We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Carotenoids are generally associated with health-beneficial effects; however, their intake patterns related to the metabolic syndrome (MetS) and its components remain controversial. This cross-sectional study investigated associations between dietary intakes of individual carotenoids, fruits and vegetables, and the MetS and its components. Dietary intakes of 1346 participants of the Observation des Risques et de la Santé Cardio-Vasculaire au Luxembourg (ORISCAV-LUX-2) study were investigated by a 174-item FFQ, and carotenoid intake was determined by linking findings using mainly the USDA food databases. Components of MetS and complementary variables, including anthropometric (BMI, waist circumferences and waist:hip ratio) and biological parameters (TAG, HDL-cholesterol, fasting blood glucose and blood pressure), were measured. Logistic (for MetS) and linear multivariable regression models (including assessing MetS as scores) adjusted for various confounders were created. α-and β-Carotene, as well as lutein + zeaxanthin, were inversely associated with MetS (also when it was measured on a continuous scale), reducing the odds for MetS by up to 48 %. However, lycopene, phytoene and phytofluene were rather positively associated with MetS scores and its components, though these adverse effects disappeared, at least for lycopene, when controlling for intakes of tomato-based convenience foods, in line with indicating a rather unhealthy/westernised diet. All these associations remained significant when including fruits and vegetables as confounders, suggesting that carotenoids were related to MetS independently from effects within fruits and vegetables. Thus, a high intake of carotenoids was bidirectionally associated with MetS, its severity, risk and its components, depending on the type of carotenoid. Future investigations are warranted to explore the inverse role that tomato-based carotenoids appear to suggest in relation to the MetS.
Low birth weight (BW) is consistently correlated with increased parental risk of subsequent cardiovascular disease, but the links with offspring placental weight (PW) are mostly unexplored. We have investigated the associations between parental coronary heart disease (CHD) and offspring BW and PW using the Walker cohort, a collection of 48,000 birth records from Dundee, Scotland, from the 1950s and 1960s. We linked the medical history of 13,866 mothers and 8,092 fathers to their offspring’s records and performed Cox survival analyses modelling maternal and paternal CHD risk by their offspring’s BW, PW, and the ratio between both measurements. We identified negative associations between offspring BW and both maternal (hazard ratio [HR]: 0.91, 95% confidence interval [CI]: 0.88–0.95) and paternal (HR: 0.96, 95% CI: 0.93–1.00) CHD risk, the stronger maternal correlation being consistent with previous reports. Offspring PW to BW ratio was positively associated with maternal CHD risk (HR: 1.14, 95% CI: 1.08–1.21), but the associations with paternal CHD were not significant. These analyses provide additional evidence for intergenerational associations between early growth and parental disease, identifying directionally opposed correlations of maternal CHD with offspring BW and PW, and highlight the importance of the placenta as a determinant of early development and adult disease.
The purpose of this research was to determine the frequency of mutation of the cytochrome CYP3A5 genes and transport proteins SLCO1B1 and MDR1 in patients with coronary heart disease in the Kazakh nation. A prospective cohort clinical and genetic study was conducted. The study was conducted in 2017−2019. Medical records containing information about drug prescription conducted in hospitals and outpatient departments were carefully analyzed. In the examined group of 178 patients treated with statins, a significant frequency of genetic variants that determine the increased risk of complications of statin use was revealed. There was a tendency toward an increase in the activity of creatine phosphokinase (CPK) in the blood upon detection of the A6986G mutation of the cytochrome gene and SLCO1B1 (c.521T>C) gene of the transport protein OATP1B1. In the studied Kazakh population, the presence of a homozygous mutant SLCO1B1 gene of the transport protein can be recommended as a genetic marker for the undesirability of using antihypercholesterolemic therapy with statins, which simultaneously leads to a decrease in the effectiveness of treatment and an increase in the risk of side effects.
