Prognostic value of ST-T abnormalities and left high R waves with cardiovascular mortality in Japanese (24-year follow-up of NIPPON DATA80)

Little is known about the prognostic value of ST-segment depression and/or T wave (ST-T abnormalities) with or without left high R waves on electrocardiogram recorded at rest for death from cardiovascular disease (CVD) in Asian populations. Japanese participants without a history of CVD and free of major electrocardiographic (ECG) abnormalities were followed for 24 years. Subjects were divided into 4 groups based on baseline ECG findings: isolated left high R waves, isolated ST-T abnormalities, ST-T abnormalities with left high R waves, and normal electrocardiogram. Cox proportional hazard model was used to estimate risk of CVD mortality in groups with ECG abnormalities compared to the normal group. Of 8,572 participants (44.4% men, mean age 49.5 years; 55.6% women, mean age 49.4 years), 1,142 had isolated left high R waves, 292 had isolated ST-T abnormalities, and 128 had ST-T abnormalities with left high R waves at baseline. Multivariable-adjusted hazard ratios of ST-T abnormalities with left high R waves for CVD mortality were 1.95 (95% confidence interval 1.25 to 3.04) in men and 2.68 (95% confidence interval 1.81 to 3.97) in women. Isolated ST-T abnormalities increased the risk for CVD death by 1.66 times (95% confidence interval 1.01 to 2.71) in men and 1.62 times (95% confidence interval 1.18 to 2.24) in women. Association of ECG abnormalities with CVD mortality was independent of age, body mass index, systolic blood pressure, serum cholesterol, blood glucose, smoking and drinking, and antihypertensive medication. In conclusion, ST-T abnormalities with or without left high R waves on electrocardiogram recorded at rest constitute an independent predictor of CVD mortality in Japanese men and women.     

Transthoracic echocardiographic abnormalities in asymptomatic diabetic patients: association with microalbuminuria and silent coronary artery disease

Aims

This study aimed to assess, on routine echocardiography, cardiac left ventricular (LV) disorders, their determinants and their role in the screening process of silent myocardial ischaemia (SMI) in asymptomatic diabetic patients.

Methods

A total of 586 asymptomatic diabetic patients with one or more additional cardiovascular risk factors, but no history of heart failure or myocardial infarction, prospectively underwent rest echocardiography and myocardial scintigraphy. Those with SMI (abnormal scintigraphy) were subsequently screened for angiographic coronary artery disease (CAD).

Results

LV hypertrophy, LV dilatation, systolic dysfunction and hypokinesia were found in 33.6, 8.6, 3.2 and 6.1%, respectively, of the study population. SMI was found in 156 (26.6%) patients, 55 of whom had silent CAD. On multivariate analysis, age (OR: 1.03 [1.00–1.05], P = 0.02), microalbuminuria (OR: 2.2 [1.4–3.2], P < 0.0001) and silent CAD (OR: 2.4 [1.3–4.6], P = 0.007) were predictive of LV hypertrophy. Creatinine clearance (OR: 0.97 [0.96–0.99], P = 0.002) and silent CAD (OR: 3.7 [1.3–10.0]) were associated with LV dilatation. LV systolic dysfunction was associated with microalbuminuria (OR: 3.8 [1.3–11.4], P = 0.02) and silent CAD (OR: 3.8 [1.1–12.6], P = 0.03). Hypokinesia was associated with retinopathy (OR: 2.4 [1.1–5.4], P = 0.04), microalbuminuria (OR: 2.3 [1.1–5.0], P = 0.04) and LV dilatation (OR: 3.0 [1.1–8.1], P = 0.03). In patients with SMI, the positive predictive value of LV hypertrophy associated with another echocardiographic abnormality (n = 19) for CAD was 63.2%.

Conclusion

LV hypertrophy was found in one-third of asymptomatic diabetic patients, while LV dilatation, systolic dysfunction or hypokinesia was seen in < 10%. The main predictors of LV abnormalities were microalbuminuria and silent CAD. The presence of LV hypertrophy with another abnormality should raise the possibility of the presence of silent CAD.     

