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Background The associations of age at orthostatic hypotension onset with incident myocardial infarction (MI), stroke, and dementia remain unknown. This study aimed to examine whether younger onset age of orthostatic hypotension was associated with higher risks of incident MI, stroke, and dementia. Methods Data were obtained from the UK Biobank. Information on the diagnosis of orthostatic hypotension, MI, stroke, and dementia was collected at baseline (2006–2010) and follow-ups (median = 13 years). The propensity score matching method and the Cox proportional hazard models were employed. Results A total of 448 374 adults (mean age: 56.8 ± 8.1 years), of whom 3 795 had orthostatic hypotension, were included. orthostatic hypotension patients exhibited higher risks of developing MI, stroke, and dementia than non-orthostatic hypotension participants. Importantly, among orthostatic hypotension patients, younger onset age (per 10-year decrement) was significantly associated with high risks of MI (HR = 3.15, 95% CI: 2.54–3.90, p  < .001), stroke (HR = 1.72, 95% CI: 1.33–2.23, p  < .001), and dementia (HR = 1.26, 95% CI: 1.02–1.57, p  = .034). After propensity score matching, orthostatic hypotension patients had significantly higher risks of MI, stroke, and dementia than matched controls among all onset age groups, and the HRs gradually increased with descending onset age. Conclusions Younger onset age of orthostatic hypotension was associated with higher risks of incident MI, stroke, and dementia, underscoring the necessity to pay additional attention to the cardiovascular health and neurocognitive status of individuals diagnosed with orthostatic hypotension at younger ages to attenuate subsequent risks of incident cardiovascular diseases and dementia. [ABSTRACT FROM AUTHOR]

Introduction The global disease burden may be exacerbated by exposure to passive smoking (SHS), with the workplace being a primary location for such exposure. Numerous epidemiological studies have identified SHS as a risk factor for diseases affecting various systems, including cardiovascular, respiratory, immune, endocrine, and nervous systems. The conventional observational study has certain methodological constraints that can be circumvented through a Mendelian randomization (MR) study. Our MR study intends to investigate the causal link between workplace exposure to SHS and the potential associated diseases. Aim and Methods Summary statistics data involving European participants were sourced from three databases: the UK Biobank, the FinnGen study, and the European Bioinformatics Institute. Genetic variants linked with exposure to SHS in the workplace were identified as instrumental variables. The MR was carried out using inverse variance weighted (IVW), MR-Egger, and weighted median methods. Sensitivity tests were also undertaken within the MR to evaluate the validity of the causality. Results According to the IVW model, genetically determined atrial fibrillation (AF) and stroke (p = 6.64E−04 and 5.68E−07, odds ratio = 2.030 and 2.494, 95% confidence interval = 1.350 to 3.051 and 1.743 to 3.569) were robustly associated with exposure to SHS in the workplace. Suggestive associations were found between workplace SHS and myocardial infarction (MI), asthma, and depression. Conclusions The MR study demonstrates that exposure to SHS in the workplace is a significant risk factor for AF and stroke in European individuals. Whether workplace exposure to SHS influences other diseases and the causality between them requires further exploration. Implications This study explored the causality between exposure to SHS in the workplace and potential associated diseases in multiple systems, including MI, AF, stroke, lung cancer, asthma, allergic disease, type 2 diabetes, and depression, using an MR study. The MR study can circumvent the methodological constraints of observational studies and establish a causal relationship. The two-sample MR analysis provides evidence supporting the causal association of frequent workplace SHS with AF and stroke. Individuals exposed to SHS in the workplace may also have a heightened risk of MI, asthma, and depression. However, whether SHS affects other diseases and the causality between them requires further investigation. To our knowledge, this is the first two-sample MR study to determine the causal relationship between SHS and potential diseases. Exposure to SHS in the workplace is a prevalent issue and may contribute to a global disease burden. The reduction of exposure following the introduction of smoke-free laws has led to a decrease in the admission rate for cardiac events and an improvement in health indicators. It is crucial to further advance smoke-free policies and their implementation. [ABSTRACT FROM AUTHOR]