In studies that contain repeated measures of variables, longitudinal analysis accounting for time-varying covariates is one of the options. We aimed to explore longitudinal association between diet quality (DQ) and non-communicable diseases (NCDs). Participants from the 1973–1978 cohort of the Australian Longitudinal Study on Women’s Health (ALSWH) were included, if they; responded to survey 3 (S3, 2003, aged 25–30 years) and at least one survey between survey 4 (S4, 2006) and survey 8 (S8, 2018), were free of NCDs at or before S3, and provided dietary data at S3 or S5. Outcomes were coronary heart disease (CHD), hypertension (HT), asthma, cancer (except skin cancer), diabetes mellitus (DM), depression and/or anxiety, and multimorbidity (MM). Longitudinal modelling using generalised estimation equation (GEE) approach with time-invariant (S4), time-varying (S4–S8) and lagged (S3–S7) covariates were performed. The mean (± standard deviation) of Alternative Healthy Eating Index-2010 (AHEI-2010) of participants (n = 8022) was 51·6 ± 11·0 (range: 19–91). Compared to women with the lowest DQ (AHEI-2010 quintile 1), those in quintile 5 had reduced odds of NCDs in time-invariant model (asthma: OR (95 % CI): 0·77 (0·62–0·96), time-varying model (HT: 0·71 (0·50–0·99); asthma: 0·62 (0·51–0·76); and MM: 0·75 (0·58–0·97) and lagged model (HT: 0·67 (0·49–0·91); and asthma: 0·70 (0·57–0·85). Temporal associations between diet and some NCDs were more prominent in lagged GEE analyses. Evidence of diet as NCD prevention in women aged 25–45 years is evolving, and more studies that consider different longitudinal analyses are needed.
Over the years, numerous observational studies have substantiated that various dietary choices have opposing effects on CVD. However, the causal effect has not yet been established. Thus, we conducted a Mendelian randomisation (MR) analysis to reveal the causal impact of dietary habits on CVD. Genetic variants strongly associated with 20 dietary habits were selected from publicly available genome-wide association studies conducted on the UK Biobank cohort (n 449 210). Summary-level data on CVD were obtained from different consortia (n 159 836–977 323). The inverse-variance weighted method (IVW) was the primary outcome, while MR-Egger, weighted median and MR Pleiotropy RESidual Sum and Outlier were used to assess heterogeneity and pleiotropy. We found compelling evidence of a protective causal effect of genetic predisposition towards cheese consumption on myocardial infarction (IVW OR = 0·67; 95 % CI = 0·544, 0·826; P = 1·784 × 10−4) and heart failure (IVW OR = 0·646; 95 % CI = 0·513, 0·814; P = 2·135 × 10−4). Poultry intake was found to be a detrimental factor for hypertension (IVW OR = 4·306; 95 % CI = 2·158, 8·589; P = 3·416 × 10−5), while dried fruit intake was protective against hypertension (IVW OR = 0·473; 95 % CI = 0·348, 0·642; P = 1·683 × 10−6). Importantly, no evidence of pleiotropy was detected. MR estimates provide robust evidence for a causal relationship between genetic predisposition to 20 dietary habits and CVD risk, suggesting that well-planned diets may help prevent and reduce the risk of CVD.
Since the work of R.H. Rosenman and Meyer Friedman in 1959, a correlation has been established between type A behavioral patterns and the occurrence of coronary heart disease. Type A personality has been found to be more of a coronary risk factor than a poor prognostic factor once coronary disease has set in. Subsequent studies have not supported such a relationship.
Objectives
The objective of our work was to investigate the association between type A personalities and coronary heart disease.
Methods
We conducted a retrospective study involving a sample of 200 patients recruited at the Mohamed Tahar Maâmouri Hospital in Nabeul. Our sample was composed of 100 coronary patients hospitalized or followed as outpatients in the cardiology department and 100 controls hospitalized or followed as outpatients in the general surgery or orthopedics department respectively. The study was conducted between April 15 and June 30, 2014. Personality type A was assessed according to the Bortner questionnaire.
Results
After performing a binary logistic regression to adjust for the associations looked for, and taking into account confounding factors, we did not observe a statistically significant association between type A personality and coronary pathology (p=0.123). In addition, type A personality was significantly associated with the following factors: diabetes (p=0.040), hypertension (p=0.049), and age <49 years (p=0.002) in coronary heart disease.
Conclusions
Future large-scale, multicenter, longitudinal studies with follow-up over time of patients would be necessary to consolidate our findings.
