European Journal of Preventive Cardiology

Short-term exposure to traffic-related air pollution (TRAP) has been associated with adverse cardiovascular outcomes. Physical activity (PA) in polluted air may increase pollutant uptake and increase these effects.

Crossover real-world exposure study in 28 healthy participants comparing systolic (SBP) and diastolic blood pressure (DBP) responses to four different exposure scenarios: 2 h exposure in high or low-TRAP environment, each at rest and combined with intermittent moderate PA consisting of 15 min intervals alternating rest and cycling on a stationary bicycle. Data was analyzed using mixed effect models for repeated measures.

Exposure to high TRAP was associated with higher DBP (1.1 mm/Hg, p = 0.002) post-exposure, irrespective of exercise status. Ultrafine particles (UFP) increased DBP post-exposure (0.9 mm/Hg, p = 0.004). Interquartile increases in black carbon (BC), fine particulate matter (PM₁₀ and PM_coarse), UFP, and nitric oxides (NO_x) were associated with statistically significantly higher SBP post-exposure (1.2, 1.0, 1.1, and 1.1 mm/Hg, respectively). Intermittent PA compared with rest was associated with lower SBP post-exposure (−2.4 mm/Hg, p < 0.001). PA lowered SBP more after exposure to the low-TRAP site (−2.3 mm/Hg) compared with the high-TRAP site (−1.6 mm/Hg). We only found evidence of an interaction between PA and both PM₁₀ and PM_coarse, increasing SBP.

Both SBP and DBP increase after exposure to TRAP. Intermittent PA attenuates the TRAP-related increases in SBP, with the exception of PM₁₀ and PM_coarse, which potentiate these increases. We showed that in low-TRAP environments intermittent PA has stronger beneficial effects on SBP than in high-TRAP environments.

Renal denervation (RDN) is believed to reduce sympathetic nerve activity and is a potential treatment for resistant hypertension. The present study investigated the effects of RDN on end organ damage (EOD).

The present study was a prospective cohort study (registered as NCT01427049).

Uncontrolled hypertensive patients underwent a work-up prior to and one year after RDN. Cardiac magnetic resonance (CMR) imaging was used to determine left ventricular (LV)-mass; pulse wave analysis and pulse wave velocity (PWV) were used for evaluation of central blood pressure (BP) and arterial stiffness and 24-hour urine was collected for assessment of urinary albumin excretion. The 24-hour ambulatory BP measurement (ABPM) was used to evaluate the effect of RDN on BP.

Fifty-four patients gave informed consent for study participation. Mean age was 58 ± 10 years, 50% were male. One year after RDN, mean ABPM decreased by 7 ± 18/5 ± 11 mm Hg (p = 0.01/p < 0.01). In the patients followed-up in a standardised fashion ABPM decreased by 5 ± 18/4 ± 12 mm Hg (n = 34; p = 0.11/p = 0.09). Mean body surface area indexed LV-mass decreased by 3.3 ± 11.5 g/m² (corresponding to a 3 ± 11% reduction; p = 0.09). PWV increased by 2.9 (−2.2 to +6.1) m/s (p = 0.04). Augmentation index corrected for 75 beats per min did not change (median increase 3.0 (−7 to +17) mm Hg; p = 0.89). Urinary albumin excretion did not change during follow-up (mean decrease 10 ± 117 mg/24 hour; p = 0.61).

In the current study, we observed a modest effect from renal denervation. Moreover, RDN did not result in a statistical significant effect on end organ damage 12 months after treatment.

Transcatheter aortic-valve implantation (TAVI) is an established alternative therapy in patients with severe aortic stenosis and a high surgical risk. Despite a rapid growth in its use, very few data exist about the efficacy of cardiac rehabilitation (CR) in these patients. We assessed the hypothesis that patients after TAVI benefit from CR, compared to patients after surgical aortic-valve replacement (sAVR).

From September 2009 to August 2011, 442 consecutive patients after TAVI (n = 76) or sAVR (n = 366) were referred to a 3-week CR. Data regarding patient characteristics as well as changes of functional (6-min walk test. 6-MWT), bicycle exercise test), and emotional status (Hospital Anxiety and Depression Scale) were retrospectively evaluated and compared between groups after propensity score adjustment.

