Background: Atrial fibrillation (AF) is a major preventable risk factor for stroke and may be silent in elderly individuals who are at especially high risk. This paper describes the first phase of implementation of a clinical AF detection programmein a community setting. Objectives were (i) to determine the feasibility of using a handheld ECG recording system for AF detection among individuals aged 65 years or more, who have cardiovascular risk factors. (ii) to estimate the yield of previously undiagnosed atrial fibrillation cases, and the proportion of these who would be suitable for oral anticoagulation. Methods: a handheld ECG monitor was placed in each of 23 primary care practices across Scotland. Eligible patients attending for annual health checks had ECGs recorded, and the ECGs were transmitted and interpreted by two senior cardiologists. ECG quality was rated, and an adjudication made on the rhythm. For patients confirmed with AF, stroke and bleeding risk were estimated using CHA2DS2-VASc and HAS-BLED scoring tools. Results: single lead ECGs were recorded in 1805 patients (703 female and 1102 male), mean (SD) age 74.9 (7.1) years. Rhythmregularity could be assessed in 98.7% of ECGs recorded. 92 patients (5.1%) were found to have AF. Median [range] CHA2DS2-VASc score was 4 ([2-7) and median [range] HAS-BLED score was 2 (1-5). Conclusion: handheld ECG recording can be used to identify AF in the primary care setting, withminimal training. The yield was relatively high. Crown Copyright (c) 2019 Published by Elsevier B. V. All rights reserved.

The Medtronic Reveal underwent a redesign in recent years to an injectable device that could be implanted outwith a theatre environment. Given the increasing demand for monitoring we developed a cardiac physiology-led implantation and follow up service. Referrals from consultant cardiologists are

INTRODUCTION:Amiodarone is associated with significant long-lasting adverse drug reactions (ADRs). Guidelines recommend laboratory monitoring during long-term use. However, data of compliance with laboratory monitoring are lacking. AIMS:The aim of this study was to assess laboratory monitoring of liver and thyroid function during amiodarone prescribing from 1989 to 2011 in the Tayside, UK, population (approximately 400 000) in relation to National Guidelines recommending laboratory monitoring every 6 months. We also report the population-level incidence of abnormal liver and thyroid function in relation to total exposure of amiodarone. METHODS:Utilizing well-established record-linkage database, a longitudinal retrospective analysis of 1413 patients on long-term amiodarone was carried out, analyzing prescribing, biochemical, and clinical data. RESULTS:Forty-six percent (46%), 28%, and 21% of patients underwent liver, thyroid, and combined testing, respectively, in accordance with guideline recommendations. Thirteen percent and 17% of patients did not have any ALT or TSH testing, respectively. During follow-up, 117 (9.5%) patients had an ALT 3×ULN and 16% patients had an abnormal TSH, (n=125, <0.4 mU/L and n=28, >10 mU/L). One hundred and forty patients (10%) required thyroxine replacement therapy, and 40 (3%) required on hyperthyroid medication. Total amiodarone exposure increased the likelihood of abnormal biochemical testing 2.5-fold after 4 years therapy for liver and thyroid function (P<.0005). CONCLUSION:In this population-based study, adherence to laboratory monitoring guidelines was suboptimal. There was a positive correlation with total amiodarone exposure and biochemical abnormalities and development of thyroid disease compared to the general population, highlighting the need for improvement and continued amiodarone monitoring.

Cardiology patients undergo a number of investigations as part of their management. Follow-up of all these disparate investigations can be difficult in many existing hospital systems. A new system, agnostic of manufacturer, was therefore developed to integrate these results into one place. The

