Journal of the American Heart Association
SCIE-ISI SCOPUS (2012-2023)
2047-9980
Anh Quốc
Cơ quản chủ quản: WILEY , Wiley-Blackwell Publishing Ltd
Lĩnh vực:
Cardiology and Cardiovascular Medicine
Các bài báo tiêu biểu
Risk of Death Following Application of Paclitaxel‐Coated Balloons and Stents in the Femoropopliteal Artery of the Leg: A Systematic Review and Meta‐Analysis of Randomized Controlled Trials
Background
Several randomized controlled trials (
RCT
s) have already shown that paclitaxel‐coated balloons and stents significantly reduce the rates of vessel restenosis and target lesion revascularization after lower extremity interventions.
Methods and Results
A systematic review and meta‐analysis of
RCT
s investigating paclitaxel‐coated devices in the femoral and/or popliteal arteries was performed. The primary safety measure was all‐cause patient death. Risk ratios and risk differences were pooled with a random effects model. In all, 28
RCT
s with 4663 patients (89% intermittent claudication) were analyzed. All‐cause patient death at 1 year (28
RCT
s with 4432 cases) was similar between paclitaxel‐coated devices and control arms (2.3% versus 2.3% crude risk of death; risk ratio, 1.08; 95% CI, 0.72–1.61). All‐cause death at 2 years (12
RCT
s with 2316 cases) was significantly increased in the case of paclitaxel versus control (7.2% versus 3.8% crude risk of death; risk ratio, 1.68; 95%
CI,
1.15–2.47; —number‐needed‐to‐harm, 29 patients [95%
CI
, 19–59]). All‐cause death up to 5 years (3
RCT
s with 863 cases) increased further in the case of paclitaxel (14.7% versus 8.1% crude risk of death; risk ratio, 1.93; 95%
CI
, 1.27–2.93; —number‐needed‐to‐harm, 14 patients [95%
CI
, 9–32]). Meta‐regression showed a significant relationship between exposure to paclitaxel (dose‐time product) and absolute risk of death (0.4±0.1% excess risk of death per paclitaxel mg‐year;
P
<0.001). Trial sequential analysis excluded false‐positive findings with 99% certainty (2‐sided α, 1.0%).
Conclusions
There is increased risk of death following application of paclitaxel‐coated balloons and stents in the femoropopliteal artery of the lower limbs. Further investigations are urgently warranted.
Clinical Trial Registration
URL
:
www.crd.york.ac.uk/PROSPERO
. Unique identifier:
CRD
42018099447.
Tập 7 Số 24 - 2018
Relationship of Sleep Duration With All‐Cause Mortality and Cardiovascular Events: A Systematic Review and Dose‐Response Meta‐Analysis of Prospective Cohort Studies
Background
Effects of extreme sleep duration on risk of mortality and cardiovascular outcomes remain controversial. We aimed to quantify the dose‐response relationships of sleep duration with risk of all‐cause mortality, total cardiovascular disease, coronary heart disease, and stroke.
Methods and Results
PubMed and Embase were systematically searched for prospective cohort studies published before December 1, 2016, that examined the associations between sleep duration and at least 1 of the 4 outcomes in generally healthy populations. U‐shaped associations were indicated between sleep duration and risk of all outcomes, with the lowest risk observed for ≈7‐hour sleep duration per day, which was varied little by sex. For all‐cause mortality, when sleep duration was <7 hours per day, the pooled relative risk (RR) was 1.06 (95%
CI
, 1.04–1.07) per 1‐hour reduction; when sleep duration was >7 hours per day, the pooled
RR
was 1.13 (95%
CI
, 1.11–1.15) per 1‐hour increment. For total cardiovascular disease, the pooled
RR
was 1.06 (95%
CI
, 1.03–1.08) per 1‐hour reduction and 1.12 (95%
CI
, 1.08–1.16) per 1‐hour increment of sleep duration. For coronary heart disease, the pooled
RR
was 1.07 (95%
CI
, 1.03–1.12) per 1‐hour reduction and 1.05 (95%
CI
, 1.00–1.10) per 1‐hour increment of sleep duration. For stroke, the pooled
RR
was 1.05 (95%
CI
, 1.01–1.09) per 1‐hour reduction and 1.18 (95%
CI
, 1.14–1.21) per 1‐hour increment of sleep duration.
