （CI） for HF incidence were included. The pooled RR and 95%C/were calculated using a fixed or random-effects model. The generalized least squares regression model was used to quantify the dose-response relationship between fish consumption and HF incidence. Results Five prospective cohort studies including 4750 HF events of 170 231 participants with an average of 9.7-year follow-up were selected and identified. Compared with those who never ate fish, individuals with higher fish consumption had a lower HF incidence. The pooled RRs for HF incidence was 0.99 （95%CI, 0.91 to 1.08） for fish consumption 1 to 3 times per month, 0.91 （95%CI, 0.84 to 0,99） for once a week, 0.87 （95%CI, 0.81 to 0.95） for 2 to 4 times per week, and 0.86 （95% CI, 0.84 to 0.99） for 5 or more times per week. An increment of 20 g of daily fish intake was related to a 6% lower risk of HF （RR： 0.94, 95% CI, 0.90 to 0.97; P for trend = 0.001）. Conclusions This meta-analysis suggests that there is a dose-dependent inverse relationship between fish consumption and HF incidence. Fish intake once or more times a week could reduce HF incidence.展开更多
Marfan syndrome is a systemic disorder of connective tissue, caused by mutations in the FBN1, TGFBR1 or TGFBR2 genes. This syndrome is characterized by involvement of three major systems, skeletal, ocular, and cardiov...Marfan syndrome is a systemic disorder of connective tissue, caused by mutations in the FBN1, TGFBR1 or TGFBR2 genes. This syndrome is characterized by involvement of three major systems, skeletal, ocular, and cardiovascular. The continuing improvements in molecular biology and increasing availability of molecular diagnosis in clinical practice allow recognition of Marfan syndrome in patients with incomplete phenotypes. Additionally, molecular analyses could also be used for preimplantation genetic diagnosis. The identification of a mutation allows for early diagnosis, prognosis, genetic counseling, preventive management of carriers and reassurance for unaffected relatives. The importance of knowing in advance the location of the putative family mutation is highlighted by its straightforward application to prenatal and postnatal screening.展开更多
文摘Background A few recent studies have reported that inflammation is associated with the prognosis of acute aortic dissection （AD）. There is, however, no systemic investigation regarding the role of plasma C-reactive protein （CRP） and white blood cell （WBC） levels in predicting in-hospital clinical events of acute type AAD. Methods The levels of high-sensitivity CRP and WBC counts were systemically determined after admission in 36 patients with acute type A AD. The variations of plasma CRP and WBC levels in different time windows （admission, 1, 2, 3, 4, 6, 8 days） in patients with acute type AAD were analyzed between patients with events and without events. Results During hospitalization, five patients died, and increased levels of CRP and WBC were found in patients died with acute type A AD compared with patients survived （P 〈0.01, respectively）. Medical treatment may significantly decrease inflammatory response in survived patients with acute type A AD. Additionally, patients with complication of pleural effusion showed higher CRP and WBC levers （P=0.046, P=-0.018, respectively）. Lower WBC levels were found in survived patients treated medically （P=-0.001）. Moreover, mean CRP and WBC levels had positive correlations with aortic diameter （r=0.364, P--0.000; r=0.333, P=0.000, respectively） and age （r=0.270, P=0.000, respectively）, while negative correlations with the time from onset of symptoms to hospital admission （r= -0.229, P=0.000, r= -0.200, P=0.002, respectively）. Univariate analysis showed that age 〉65 years, CRP zl 2.05 rag/L, WBC 〉12.16×10^9/L, aortic diameter 〉48 mm, pleural effusion and diastolic blood pressure 〉105 mmHg were associated with hospital mortality. While CRP 〉12.05 mg/L, WBC ≥12.16×10^9/L, aortic diameter 〉48 mm were strongly associated with hospital mortality in multiple Logistic regression analysis. Conclusions The results suggested that CRP and WBC were preferred markers for predicting the clinical events in patients with acute type A AD, especially death during hospitalization. Therefore, further study enrolling larger cohort, prospective study would be warranted.