AimsControversy exists regarding the importance of glycaemic control in patients with type 2 diabetes mellitus (T2DM) and chronic heart failure (CHF) based on conflicting reports using single baseline glycosyated haemoglobin (HbA1c). Using the time‐weighted mean of serial HbA1c measurements has been found to be a better predictor of diabetic complications as it reflects the glycaemic burden for that individual over time. We therefore sought to confirm this in a large cohort of patients with T2DM and incident CHF.Methods and resultsA time‐weighted mean HbA1c was calculated using all HbA1c measurements following CHF diagnosis. Patients were grouped into five categories of HbA1c (≤6.0%, 6.1–7.0%, 7.1–8.0%, 8.1–9.0%, and >9.0%). The relationship between time‐weighted mean HbA1c and all‐cause death after CHF diagnosis was assessed. A total of 1447 patients with T2DM met the study criteria. During a median follow‐up of 2.8 years, there were 826 (57.1%) deaths, with a crude death rate of 155 deaths per 1000 person‐years [95% confidence interval (CI) 144–166]. A Cox regression model, adjusted for all significant predictors, with the middle HbA1c category (7.1–8.0%) as the reference, showed a U‐shaped relationship between HbA1c and outcome [HbA1c <6.0%, hazard ratio (HR) 2.5, 95% CI 1.8–3.4; HbA1c 6.1–7.0%, HR 1.4, 95% 1.1–1.7; HbA1c 8.1–9.0%, HR 1.3, 95% CI 1.0–1.6; and HbA1c >9.0%, HR 1.8, 95% CI 1.4–2.3]. Further analysis revealed a protective effect of insulin sensitizers (i.e. metformin) (HR 0.7, 95% CI 0.61–0.93) but not other drug classes.ConclusionsIn patients with T2DM and CHF, our study shows a U‐shaped relationship between HbA1c and mortality, with the lowest risk in patients with modest glycaemic control (HbA1c 7.1–8.0%) and those treated with insulin sensitizers.

Left ventricular hypertrophy (LVH) is a significant cardiac risk factor, associated with increased mortality. The impact of LVH on mortality in chronic obstructive pulmonary disease (COPD) is unknown. We evaluated the impact of LVH on mortality in COPD patients by measurement of left ventricular dimensions by echocardiography.

Background—Type 2 diabetes mellitus is an independent risk factor for heart failure development, but the relationship between incident heart failure and antecedent glycemia has not been evaluated. Methods and Results—The Genetics of Diabetes Audit and Research in Tayside Study study holds data for 8683 individuals with type 2 diabetes mellitus. Dispensed prescribing, hospital admission data, and echocardiography reports were linked to extract incident heart failure cases from December 1998 to August 2011. All available HbA1c measures until heart failure development or end of study were used to model HbA1c time-dependently. Individuals were observed from study enrolment until heart failure development or end of study. Proportional hazard regression calculated heart failure development risk associated with specific HbA1c ranges accounting for comorbidities associated with heart failure, including blood pressure, body mass index, and coronary artery disease. Seven hundred and one individuals with type 2 diabetes mellitus (8%) developed heart failure during follow up (mean 5.5 years, ±2.8 years). Time-updated analysis with longitudinal HbA1c showed that both HbA1c <6% (hazard ratio =1.60; 95% confidence interval, 1.38–1.86; P value <0.0001) and HbA1c >10% (hazard ratio =1.80; 95% confidence interval, 1.60–2.16; P value <0.0001) were independently associated with the risk of heart failure. Conclusions—Both high and low HbA1c predicted heart failure development in our cohort, forming a U-shaped relationship.

Controversy exists regarding the importance of glycaemic control in patients with type 2 diabetes mellitus (T2DM) and chronic heart failure (CHF) based on conflicting previous reports that had used a single baseline HbA1c. HbA1c variability has also been linked to vascular complications in T2DM. We

AIMS:To identify the prevalence and characteristics of recently hospitalized chronic heart failure (CHF) patients in community care who meet the indication for ivabradine.METHODS:A retrospective clinical audit of CHF patients recently hospitalized with acute decompensated heart failure (ADHF) and subsequently referred to the Tayside Heart Failure Nurse Liaison Service (THFNLS), a Scottish nurse-led community heart failure liaison service. Inclusion criteria were previous hospitalization with ADHF, subsequent referral to the THFNLS, data for ≥ 2 nurse visits, and a recorded pulse. The main outcome measure was the proportion of patients who meet the indicated criteria for ivabradine.RESULTS:In the UK, ivabradine is indicated for CHF with systolic dysfunction in patients in sinus rhythm, with a heart rate ≥ 75 bpm, and NYHA class II-class IV. After up-titration of a beta-blocker, 19.0% of patients in the full dataset (158 of 830) met the indication for ivabradine at the last visit. Of these "ivabradine-suitable" patients, 101 of 158 (63.9%) received bisoprolol "at any time" during the study period; 20 of 158 (12.7%) achieved the target dose (10 mg daily); 52 of 158 (32.9%) received 5 mg or 7.5 mg daily; and 93 of 158 (58.9%) received <5 mg daily.CONCLUSIONS:In this group of Scottish patients previously hospitalized with ADHF and under the care of a protocol-driven clinic, 19% met the indication for ivabradine and may benefit from the increased control of CHF that ivabradine can provide. Among these "ivabradine-suitable" patients, <15% achieved the target dose of beta-blockers, illustrating the substantial clinical need for a well-tolerated and effective therapy such as ivabradine.