Background Telomere length has been linked to various health outcomes. To comprehensively investigate the causal effects of telomere length throughout the human disease spectrum, we conducted a phenome-wide Mendelian randomization study (MR-PheWAS) and a systematic review of MR studies. Methods We conducted a PheWAS to screen for associations between telomere length and 1 035 phenotypes in the UK Biobank (n = 408 354). The exposure of interest was the genetic risk score (GRS) of telomere length. Observed associations passing multiple testing corrections were assessed for causality by 2-sample MR analysis. A systematic review of MR studies on telomere length was performed to harmonize the published evidence and complement our findings. Results Of the 1 035 phenotypes tested, PheWAS identified 29 and 78 associations of telomere length GRS at a Bonferroni- and false discovery rate-corrected threshold; 24 and 66 distinct health outcomes were causal in the following principal MR analysis. The replication MR using data from the FinnGen study provided evidence of causal effects of genetically instrumented telomere length on 28 out of 66 outcomes, including decreased risks of 5 diseases in respiratory diseases, digestive diseases, and myocardial infarction, and increased risks of 23 diseases, mainly comprised neoplasms, diseases of the genitourinary system, and essential hypertension. A systematic review of 53 MR studies found evidence to support 16 out of the 66 outcomes. Conclusions This large-scale MR-PheWAS identified a wide range of health outcomes that were possibly affected by telomere length, and suggested that susceptibility to telomere length may vary across disease categories. [ABSTRACT FROM AUTHOR]

Aims Treatment with sodium-glucose co-transporter 2 (SGLT2)-inhibitors reduces the risk of cardiovascular disease and mortality, but the mechanism is unclear. We hypothesized that a functional genetic variant in solute carrier family 5 member 2 (SLC5A2), known to be associated with familial renal glucosuria, would mimic pharmacological SGLT2-inhibition, and thus provide an opportunity to examine potential mediators of the effects on lower risk of cardiovascular disease and mortality. Methods and results We examined 112 712 individuals from the Copenhagen City Heart Study and Copenhagen General Population Study (CCHS + CGPS), 488 687 from the UK Biobank, and 342 499 from FinnGen, genotyped for SLC5A2 rs61742739, c.1961A > G; p.(Asn654Ser). The 2.0% heterozygotes and 0.01% homozygotes were pooled as carriers and compared with the 98% non-carriers. First, we examined the risk of cardiovascular disease and mortality; second, whether carrying the variant was associated with potential mediators of the effect; and third, whether identified potential mediators could explain the observed reduced risk of cardiovascular disease and mortality. In the CCHS + CGPS, carriers vs. non-carries had a 31% lower risk of heart failure, 21% lower risk of myocardial infarction, 16% lower risk of ischaemic heart disease, and 22% lower risk of all-cause mortality. Corresponding values in meta-analyses of the three studies combined were lower risk by 10%, 6%, 6%, and 10%, respectively. The SLC5A2 rs61742739 variant was not associated with a risk of ischaemic stroke or cardiovascular mortality. Of the lower risks observed in CCHS + CGPS, lower plasma glucose mediated 2.0%(P = 0.004) on heart failure, 3.1%(P = 0.09) on myocardial infarction, 4.1%(P = 0.02) on ischaemic heart disease, and 6.0%(P = 0.39) on all-cause mortality; corresponding values in the UK Biobank were 2.9%(P = 0.70), 1.5%(P = 0.77), 4.1%(P = 0.23), and 3.1%(P = 0.21), respectively. Conclusion A functional genetic variant in SLC5A2 , mimicking SGLT2-inhibition, was associated with a lower risk of heart failure, myocardial infarction, ischaemic heart disease, and all-cause mortality. These effects were at most minimally mediated through lower plasma glucose. [ABSTRACT FROM AUTHOR]