Conclusions
Our findings indicate that both short and long sleep duration is associated with an increased risk of all‐cause mortality and cardiovascular events.
Tập 6 Số 9 - 2017
Association of Anxiety and Depression With All‐Cause Mortality in Individuals With Coronary Heart Disease
Background
Depression has been related to mortality in coronary heart disease (
CHD
) patients, but few studies have evaluated the role of anxiety or the role of the co‐occurrence of depression and anxiety. We examined whether anxiety is associated with increased risk of mortality after accounting for depression in individuals with established
CHD
.
Methods and Results
The cohort was composed of 934 men and women with confirmed
CHD
(mean age, 62±11 years) who completed the Hospital Anxiety and Depression scale (
HADS
) during hospitalization for coronary angiography. Over the 3‐year follow‐up period, there were 133 deaths. Elevated scores on the
HADS
anxiety subscale (
HADS
‐A≥8) were associated with increased risk of mortality after accounting for established risk factors including age, congestive heart failure, left ventricular ejection fraction, 3‐vessel disease, and renal disease (hazard ratio [
HR
], 2.27; 95%
CI
, 1.55 to 3.33;
P
<0.001). Elevated scores on the
HADS
depression subscale (
HADS
‐D≥8) were also associated with increased risk of mortality (
HR
, 2.18; 95%
CI
, 1.47 to 3.22;
P
<0.001). When both psychosocial factors were included in the model, each maintained an association with mortality (anxiety,
HR
, 1.83; 95%
CI
, 1.18 to 2.83;
P
=0.006; depression,
HR
, 1.66; 95%
CI
, 1.06 to 2.58;
P
=0.025). Estimation of the
HR
for patients with both anxiety and depression versus those with neither revealed a larger
HR
than for patients with either factor alone (
HR
, 3.10; 95%
CI
, 1.95 to 4.94;
P
<0.001).
Conclusions
Anxiety is associated with increased risk of mortality in
CHD
patients, particularly when comorbid with depression. Future studies should focus on the co‐occurrence of these psychosocial factors as markers of increased mortality risk.
Tập 2 Số 2 - 2013
DNA Hypomethylation, Ambient Particulate Matter, and Increased Blood Pressure: Findings From Controlled Human Exposure Experiments
Background
Short‐term exposures to fine (<2.5 μm aerodynamic diameter) ambient particulate‐matter (
PM
) have been related with increased blood pressure (
BP
) in controlled‐human exposure and community‐based studies. However, whether coarse (2.5 to 10 μm)
PM
exposure increases
BP
is uncertain. Recent observational studies have linked
PM
exposures with blood
DNA
hypomethylation, an epigenetic alteration that activates inflammatory and vascular responses. No experimental evidence is available to confirm those observational data and demonstrate the relations between
PM
, hypomethylation, and
BP
.