Introduction Amiodarone is associated with significant adverse drug reactions (ADRs) and guidelines recommend continued monitoring for ADRs during long-term use. However data of compliance with monitoring guidelines is lacking. The aim of this study was to assess the monitoring of liver and thyroid function on long-term amiodarone over 22-years in Tayside and secondly, to determine the incidence of abnormal biochemical results in relation to total exposure of amiodarone. Methods Uutilizing the well-established record linkage database and the prescription-record linkage database available in Tayside, all patients who were prescribed amiodarone over the 22 years were identified. Long-term prescribing of amiodarone was defined as exposure greater than 6 months, baseline testing was defined as blood tests 6 months before or one month after commencing amiodarone and frequency of testing was performed looking at the mean number of days between testing. The test with closest temporal proximity to the commencement of amiodarone was used to identify patients with abnormal liver or/and thyroid function. Patients with baseline biochemical liver and thyroid abnormalities were excluded from the analysis. Results A total of 1413 patients (mean age 71 ± 11, 57% male) on regularly prescribed amiodarone for more than 6 months were included for final analysis. Only 46%, 27% and 21% of patients had liver, thyroid, and combined testing respectively in accordance with national guidance, though monitoring had significantly improved over the last 22 years (p < 0.0005). Importantly our data also shows that, despite monitoring guidance, patients on long-term amiodarone are at risk of hepatic and thyroid toxicity (9.5% and 16% of patients respectively) and are more likely to develop thyroid disease compared to the general population. There was a positive correlation between duration of amiodarone exposure and percentage of patients with an abnormal result (2.46 and 2.5 fold increase over 4 years for liver and thyroid dysfunction respectively .0005). Discussion Risks of developing ADR on amiodarone increase with continued exposure. Our study highlights the need for awareness and continued surveillance.

BackgroundThe use of oral anticoagulation in patients with heart failure in sinus rhythm remains controversial as previous large randomized controlled trials (RCTs) have not shown a survival benefit. However, heterogeneity exists among heart failure patients and it is possible that high‐risk subgroups may benefit from anticoagulation (warfarin). We hypothesize that one such subgroup are patients with heart failure and pulmonary hypertension (PH), conditions associated with coagulation abnormalities.MethodsWe conducted a retrospective, population‐based, longitudinal cohort study in patients with left ventricular systolic dysfunction (LVSD) and PH [defined as a right ventricular systolic pressure (RVSP) >35 mmHg] identified from echocardiograms performed between January 1994 to May 2011. This data was linked using a unique patient‐specific identifier to community‐dispensed prescriptions, hospital admissions, and mortality data. For comparison, we included patients with LVSD and no PH.ResultsA total of 2619 subjects with LVSD and a measurable RVSP were identified (mean ± SD age of 73 ± 12 years); 1606 out of 2619 had PH and 1013 out of 2619 had no PH. The overall mean follow‐up period was 2.56 ± 3.0 years. In patients with LVSD and PH, the use of warfarin was associated with an improved survival [hazard ratio (HR) = 0.72 95% confidence interval (CI) 0.58–0.90, P = 0.0003], fewer non‐cardiovascular disease‐related deaths (HR = 0.65, 95%CI 0.49–0.87, P = 0.0033 and showed a trend towards reduced cardiovascular disease‐associated mortality (HR = 0.72, 95%CI 0.51–1.02). Warfarin did not improve survival in those with LVSD with no PH.ConclusionsIn patients with both LVSD and PH, the use of warfarin is associated with a 28% reduction in mortality. Further prospective trials are required to confirm our findings.