Prevalence of ECG abnormalities in people with type 2 diabetes: The Hoorn Diabetes Care System cohort

AimsThe American Diabetes Association, and the joint European Society of Cardiology and European Association for the Study of Diabetes guidelines recommend a resting ECG in people with type 2 diabetes with hypertension or suspected cardiovascular disease (CVD). However, knowledge on the prevalence of ECG abnormalities is incomplete. We aimed to analyse the prevalence of ECG abnormalities and their cross-sectional associations with cardiovascular risk factors in people with type 2 diabetes.MethodsWe used data of the Diabetes Care System cohort obtained in 2018. ECG abnormalities were defined using the Minnesota Classification and categorised into types of abnormalities. The prevalence was calculated for the total population (n = 8068) and the subgroup of people without a history of CVD (n = 6494). Logistic regression models were used to asses cross-sectional associations.ResultsApproximately one-third of the total population had minor (16.0%) or major (13.1%) ECG abnormalities. Of the participants without a CVD history, approximately one-quarter had minor (14.9%) or major (9.1%) ECG abnormalities, and for those with hypertension or very high CVD risk, the prevalence was 27.5% and 39.6%, respectively. ECG abnormalities were significantly and consistently associated with established CVD risk factors.ConclusionsResting ECG abnormalities are common in all people with type 2 diabetes (29.1%), including those without a history of CVD (24.0%), and their prevalence is related to traditional cardiovascular risk factors such as older age, male sex, hypertension, lower HDL cholesterol, higher BMI, and smoking behaviour.     

Association between sleep apnea, snoring, incident cardiovascular events and all-cause mortality in an adult population: MESA

Background

We assessed the association between sleep apnea, snoring, incident cardiovascular (CV) events and all-cause mortality in the Multi Ethnic Study of Atherosclerosis (MESA) cohort.

Methods

Out of 5338 respondents to a sleep questionnaire administered during the second MESA exam period, 208 had physician diagnosed sleep apnea (PDSA), 1452 were habitual snorers (HS) and 3678 were neither a habitual snorer nor had PDSA (normal participants). Cox proportional hazard analysis was used to assess the associations adjusting for age, gender, race/ethnicity, smoking, diabetes mellitus, total cholesterol, HDL, triglycerides, BMI, current alcohol use, benzodiazepine use, BP medications and statin use.

Results

Over a 7.5 year average follow-up period, 310 adjudicated CV events including MI, stroke, angina, resuscitated cardiac arrest, stroke death and CVD death and 189 deaths occurred. Compared to HS, PDSA was associated with higher incident CV rates in both univariate and multivariable models [hazard ratio (95%); 1.89 (1.22–2.93), p = 0.004 and 1.91 (1.20–3.04), p = 0.007, respectively]. PDSA was also associated with a higher death rates compared with HS [hazard ratio (95%); 2.13 (1.25–3.63), p = 0.006 and 2.70 (1.52–4.79), p = 0.007, respectively]. Compared with normal participants, PDSA had higher incident CV event rates in both univariate and multivariable models [hazard ratio (95%); 2.23 [1.39–3.60], p = 0.001 and 2.16 [1.30–3.58], p = 0.003, respectively]. Similarly, PDSA had a higher death rate compared with normal participants in both the univariate and multivariable models [hazard ratio (95% CI); 2.44 (1.36–4.37), p = 0.003 and 2.71 (1.45–5.08), p = 0.002, respectively]. Habitual snorers had similar incident CV event rates and death rates in both univariate and multivariable models compared with normal participants.

Conclusion

PDSA but not habitual snoring was associated with high incident CV events and all-cause mortality in a multi-ethnic population based study of adults free of clinical CV disease at baseline.     

Effect of intensive lipid‐lowering therapy on cardiovascular outcome in patients with and those without inflammatory joint disease

Objective

To examine the effect of intensive lipid‐lowering therapy on a composite cardiovascular outcome (cardiovascular disease [CVD]), consisting of mortality and morbidity end points, in patients with inflammatory joint disease (rheumatoid arthritis [RA], ankylosing spondylitis [AS], or psoriatic arthritis [PsA]) by post hoc analysis of 2 prospective trials of statins with a secondary end point of CVD outcome (the Treating to New Targets [TNT] and Incremental Decrease in End Points Through Aggressive Lipid Lowering [IDEAL] studies).