基金The study was supported by a grant from the National Natural Science Foundation of China （No. 81100160）
文摘Background Left ventricular hypertrophy （LVH） and geometric abnormality are associated with morbidity and mortality of cardiovascular disease and stroke. Hypertension is the major cause of LVH. Yet the prevalence and other risk factors of LVH and geometric abnormality in Chinese hypertensive population are unknown. The objective of this study was to investigate the prevalence and risk factors of LVH and geometric abnormality in community-based Chinese hypertensive population. Methods The study was a community-based cross-sectional study, and comprised 4270 hypertension patients with integrated clinical and echocardiographic data. Left ventricular mass was measured by transthoracic echocardiography. LVH was diagnosed by using the criteria of over 49.2 g/m^2.7 for men and 46.7 g/m^2.7 for women. LV geometric patterns （normal, concentric remodeling, concentric or eccentric hypertrophy） were calculated according to LVH and relative wall thickness. Logistic regression model was used to determine the odds ratio （OR） and 95% confidence intervals （CI） of the risk factors of LVH. Results The prevalence of LVH was 42.7% in 4270 hypertensive patients, with 37.4% in males and 45.4% in females, respectively. The prevalence of concentric remodeling, concentric or eccentric hypertrophy was 24.7%, 20.2%, and 22.6%, respectively. In Logistic regression model, female （OR 1.3, 95%C/ 1.1-1.5, P 〈0.01）, age （OR 1.02, 95%C/ 1.01-1.03, P 〈0.01）, body mass index （OR 1.2, 95%C/1.15-1.20, P 〈0.01）, systolic blood pressure （OR 1.02, 95%C/ 1.01-1.03, P 〈0.01 ）, and serum triglyceride （OR 1.10, 95% CI 1.00-1.20, P 〈0.01 ） were risk factors of LVH. Female, age, body mass index, systolic blood pressure and serum triglyceride were also risk factors of left ventricular geometric abnormality. Conclusions The echocardiographic LVH is the major complication of patients with hypertension in rural area of China, especially for women. To effectively treat hypertension, weight loss and control of serum triglyceride may help to prevent LVH in hypertensive population.
文摘Background Even carrying an identical gene mutation, inter- and intra-family variations have been noticed worldwide in the presence and the severity of left ventricular hypertrophy and sudden death in patients with hypertrophic cardiomyopathy （HCM）. Modifier genes may contribute to the diversity. Angiotensin-converting enzyme 2 （ACE2） gene has been established to be associated with parameters of left ventricular hypertrophy in community based male subjects. The objective of the present study was to investigate the association of ACE2 gene polymorphisms with the phenotype of HCM. Methods A total of 261 consecutive HCM patients and 609 healthy controls were enrolled into this study. The polymorphism of rs2106809 and rs6632677 were genotyped by polymerase chain reaction-restriction fragment length polymorphism （PCR-RFLP） and confirmed by sequencing. Logistic regression model and multivariate analysis were used to determine the odds ratio （OR） and 95% confidence intervals （CO of variations of ACE2 for HCM. Results The T allele of rs2106809 and C allele of rs6632677 conferred increasing risk for HCM （OR 1.34, 95%C/ 1.01-1.77, P=0.04; OR 1.11, 95%C/ 1.03-1.21, P=0.002, respectively）, and the 2 single nucleotide polymorphisms （SNPs） were in strong linkage disequilibrium （LD）, the TC haplotype was independently associated with a higher OR for HCM （OR=1.59, 95%C/1.21-1.87） after adjusted for conventional risk factors. And the risk alleles were associated with thicker interventricular septal thickness of HCM （（20.0±6.3） mm vs （17.9±5.5） mm, P=0.03 and （21.3±5.9） mm vs （17.9±5.8） mm, P=0.04, respectively）. No association was found between the two polymorphisms with female patients with HCM. Conclusion Minor alleles of ACE2 gene might be the genetic modifier for the magnitude of left ventricular hypertrophy in male patients with HCM.