To date, there is limited evidence for health care providers regarding the determinants of early assessment of poor outcomes of adult in-patients due to earthquakes. This study aimed to explore factors related to early assessment of adult earthquake trauma patients (AETPs).
Methods:
The data on 29,933 AETPs in the West China Earthquake Patients Database (WCEPD) were analyzed retrospectively. Then, 37 simple variables that could be obtained rapidly upon arrival at the hospital were collected. The least absolute shrinkage and selection operator (LASSO) regression analyses were performed. A nomogram was then constructed.
Results:
Nine independent mortality-related factors that contributed to AETP in-patient mortality were identified. The variables included age (OR:1.035; 95%CI, 1.027-1.044), respiratory rate ([RR]; OR:1.091; 95%CI, 1.050-1.133), pulse rate ([PR]; OR:1.028; 95%CI, 1.020-1.036), diastolic blood pressure ([DBP]; OR:0.96; 95%CI, 0.950-0.970), Glasgow Coma Scale ([GCS]; OR:0.666; 95%CI, 0.643-0.691), crush injury (OR:3.707; 95%CI, 2.166-6.115), coronary heart disease ([CHD]; OR:4.025; 95%CI, 1.869-7.859), malignant tumor (OR:4.915; 95%CI, 2.850-8.098), and chronic kidney disease ([CKD]; OR:5.735; 95%CI, 3.209-10.019).
Conclusions:
The nine mortality-related factors for ATEPs, including age, RR, PR, DBP, GCS, crush injury, CHD, malignant tumor, and CKD, could be quickly obtained on hospital arrival and should be the focal point of future earthquake response strategies for AETPs. Based on these factors, a nomogram was constructed to screen for AETPs with a higher risk of in-patient mortality.
Cardiac injury is associated with poor prognosis of 2019 novel coronavirus disease 2019 (COVID-19), but the risk factors for cardiac injury have not been fully studied. In this study, we carried out a systematic analysis of clinical characteristics in COVID-19 patients to determine potential risk factors for cardiac injury complicated COVID-19 virus infection.
Methods
We systematically searched relevant literature published in Pubmed, Embase, Europe PMC, CNKI and other databases. All statistical analyses were performed using STATA 16.0.
Results
We analysed 5726 confirmed cases from 17 studies. The results indicated that compared with non-cardiac-injured patients, patients with cardiac injury are older, with a greater proportion of male patients, with higher possibilities of existing comorbidities, with higher risks of clinical complications, need for mechanical ventilation, ICU transfer and mortality. Moreover, C-reactive protein, procalcitonin, D-dimer, NT-proBNP and blood creatinine in patients with cardiac injury are also higher while lymphocyte counts and platelet counts decreased. However, we fortuitously found that patients with cardiac injury did not present higher clinical specificity for chest distress (P = 0.304), chest pain (P = 0.334), palpitations (P = 0.793) and smoking (P = 0.234). Similarly, the risk of concomitant arrhythmia (P = 0.103) did not increase observably either.
Conclusion
Age, male gender and comorbidities are risk factors for cardiac injury complicated COVID-19 infection. Such patients are susceptible to complications and usually have abnormal results of laboratory tests, leading to poor outcomes. Contrary to common cardiac diseases, cardiac injury complicated COVID-19 infection did not significantly induce chest distress, chest pain, palpitations or arrhythmias. Our study indicates that early prevention should be applied to COVID-19 patients with cardiac injury to reduce adverse outcomes.
Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF).
Methods:
The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment.
Results:
Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS.
Conclusion:
Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.