Methods

Of the 18,889 patients participating in the 2 trials, 199 had RA, 46 had AS, and 35 had PsA. Lipid‐lowering therapy consisted of an intensive regimen of atorvastatin 80 mg or a conventional/low‐dose regimen of atorvastatin 10 mg or simvastatin 20–40 mg. The median duration of followup was nearly 5 years. Changes in lipid levels were examined by analyses of covariance. The effect on CVD was examined by Cox regression analyses, and heterogeneity tests were performed.

Results

Patients with RA and those with AS had lower baseline cholesterol levels than patients without inflammatory joint disease (least squares mean ± SEM 180.7 ± 2.3 mg/dl and 176.5 ± 4.7 mg/dl, respectively, versus 185.6 ± 0.2 mg/dl; P = 0.03 and P = 0.05, respectively). Statin treatment led to a comparable decrease in lipid levels and a 20% reduction in overall risk of CVD in both patients with and those without inflammatory joint disease.

Conclusion

Our findings indicate that patients with and those without inflammatory joint disease experience comparable lipid‐lowering effects and CVD risk reduction after intensive treatment with statins.

     

Association of IL-6 and a Functional Polymorphism in the IL-6 Gene with Cardiovascular Events in Patients with CKD

Background and objectives

High serum IL-6 is a major risk factor for cardiovascular disease (CVD) in the general population. This cytokine is substantially increased in patients with CKD, but it is still unknown whether the link between IL-6 and CVD in CKD is causal in nature.

Design, setting, participants, & measurements

In a cohort of 755 patients with stages 2–5 CKD, consecutively recruited from 22 nephrology units in southern Italy, this study assessed the relationship of serum IL-6 with history of CVD, as well as with incident cardiovascular (CV) events (mean follow up±SD, 31±10 months) and used the functional polymorphism (−174 G/C) in the promoter of the IL-6 gene to investigate whether the link between IL-6 and CV events is causal.

Results

In adjusted analyses, serum IL-6 above the median value was associated with history of CVD (P<0.001) and predicted the incidence rate of CV events (hazard ratio, 1.66; 95% confidence interval [95% CI], 1.11 to 2.49; P=0.01). Patients homozygous for the risk allele (C) of the −174 G/C polymorphism had higher levels of IL-6 than did those with other genotypes (P=0.04). Homozygous CC patients more frequently had a history of CVD (odds ratio, 2.15; 95% CI, 1.15 to 4.00; P=0.02) as well as a 87% higher rate of incident CV events (hazard ratio, 1.87; 95% CI, 1.02 to 3.44; P=0.04) compared with other genotypes.

Conclusions

In patients with stages 2–5 CKD, high serum IL-6 is associated with history of CVD and predicts incident CV events. The parallel relationship with history of CVD and incident CV events of the −174 G/C polymorphism in the IL-6 gene suggests that IL-6 may be causally involved in the high CV risk in this population.     

Factors associated with failure to identify the culprit artery by the electrocardiogram in inferior ST-elevation myocardial infarction

Background

Right and left circumflex coronary artery occlusions cause inferior myocardial infarction. To improve the targeting of diagnostic and therapeutic measures individually, factors interfering with identification of the culprit artery by the electrocardiogram (ECG) were explored.

Methods

Patients with inferior preinfarction syndrome (n = 266) were included to the Danish Trial in Acute Myocardial Infarction-2 substudy. The culprit vessel was predicted by the ECG, and findings were correlated with angiography. Factors associated with false identification of the culprit artery by the ECG were examined.

Results

Electrocardiogram criteria for right coronary artery occlusion to predict coronary angiography findings had sensitivity, specificity, and positive and negative predictive values of 95%, 52%, 84%, and 81%. For left circumflex coronary artery occlusion, the corresponding values were 51%, 93%, 70%, and 85%, respectively. False ECG identification of the culprit artery was independently associated with left coronary dominance (P < .001; odds ratio [OR], 22.0; 95% confidence interval [CI], 7.2-67.0), multivessel disease (P = .035; OR, 2.2; 95% CI, 1.1-4.7), and absence of proximal occlusion pattern in the ECG (P = .003; OR, 4.0; 95% CI, 1.6-9.8).