Patients after TAVI were significantly older (p < 0.001), more female (p < 0.001), and had more often coronary artery disease (p = 0.027), renal failure (p = 0.012) and a pacemaker (p = 0.032). During CR, distance in 6-MWT (both groups p ≤ 0.001) and exercise capacity (sAVR p ≤ 0.001, TAVI p ≤ 0.05) significantly increased in both groups. Only patients after sAVR demonstrated a significant reduction in anxiety and depression (p ≤ 0.001). After propensity scores adjustment, changes were not significantly different between sAVR and TAVI, with the exception of 6-MWT (p = 0.004).

Patients after TAVI benefit from cardiac rehabilitation despite their older age and comorbidities. CR is a helpful tool to maintain independency for daily life activities and participation in socio-cultural life.

In coronary artery disease (CAD), circulating angiogenic factors have been seen to increase, possibly as a response to ischaemia. Regular physical activity (PA) is recommended for prevention and treatment of CAD, but more research is needed to optimise PA regimes. We investigated the effect of home-based high frequency exercise (HFE) on angiogenic cytokines and cardiac markers in patients with stable CAD.

This was a randomised case-control study

Sixty-two patients, with stable CAD, were randomised to HFE (n = 33), (aerobic exercise 70% of max, 30 min, five times/week and resistance exercise three times/week), performed at home, or usual lifestyle (control, n = 29). After eight weeks, percutaneous coronary intervention (PCI) was performed in both groups, and the HFE group continued another six months of exercise. Serum vascular endothelial growth factor (VEGF) and stromal derived factor-1 (SDF-1), plasma N-terminal-brain natriuretic peptide (NT-proBNP), high-sensitive troponin T (TnT) and copeptin were analysed.

Data are presented as median (25^th, 75^th percentile) of relative changes (%) from baseline. Values of p are given for the difference between the HFE and controls. HFE decreased circulating VEGF levels, before PCI (−5% (−15%, −2%)), while VEGF levels increased in the control group (5% (−3%, 20%) p = 0.004). A significant difference in VEGF remained at three months post-PCI (HFE (−1%(−12%, 5%), control (7% (0%, 14%), p = 0.04), but not at six months after PCI. SDF-1, NT-proBNP, TnT and copeptin levels did not differ significantly. In addition, VEGF levels were positively correlated to NT pro-BNP.

Home-based HFE decreased circulating VEGF in patients with stable CAD, suggesting a reduced ischaemic burden. HFE does not increase markers of cardiac dysfunction, suggesting that it is a safe therapeutic intervention in these patients.

Despite suffering from poor prognosis, progressive exercise intolerance, and impaired quality of life (QoL), effective therapeutic strategies in heart failure with preserved ejection fraction (HFpEF) are sparse. Exercise training (ET) improves physical QoL in HFpEF, but the effects on other aspects of QoL are unknown.

The multicentre, prospective, randomized, controlled Exercise training in Diastolic Heart Failure Pilot study included 64 HFpEF patients (65 ± 7 years, 56% female). They were randomized to supervised endurance/resistance training in addition to usual care (ET, n = 44) or usual care alone (UC, n = 20). At baseline and after 3 months, QoL was assessed (36-item Short-form Health Survey (SF-36), Minnesota Living With Heart Failure Questionnaire (MLWHFQ), and Patient Health Questionnaire (PHQ-9).

Exercise improved the following SF-36 dimensions: physical functioning (p < 0.001, p = 0.001 vs. UC), bodily pain (p = 0.046), general health perception (p < 0.001, p = 0.016 vs. UC), general mental health (p =  0.002), vitality (p = 0.003), social functioning (p < 0.001) physical (p < 0.001, p = 0.001 vs. UC), and mental component score (p = 0.030). ET did not improve role limitations due to physical and emotional problems. The MLWHFQ total scale (p < 0.001) and the MLWHFQ physical limitation scale (p < 0.001, p = 0.04 vs. UC) also improved with ET. The MLWHFQ emotional limitation scale did not change with ET. With ET, also the PHQ-9 total score improved significantly (p = 0.004, p = 0.735 vs. UC).

In patients with HFpEF, exercise training improved emotional status, physical and social dimensions of QoL as well as symptoms of depression from pre to post test. Physical dimensions of QoL and general health perception also improved significantly with exercise in comparison to usual care.

Low vitamin D status is associated with increased risk of cardiovascular disease and may be involved in atherosclerosis. Our aim was to assess the association between vitamin D status and the progression of coronary artery disease (CAD).