Methods and Results
We conducted a cross‐over trial of controlled‐human exposure to concentrated ambient particles (
CAP
s). Fifteen healthy adult participants were exposed for 130 minutes to fine
CAP
s, coarse
CAP
s, or
HEPA
‐filtered medical air (control) in randomized order with ≥2‐week washout. Repetitive‐element (
Alu
, long interspersed nuclear element‐1 [
LINE
‐1]) and candidate‐gene (
TLR4
,
IL‐12
,
IL‐6
,
iNOS
) blood methylation, systolic and diastolic
BP
were measured pre‐ and postexposure. After adjustment for multiple comparisons, fine
CAP
s exposure lowered
Alu
methylation (β‐standardized=−0.74, adjusted‐
P
=0.03); coarse
CAP
s exposure lowered
TLR4
methylation (β‐standardized=−0.27, adjusted‐
P
=0.04). Both fine and coarse
CAP
s determined significantly increased systolic
BP
(β=2.53 mm Hg,
P
=0.001; β=1.56 mm Hg,
P
=0.03, respectively) and nonsignificantly increased diastolic
BP
(β=0.98 mm Hg,
P
=0.12; β=0.82 mm Hg,
P
=0.11, respectively). Decreased
Alu
and
TLR4
methylation was associated with higher postexposure
DBP
(β‐standardized=0.41,
P
=0.04; and β‐standardized=0.84,
P
=0.02; respectively). Decreased
TLR4
methylation was associated with higher postexposure
SBP
(β‐standardized=1.45,
P
=0.01).
Conclusions
Our findings provide novel evidence of effects of coarse
PM
on
BP
and confirm effects of fine
PM
. Our results provide the first experimental evidence of
PM
‐induced
DNA
hypomethylation and its correlation to
BP
.
Tập 2 Số 3 - 2013
Clinical Implications of the New York Heart Association Classification
Background
The New York Heart Association (
NYHA
) classification has served as a fundamental tool for risk stratification of heart failure (
HF
) and determines clinical trial eligibility and candidacy for drugs and devices. However, its ability to adequately stratify risk is unclear.
Methods and Results
To compare
NYHA
class with objective assessments and survival in patients with
HF
, we performed secondary analyses of 4 multicenter National Institutes of Health–funded
HF
clinical trials that included patients classified as
NYHA
class
II
or III: TOPCAT (Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist), DIG (The Effect of Digoxin on Mortality and Morbidity in Patients With Heart Failure), HF‐ACTION (Efficacy and Safety of Exercise Training in Patients With Chronic Heart Failure), and GUIDE‐IT (Guiding Evidence‐Based Therapy Using Biomarker Intensified Treatment in Heart Failure). Twenty‐month cumulative survival was compared between classes using Kaplan–Meier curves and the log rank test.
NT
‐proBNP (N‐terminal pro–B‐type natriuretic peptide), Kansas City Cardiomyopathy Questionnaire (
KCCQ
) scores, 6‐minute walk distances, left ventricular ejection fraction, and cardiopulmonary test parameters were compared using Wilcoxon rank sum tests and percentage overlap using kernel density estimations. Cumulative mortality varied significantly across
NYHA
classes and
HF
clinical trials (likelihood ratio,
P
<0.001). Mortality at 20 months for
NYHA
class
II
ranged from 7% for patients in
HF
‐
ACTION
to 15% in
GUIDE
‐
IT
, whereas mortality for
NYHA
class
III
ranged from 12% in
TOPCAT
to 26% in
GUIDE
‐
IT
. There was substantial percentage overlap in values for
NT
‐pro
BNP
levels (79% and 69%),
KCCQ
scores (63% and 54%), 6‐minute walk distances (63% and 54%), and left ventricular ejection fraction (88% and 83%). Similarly, there was substantial overall in values for minute ventilation–carbon dioxide production relationship (71%), maximal oxygen uptake (54%), and exercise duration (53%).
Conclusions
The
NYHA
system poorly discriminates
HF
patients across the spectrum of functional impairment. These findings raise important questions about the need for improved phenotyping of these patients to facilitate risk stratification and response to interventions.
Tập 8 Số 23 - 2019
Impact of Fine Particulate Matter (PM 2.5 ) Exposure During Wildfires on Cardiovascular Health Outcomes
Background
Epidemiological studies investigating the role of fine particulate matter (
PM
2.5
; aerodynamic diameter <2.5 μm) in triggering acute coronary events, including out‐of‐hospital cardiac arrests and ischemic heart disease (
IHD
), during wildfires have been inconclusive.