Background Sex hormone-binding globulin (SHBG), testosterone and oestradiol have been associated with many diseases in observational studies; however, the causality of associations remains unestablished. Methods A phenome-wide Mendelian randomization (MR) association study was performed to explore disease outcomes associated with genetically proxied circulating SHBG, testosterone and oestradiol levels by using updated genetic instruments in 339 197 unrelated White British individuals (54% female) in the UK Biobank. Two-sample MR analyses with data from large genetic studies were conducted to replicate identified associations in phenome-wide MR analyses. Multivariable MR analyses were performed to investigate mediation effects of hormone-related biomarkers in observed associations with diseases. Results Phenome-wide MR analyses examined associations of genetically predicted SHBG, testosterone and oestradiol levels with 1211 disease outcomes, and identified 28 and 13 distinct phenotypes associated with genetically predicted SHBG and testosterone, respectively; 22 out of 28 associations for SHBG and 10 out of 13 associations for testosterone were replicated in two-sample MR analyses. Higher genetically predicted SHBG levels were associated with a reduced risk of hypertension, type 2 diabetes, diabetic complications, coronary atherosclerotic outcomes, gout and benign and malignant neoplasm of uterus, but an increased risk of varicose veins and fracture (mainly in females). Higher genetically predicted testosterone levels were associated with a lower risk of type 2 diabetes, coronary atherosclerotic outcomes, gout and coeliac disease mainly in males, but an increased risk of cholelithiasis in females. Conclusions These findings suggest that sex hormones may causally affect risk of several health outcomes. [ABSTRACT FROM AUTHOR]

As people age they are at increased risk of cardiovascular disease, the leading cause of mortality and morbidity worldwide. Understanding cardiovascular ageing is essential to preserving healthy ageing and preventing serious health outcomes. This collection of papers published in Age and Ageing since 2011 cover key themes in cardiovascular ageing, with a separate collection on stroke and atrial fibrillation planned. Treating high blood pressure remains important as people age and reduces strokes and heart attacks. That said, a more personalised approach to blood pressure may be even more important as people age to lower blood pressure to tight targets where appropriate but avoid overtreatment in vulnerable groups. As people age, more people experience blood pressure drops on standing (orthostatic hypotension), particularly as they become frail. This can predispose them to falls. The papers in this collection provide an insight into blood pressure and orthostatic hypotension. They highlight areas for further research to understand blood pressure changes and management in the ageing population. Inpatient clinical care of older people with heart attacks differs from younger people in UK national audit data. People aged over 80 had improved outcomes in survival after heart attack over time, but had lower rates of specialist input from cardiology compared with younger people. This may partly reflect different clinical presentations, with heart attacks occurring in the context of other health conditions, frailty and multimorbidity. The care and outcomes of acute and chronic cardiovascular disease are impacted by the frailty and health status of an individual at baseline. The research included in this collection reinforces the wide variations in the ageing population and the necessity to focus on the individual needs and priorities, and provide a person-centred multidisciplinary approach to care. [ABSTRACT FROM AUTHOR]