We measured 25-hydroxyvitamin D3 (25OHD3) by liquid chromatography tandem mass spectrometry (LC-MS/MS) in plasma from 348 participants with established CAD (84% males, mean ± standard deviation (SD) age 60 ± 10 years) of the Western Norway B-vitamin Intervention Trial (WENBIT, 1999–2006). The patients underwent invasive coronary angiography (CA) and percutaneous coronary intervention at baseline and a second CA after 302 ± 79 days of follow-up. From the angiograms, minimal lumen diameter (MLD) and diameter stenosis (DS) of atherosclerotic lesions were obtained. Significant CAD in non-intervened vessels was found in 309 coronary arteries from 183 participants either at baseline and/or at follow-up. To assess the association between levels of 25OHD3 and CAD progression in non-intervened vessels, we applied a linear quantile fitted mixed effects model with MLD or DS measured at follow-up as a function of continuous 25OHD3 concentrations.

There were no statistically significant associations between plasma 25OHD3 concentrations (median: 63.9, 95% confidence interval (CI): 48.1–78.5 nmol/l) measured at baseline and the follow-up measures of either MLD (estimated effect per 10 nmol/l increase of 25OHD3 and 95% CI: –0.015 (−0.032–0.002) mm, p = 0.088) or DS (0.225 (−0.354–0.804) percentage points, p = 0.444). Multivariate adjustment did not alter these results.

Plasma 25OHD3 levels were not associated with ‘one-year’ progression of CAD, assessed by CA in statin-treated patients.

To assess the gender differences in correlation lipoprotein(a) concentration with the extent of coronary artery disease in patients with established coronary artery disease.

Blood lipids and lipoprotein(a) concentrations were measured in 351 consecutive patients (256 men and 95 women) who underwent coronary angiography between January and May 2010, and who had established coronary atherosclerosis (angiography score >1). A modified angiographic Gensini Score was used.

Mean angiographic score was 19.6 in men and 15.0 in women. Men had lower mean high-density lipoprotein cholesterol level than women (1.05 vs. 1.18 mmol/l) and lower mean apolipoprotein A level (1.41 vs. 1.53 g/l). Mean lipoprotein(a) level was higher in men than women (307.1 vs. 282.7 mg/l). Significant inverse correlation between high-density lipoprotein cholesterol and apoA with angiographic score was identified in women (r = −0.23, p = 0.028 and r = −0.26, p = 0.025), but not in men. Lipoprotein(a) level correlated significantly with angiographic score only in men (r = 0.168, p = 0.0185).

Gender differences were identified in patients with established coronary atherosclerosis in the relation of blood lipids and lipoprotein(a) levels with the extent of coronary artery disease.

Plasma choline has been associated with cardiovascular disease and nonalcoholic steatohepatitis.

We sought to study relations of plasma choline and its metabolite betaine to long-term risk of acute myocardial infarction (AMI) and all-cause mortality according to smoking status, in patients undergoing coronary angiography for stable angina pectoris.

Samples were obtained before angiography from 2568 patients who were subsequently randomized in the Western Norway B-Vitamin Intervention Trial (WENBIT). Hazard ratios (HR) were calculated using multivariate Cox-regression and p-values were reported for trends over quartiles.

Plasma concentrations of choline, but not betaine, were lower in smokers, and choline was positively associated with C-reactive protein and troponin T in nonsmokers, but not in smokers (p for interaction <0.03). During a follow up of 4.8 ± 1.4 (mean ± SD) years, 8.3% suffered from AMI and 6.1% died. In the total population, choline was not associated with AMI or all-cause mortality. However, comparing the highest vs. the lowest quartiles, plasma choline was associated with increased risk of AMI in nonsmokers (HR 2.63, 95% CI 1.56 to 5.51; p for trend = 0.013) and no risk in smokers (p for interaction < 0.001). Plasma choline significantly improved discrimination and reclassification when added to established cardiovascular risk factors. Plasma betaine was not associated with either endpoint.

In patients with stable angina pectoris, elevated plasma choline is associated with elevated troponin levels and increased risk of AMI in nonsmokers. These results motivate further research into the relation between choline metabolism, smoking, and atherothrombosis.