文摘Background Severe bilateral carotid stenosis caused by atherosclerosis has not been unusual in the elderly. Such patients have high stroke risk. Many studies show that carotid artery stenting （CAS） is an alternative to treat unilateral carotid stenosis. However, the optimal procedural strategy of bilateral carotid stenosis remains unclear. The purpose of our study was to evaluate the safety of simultaneous bilateral carotid artery stenting （SBCAS） compared with unilateral carotid artery stenting （UCAS）. Methods In this single-center retrospective study, we analyzed 234 consecutive patients who underwent carotid stenting from January 2005 to December 2009. Thirty-nine patients （16.7%） of them underwent SBCAS, and the others （n=195） underwent UCAS. Indication for CAS was defined as carotid artery diameter reduction 〉60% （symptomatic） or 〉80% （asymptomatic）. Six-month and 30-day hemodynamic depression （HD）, hyperperfusion syndrome （HPS）, stroke, death and myocardial infarction （MI） after carotid stenting were assessed. Results SBCAS group had no more HD and HPS compared with UCAS group at 30 days （HD： 28.2% vs. 20.0%, P=0.396; HPS： 2.6% vs. 2.1%, P=0.262）. Moreover, there was no statistically significant difference between SBCAS group and UCAS group in major stroke, death, MI and their combinations within 30 days （major stroke： 0 vs. 3.6%, P=0.604; death： 2.6% vs. 1.5%, P=0.520; MI： 2.6% vs. 0.5%, P=0.306; and their combinations： 5.1% vs. 4.6%, P=1.000） and 6 months （major stroke： 0 vs. 3.6%, P=0.604; death： 5.1% vs. 2.1%, P=0.262; MI： 5.1% vs.1.0%, P=0.130 and their combinations： 7.7% vs. 5.1%, P=0.459）. Conclusions The patients undergoing SBCAS had no more events than those undergoing UCAS in 30-day and 6-month follow-up. Our finding suggests that SBCAS appears to be as safe as UCAS.
文摘Background Tumor necrosis factor-induced protein 3 （TNFAIP3） gene has been shown important in cardiac remodeling. The aim of the present study was to investigate whether the variants of TNFAIP3 gene are associated with left ventricular hypertrophy （LVH） in hypertensive patients.Methods Four representatives of all the other single nucleotide polymorphisms （SNPs） in TNFAIP3 gene were tested for association with hypertrophy in two independent hypertensive populations （n=2120 and n=324）.Results We found that only the tag SNP （rs5029939） was consistently lower in the hypertensives with cardiac hypertrophy than in those without cardiac hypertrophy in the two study populations, indicating a protective effect on LVH （odds ratio （OR） （95% confidence interval （CI））0.58 （0.358-0.863）, P=0.035; OR （95% CI）=0.477 （0.225-0.815）, P〈0.05,respectively）. Multiple regression analyses confirmed that the patients with G allele of rs5029939 had less thickness in inter-ventricular septum, left ventricular posterior wall, relative wall thickness and left ventricular mass index than did those with CC allele in the hypertensive patients in both study populations （all P〈0.01）.Conclusion These findings indicate that the SNP （rs5029939） in the TNFAIP3 gene may serve as a novel protective genetic marker for the development of LVH in patients with hypertension
文摘Background The association between fish consumption and heart failure （HF） incidence is inconsistent. Methods We performed a systematic search of Pubmed and Embase （from 1953 to June 2012） using key words related to fish and HF. Studies with at least three categories of fish consumption reporting both relative risk （RR） and corresponding 95% confidence interval （CI） for HF incidence were included. The pooled RR and 95%C/were calculated using a fixed or random-effects model. The generalized least squares regression model was used to quantify the dose-response relationship between fish consumption and HF incidence. Results Five prospective cohort studies including 4750 HF events of 170 231 participants with an average of 9.7-year follow-up were selected and identified. Compared with those who never ate fish, individuals with higher fish consumption had a lower HF incidence. The pooled RRs for HF incidence was 0.99 （95%CI, 0.91 to 1.08） for fish consumption 1 to 3 times per month, 0.91 （95%CI, 0.84 to 0,99） for once a week, 0.87 （95%CI, 0.81 to 0.95） for 2 to 4 times per week, and 0.86 （95% CI, 0.84 to 0.99） for 5 or more times per week. An increment of 20 g of daily fish intake was related to a 6% lower risk of HF （RR： 0.94, 95% CI, 0.90 to 0.97; P for trend = 0.001）. Conclusions This meta-analysis suggests that there is a dose-dependent inverse relationship between fish consumption and HF incidence. Fish intake once or more times a week could reduce HF incidence.
文摘Marfan syndrome is a systemic disorder of connective tissue, caused by mutations in the FBN1, TGFBR1 or TGFBR2 genes. This syndrome is characterized by involvement of three major systems, skeletal, ocular, and cardiovascular. The continuing improvements in molecular biology and increasing availability of molecular diagnosis in clinical practice allow recognition of Marfan syndrome in patients with incomplete phenotypes. Additionally, molecular analyses could also be used for preimplantation genetic diagnosis. The identification of a mutation allows for early diagnosis, prognosis, genetic counseling, preventive management of carriers and reassurance for unaffected relatives. The importance of knowing in advance the location of the putative family mutation is highlighted by its straightforward application to prenatal and postnatal screening.
