Body mass index and total and cardiovascular mortality in men with a history of cardiovascular disease

BACKGROUND: Previous studies designed to identify an association between body mass index (BMI) (calculated as weight in kilograms divided by the square of height in meters) and cardiovascular or total mortality in populations with known atherosclerotic disease have shown conflicting results. In this study, we used the Physicians' Health Study enrollment cohort to examine the risk of total and cardiovascular mortality among men reporting a history of myocardial infarction or stroke, excluding those who reported a history of cancer. METHODS: Cause-specific death was ascertained for 5010 men during a mean follow-up of 5.0 years. End points were classified as total deaths and deaths due to cardiovascular causes. Four BMI categories (<22.0, 22.0-24.9 [referent], 25.0-27.9, and > or =28.0) were created a priori. We used proportional hazards models to calculate age and multivariate-adjusted relative risks (RRs) for each BMI category for each end point. RESULTS: Compared with men with a BMI of 22.0 to 24.9, men with a BMI of 28.0 or greater had an age-adjusted RR of 1.11 (95% confidence interval [CI], 0.91-1.36), a multivariate RR of 1.04 (95% CI, 0.84-1.28) in a model that did not include biological mediators of obesity, and a multivariate RR of 1.06 (95% CI, 0.78-1.44) in a model that included these mediators. The RRs for cardiovascular mortality were similar, at 1.07 (95% CI, 0.85-1.35), 1.01 (95% CI, 0.79-1.29), and 1.01 (95% CI, 0.71-1.43), respectively. A BMI of less than 22.0 was associated with a small increased risk of total mortality and cardiovascular mortality. CONCLUSION: These findings indicate that elevated BMI may not be strongly associated with total or cardiovascular mortality among men with previously manifested coronary artery disease.     

Lipoprotein (a) in childhood: correlations with family history of cardiovascular disease

The association between lipoprotein (a) [Lp(a)] and cardiovascular diseases is well known. Lp(a) is an independent risk factor for the development of atherosclerosis. Little information concerning Lp(a) during childhood is available. The aim of the present investigation was to determine the Lp(a) concentration in a cohort of children aged between 4 and 15 yr and to correlate Lp(a) with: a) overweight status; b) body fat distribution; c) family history of vascular diseases in their parents and grandparents. Six hundred and eighty-nine children (350 males, 339 females), were enrolled in the study. BMI as index of being overweight was calculated; the waist-to-hip ratio (WHR) and the waist-to-thigh ratio (WTR) were calculated to obtain two anthropometric indexes for the pattern of body fat distribution. The areas of visceral (VAT) and subcutaneous adipose tissue (SAT) were evaluated by MRI at the L4-L5 level in only 30 overweight subjects. The serum of Lp(a), total cholesterol (TC), HDL-cholesterol, LDL-cholesterol and triglycerides were evaluated in the whole population. Moreover, the same biochemical study was performed in 70 children's parents randomly chosen. A structured questionnaire was administered to the children's parents to investigate the presence of cardiovascular disease (CVD) in family stories. Our data show no Lp(a) serum differences between children according to sex, age and body composition. The strong correlation between the children's and the parents' Lp(a) concentrations and the occurrence of CVD in their grandparents suggests that Lp(a) represents an important independent early risk factor for the development of CVD in adulthood. Measurements of Lp(a) in childhood may help to evaluate this risk in subjects with family history of cardiovascular diseases.     

The association of ulceration of the foot with cardiovascular and all-cause mortality in patients with diabetes: a meta-analysis

Aims/hypothesis  

It is well established that diabetes mellitus increases the risk of cardiovascular disease (CVD) and all-cause mortality. Observational studies suggest that a history of diabetic foot ulceration (DFU) may increase this risk further still. We sought to determine to what extent DFU is associated with excess risk over and above diabetes.     

Association of obstructive sleep apnea with cardiometabolic diseases and cardiovascular mortality

Background

Obstructive sleep apnea (OSA) is one of the leading respiratory disorders, increasing the risk of cardiometabolic diseases. In the study, we investigated the association between OSA and the risk of cardiometabolic diseases and all-cause and cardiovascular mortality in adults.

Methods

Participants were enrolled in the National Health and Nutrition Examination Survey. The baseline covariates were compared between participants with and without OSA status. Multivariable logistic regression was performed to explore the association between OSA and cardiometabolic diseases, while Cox proportional regression was performed for all-cause and cardiovascular mortality.