This study was performed to evaluate the effects of vitamin D and n-3 fatty acids’ co-supplementation on markers of cardiometabolic risk in diabetic patients with CHD. This randomised, double-blinded, placebo-controlled trial was conducted among sixty-one vitamin D-deficient diabetic patients with CHD. At baseline, the range of serum 25-hydroxyvitamin D levels in study participants was 6·3–19·9 ng/ml. Subjects were randomly assigned into two groups either taking 50 000 IU vitamin D supplements every 2 weeks plus 2× 1000 mg/d n-3 fatty acids from flaxseed oil (n 30) or placebo (n 31) for 6 months. Vitamin D and n-3 fatty acids’ co-supplementation significantly reduced mean (P = 0·01) and maximum levels of left carotid intima–media thickness (CIMT) (P = 0·004), and mean (P = 0·02) and maximum levels of right CIMT (P = 0·003) compared with the placebo. In addition, co-supplementation led to a significant reduction in fasting plasma glucose (β −0·40 mmol/l; 95 % CI −0·77, −0·03; P = 0·03), insulin (β −1·66 μIU/ml; 95 % CI −2·43, −0·89; P < 0·001), insulin resistance (β −0·49; 95 % CI −0·72, −0·25; P < 0·001) and LDL-cholesterol (β −0·21 mmol/l; 95 % CI −0·41, −0·01; P = 0·04), and a significant increase in insulin sensitivity (β +0·008; 95 % CI 0·004, 0·01; P = 0·001) and HDL-cholesterol (β +0·09 mmol/l; 95 % CI 0·01, 0·17; P = 0·02) compared with the placebo. Additionally, high-sensitivity C-reactive protein (β −1·56 mg/l; 95 % CI −2·65, −0·48; P = 0·005) was reduced in the supplemented group compared with the placebo group. Overall, vitamin D and n-3 fatty acids’ co-supplementation had beneficial effects on markers of cardiometabolic risk.
We aimed to develop, deliver and evaluate a brief training programme for primary care mental health staff in NW London focussing on long-term physical health conditions (LTCs). The objective was to improve participants’ knowledge, understanding and confidence (self-efficacy) in providing effective support to people with LTCs. The second objective was to develop an online version to be made available more widely.
Background
The project was commissioned by NW London Collaboration of Clinical Commissioning Groups as part of a strategy to develop more joined up care and support for people with mental health needs. Training was developed by a team of experts, with input from commissioners, service users, clinicians and service managers.
Methods
Training was delivered via two-day interactive workshops providing: (i) key facts (informed by a review of published research and publically available health information); (ii) opportunity to engage with the ‘lived experience’ of people with LTCs (via videos, role plays, case studies and group discussion); (iii) skills-based training (in specific assessment and intervention methods). Knowledge, understanding and confidence (with respect to supporting people with LTCs) were assessed at the start and end of the training. An online training programme (with embedded evaluation questionnaire) was also developed, covering the same themes as the workshop.
Findings
Mental health staff (n=60) reported limited knowledge, understanding and confidence before the workshop, underlining the need for training. Knowledge of LTCs improved significantly following training (P<0.0001), along with awareness of the impact of poor psychological wellbeing on physical health (P<0.05) and the role of psychological therapies in supporting people with LTCs (P<0.0001). Self-efficacy also improved (P<0.001). Online training was accessed by 894 participants in the first six months and 187 provided feedback via the evaluation questionnaire. Responses indicated that participants found the training useful (88%), interesting (91%) and easy to understand (97%).
The theory, in brief outline here, implicating deficiency of Cu in the aetiology and pathophysiology of IHD explains more attributes of the disease than any other theory. This theory satisfies several of Hill’s criteria of a half-century ago for deducing association between an environmental feature and presence of an illness. Most important is the temporal association between the rise of IHD and the decrease in dietary Cu since the 1930s along with a parallel increase in the supplementation of pregnant women with Fe, a Cu antagonist. There are more than eighty anatomical, chemical and physiological similarities between animals deficient in Cu and individuals with IHD. Few of these similarities have been produced by other dietary manipulations because feeding cholesterol induces Cu deficiency in animals. The most recent of these to be identified is decreased serum dehydroepiandrosterone. Some concomitant aspects of Cu metabolism and utilisation have been identified in other theories about heart disease: fetal programming, homocysteine, and Fe overload.
Substantial healthcare resources are devoted to panic disorder (PD) and coronary heart disease (CHD); however, the association between these conditions remains controversial. Our objective was to conduct a systematic review of studies assessing the association between PD, related syndromes, and incident CHD.
Method.
Relevant studies were retrieved from Medline, EMBASE, SCOPUS and PsycINFO without restrictions from inception to January 2015 supplemented with hand-searching. We included studies that reported hazard ratios (HR) or sufficient data to calculate the risk ratio and 95% confidence interval (CI) which were pooled using a random-effects model. Studies utilizing self-reported CHD were ineligible. Twelve studies were included comprising 1 131 612 persons and 58 111 incident CHD cases.