Conclusions

Left coronary artery dominance, multivessel disease, and absence of ECG signs of proximal culprit lesion are associated with failure to predict the culprit artery of inferior myocardial infarction by the 12-lead ECG.     

Long-term favorable cardiovascular risk profile and 39-year development of major and minor electrocardiographic abnormalities – The Chicago Healthy Aging Study (CHAS)

Background

Data are limited on long-term associations of favorable cardiovascular risk profile (i.e., low-risk) and changes in risk profile with ECG abnormality development.

Defining unrecognized myocardial infarction: a call for standardized electrocardiographic diagnostic criteria

Background

Unrecognized myocardial infarctions (UMI) are detected by surveillance electrocardiograms (ECGs). In epidemiologic studies, different sets of ECG criteria have been used to define myocardial infarction, possibly contributing to significant differences in prevalence estimates and risk factor associations. We sought to summarize the rationale behind the various UMI-ECG definitions and to suggest an approach to develop uniform criteria.

Methods

A comprehensive review of relevant publications from 1966 to 2002 was conducted.

Results

Out of 14 major studies, the occurrence of UMI as a proportion of all infarctions varied from 4% to 44%, with markedly varying ECG criteria. No study directly addressed the rationale behind selection of ECG criteria. Computerized ECG analysis appears superior to visual reading due to better reliability, speed and cost while maintaining a similar predictive validity. Criteria requiring only major Q waves have the highest specificity for ECG-MI and for prediction validity for future coronary heart disease in middle-aged white men. The addition of minor Q waves and ST-T abnormalities improves predictive validity in middle-aged women and elderly men. Minor Q waves can have their diagnostic accuracy improved by several strategies, including use of ST-T wave changes, Washington Code, vector cardiogram, chronic obstructive pulmonary disease-ECG criteria, and serial ECG analysis.

Conclusion

Currently the most cost-effective and valid method for detecting UMI in epidemiologic studies appears to be computerized ECG analysis using major Q waves in middle-aged white men. Issues needing further research include morphologic validation of ECG-UMI criteria and the influence of age, sex, and race on ECG-MI criteria.     

Increased frequency of DRB1*11:01 in anti–hydroxymethylglutaryl‐coenzyme A reductase–associated autoimmune myopathy

Objective

To investigate the association of anti–hydroxymethylglutaryl‐coenzyme A reductase (anti‐HMGCR) myopathy with HLA class I and II antigens.

Methods

HLA antigens were determined in 1) 20 white and 8 African American anti‐HMGCR patients, 2) 487 white and 167 African American controls, and 3) 51 white subjects with mild self‐limited statin intolerance.

Results

White anti‐HMGCR patients had a higher frequency of the combination HLA–DR11, DQA5, and DQB7 than controls or statin‐intolerant subjects (70% versus 17%; odds ratio [OR] 11.7 [95% confidence interval (95% CI) 4.0–35.3], P = 4.1 × 10^?7 and 70% versus 21%; OR 8.3 [95% CI 2.2–33.9], P = 5.4 × 10^?4, respectively). This combination was not increased in African American anti‐HMGCR subjects compared to controls (13% versus 3%; OR 4.6 [95% CI 0.2–53.3], P = 0.2). However, DR11 was increased in African American anti‐HMGCR patients compared to controls (88% versus 21%; OR 26.4 [95% CI 3.1–590.3], P = 0.0002). High‐resolution mapping showed that 95% with DR11 had DRB1*11:01. DQA1 and DQB6 were less frequent in white anti‐HMGCR–positive patients compared to controls (25% versus 65%; OR 0.2 [95% CI 0.1–0.5], P = 5.5 × 10^?4 and 0% versus 45%; OR 0.0 [95% CI 0.0–0.3], P = 2.1 × 10^?5, respectively). DRB11 was not associated with particular disease features.