Results

OSA status was positively associated with higher risks of cardiometabolic diseases, including hypertension (odds ratio [OR] 1.28, 95% confidence interval [CI] 1.14–1.45; p < 0.001), diabetes (OR 1.46, 95% CI 1.22–1.76; p < 0.001), and cardiovascular diseases (OR 1.29, 95% CI 1.08–1.54; p = 0.006) after adjusting for numerous covariates. However, no associations of OSA with all-cause or cardiovascular mortality were observed.

Conclusion

OSA was associated with a higher risk of hypertension, diabetes, and cardiovascular diseases, but had no significant association with all-cause or cardiovascular mortality in adults.     

Patients with premature cardiovascular disease and a positive family history for cardiovascular disease are prone to recurrent events

Background: Premature cardiovascular disease (CVD) is treated in the same way as CVD of advanced age. However, in patients with premature CVD and a family history of CVD, different —possibly genetic— mechanisms may underlie this disease, which current medical treatment is not targeted to. This suggests that subjects with a genetic predisposition to CVD are more likely to have recurrent cardiovascular events.Methods: We retrospectively investigated 291 patients with premature CVD and assessed the amount of recurrent events according to family history in a follow-up period of 31 years. Premature CVD was defined as an event < 51 years for men or < 56 for women. We used a Cox proportional hazards model to estimate the relationship between a positive family history and recurrence of cardiovascular events.Results: Patients with recurrent events had more often a positive family history (60.0% vs. 47.1%; p < 0.05), were more often smokers (85.2% vs. 70.7%; p < 0.05), had more often hypertension (36.3% vs. 23.6%; p < 0.05) and had a longer follow-up period (10.0 years vs. 5.4 years; p < 0.001) than patients without recurrent events. After adjusting for these differences and modelling time to events, a positive family history was independently associated with recurrent events (Hazard ratio 1.31 (95% confidence intervals (CI) 1.01-1.72; p < 0.05)).Conclusions: Patients with a genetic predisposition for CVD are at risk for recurrent events, after adjusting for risk factors and other confounders. This might imply that in subjects with a genetic predisposition for CVD different pathophysiological mechanisms are active, leading to recurrent events.     

Interleukin family member ST2 and mortality in acute dyspnoea

Abstract. Socrates T, deFilippi C, Reichlin T, Twerenbold R, Breidhardt T, Noveanu M, Potocki M, Reiter M, Arenja N, Heinisch C, Meissner J, Jaeger C, Christenson R, Mueller C. (Department of Internal Medicine, University Hospital Basel, Basel, Switzerland; University of Maryland, School of Medicine, Baltimore, MD, USA). Interleukin family member ST2 and mortality in acute dyspnoea. J Intern Med 2010; 268 : 493–500. Objectives. The study objective was to investigate the prognostic utility and patient‐specific characteristics of ST2 (suppression of tumorigenicity 2), assessed with a novel sensitive assay. Background. Suppression of tumorigenicity 2 signalling has been shown to be associated with death in cardiac and pulmonary diseases. Design/Subjects. In an international multicentre cohort design, we prospectively enrolled 1091 patients presenting with acute dyspnoea to the emergency department (ED). ST2 was measured in a blinded fashion using a novel assay and compared to B‐type natriuretic peptide (BNP) and NT‐proBNP. The primary end‐point was mortality within 30 days and 1 year. The prognostic value of ST2 was evaluated in comparison and in addition to BNP and NT‐proBNP. Results. Suppression of tumorigenicity 2 concentrations was higher amongst decedents than among survivors (median 85 vs. 43 U mL^?1, P < 0.001) and also higher in patients with impaired left ventricular ejection fraction (LVEF) when compared with preserved LVEF (P < 0.001). In receiver operator characteristics analysis, the area under the curve (AUC) for ST2, BNP and NT‐proBNP to predict 30‐day and 1‐year mortality were 0.76, 0.63 and 0.71, and 0.72, 0.71 and 0.73, respectively. The combinations of ST2 with BNP or NT‐proBNP improved prediction of mortality provided by BNP or NT‐proBNP alone. After multivariable adjustment, ST2 values above the median (50 U mL^?1) significantly predicted 1‐year mortality (HR 2.3, P < 0.001). Conclusion. In patients presenting to the ED with acute dyspnoea, ST2 is a strong and independent predictor of 30‐day and 1‐year mortality and might improve risk stratification already provided by BNP or NT‐proBNP.     