Background Associations between human herpesviruses (HHVs) and cardiovascular disease/mortality have been reported, but evidence is inconsistent. We investigated associations between 3 common herpesviruses and (1) incident stroke or myocardial infarction (MI) and (2) all-cause mortality. Methods We included participants from the UK Biobank Infectious Disease pilot study with valid serum antibody (IgG) measurements taken at cohort entry (2006–2010) for herpes simplex virus type 1 (HSV1), varicella zoster virus (VZV), and cytomegalovirus (CMV). Linked hospital and mortality records up to December 30 2019 provided information on rates of (1) incident first stroke or MI and (2) all-cause mortality. Hazard ratios (HRs) from Cox proportional hazards regression models were used to assess relationships between (1) HHV seropositivity, (2) HHV titer and incident stroke/MI, and death outcomes. Fully adjusted models accounted for sociodemographic information (age, sex, ethnicity, education, deprivation quintile, birthplace, population density), baseline comorbidities (including diabetes and hypertension), smoking status, body mass index, and serum cholesterol. Results Of 9429 study participants (56% female, 95% White, median age 58 years), 41% were seropositive for all 3 HHVs. Human herpesvirus seropositivity was not associated with stroke/MI (fully adjusted HRs and 95% confidence intervals [CIs]: HSV1 = 0.93 [CI, 0.72–1.22], VZV = 0.78 [CI, 0.51–1.20], CMV = 0.91 [CI, 0.71–1.16]) or all-cause mortality (HSV1 = 1.21 [CI, 1.00–1.47], VZV = 0.79 [CI, 0.58–1.07], CMV = 0.90 [CI, 0.76–1.06]). Human herpesvirus titers were not associated with outcomes. Conclusions In this mostly White UK Biobank subset, neither HHV seropositivity nor titers were associated with stroke/MI or all-cause mortality. [ABSTRACT FROM AUTHOR]

Background: It is commonly assumed that high oestradiol levels in women are cardioprotective. We assessed the association between oestradiol and the risk of incident myocardial infarction (MI) in women.Methods: We used data from 263 295 female UK Biobank participants [mean age 56.2; standard deviation (SD) 8.0 years] without previous cardiovascular disease (CVD). Associations of oestradiol with age and other cardiovascular risk factors were assessed. Cox proportional hazards models estimated crude, ag- and multiple-adjusted hazard ratios (HR) for MI associated with oestradiol levels.Results: After a mean follow-up of 9 years, 2206 incident cases of MI had been recorded, including 230 events among the 57 204 women (mean age 48) with detectable oestradiol levels. In the unadjusted analyses, a unit higher in log-transformed oestradiol was associated with an HR [95% confidence interval (CI) for MI of 0.73 (0.58; 0.92)]. After adjusting for age, this HR became 0.94 (0.75; 1.17), and after further adjusting for classical CVD risk factors, it was 1.05 (0.83; 1.31. Results were similar in subgroup analyses defined by age, menopausal status, socioeconomic status, contraceptive pill use and the use of hormone replacement therapy. The multivariable-adjusted HR for the 171 431 women (mean age 59) with undetectable levels of oestradiol, compared with those with detectable levels, was 0.97 (0.92; 1.02).Conclusions: Higher levels of oestradiol were not associated with a decreased risk of MI. The presumed cardioprotective effects of oestradiol seem to be largely confounded by age and further confounded by other cardiovascular risk factors. [ABSTRACT FROM AUTHOR]

This case report explores the interesting case of a 71-year-old gentleman who presented with a testicular lump following trauma. Ultrasound imaging of the testicle demonstrated malignancy and subsequently orchidectomy was listed. Due to a scheduling difficulty, this was prioritized ahead of his whole-body computed tomography scan. Intraoperatively, he developed electrocardiogram changes suggestive of a non-ST elevated myocardial infarction. Post-operative imaging demonstrated a diffuse large B-cell lymphoma encroaching the heart and greater vessels. This case report highlights the importance of preoperative imaging, even where it may prove challenging. We assess the adequacy of current guidelines within the UK on imaging for new testicular malignancies. [ABSTRACT FROM AUTHOR]