Conclusion

DRB1*11:01 is associated with an increased risk of anti‐HMGCR myopathy in whites and African Americans. These findings suggest a mechanistic link between statin exposure, increased HMGCR expression, and the possible presentation of HMGCR‐derived peptide(s) by DRB1*11:01.

     

Heritability of vasculopathy,autoimmune disease,and fibrosis in systemic sclerosis: A population‐based study

Objective

To investigate the familiality of systemic sclerosis (SSc) in relation to Raynaud's phenomenon (RP) (a marker of vasculopathy), other autoimmune inflammatory disease, and fibrotic interstitial lung disease (ILD).

Methods

A genealogic resource, the Utah Population Database (UPDB), was used to test heritability of RP, other autoimmune disease, and ILD. Diseases were defined by International Classification of Diseases, Ninth Revision codes and identified from statewide discharge data, the University of Utah Health Science Center Enterprise Data Warehouse, and death certificates and were linked to the UPDB for analysis. Familial standardized incidence ratio (FSIR), relative risks (RRs) to first‐, second‐, third‐, and fourth‐degree relatives for SSc, RP, other autoimmune disease, and ILD (with 95% confidence intervals [95% CIs]), and population attributable risk (PAR) were calculated.

Results

A software kinship analysis tool was used to analyze 1,037 unique SSc patients. Fifty SSc families had significant FSIRs, ranging from 2.07 to 17.60. The adjusted PAR was ∼8%. The RRs were significant for other autoimmune disease in the first‐degree relatives (2.49 [95% CI 1.99–3.41], P = 2.42 × 10⁻¹⁵) and second‐degree relatives (1.48 [95% CI 1.34–2.39], P = 0.002), for RP in first‐degree relatives (6.38 [95% CI 3.44–11.83], P = 4.04 × 10⁻⁹) and second‐degree relatives (2.39 [95% CI 1.21–4.74], P = 0.012), and for ILD in first‐degree relatives (1.53 [95% CI 1.04–2.26], P = 0.03), third‐degree relatives (1.47 [95% CI 1.18–1.82], P = 0.0004), and fourth‐degree relatives (1.2 [95% CI 1.06–1.35], P = 0.004).

Conclusion

These data suggest that SSc pedigrees include more RP, autoimmune inflammatory disease, and ILD than would be expected by chance. In SSc pedigrees, genetic predisposition to vasculopathy is the most frequent risk among first‐degree relatives.

     

Prevalence of electrocardiographic abnormalities in a middle-aged, biracial population: Coronary Artery Risk Development in Young Adults study

Background

Few studies to date have described the prevalence of electrocardiographic (ECG) abnormalities in a biracial middle-aged cohort.

Methods and Results

Participants underwent measurement of traditional risk factors and 12-lead ECGs coded using both Minnesota Code and Novacode criteria. Among 2585 participants, of whom 57% were women and 44% were black (mean age 45 years), the prevalence of major and minor abnormalities was significantly higher (all P < .001) among black men and women compared to whites. These differences were primarily due to higher QRS voltage and ST/T-wave abnormalities among blacks. There was also a higher prevalence of Q waves (Minnesota Code 1-1, 1-2, 1-3) than described by previous studies. These racial differences remained after multivariate adjustment for traditional cardiovascular (CV) risk factors.

Conclusions

Black men and women have a significantly higher prevalence of ECG abnormalities, independent of traditional cardiovascular risk factors, than whites in a contemporary cohort of middle-aged participants.     

Nonconcordance between subclinical atherosclerosis and the calculated Framingham risk score in HIV‐infected patients: relationships with serum markers of oxidation and inflammation

Objectives

HIV‐infected patients show an increased cardiovascular disease (CVD) risk resulting, essentially, from metabolic disturbances related to chronic infection and antiretroviral treatments. The aims of this study were: (1) to evaluate the agreement between the CVD risk estimated using the Framingham risk score (FRS) and the observed presence of subclinical atherosclerosis in HIV‐infected patients; (2) to investigate the relationships between CVD and plasma biomarkers of oxidation and inflammation.