Another Swedish family with complete properdin deficiency: association with fulminant meningococcal disease in one male family member

Inherited deficiency of the complement component properdin is described in a Swedish family without any previous history of meningococcal infections. The properdin-deficient index patient died from a fulminant infection caused by Neisseria meningitidis serogroup Y. Family investigation revealed properdin deficiency in the patient's half-brother and in the maternal grandfather. The half-brother had a history of pneumococcal pneumonia and meningitis probably caused by Borrelia burgdorferi. Opsonic and bactericidal functions of serum were examined in the half-brother after immunization with tetravalent meningococcal vaccine. Vaccination promoted opsonization of N. meningitidis serogroups C and Y but not of serogroups A and W-135. The serum bactericidal activity increased against serogroup C and to some extent against serogroup W-135. This report emphasizes the importance of investigating the complement system even in families with single cases of fulminant meningococcal disease. Individuals with properdin deficiency might be protected from infection by immunization.     

The association between low bone mass at the menopause and cardiovascular mortality

BACKGROUND: Low bone mineral density in late postmenopausal women has been associated with increased nontrauma mortality. We investigated whether bone mass in women soon after menopause was also associated with the risk of mortality in later life. METHODS: Between 1977 and 1988, two samples of healthy women were enrolled; one group soon after the menopause (age 50 +/- 2 years [mean +/- SD], n = 309) and another later after menopause (age 70 +/- 2 years, n = 754). The baseline visit included a medical examination and a measurement of bone mineral content in the distal forearm. In 1994, vital status was checked. All causes of death were registered, excluding those that were due to trauma or suicide. Multivariate relative risks (RR) and 95% confidence intervals (CI) were determined. RESULTS: In the early postmenopausal group, each decrease of one SD (0.4 g/cm) in bone mineral content was associated with a 43% increase in mortality (RR = 1.4; 95% CI 1.0 to 2.0; P < 0.05). When only cardiovascular death was considered, the relative risk of dying within 17 years of the menopause was increased 2.3-fold (95% CI 1.0 to 5.3; P < 0.05). Correspondingly, a 70-year-old woman with a bone mineral content 1 SD below the mean for her age had a 1.8-fold increased risk of dying from cardiovascular disease (95% CI 1.0 to 3.2; P = 0.06). Expressed as quartiles, women with bone mass in the lowest quartile had twice the risk of cardiovascular death compared with those in the highest quartile. A prevalent vertebral compression fracture in the late postmenopausal group was independently associated with cardiovascular death (RR = 2.0; 95% CI 1.4 to 3.3; P = 0.004). CONCLUSION: Low bone mineral content at the menopause is a risk factor for increased mortality in later life, especially from cardiovascular disease.     

Gout:A clinical overview and its association with cardiovascular diseases

Gout is a common disease caused by the deposition of monosodium urate(MSU) crystals in patients with hyperuricemia, and characterized by very painful recurrent acute attacks of arthritis. The gold standard for diagnosing gout is the identification of MSU crystals in synovial fluid by polarization light microscopy. Arthritis attacks can be treated with anti-inflammatory medications, such as non-steroidal anti-inflammatory drugs, colchicine, oral prednisone, or intra-articular or intramuscular glucocorticoids. To prevent gout uric acid lowering therapy with for example allopurinol can be prescribed. When gout is adequately treated, the prognosis is good. Unfortunately, the management of gout patients is often insufficient. Gout is associated with dietary factors, the use of diuretics, and several genetic factors. Comorbidities as hypertension, chronic kidney disease, cardiovascular diseases, the metabolic syndrome, diabetes, obesity, hyperlipidemia, and early menopause are associated with a higher prevalence of gout. Xanthine oxidase and chronic systemic inflammation seem to play an important role in the pathophysiology of the association between gout and cardiovascular diseases. To prevent cardiovascular diseases goutpatients must be early screened for cardiovascular risk factors.     

The association between mortality from ischaemic heart disease and mortality from leading chronic diseases.