OBJECTIVE:To determine all-cause mortality in patients with a first myocardial infarct who were treated with simvastatin compared with high-potency statin and simvastatin/ezetimibe combination. BACKGROUND:Despite statin use, residual cardiovascular risk remains. Therapeutic options include more potent statins or addition of ezetimibe. There is no clinical outcome data on the use of ezetimibe in such patients. METHODS:Retrospective longitudinal study using the United Kingdom General Practice Research Database. Patients who had survived 30 days after their first acute myocardial infarct (AMI), had not received prior statin or ezetimibe therapy and were started on a statin within 30 days of AMI were included. Three groups were identified according to their follow-up: (i) simvastatin monotherapy; (ii) high-potency statin group (patients who started on simvastatin and switched to atorvastatin or rosuvastatin); and (iii) ezetimibe/statin combination group (patients who received ezetimibe in addition to statin). RESULTS:9597 patients (57% male, mean age of 65 ± 13 years) matched study criteria: simvastatin (n=6990 (72.8%)); high-potency statin (n=1883, (19.6%)); and ezetimibe/statin combination (n=724 (7.5%)). During a mean follow-up of 3.2 years, there were 1134 (12%) deaths. In the multivariate proportional hazards model, the adjusted HR for high-potency statin and ezetimibe group were 0.72 (95% CI 0.59 to 0.88, p<0.001) and 0.96 (95% CI 0.64 to 1.43, p=0.85), respectively. A similar result was also obtained in the propensity score analysis that took into account covariates that predicted drug treatment groups. CONCLUSIONS:Patients switched to a high-potency statin had a significantly reduced mortality compared with simvastatin monotherapy. There was no observed mortality benefit in the ezetimibe group.

Background Hyperglycaemia is associated with increased risk of cardiovascular events in diabetic individuals. The relationship between glycaemic control and the development of chronic heart failure (CHF) is undefined and may have a genetic component. In this study, we aim to assess the relationship between glycaemic control and the development of CHF and examine whether genes predicting glycosylated haemoglobin levels also predicted time to development of CHF. Methods This study was carried out in the Go-DARTS population of Tayside, Scotland, using demographic, echocardiographic and prescribing data maintained by the University of Dundee. CHF incidence, determined during the study period October 1999 to August 2011, was identified by either the presence of a hospital discharge code for CHF or echocardiogram showing left ventricular systolic dysfunction and prescription of a loop diuretic. CHF cases and non-CHF controls were matched for gender and age at diabetes diagnosis. Development of CHF was modelled using conditional logistic regression using updated mean HbA1c during the study period, using age, gender and duration of diabetes as covariates. Proportional hazard regression analysis was used to determine whether published single nucleotide polymorphisms (SNPs) associated with glycaemic control predicted time to development of CHF in this population. Results Out of 8890 diabetic individuals, 759 developed CHF during the study period (mean age at diagnosis 74.2±9.6 years, 60.6% males). The adjusted OR for developing CHF in those with updated mean HbA1C greater than 6.9 was 2.14 (95% CI 1.64 to 2.8, p<0.01). Three SNPs previously associated with glycaemic control predicted time to CHF development rs6474359 (p=1.67×10–4, HR 1.90, 95% CI 1.36 to 2.67), rs7800094 (p=9.46×10–3, HR 1.23, 95% CI 1.05 to 1.45) and rs10885122 (p=0.02, HR 1.34, 95% CI 1.05 to 1.70). Conclusions These data suggest that glycaemic control is an independent risk factor for incident CHF in individuals with T2DM. Since SNPs associated with glycaemic control were also associated with CHF development this increased risk may have a genetic component.

In diabetes, hyperglycemia increases the risk of cardiovascular events. However, intensive glycemic control predicted worse outcome in recent studies. We assessed the link between glycemic control and chronic heart failure (CHF) development. We studied the diabetic population of Go-DARTS (n=8 890)

Aortic valve disease (AVD) is the most common form of valvular heart disease in the western world. The only proven therapy for severe AVD is open aortic valve replacement, with trans-catheter aortic valve implantation emerging as a promising modality to treat severe aortic stenosis in a selected group of patients. AVD has a long asymptomatic phase with symptoms occurring late in the disease and once symptoms develop, prognosis is poor. There is a growing appreciation that aortic valvular heart disease incorporates a disease process that extends beyond the valve itself leading to an aortic valvular 'heart' disease. The renin-angiotensin system is known to modulate adverse left ventricular remodeling and myocardial fibrosis, which could be caused by increased load caused by the AVD. In this review, the authors explore evidence that suggest that drugs that target the renin-angiotensin system may have a potential therapeutic role in AVD.