The association between use of aromatase inhibitors (AIs) and cardiovascular outcomes is controversial. While some observational studies have assessed the cardiovascular safety of AIs as upfront treatments, their cardiotoxicity as sequential treatments with tamoxifen remains unknown. Thus, we conducted a population-based cohort study using data from the United Kingdom Clinical Practice Research Datalink linked to the Hospital Episode Statistics and Office for National Statistics databases. We employed a prevalent new-user design to propensity-score match, in a 1:2 ratio, patients switching from tamoxifen to AIs with patients continuing tamoxifen between 1998 and 2016. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals for the study outcomes (myocardial infarction, ischemic stroke, heart failure, and cardiovascular mortality). Overall, 1,962 patients switching to AIs were matched to 3,874 patients continuing tamoxifen. Compared with tamoxifen, AIs were associated with an increased risk of myocardial infarction (hazard ratio (HR) = 2.08, 95% confidence interval (CI): 1.02, 4.27). The hazard ratios were elevated for ischemic stroke (HR = 1.58, 95% CI: 0.85, 2.93) and heart failure (HR = 1.69, 95% CI: 0.79, 3.62) but not cardiovascular mortality (HR = 0.87, 95% CI: 0.49, 1.54), with confidence intervals including the null value. The elevated hazard ratios observed for the cardiovascular outcomes should be corroborated in future large observational studies. [ABSTRACT FROM AUTHOR]

Aims To compare ST-segment elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI) mortality between Sweden and the UK, adjusting for background population rates of expected death, case mix, and treatments. Methods and results National data were collected from hospitals in Sweden [ n  = 73 hospitals, 180 368 patients, Swedish Web-system for Enhancement and Development of Evidence-based care in Heart disease Evaluated According to Recommended Therapies (SWEDEHEART)] and the UK [ n  = 247, 662 529 patients, Myocardial Ischaemia National Audit Project (MINAP)] between 2003 and 2013. There were lower rates of revascularization [STEMI (43.8% vs. 74.9%); NSTEMI (27.5% vs. 43.6%)] and pharmacotherapies at time of hospital discharge including [aspirin (82.9% vs. 90.2%) and (79.9% vs. 88.0%), β-blockers (73.4% vs. 86.4%) and (65.3% vs. 85.1%)] in the UK compared with Sweden, respectively. Standardized net probability of death (NPD) between admission and 1 month was higher in the UK for STEMI [8.0 (95% confidence interval 7.4–8.5) vs. 6.7 (6.5–6.9)] and NSTEMI [6.8 (6.4–7.2) vs. 4.9 (4.7–5.0)]. Between 6 months and 1 year and more than 1 year, NPD remained higher in the UK for NSTEMI [2.9 (2.5–3.3) vs. 2.3 (2.2–2.5)] and [21.4 (20.0–22.8) vs. 18.3 (17.6–19.0)], but was similar for STEMI [0.7 (0.4–1.0) vs. 0.9 (0.7–1.0)] and [8.4 (6.7–10.1) vs. 8.3 (7.5–9.1)]. Conclusion Short-term mortality following STEMI and NSTEMI was higher in the UK compared with Sweden. Mid- and longer-term mortality remained higher in the UK for NSTEMI but was similar for STEMI. Differences in mortality may be due to differential use of guideline-indicated treatments. [ABSTRACT FROM AUTHOR]

Objectives To compare the prevalence and incidence of chronic co-morbidities in people with inflammatory rheumatic and musculoskeletal diseases (iRMDs), and to determine whether the prevalent co-morbidities are associated with physical activity levels in people with iRMDs and in those without iRMDs. Methods Participants were recruited to the UK Biobank; a population-based cohort. Data were collected about demographics, physical activity, iRMDs (RA, PsA, AS, SLE) and other chronic conditions, including angina, myocardial infarction, stroke, hypertension, pulmonary disease, diabetes and depression. The standardized prevalence of co-morbidities in people with iRMDs was calculated. Cox regression was used to determine the relationship between the presence of an iRMD and an incident co-morbidity. The relationship between the presence (versus absence) of a (co-)morbidity and physical activity level (low, moderate, high) in people with iRMDs and in those without was assessed using multinomial logistic regression. Results A total of 488 991 participants were included. The estimated prevalence of each co-morbidity was increased in participants with an iRMD, compared with in those without, particularly for stroke in participants with SLE (standardized morbidity ratio (95% CI), 4.9 (3.6, 6.6). Compared with people with no iRMD and no morbidity, the odds ratios (95% CI) for moderate physical activity were decreased for: no iRMD and morbidity, 0.87 (0.85, 0.89); iRMD and no co-morbidity, 0.71 (0.64, 0.80); and iRMD and co-morbidity, 0.58 (0.54, 0.63). Conclusion Having a (co-)morbidity is associated with reduced physical activity in the general population, and to a greater extent in participants with an iRMD. Optimal management of both iRMDs and co-morbidities may help to reduce their impact on physical activity. [ABSTRACT FROM AUTHOR]