Low ankle–brachial index (ABI) is a predictor of increased mortality. The impact of a high ABI on mortality is less studied. Moreover, diabetes is frequently associated with high ABI and, because of specific mechanisms in diabetic vascular diseases, the relationship with prognosis may be unique. Therefore, our aim was to compare mortality in individuals with and without diabetes according to abnormally low and high ABI.

We studied the association between ABI and all-cause and cardiovascular mortality in 6986 participants from the REACH registry, a cohort of 45 years and older stable outpatients at high cardiovascular risk (2875 (41.1%) with diabetes) followed for 4 years.

ABI was normal (0.91–1.29) in 49.5%, low (≤0.9) in 47.5%, and high (≥1.3) in 2.9% of participants. During follow up, 9.9% of participants died (6.5% from cardiovascular causes). A low ABI was associated with cardiovascular mortality (adjusted hazard ratio, HR, 1.98, 95% CI 1.62–2.41) and all-cause mortality (HR 2.01, 95% CI 1.72–2.36), without heterogeneity according to diabetes. In contrast, high ABI was associated with higher risk of all-cause mortality in individuals with diabetes (HR 2.11, 95% CI 1.16–3.84), but not without diabetes (HR 0.82, 95% CI 0.36–1.85; p-value for interaction 0.07). The trend was similar for cardiovascular mortality (HR 2.13, 95% CI 1.03–4.44 and HR 1.05, 95% CI 0.43–2.59 with and without diabetes, respectively; p-value for interaction 0.24).

In the REACH registry, low ABI was associated with mortality, similarly in individuals without and with diabetes, whereas the association with high ABI was only observed in patients with diabetes.

Since decades, oral anticoagulation (OAC) with vitamin K antagonists (VKA) is an established therapy for both prevention and treatment of thromboembolism in daily clinical routine. Increasing life expectancy, demographic changes, and novel oral anticoagulants have led to an increasing complexity of medical therapy. However, data on quality and management of VKA therapy with phenprocoumon in current medical care are limited. Our aim is to investigate the quality of OAC with VKA in current health care and to evaluate the potential for improvements.

The investigator-initiated thrombEVAL study programme comprises two cohorts of patients treated with vitamin K antagonists for oral anticoagulation therapy in real-life settings: a multicentre cohort of patients in regular medical care and a multilocal, single-centre cohort of patients in a telemedicine-based coagulation service. The study programme is expected to enrol a total number of approximately 2000 to 2500 patients. Both cohorts will build on a detailed clinical assessment of participants and anticoagulation therapy at study enrolment. Subsequently active and passive follow-up investigations are carried out to document and validate complications of the treatment. The primary short-term outcome is the distribution of time in therapeutic range; the primary long-term outcome comprises the composite of stroke, systemic embolism, myocardial infarction, major and clinically relevant bleeding, and death.

The thrombEVAL project will provide a large prospective observational cohort of patients predominantly treated with phenprocoumon. It will evaluate the quality of oral anticoagulation in regular medical care and a telemedicine-based coagulation service.

Although substantial evidence relates reduced exercise heart rate (HR) reserve and recovery to a higher risk of all-cause mortality, a combined indicator of these variables has not been explored. Our aim was to combine HR reserve and recovery into a single index and to assess its utility to predict all-cause mortality.

Retrospective cohort analysis.

Participants were 1476 subjects (937 males) aged between 41 and 79 years who completed a maximal cycle cardiopulmonary exercise test while not using medication with negative chronotropic effects or having an implantable cardiac pacemaker. HR reserve (HR maximum – HR resting) and recovery (HR maximum – HR at 1-min post exercise) were calculated and divided into quintiles. Quintile rankings were summed yielding an exercise HR gradient (EHRG) ranging from 2 to 10, reflecting the magnitude of on- and off-HR transients to exercise. Survival analyses were undertaken using EHRG scores and HR reserve and recovery in the lowest quintiles (Q1).

During a mean follow up of 7.3 years, 44 participants died (3.1%). There was an inverse trend for EHRG scores and death rate (p < 0.05) that increased from 1.2% to 13.5%, respectively, for scores 10 and 2. An EHRG score of 2 was a better predictor of all-cause mortality than either Q1 for HR reserve (<80 bpm) or HR recovery alone (<27 bpm): age-adjusted hazard ratios: 3.53 (p = 0.011), 2.52 (p < 0.05), and 2.57 (p < 0.05), respectively.