Methods

Atherosclerosis was evaluated in 187 HIV‐infected patients by measuring the carotid intima‐media thickness (CIMT). CVD risk was estimated using the FRS. We also measured the circulating levels of interleukin‐6, monocyte chemoattractant protein‐1 (MCP‐1) and oxidized low‐density lipoprotein (LDL), and paraoxonase‐1 activity and concentration.

Results

There was a weak, albeit statistically significant, agreement between FRS and CIMT (κ=0.229, P<0.001). A high proportion of patients with an estimated low risk had subclinical atherosclerosis (n=66; 56.4%). In a multivariate analysis, the presence of subclinical atherosclerosis in this subgroup of patients was associated with age [odds ratio (OR) 1.285; 95% confidence interval (CI) 1.084–1.524; P=0.004], body mass index (OR 0.799; 95% CI 0.642–0.994; P=0.044), MCP‐1 (OR 1.027; 95% CI 1.004–1.050; P=0.020) and oxidized LDL (OR 1.026; 95% CI 1.001–1.051; P=0.041).

Conclusion

FRS underestimated the presence of subclinical atherosclerosis in HIV‐infected patients. The increased CVD risk was related, in part, to the chronic oxidative stress and inflammatory status associated with this patient population.

     

Biomarkers of inflammation and development of rheumatoid arthritis in women from two prospective cohort studies

Objective

To examine the association of biomarkers of inflammation with preclinical rheumatoid arthritis (RA).

Methods

A nested case–control study was performed using samples from 2 large, prospectively studied cohorts of women (the Women's Health Study [WHS] and the Nurses' Health Study [NHS]). Blood samples obtained prior to symptom onset in women who later developed RA were selected as incident RA cases, and 3 controls per case were randomly chosen, matched for age, menopausal status, postmenopausal hormone use, and day, time, and fasting status at the time of collection. Plasma was tested for levels of interleukin‐6 (IL‐6), soluble tumor necrosis factor receptor II (sTNFRII) (as a proxy for TNFα), and high‐sensitivity C‐reactive protein. Relationships between biomarkers and RA were assessed using conditional logistic regression models, adjusting for age, body mass index, smoking habits, ethnicity, and reproductive factors.

Results

In 93 incident cases in the NHS and 77 incident cases in the WHS, the mean time between blood collection and the onset of RA symptoms was 5.2 years (range 0.3–12 years). Median IL‐6 and sTNFRII levels were significantly higher in preclinical RA cases compared with matched controls in the NHS (P = 0.03 and P = 0.003, respectively) though not in the WHS. Pooled analysis of the NHS and WHS cohorts demonstrated significant association of sTNFRII with RA (relative risk 2.0 [95% confidence interval 1.1–3.6], P for trend = 0.004), and a modest association of IL‐6 with RA (relative risk 1.4 [95% confidence interval 0.8–2.5], P for trend = 0.06).

Conclusion

Levels of sTNFRII, a biomarker typically associated with active RA, were elevated up to 12 years prior to the development of RA symptoms and were positively associated with incident RA in these nested case–control studies. Studies with repeated assessments of biomarkers prior to RA development may provide further insight into the timing of biomarker elevation in preclinical RA.

     

The 12-lead ECG in peripartum cardiomyopathy

Background

The value of the 12-lead electrocardiogram (ECG) to provide prognostic information in the deadly and disabling syndrome peripartum cardiomyopathy (PPCM) is unknown.

Aims

To determine the prevalence of major and minor ECG abnormalities in PPCM patients at the time of diagnosis, and to establish whether there are ECG correlates of persistent left ventricular dysfunction and/or clinical stability at six months of follow up, where available.

Methods

Twelve-lead ECGs were performed at the point of diagnosis on 78 consecutive women presenting with PPCM to two tertiary centres in South Africa and 44 cases (56%) at the six-month follow up. Blinded Minnesota coding identified major ECG abnormalities and minor ECG changes.