Methods and Results
We examined the associations of out‐of‐hospital cardiac arrests,
IHD
, acute myocardial infarction, and angina (hospital admissions and emergency department attendance) with
PM
2.5
concentrations during the 2006–2007 wildfires in Victoria, Australia, using a time‐stratified case‐crossover study design. Health data were obtained from comprehensive health‐based administrative registries for the study period (December 2006 to January 2007). Modeled and validated air exposure data from wildfire smoke emissions (daily average
PM
2.5
, temperature, relative humidity) were also estimated for this period. There were 457 out‐of‐hospital cardiac arrests, 2106 emergency department visits, and 3274 hospital admissions for
IHD
. After adjusting for temperature and relative humidity, an increase in interquartile range of 9.04 μg/m
3
in
PM
2.5
over 2 days moving average (lag 0‐1) was associated with a 6.98% (95% CI 1.03% to 13.29%) increase in risk of out‐of‐hospital cardiac arrests, with strong association shown by men (9.05%,95%CI 1.63% to 17.02%) and by older adults (aged ≥65 years) (7.25%, 95%
CI
0.24% to 14.75%). Increase in risk was (2.07%, 95%
CI
0.09% to 4.09%) for
IHD
‐related emergency department attendance and (1.86%, 95%
CI
: 0.35% to 3.4%) for
IHD
‐related hospital admissions at lag 2 days, with strong associations shown by women (3.21%, 95%
CI
0.81% to 5.67%) and by older adults (2.41%, 95%
CI
0.82% to 5.67%).
Conclusion
PM
2.5
exposure was associated with increased risk of out‐of‐hospital cardiac arrests and
IHD
during the 2006–2007 wildfires in Victoria. This evidence indicates that
PM
2.5
may act as a triggering factor for acute coronary events during wildfire episodes.
Tập 4 Số 7 - 2015
Using Mobile Technology for Cardiac Rehabilitation: A Review and Framework for Development and Evaluation
Tập 2 Số 6 - 2013
Cardiovascular Effects of Long‐Term Exposure to Air Pollution: A Population‐Based Study With 900 845 Person‐Years of Follow‐up
Background
Studies have shown that long‐term exposure to air pollution such as fine particulate matter (≤2.5 μm in aerodynamic diameter [
PM
2.5
]) increases the risk of all‐cause and cardiovascular mortality. To date, however, there are limited data on the impact of air pollution on specific cardiovascular diseases. This study aimed to evaluate cardiovascular effects of long‐term exposure to air pollution among residents of Seoul, Korea.
Methods and Results
Healthy participants with no previous history of cardiovascular disease were evaluated between 2007 and 2013. Exposure to air pollutants was estimated by linking the location of outdoor monitors to the
ZIP
code of each participant's residence. Crude and adjusted analyses were performed using Cox regression models to evaluate the risk for composite cardiovascular events including cardiovascular mortality, acute myocardial infarction, congestive heart failure, and stroke. A total of 136 094 participants were followed for a median of 7.0 years (900 845 person‐years). The risk of major cardiovascular events increased with higher mean concentrations of
PM
2.5
in a linear relationship, with a hazard ratio of 1.36 (95% confidence interval, 1.29–1.43) per 1 μg/m
3
PM
2.5
. Other pollutants including
PM
2.5–10
of
CO
,
SO
2
, and
NO
2
, but not O
3
, were significantly associated with increased risk of cardiovascular events. The burden from air pollution was comparable to that from hypertension and diabetes mellitus.
Conclusions
This large‐scale population‐based study demonstrated that long‐term exposure to air pollution including
PM
2.5
increases the risk of major cardiovascular disease and mortality. Air pollution should be considered an important modifiable environmental cardiovascular risk factor.
Tập 6 Số 11 - 2017
Prediction of Thrombotic and Bleeding Events After Percutaneous Coronary Intervention: CREDO‐Kyoto Thrombotic and Bleeding Risk Scores
Background
Prediction of thrombotic and bleeding risk is important to optimize antithrombotic therapy after percutaneous coronary intervention.