AIMS: Coronary risk factors raise the risk of other chronic disorders. We therefore tested the hypothesis that the geographic distribution of ischaemic heart disease mortality is associated with that of other chronic diseases with which it shares risk factors. METHODS AND RESULTS: For the 50 provinces of Spain, we collected mortality data for the period 1980-1995 from the national vital statistics. We calculated age-adjusted mortality rates for the leading causes of death in quintiles of provincial distribution of ischaemic heart disease mortality, and correlation coefficients with respect to provincial ischaemic heart disease mortality. As expected, because they share risk factors with ischaemic heart disease, mortality from cerebrovascular disease, malignant tumours, lung cancer, respiratory diseases, chronic obstructive pulmonary disease, diseases of the digestive system, cirrhosis of the liver and all causes, increase with the rise from lower to higher quintiles of ischaemic heart disease mortality. Ischaemic heart disease mortality registered correlations over 0.5 (P<0.001) with mortality from many of the above diseases in the periods 1980-1984 and 1991-1995. Expectations were similarly borne out for disorders not sharing risk factors with ischaemic heart disease, in that mortality from prostate and breast cancer, injury and poisoning, traffic accidents and ill-defined causes in most cases did not show a provincial association with ischaemic heart disease mortality. In general, these results were observed for both sexes and across all age groups. CONCLUSION: Ischaemic heart disease mortality is associated with mortality from chronic diseases which share coronary risk factors, across provinces of Spain over the period 1980-1995. This suggests that the geographic variation in such chronic diseases is due to common factors, potentially susceptible to similar preventive interventions.     

The association between AST/ALT ratio and all-cause and cardiovascular mortality in patients with hypertension

Previous studies had shown that an increased aspartate aminotransferase to alanine aminotransferase ratio (AST/ALT ratio) was associated with cardiovascular disease. This study aimed to assess the relationship between AST/ALT ratio and all-cause and cardiovascular mortality in patients with hypertension.By March 31, 2020, a cohort of 14,220 Chinese hypertensive patients was followed up. The end point was all-cause and cardiovascular death. Hazard ratios (HRs) and 95% CIs were calculated for mortality associated with AST/ALT ratio, using Cox proportional hazards models and competing risk model.In an average of 1.7 years of follow-up, 1.39% (n = 198) of patients died, 55.5% (n = 110) of whom from cardiovascular disease. AST/ALT ratio was associated with increased risk of all-cause death (HR:1.37, 95% CI:1.15–1.63) and cardiovascular death (HR:1.32, 95% CI:1.03–1.68) after adjustment for other potential confounders. Compared with low AST/ALT ratio (Tertile 1), high AST/ALT ratio was associated with high cause mortality (Tertile 2: HR:1.35, 95% CI:0.86–2.10; Tertile 3: HR:2.10, 95% CI:1.37–3.21; P for trend <.001). Compared with low AST/ALT ratio (Tertile 1), a statistically significant increased risk of cardiovascular mortality was also observed (Tertile 2: HR:1.27, 95% CI:0.70–2.29; Tertile 3: HR:1.92, 95% CI:1.09–3.37; P for trend <.001). High AST/ALT ratio was also associated with high cardiovascular mortality (Tertile 2: HR:1.27, 95% CI:0.70–2.29; Tertile 3: HR:1.92, 95% CI:1.09–3.37; P for trend <.001).Present study indicated that increased AST/ALT ratio levels were predictive of all-cause and cardiovascular mortality among Chinese hypertensive patients.Trial registration: CHICTR, CHiCTR1800017274. Registered 20 July 2018.     

Frequency of replication errors in colorectal cancer and their association with family history

Background—Replication errors (RERs) characterisetumours of hereditary non-polyposis colorectal cancer (HNPCC). RERstatus may therefore improve identification of such families previously diagnosed by family history alone.
Aims—To assess RER and HNPCC frequency within apopulation of colorectal cancer patients and a regional population offamily history defined (Amsterdam criteria) HNPCC families.
Methods—Family history was assessed by personalinterview in a population of 479 patients with colorectal cancerattending one follow up clinic. Seven fluorescently labelledmicrosatellites were used to investigate RER frequency in colorectalcancers from 89 patients of this population with varying degrees offamily history and 20 Amsterdam criteria positive families (four with aknown germline mutation, 16 with unknown mutation status) from theregional population.
Results—Only four of the follow up population(0.8%) came from families meeting the Amsterdam criteria with only oneshowing RERs. The frequency of RERs was similar in the early onsetcancer group (less than 50 years of age), those with a family history, and those with no family history of colorectal cancer. From the regional population, RERs were identified in 4/4 families with amutation but only 8/16 families with unknown mutation status.
Conclusions—No correlation was seen between RERstatus and strength of family history except in HNPCC families. Resultsalso indicate that half of the Amsterdam criteria defined families donot exhibit RERs, perhaps suggesting a different mechanism of tumorigenesis.