Background: Left ventricular hypertrophy has multiple aetiologies including diabetes and genetic factors. We aimed to identify genetic variants predicting left ventricular hypertrophy in diabetic individuals.Methods: Demographic, echocardiographic, prescribing, morbidity, mortality and genotyping databases connected with the Genetics of Diabetes Audit and Research in Tayside, Scotland project were accurately linked using a patient-specific identifier. Left ventricular hypertrophy cases were identified using echocardiographic data. Genotyping data from 973 cases and 1443 non-left ventricular hypertrophy controls were analysed, investigating whether single nucleotide polymorphisms associated with left ventricular hypertrophy in previous Genome Wide Association Studies predicted left ventricular hypertrophy in our population of individuals with type 2 diabetes. Meta-analysis assessed overall significance of these single nucleotide polymorphisms, which were also used to create gene scores. Logistic regression assessed whether these scores predicted left ventricular hypertrophy.Results: Two single nucleotide polymorphisms previously associated with left ventricular hypertrophy were significant: rs17132261: OR 2.03, 95% CI 1.10-3.73, p-value 0.02 and rs2292462: OR 0.82, 95% CI 0.73-0.93 and p-value 2.26x10(-3). Meta-analysis confirmed rs17132261 and rs2292462 were associated with left ventricular hypertrophy (p=1.03x10(-8) and p=5.86x10(-10) respectively) and one single nucleotide polymorphisms in IGF1R (rs4966014) became genome wide significant upon meta-analysis although was not significant in our study. Gene scoring based on published single nucleotide polymorphisms also predicted left ventricular hypertrophy in our study.Rs17132261, within SLC25A46, encodes a mitochondrial phosphate transporter, implying abnormal myocardial energetics contribute to left ventricular hypertrophy development. Rs2292462 lies within the obesity-implicated neuromedin B gene. Rs4966014 lies within the IGF1R1 gene. IGF1 signalling is an established factor in cardiac hypertrophy.Conclusions: We created a resource to study genetics of left ventricular hypertrophy in diabetes and validated our left ventricular hypertrophy phenotype in replicating single nucleotide polymorphisms identified by previous genome wide association studies investigating left ventricular hypertrophy.

Background Improvements in medical therapy for chronic heart failure (CHF) have resulted in an increase in the number of drugs which patients have to take. As CHF patients are often elderly with multiple comorbid conditions, the resulting polypharmacy could potentially lead to non-adherence to medications. The aim of this study was to determine the prevalence of non-adherence among CHF patients and to determine if non-adherence is associated with a poor outcome. Methods We conducted a 10 year retrospective longitudinal cohort study of CHF patients from Tayside in Scotland (population of 450 000) that were started on the angiotensin-converting enzyme (ACE) inhibitor, ramipril, after their incident CHF hospitalisation utilising our established record linkage database linking dispensed prescriptions to other datasets covering socioeconomic status, age, gender, hospital admissions and mortality data. To be included, patients with incident CHF hospitalisation had to have survived their index hospitalisation and completed a month of medication and have not switched to an angiotensin receptor blocker. Adherence was calculated as Proportion of Days Covered, with <80% deemed as non-adherence. Cross-tabulation was utilised to assess the factors associated with non-adherence and its effect on the number of repeated hospitalisation. All-cause mortality was analysed with Cox Regression models. Results 702 eligible patients (mean age, 75.5±11.3 years) entered into the analysis. 35.9% (mean age, 78.1±11.3 years, 58.7% male) of the cohort were non-adherent and 64.1% (mean age, 74.1±11.1 years, 66.7% male) were considered adherent. Factors associated with non-adherence were male gender, old age (>81 years old), presence of ischaemic heart disease (IHD), chronic pulmonary obstructive disease (COPD) and chronic kidney disease (CKD). Non-adherence was associated with increased number of repeated hospitalisation (p=0.042) and was an independent predictor of all-cause mortality (risk ratio 1.58, 95% CI 1.29 to 1.95, p<0.001). Conclusions Non-adherence to ACE inhibitor therapy was highly prevalent among CHF patients. Male patients, advanced age, presence of IHD, COPD and CKD are associated with non-adherence. Non-adherence was associated with an increase in the number of repeated hospitalisation and is a predictor of all-cause mortality.