Results.
PD was associated with the primary incident CHD endpoint [adjusted HR (aHR) 1.47, 95% CI 1.24–1.74, p < 0.00001] even after excluding angina (aHR 1.49, 95% CI 1.22–1.81, p < 0.00001). High to moderate quality evidence suggested an association with incident major adverse cardiac events (MACE; aHR 1.40, 95% CI 1.16–1.69, p = 0.0004) and myocardial infarction (aHR 1.36, 95% CI 1.12–1.66, p = 0.002). The risk for CHD was significant after excluding depression (aHR 1.64, 95% CI 1.45–1.85) and after depression adjustment (aHR 1.38, 95% CI 1.03–1.87). Age, sex, length of follow-up, socioeconomic status and diabetes were sources of heterogeneity in the primary endpoint.
Conclusions.
Meta-analysis showed that PD was independently associated with incident CHD, myocardial infarction and MACE; however, reverse causality cannot be ruled out and there was evidence of heterogeneity.
This study assesses the feasibility of collecting genetic samples and self-reported outcome measures after cardiovascular risk assessment, and presenting the genetic test results to participants.
Background
Coronary heart disease (CHD) genetic tests are increasingly available through direct-to-consumer marketing, but their potential clinical impact on cardiovascular risk assessment is unclear.
Methods
Observational study in 10 British general practices in Central England. A total of 320 individuals, who had completed conventional cardiovascular risk assessment, were offered CHD genetic test, with follow-up outcome questionnaire at eight months for lifestyle change and State-Trait Anxiety.
Findings
A total of 119 (37%) participants returned genetic test specimens, with over a third reporting family history of CHD in a specified relative; 79 (66.4%) were categorized above-average risk on conventional cardiovascular risk assessment, 65 of whom (82.3%) were only average risk on genetic assessment. The dietary fat questionnaire was poorly completed while study participation was not associated with increased anxiety (mean increase in anxiety score=2.1; 95% CI −0.1–4.3; P=0.06).
Conclusion
As a feasibility study, over a third of individuals offered genetic testing in primary care, as part of CVD risk assessment, took up the offer. Although intervention did not appear to increase anxiety, this needs further evaluation. To improve generalizability and effect size, future studies should actively engage individuals from wider socio-economic backgrounds who may not have already contemplated lifestyle change. The current research suggests general practitioners will face the clinical challenge of patients presenting with direct-to-consumer genetic results that are inconsistent with conventional cardiovascular risk assessment.
Some studies have found a significant relationship between birth weight (BW) and the risk of coronary heart disease (CHD) in adulthood, but results were inconsistent. The purpose of this study was to characterize the association between BW and the risk of CHD in adults. Among 144 papers detected by our search, 27 papers provided data on the relationship between BW and CHD, of which 23 papers considered BW as a continuous variable, and 14 articles considered BW as a categorical variable for this meta-analysis. Based on 23 papers, the mean weighted estimate for the association between BW and the combined outcome of non-fatal and fatal CHD was 0.83 [95% confidence interval (CI), 0.80–0.86] per kilogram of BW (P<0.0001). Low birth weight (LBW<2500 g) was associated with increased risk of CHD [odds ratio (OR), 1.19; 95% confidence interval (CI), 1.11–1.27] compared with subjects with BW⩾2500 g. LBW, as compared with normal BW (2500–4000 g), was associated with increased risk of CHD (OR, 1.16; 95% CI, 1.08–1.25). High birth weight (HBW⩾4000 g) was associated with decreased risk of CHD (OR, 0.89; 95% CI, 0.81–0.98) compared with subjects with BW<4000 g. In addition, there was an indication (not quite significant) that HBW was associated with a lower risk of CHD (OR, 0.89; 95% CI, 0.79–1.01), as compared with normal BW. No significant evidence of publication bias was present. These results suggest that LBW is significantly associated with increased risk of CHD and a 1 kg higher BW is associated with a 10–20% lower risk of CHD.
Antidepressants reduce depressive symptoms in patients with coronary heart disease, but they may be associated with increased mortality. This study aimed to examine whether the use of tricyclic antidepressants (TCA) or selective serotonin reuptake inhibitors (SSRI) is associated with mortality in patients with coronary heart disease, and to determine whether this association is mediated by autonomic function.