Objective. To evaluate the associations between GCA and vascular diseases and other comorbidities in patients with GCA compared with non-vasculitis patients. Methods. Using the UK-based Clinical Practice Research Datalink we identified 9778 newly diagnosed GCA patients in 1990-2014, and up to 10 non-vasculitis patients randomly matched to each case on age, sex, practice and years of history before cohort entry. We compared the distributions of 9 different preexisting vascular diseases and 11 other comorbidities, and risks of incident vascular diseases and other comorbidities after cohort entry between GCA and non-vasculitis patients. Results. Patients with GCA were more likely to have a history of vascular diseases and other comorbidities except myocardial infarction, type 2 diabetes, obesity and cancer, compared with non-vasculitis patients. Patients with GCA had increased risks for all types of incident vascular disease compared with non-vasculitis patients: adjusted hazard ratios were 1.57 (95% CI: 1.36, 1.82) for myocardial infarc-tion, 1.41 (95% CI: 1.29, 1.55) for stroke, 1.75 (95% CI: 1.49, 2.06) for peripheral vascular disease, 1.98 (95% CI: 1.50, 2.62) for aortic aneurysm and 2.03 (95% CI: 1.77, 2.33) for venous thromboembolism. Patients with GCA also had increased risks for other incident comorbidities (type 2 diabetes, depression, etc.), but not for cancer. Conclusion. Patients with GCA had more prior vascular diseases and other comorbidities before the diagnosis and they also had increased risks for incident vascular diseases and many other incident comorbidities after the diagnosis compared with non-vasculitis population. [ABSTRACT FROM AUTHOR]

Objectives. RA is associated with early ischaemic heart disease. This appears to be driven largely by the presence of chronic inflammation. Studies suggest that treatment with disease-modifying drugs such as MTX may reduce the incidence of cardiovascular events in RA. Anti-TNF therapies significantly reduce inflammation in RA. However, the extent to which these agents also reduce cardiovascular disease (CVD) is uncertain. The purpose of this study was to explore the effect of anti-TNF agents on CVD in RA using a systematic literature review.Methods. We searched for studies of adults with RA treated with TNF antagonists where cardiovascular outcomes were recorded using MEDLINE, EMBASE, Cochrane Database, Database of Abstracts and Reviews of Effects, Health Technology Appraisal, Science Citation Index and Clinical Evidence from 1989 to 2010. Conference proceedings for the British Society of Rheumatology, ACR and EULAR between 2005 and 2009 were hand searched. Two reviewers assessed abstracts for inclusion and then quality of selected papers was assessed.Results. A total of 1840 abstracts were identified and 20 articles were suitable for inclusion. Information was obtained on the effect of TNF antagonists on overall CVD events, myocardial infarction, strokes and heart failure.Conclusion. In many studies, TNF antagonists appear to reduce the likelihood of CVD in individuals with RA. Reassuringly, there does not appear to be an increased risk of cardiac failure. However, the reduction in CVD is not as consistently seen as with studies of MTX. [ABSTRACT FROM PUBLISHER]