EHRG, a novel index combining HR reserve and HR recovery, is a better indicator of mortality risk than either response alone.

a negative peak supine bicycle exercise stress echocardiography (ESE) was shown to have a long-term favourable prognostic value. Data on the long-term prognosis of ischaemic electrocardiographic (ISECG) changes in the setting of a negative peak supine bicycle ESE are lacking.

we evaluated the prognostic value of negative peak supine bicycle ESE with or without concomitant ISECG changes in a referral population evaluated for chest pain after an inconclusive first-line work-up including clinical evaluation and exercise ECG stress.

from 2003 to 2010, patients who underwent a peak supine bicycle ESE and were deemed to be negative were evaluated. Two groups based on concomitant stress ECG tracing were analysed – those with normal stress ECG and those with ISECG changes. The primary endpoint was cumulative incidence of cardiovascular death, hospitalizations for acute coronary syndrome and coronary revascularizations.

a total of 371 patients (mean age 59.1 ± 12.1 years, 49.9% women) were studied. Of those, 141 (38.0%) had concomitant ISECG changes. Mean follow-up was 3.46 ± 1.76 years. The primary endpoint occurred in 3.0% of patients, (2.2% in those with normal stress ECG, and in 4.3% with ISECG changes, p = 0.251); with unadjusted hazard ratio for primary endpoint of 2.04 (95%CI 0.62–6.69, p = 0.239) in patients with ISECG changes compared to those with normal stress ECG.

in an outpatient population without known CAD evaluated for chest pain after inconclusive first-line work-up, a negative peak supine bicycle ESE confers an excellent prognosis regardless of the nature of concomitant stress ECG abnormalities.

heart failure is a major risk factor for cardiovascular mortality, for which n-3 fatty acids may have beneficial effects. We examined the effect of marine eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and plant-derived alpha-linolenic acid (ALA) on N-Terminal-pro Brain Natriuretic Peptide (NT-proBNP), a biomarker of heart failure.

we randomly assigned 4837 post-myocardial infarction patients, aged 60–80 years (82% men), to margarines supplemented with a targeted additional intake of 400 mg/day EPA and DHA, 2 g/day ALA, EPA-DHA plus ALA, or placebo for 40 months. In a random selection of 639 patients, NT-proBNP was determined both at baseline and at the end of follow-up. NT-proBNP was log_e-transformed and analysed by type of treatment using analysis of covariance adjusting for baseline NT-proNBP.

patients consumed on average 19.8 g margarine/day, providing an additional amount of 238 mg/day EPA with 158 mg/day DHA, 1.98 g/day ALA, or both, in the active-treatment groups. In the placebo group, the geometric mean level NT-proBNP increased from 245 ng/l (95%-confidence interval [CI]: 207–290) to 294 ng/l (95%-CI: 244–352) after 40 months (p = 0.001). NT-proBNP levels were not affected by ALA (+8% versus placebo; 95%-CI: −8% to +25%; p = 0.34), EPA-DHA (+2% versus placebo; 95%-CI: −14% to +18%; p = 0.78), nor EPA-DHA plus ALA (+9% versus placebo; 95%-CI: −8% to +25%; p = 0.31) treatment.

supplementation with modest amounts of EPA-DHA, with or without ALA, did not have a significant effect on NT-proBNP levels in patients with a history of myocardial infarction.

Physical activity has long been proposed as an important modifiable cardiovascular risk factor in adults. We assessed whether physical activity already has an effect on childhood vasculature.

In the Wheezing-Illnesses-Study-in-Leidsche-Rijn birth cohort, we performed vascular ultrasound to measure carotid intima–media thickness (cIMT) and functional properties (distensibility, elastic modulus) at 5 and 8 years of age. Child typical physical activities were inquired using a questionnaire completed by parents. Linear regression was used with physical activity level, expressed as a standardized value of time-weighted metabolic equivalent (MET) as the independent variable and vascular properties as dependent variables with further confounder adjustment and evaluation for possible body mass index and sex effect modifications.

In 595 5-year-old children and in 237 of those who had reached the age of 8 years, we did not find statistically significant associations between total time-weighted MET and each vascular parameter, neither in pooled nor stratified analysis. However, sport activities were associated with thinner cIMT (−3.20 µm/SD, 95% CI −6.34, −0.22, p = 0.04) at 5 years of age; a similar pattern was seen for organized sport. This effect was strongest in children in the highest body mass index tertile (−5.38 µm/SD, 95% CI −10.54, −0.19, p = 0.04). At the age of 8 years, higher sport level tended to be associated with higher vascular distensibility (2.64 × 10³ kPa/SD, 95% CI −0.18, 5.45, p = 0.07) although this was not statistically significant.