Method
A total of 956 patients with coronary heart disease were followed for a mean duration of 7.2 years. Autonomic function was assessed as heart rate variability, and plasma and 24-h urinary norepinephrine.
Results
Of 956 patients, 44 (4.6%) used TCA, 89 (9.3%) used SSRI, and 823 (86.1%) did not use antidepressants. At baseline, TCA users exhibited lower heart rate variability and higher norepinephrine levels compared with SSRI users and antidepressant non-users. At the end of the observational period, 52.3% of the TCA users had died compared with 38.2% in the SSRI group and 37.3% in the control group. The adjusted hazard ratio (HR) for TCA use compared with non-use was 1.74 [95% confidence interval (CI) 1.12–2.69, p = 0.01]. Further adjustment for measures of autonomic function reduced the association between TCA use and mortality (HR = 1.27, 95% CI 0.67–2.43, p = 0.47). SSRI use was not associated with mortality (HR = 1.15, 95% CI 0.81–1.64, p = 0.44).
Conclusions
The use of TCA was associated with increased mortality. This association was at least partially mediated by differences in autonomic function. Our findings suggest that TCA should be avoided in patients with coronary heart disease.
This study aimed to determine whether depression in patients with long-term conditions is associated with the number of morbidities or the type of co-morbidity.
Method
A cohort study of 299 912 participants aged 30–100 years. The prevalence of depression, rates of health-care utilization and costs were evaluated in relation to diagnoses of diabetes mellitus (DM), coronary heart disease (CHD), stroke and colorectal cancer.
Results
The age-standardized prevalence of depression was 7% in men and 14% in women with no morbidity. The frequency of depression increased in single morbidities including DM (men 13%, women 22%), CHD (men 15%, women 24%), stroke (men 14%, women 26%) or colorectal cancer (men 10%, women 21%). Participants with concurrent diabetes, CHD and stroke had a very high prevalence of depression (men 23%, women 49%). The relative rate of depression for one morbidity was 1.63 [95% confidence interval (CI) 1.59–1.66], two morbidities 1.96 (95% CI 1.89–2.03) and three morbidities 2.35 (95% CI 2.03–2.59). Compared to those with no morbidity, depression was associated with higher rates of health-care utilization and increased costs at any level of morbidity. In women aged 55 to 64 years without morbidity, the mean annual health-care cost was £513 without depression and £1074 with depression; when three morbidities were present, the cost was £1495 without depression and £2878 with depression.
Conclusions
Depression prevalence and health-care costs are more strongly associated with the number of morbidities than the nature of the co-morbid diagnosis.
Depression is common in chronic illness and screening for depression has been widely recommended. There have been no large studies of screening for depression in routine care for patients with chronic illness.
Method
We performed a retrospective cohort study to examine the timing of new depression diagnosis or treatment in relation to annual screening for depression in patients with coronary heart disease (CHD) or diabetes. We examined a database derived from 1.3 million patients registered with general practices in Scotland for the year commencing 1 April 2007. Eligible patients had either CHD or diabetes, were screened for depression during the year and either received a new diagnosis of depression or commenced a new course of antidepressant (excluding those commonly used to treat diabetic neuropathy). Analysis was by the self-controlled case-series method with the outcome measure being the relative incidence (RI) in the period 1–28 days after screening compared to other times.
Results
A total of 67358 patients were screened for depression and 2269 received a new diagnosis or commenced treatment. For the period after screening, the RI was 3.03 [95% confidence interval (CI) 2.44–3.78] for diagnosis and 1.78 (95% CI 1.54–2.05) for treatment. The number needed to screen was 976 (95% CI 886–1104) for a new diagnosis and 687 (95% CI 586–853) for new antidepressant treatment.
Conclusions
Systematic screening for depression in patients with chronic disease in primary care results in a significant but small increase in new diagnosis and treatment in the following 4 weeks.
This paper was originally written for a conference entitled ‘The Future of Medical History. Now it ought to be clear – certainly to historians – that the future of anything is hard to predict; but at least in the short term, any future for medical history seems likely to include the history of disease, and the history of coronary heart disease (CHD) provides an excellent example of what the history of disease has to offer to a wide range of audiences.