Results

The cohort mainly comprised young women of black African ancestry (90%) [mean age 29 ± 7 years and median body mass index 24.3 (IQR: 22.7–27.5) kg/m²]. The majority of cases (n = 70; 90%) presented in sinus rhythm (mean heart rate 100 ± 21 beats/min). At baseline, at least one ECG abnormality/variant was detected in 96% of cases. Major ECG abnormalities and minor changes were detected in 49% (95% CI: 37–60%) and 62% (95% CI: 51–74%) of cases, respectively; the most common being T-wave changes (59%), p-wave abnormality (29%) and QRS-axis deviation (25%).Of the 44 cases (56%) reviewed at six months, normalisation of the 12-lead ECG occurred in 25%; the most labile ECG features being heart rate (mean reduction of 27 beats/min; p < 0.001) and abnormal QRS axis (36 vs 14%; p = 0.014). On an adjusted basis, major T-wave abnormalities on the baseline 12-lead ECG were associated with lower left ventricular ejection fraction (LVEF) at baseline (average of –9%, 95% CI: –1 to –16; p = 0.03) and at six months (–12%; 95% CI: –4 to –24; p = 0.006). Similarly, baseline ST-segment elevation was also associated with lower LVEF at six months (–25%; 95% CI: –0.7 to –50; p = 0.04).

Conclusions

In this unique study, we found that almost all women suffering from PPCM had an ‘abnormal’ 12-lead ECG. Pending more definitive studies, the ECG appears to be a useful adjunctive tool in both screening and prognostication in resource-poor settings.     

Electrocardiogram abnormalities and risk of cardiovascular mortality and all-cause mortality in old age: The Kahrizak Elderly Study (KES)

Resting electrocardioghic (ECG) abnormalities might be value for mortality prediction. The aim of this study is to evaluate whether ECG abnormalities are associated with increased mortality in older residents of Kahrizak Charity Foundation (KCF). A total of 247 participants ≥60-years of KES were enrolled in this study. Adjudicated all cause mortality was collected over 3 years between 2006 and 2009. The subjects were classified as having major, minor or no ECG abnormalities according to the Minnesota Code. The addition of ECG to risk factors were examined to predict cardiovascular diseases (CVD) and all-cause mortality by using Cox proportional hazards regression models. At baseline, 104(42.1%) had major ECG abnormalities and 73(29.6%) had minor abnormalities. During a median follow-up of 3.2 years, 73 participants died from all-cause mortality and 31deaths from CVD. Major ECG abnormalities were associated with an increased risk of CVD mortality in all models. The associations between minor ECG abnormalities at baseline and CVD mortality were not statistically significant. After adjustment for age and sex, Body mass index (BMI), smoking, diabetes, hypertension (HTN), hyperlipidemia and history of CVD, the participants with the major ECG abnormalities had higher risks of CVD mortality (HR: 3.12(95% CI, 1.02-9.57) and all-cause mortality (HR: 2.45(95% CI, 1.23–4.85) compared with those with normal ECG.     

Type 1 electrocardiographic burden is increased in symptomatic patients with Brugada syndrome

Background

Spontaneous type 1 electrocardiographic (ECG) is a risk factor for arrhythmic events in Brugada patients but the importance of the proportion of time with a type 1 ECG is unknown.

Patients and Methods

Thirty-four Brugada patients (15 symptomatic) underwent a 24-hour 12-lead ECG recording. One-minute averaged waveforms displaying ST-segment elevation above 200 μV, with descending ST-segment and negative T-wave polarity on leads V₁-V₃ were considered as type 1 Brugada ECG. The burden was defined as the percentage of type 1 Brugada waveforms.

Results

Type 1 ECG on lead V2 was more frequent in symptomatic patients (median 80.6% [15.7-96.7] vs 12.4% [0.0-69.7], P = .05). Patients with a permanent type 1 pattern on lead V₂ were more likely to be symptomatic (5/6) than patients without type 1 ECG during a 24-hour period (2/9) (P < .05).

Conclusion

Type 1 pattern is more prevalent across a 24-hour period in symptomatic Brugada patients.     

Yield of Serial Evaluation in At-Risk Family Members of Patients With ARVD/C

Background

Incomplete penetrance and variable expressivity of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) complicate family screening.

Objectives

The objective of the present study was to determine the optimal approach to longitudinal follow-up regarding: 1) screening interval; and 2) testing strategy in at-risk relatives of ARVD/C patients.