Keywords:hereditary non-polyposis colorectal cancer; replication errors

     

The association of alcohol consumption with coronary heart disease mortality and cancer incidence varies by smoking history

OBJECTIVE: To evaluate the effect of alcohol on coronary heart disease (CHD), cancer incidence, and cancer mortality by smoking history. DESIGN/SETTING: A prospective, general community cohort was established with a baseline mailed questionnaire completed in 1986. Participants: A population-based sample of 41,836 Iowa women aged 55-69 years. MEASUREMENTS: Mortality (total, cancer, and CHD) and cancer incidence outcomes were collected through 1999. Relative hazard rates (HR) were calculated using Cox regression analyses. MAIN RESULTS: Among never smokers, alcohol consumption (> or =14 g/day vs none) was inversely associated with age-adjusted CHD mortality (HR, 0.40; 95% confidence interval [CI], 0.19 to 0.84) and total mortality (HR, 0.71; 95% CI, 0.55 to 0.92). Among former smokers, alcohol consumption was also inversely associated with CHD mortality (HR, 0.45; 95% CI, 0.23 to 0.88) and total mortality (HR, 0.78; 95% CI, 0.62 to 0.97), but was positively associated with cancer incidence (HR, 1.25; 95% CI, 1.03 to 1.51). Among current smokers, alcohol consumption was not associated with CHD mortality (HR, 1.05; 95% CI, 0.73 to 1.50) or total mortality (HR, 1.07; 95% CI, 0.92 to 1.25), but was positively associated with cancer incidence (HR, 1.30; 95% CI, 1.10 to 1.54). CONCLUSIONS: Health behavior counseling regarding alcohol consumption for cardioprotection should include a discussion of the lack of a decreased risk of CHD mortality for current smokers and the increased cancer risk among former and current smokers.     

Impact of parental history on patients' cardiovascular mortality in rheumatoid arthritis

BACKGROUND: Patients with rheumatoid arthritis are at increased risk of death from cardiovascular disease (CVD). This risk is influenced by the inflammatory activity of the rheumatoid arthritis as well as by traditional risk factors for CVD. However, little is known about whether or to what extent hereditary factors for CVD contribute additional risk in patients with rheumatoid arthritis. OBJECTIVE: To assess the clinical impact of a parental history of CVD in patients with rheumatoid arthritis. METHODS: Population based cohort study of 10,805 Swedish patients with rheumatoid arthritis aged 16-67 years during follow up (1990-2000). Parents, and cardiovascular deaths among patients and parents, were identified through register linkages. Relative risk of death v the general population was assessed using standardised mortality ratios (SMR), which were compared by Poisson regression. RESULTS: Rheumatoid patients with a parental history of fatal CVD had an SMR of death from CVD of 2.9 (95% confidence interval, 2.5 to 3.4). By contrast, rheumatoid patients without a parental history of fatal CVD had an SMR of 1.7 (1.2 to 2.3). A parental death from CVD was associated with a 70% increase in the risk of fatal CVD in rheumatoid arthritis (SMR ratio = 1.7 (1.2 to 2.4), and an increase in the 10 year mortality from CVD from 5% to 10% in men and from 2% to 4% in women aged 50 to 67 years. CONCLUSIONS: Parental history of death from CVD is an important (and easily assessable) risk factor for fatal CVD in rheumatoid arthritis.     

2型糖尿病家系青少年一级亲属心血管危险因素研究

目的探讨2型糖尿病（T2DM）家族史对青少年心血管危险因素的影响。方法秦皇岛地区12～18岁青少年4023人横断面调查。根据父母有无糖尿病分为糖尿病家族史阳性组（FH＋）和阴性组（FH-）。测量腰围（WC）、血压、FPG、血脂,计算BMI。结果（1）FH＋组腰围、FPG、TC和LDL-C均高于FH-组（P〈0.05）,超重/肥胖、高SBP、高FPG检出率高于FH-组（P〈0.05）。（2）校正年龄、性别后FH＋组SBP、FPG升高、超重/肥胖的危险性分别是FH-组的1.54、2.06、1.33倍,95%CI分别是（1.10～2.16）、（1.46～2.89）、（1.12～1.59）,具有2项以上心血管危险因素的危险性是FH-组的1.72倍。结论T2DM患者的青少年一级亲属已存在心血管危险因素增加和聚集。应重视对这一人群进行早期筛查和干预,以减少心血管病的发生。     

中国不同地区糖代谢状态的心血管疾病归因死亡研究

目的 分析中国不同地区糖代谢状态的归因死亡风险和疾病负担.方法 本研究数据基于2012—2015年中国高血压调查和2013年中国居民死因监测数据.共纳入22702名35岁及以上无心血管疾病史的中国高血压调查对象,并于2018—2019年对其随访心血管死亡结局.利用Cox比例风险模型,对糖代谢状态与死亡的风险比进行估计....