In 2007, the Wellcome Trust Case Control Consortium (WTCCC) performed a genome-wide association study in 2,000 British coronary heart disease (CHD) cases and 3,000 controls after genotyping 469,557 single nucleotide polymorphisms (SNPs). Seven variants associated with CHD were initially identified, and 5 SNPs were later found in replication studies. In the current study, the authors aimed to determine whether the 12 SNPs reported by the WTCCC predicted incident CHD through 2004 in a biracial, prospective cohort study (Atherosclerosis Risk in Communities) comprising 15,792 persons aged 45–64 years who had been selected by probability sampling from 4 different US communities in 1987–1989. Cox proportional hazards models with adjustment for age and gender were used to estimate CHD hazard rate ratios (HRRs) over a 17-year period (1,362 cases in whites and 397 cases in African Americans) under an additive genetic model. The results showed that 3 SNPs in whites (rs599839, rs1333049, and rs501120; HRRs were 1.10 (P = 0.044), 1.14 (P < 0.001), and 1.14 (P = 0.030), respectively) and 1 SNP in African Americans (rs7250581; HRR = 1.60, P = 0.05) were significantly associated with incident CHD. This study demonstrates that genetic variants revealed in a case-control genome-wide association study enriched for early disease onset may play a role in the genetic etiology of CHD in the general population. [ABSTRACT FROM PUBLISHER]

Background: Cocaine is a sympathomimetic agent that can cause coronary artery vasospasm leading to myocardial ischaemia, acute coronary syndrome and acute myocardial infarction (ACS/AMI). The management of cocaine-induced ACS/AMI is different to classical atheromatous ACS/MI, because the mechanisms are different. Methods: Knowledge study—Junior medical staff were given a scenario of a patient with ACS and asked to identify potential risk factors for ACS and which ones they routinely asked about in clinical practice. Retrospective study—Retrospective notes reviews of patients with suspected and proven (elevated troponin I concentration) ACS were undertaken to determine the recording of cocaine use/non-use in clinical notes. Results: Knowledge study—There was no significant difference in the knowledge that cocaine was a risk factor compared to other "classical" cardiovascular risk factors, but juniors doctors were less likely to ask routinely about cocaine use compared to other "classical" risk factors (52.9% vs >90% ,respectively). Retrospective study—Cocaine use or non-use was documented in 3.7% (4/109) and 4% (2/50) of clinical notes of patients with suspected and proven ACS, respectively. Discussion: Although junior medical staff are aware that cocaine is a risk factor for ACS/AMI, they are less likely to ask about it in routine clinical practice or record its use/non-use in clinical notes. It is essential that patients presenting with suspected ACS are asked about cocaine use, since the management of these patients is different to those with ACS secondary to "classical" cardiovascular risk factors. [ABSTRACT FROM AUTHOR]

Abstract: Thrombolysis remains the most popular means of reperfusion following an acute ST-elevation myocardial infarction in the United Kingdom today. There is a wealth of evidence to support the early provision of thrombolysis care and a number of models of care delivery have been proposed to reduce the time delay from admission to hospital to administration of thrombolytic therapy. The movement of this treatment from the coronary care unit to the emergency department in association with the employment of specialist cardiac nurses has been associated with some time reductions. However the quality of evidence to support the employment of specialist cardiac nurses working outside the coronary care unit is limited. The author provides an overview of the main literature in this area outlining the models of care in operation and argues that there are lessons to be learned for future nursing research. [Copyright &y& Elsevier]

The National Service Framework (NSF) for coronary heart disease requires that patients with acute myocardial infarction should start thrombolytic therapy within 60 min of the patient making contact with the National Health Service. In an audit of 700 patients with suspected acute myocardial infarction, patients' first contact was most commonly with a general practitioner (GP) (505/700; 72 per cent), who attended on 88 per cent (446/505) of occasions when they were called. In 93 per cent (255/284) of cases where both GP and an ambulance attended, the GP arrived first, by 25 min (median). In the final audit period, median call‐to‐thrombolysis time was 90 min (26 per cent ≤60). We conclude that with existing physical and personnel resources in this semi‐rural area of Northern Ireland, the NSF standard for thrombolytic treatment is unlikely to be met in a majority of cases unless GPs adopt prehospital thrombolysis. [ABSTRACT FROM PUBLISHER]

This article comments on an emerging threat posed by khat, a shrub whose leaves have a central stimulatory effect, to the cardiovascular system of people in Great Britain. It discusses the clinical effects of khat, including increased blood pressure and heart rate and an increased incidence of coronary vasospasm and myocardial infarction. It also associates khat to cardiac rhythm disturbance, dilated cardiomyopathy, cerebrovascular ischemia and stroke.