Methods

We included 117 relatives (45% male, age 33.3 ± 16.3 years) from 64 families who were at risk of developing ARVD/C by virtue of their familial predisposition (72% mutation carriers [92% plakophilin-2]; 28% first-degree relatives of a mutation-negative proband). Subjects were evaluated by electrocardiography (ECG), Holter monitoring, signal-averaged ECG, and cardiac magnetic resonance (CMR). Disease progression was defined as the development of a new criterion by the 2010 Task Force Criteria (not the “Hamid criteria”) at last follow-up that was absent at enrollment.

Results

At first evaluation, 43 subjects (37%) fulfilled an ARVD/C diagnosis according to the 2010 Task Force Criteria. Among the remaining 74 subjects (63%), 11 of 37 (30%) with complete re-evaluation experienced disease progression during 4.1 ± 2.3 years of follow-up. Electrical progression (n = 10 [27%], including by ECG [14%], Holter monitoring [11%], or signal-averaged ECG [14%]) was more frequently observed than structural progression (n = 1 [3%] on CMR). All 5 patients (14%) with clinical ARVD/C diagnosis at last follow-up had an abnormal ECG or Holter monitor recording, and the only patient with an abnormal CMR already had an abnormal ECG at enrollment.

Conclusions

Over a mean follow-up of 4 years, our study showed that: 1) almost one-third of at-risk relatives have electrical progression; 2) structural progression is rare; and 3) electrical abnormalities precede detectable structural changes. This information could be valuable in determining family screening protocols.     

Impact of low-density lipoprotein cholesterol on cardiovascular outcomes in people with type 2 diabetes: A meta-analysis of prospective cohort studies

Aims

To estimate the prospective association of low-density lipoprotein (LDL) cholesterol on cardiovascular disease (CVD) risk among people with type 2 diabetes.

Methods

We used extensive literature searching strategies to locate prospective cohort studies that reported LDL cholesterol levels as a risk factor for cardiovascular events. We conducted meta-analytic procedures for two outcomes: incident CVD and CVD mortality.

Results

A total of 16 studies were included in this analysis with a mean follow-up range of 4.8–11 years. The pooled relative risk associated with a 1 mmol/L increase in LDL cholesterol in people with type 2 diabetes was 1.30 (95% confidence interval [CI], 1.19–1.43) for incident CVD, and 1.50 (95% CI, 1.25–1.80) for CVD mortality, respectively. Subgroup analyses showed that for incident CVD, the pooled relative risk was 1.28 (95% CI, 1.17–1.41) for 7 studies adjusted for blood pressure and/or glucose concentration (or insulin concentration, glycated hemoglobin) and 1.40 (95% CI, 1.05–1.86) for 3 studies that did not adjust for these variables.

Conclusions

Our study demonstrates that LDL cholesterol was associated with an increased risk for cardiovascular outcomes in people with type 2 diabetes, independent of other conventional risk factor.     

Myeloperoxidase is Independently Associated with Incident Heart Failure in Patients with Coronary Artery Disease and Kidney Disease

Chronic kidney disease (CKD) is associated with high cardiovascular risk and mortality. Myeloperoxidase (MPO) has been linked to adverse events in patients with mild-moderate CKD. We sought to investigate whether MPO levels are associated with adverse outcomes in patients with CKD. We studied participants with mild to moderate CKD in the prospective chronic renal insufficiency cohort (CRIC). We followed patients for incident heart failure (HF), death, and composite outcome (myocardial infarction, incident peripheral arterial disease, cerebrovascular accident and death). A total of 3872 patients were included (2702 without CVD, 1170 with CVD). After multiple adjustments, doubling of MPO in patients with prior CAD was associated with risk of HF (HR 1.15 [1.01-1.30], P = 0.032) and mortality (HR 1.16 [1.05-1.30], P = 0.005), and composite outcome of MI, PAD, CVA and death (HR 1.12 [1.01-1.25], P = 0.031). In this cohort of patients with mild to moderate CKD and CAD, MPO levels are independently associated with incident HF, all-cause mortality, and a composite outcome.