Sport activity may have beneficial effects on arteries of young children, particularly those with higher relative body weight.

To evaluate the impact of covariates on performance accuracy of the Beck Depression Inventory II (BDI-II) and to determine the optimal cut-off score for the BDI-II in cardiac outpatients. Differences of optimal cut-off scores were also verified across covariate subgroups.

Prospective cross-sectional study at the Department of Nuclear Medicine of the Montreal Heart Institute (Quebec, Canada).

A total of 750 adult cardiac outpatients (mean ± SD age 58 ± 10 years, 31% women) completed the BDI-II and the Primary Care Evaluation of Mental Disorders (PRIME-MD; a psychiatric interview used as the reference standard for determining diagnosis of major depressive disorder). The receiver operating characteristics (ROC) curve of the BDI-II was adjusted for age, sex, level of education, smoking status, obesity, anxiety disorder, psychotropic medication, and history of coronary artery disease. The ROC analyses were conducted to determine optimal cut-off scores.

Forty-two (6%) patients met criteria for current major depressive disorder according to the PRIME-MD. After adjusted for covariates, the area under the ROC curve was significantly smaller than the unadjusted curve (0.76, 95% CI 0.66 to 0.85 vs. 0.84, 95% CI 0.77 to 0.89; ΔAUC = −0.07, 95% CI −0.13 to −0.02). While the optimal cut-off score was 10 for the total sample (sensitivity 83%, specificity 73%), the analyses indicated different cut-off scores across covariate subgroups: e.g. sex (women 13; men 10), and anxiety disorders (yes 15; no 10).

BDI-II is a good screening instrument for depression in cardiac outpatients. However, the present results suggest that covariates can affect the classification accuracy of the BDI-II’s original recommended cut-off score. Scholars and clinicians should be aware of the principle that a screening score established in one population may not be relevant to another.

Left ventricular hypertrophy (LVH) has not been evaluated for reclassification improvement in the intermediate Framingham risk category for incident hard coronary events in a large multi ethnic population free of cardiovascular disease at baseline.

A post-hoc analysis on the Multi Ethnic Study of Atherosclerosis (MESA) dataset (n = 4921) was performed.

LVH was defined as the upper 95 th percentile of cardiac magnetic resonance imaging derived left ventricular mass (LVM) indexed based on body surface area (BSA) and height. Multivariate Cox proportional hazards models were used to assess the independent association between LVH and composite outcomes like all cardiovascular disease (CVDa) and hard coronary heart disease (CHDh) events over a mean follow-up period of 4.5 years. To assess the incremental value of LVH over traditional CV risk factors for CHDh prediction, we compared the discrimination, calibration and net reclassification index (NRI) of models comprising of traditional CV risk factors with and without LVH.

LVH derived from LVM indexed by BSA (LVH-BSA) and height^1.7(LVH-height) showed an independent association with CVDa (LVH-BSA: hazard ratio (HR) 1.52, 95% confidence interval (CI) 1.05–2.20, p = 0.03; LVH-height^1.7: HR 1.58, 95% CI 1.14–2.18, p = 0.012) and CHDh (LVH-BSA: HR 2.36, 95% CI 1.37–4.04, p = 0.002; LVH-height^1.7: HR: 1.95, 95% CI: 1.17–3.26, p = 0.01). Addition of LVH to the model based on traditional CV risk factors demonstrated no significant improvement in NRI for CHDh in either the entire cohort (LVH-BSA: NRI 1.7%, 95% CI: –8.3% to 11.7%, p = 0.74; LVH-height^1.7: NRI 2.7%, 95% CI: –5.8% to 11.3%, p = 0.62) or the intermediate risk group (LVH-BSA: NRI 12.0%, 95% CI: –5.7% to 29.8%, p = 0.19; LVH-height^1.7: NRI 14.5%, 0.1% to 28.8%, p = 0.05).

Although an independent predictor of cardiovascular events, LVH does not lead to clinically meaningful reclassification of the overall and intermediate risk population for CHDh.