OBJECTIVES The Global Registry of Acute Coronary Events (GRACE) registry reported that the in-hospital risk of death from non-ST elevation myocardial infarction (NSTEMI) is 5%, with an 11% mortality by 6 months. Prospective Registry of Acute Ischaemic Syndromes in the UK demonstrated that the overall risk of death from NSTEMI over 4 years is 25%. In GRACE, while 28% of patients received percutaneous intervention, only 10% received coronary artery bypass graft (CABG). Results of urgent CABG surgery following NSTEMI are difficult to interpret as these often include patients who have had STEMIs and urgent surgery. With increasing multidisciplinary assessment of patients with acute coronary syndromes (ACS), accurate data collection on the outcome of such patients could inform correct revascularization strategy. METHODS Three hundred and forty-two consecutive patients who had undergone urgent CABG from April 2004 to April 2009 at a single institution were identified. The GRACE predicted mortality was calculated from hospital records and patients categorized into three groups based upon their predicted risk. Late survival data were obtained from the UK Office of National Statistics. RESULTS The GRACE score could be calculated in 270 patients with a confirmed diagnosis of NSTEMI. Of the 304 probable patients with NSTEMI, there were 5 in-hospital deaths (1.6%). Survival at 6 months was higher than GRACE predicted mortality in all groups. At 6 months the predicted versus observed mortality in the low-risk group was 4 versus 2% (P = 0.05), in the medium-risk group it was 12.5 versus 1.9% (P = 0.0001) and in the high-risk group it was 25 versus 20% (P = 0.45). CONCLUSIONS In-hospital CABG performed after NSTEMI is associated with a low-mortality risk and survival significantly better than that predicted by the GRACE score. [ABSTRACT FROM AUTHOR]

Comorbidity returns have continued to improve, albeit slowly, with centres running Mediqal software having the highest rates of completeness.Diabetes as a primary renal diagnosis accounted for 20% of those starting RRT, but a further 7% had diabetes present as a comorbid condition. The incidence of smoking remained high at 17% of diabetic patients, which was similar to that found in non-diabetics.Twelve percent of the patients starting RRT had a previous myocardial infarction (MI) and 31% of those aged over 65 years starting RRT had ischaemic heart disease (IHD).Patients starting on peritoneal dialysis (PD) were on average 9 years younger than those on haemodialysis (HD) and had fewer comorbidities present.Patients starting RRT without any comorbidity present had a lower median estimated glomerular filtration rate (eGFR) than those with comorbid conditions.Patients with a previous MI or coronary artery bypass grafting (CABG), started RRT with slightly higher mean haemoglobin than those without comorbid conditions or other comorbid conditions.On univariate survival analysis, diabetes was not associated with an increased risk of death amongst patients aged over 65 years, possibly due to its close association with other comorbidities in this age group.In the multivariate survival analysis, the presence of ischaemic/neuropathic ulcers was the predictor of worst survival, followed by malignancy, previous MI and age per 10 year increment.Smoking was less common in both South Asian and black patients than whites (7 vs 17%) starting RRT. Twenty-three percent of both South Asian and white patients started RRT with IHD compared with only 12% of Black patients. [ABSTRACT FROM AUTHOR]

Examines the risks of an acute myocardial infarction on patients with thrombophilia in Great Britain. Increase on the level of mortality rate; Description on the physical condition of the patients; Level of survival.