Methods and Results
We developed the prediction rules for thrombotic and bleeding events separately in Japanese patients. Derivation and validation cohorts consisted of 4778 patients from
CREDO
‐Kyoto (Coronary Revascularization Demonstrating Outcome Study in Kyoto) registry cohort 2 and 4669 patients from RESET (Randomized Evaluation of Sirolimus‐Eluting Versus Everolimus‐Eluting Stent Trial) and NEXT (Nobori Biolimus‐Eluting Versus Xience/Promus Everolimus‐Eluting Stent Trial). Primary thrombotic and bleeding events were a composite of myocardial infarction, definite or probable stent thrombosis or ischemic stroke, and GUSTO (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) moderate or severe bleeding. The prediction rule for thrombosis assigned 2 points for severe chronic kidney disease, atrial fibrillation, peripheral vascular disease, and anemia and 1 point for age ≥75 years, heart failure, diabetes mellitus, and chronic total occlusion. The prediction rule for bleeding assigned 2 points for thrombocytopenia, severe chronic kidney disease, peripheral vascular disease, and heart failure and 1 point for prior myocardial infarction, malignancy, and atrial fibrillation. In derivation and validation cohorts, area under the curve was 0.68 and 0.64, respectively, for thrombosis and 0.66 and 0.66, respectively, for bleeding. In the validation cohort, a high thrombosis risk score (≥4, n=682) was associated with higher 3‐year incidence of thrombotic events than a score that was intermediate (2–3, n=1178) or low (0–1, n=2809) (7.6%, 3.7%, versus 2.4%, respectively;
P
<0.0001). A high bleeding risk score (≥3, n=666) was associated with higher incidence of bleeding than scores that were intermediate (1–2, n=1802) or low (0, n=2201) (8.8%, 4.1%, versus 2.3%, respectively;
P
<0.0001). Among 682 patients at high thrombotic risk, only 39 (5.7%) had low bleeding risk, whereas 401 (58.8%) had high bleeding risk with very high incidence of bleeding (11.6%).
Conclusions
CREDO
‐Kyoto thrombotic and bleeding risk scores demonstrated modest accuracy in stratifying thrombotic and bleeding risks; however, a large proportion of patients at high thrombotic risk also had high bleeding risk.
Tập 7 Số 11 - 2018
Duration of Reproductive Life Span, Age at Menarche, and Age at Menopause Are Associated With Risk of Cardiovascular Disease in Women
Background
Although the timing of menarche and menopause may be associated with cardiovascular disease (CVD), the entire reproductive life span has not been considered comprehensively as risk for
CVD
. We investigate the associations of reproductive life span duration and ages at menarche and menopause, induced by natural means or surgical bilateral oophorectomy, with incident
CVD
in women.
Methods and Results
Prospective cohort study of 73 814 Nurses' Health Study following participants without
CVD
, defined as incident coronary heart disease or stroke, from 1980 through 2012. Duration of reproductive life span was generated by subtracting age at menarche from age at menopause. A shorter reproductive life span was associated with a higher risk of incident
CVD
after multivariable adjustment (relative risk, 1.32 [95% confidence interval, 1.16–1.49] comparing duration <30 with ≥42 years;
P
trend<0.0001). Early age at menopause was associated with higher multivariable‐adjusted
CVD
risk (1.32 [1.16–1.51] comparing age <40 with 50 to <55 years;
P
trend<0.0001), with excess risk for both natural and surgical menopause. Compared with women with menarche at 13 years, the multivariable‐adjusted
CVD
risk for early menarche at ≤10 years was 1.22 (1.09–1.36). The association between reproductive life span and
CVD
remained significant in sensitivity analyses excluding women who experienced extreme early age at menarche or who used hormone therapy.
Conclusions
A shorter duration of reproductive life span is associated with a higher risk of
CVD
, which is likely driven by the timing of menopause induced either naturally or surgically. Extremely early age at menarche is also associated with a higher risk of
CVD
.
Tập 6 Số 11 - 2017