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
Simple Risk Model Predicts Incidence of Atrial Fibrillation in a Racially and Geographically Diverse Population: the CHARGE‐AF Consortium
Background
Tools for the prediction of atrial fibrillation (
AF
) may identify high‐risk individuals more likely to benefit from preventive interventions and serve as a benchmark to test novel putative risk factors.
Methods and Results
Individual‐level data from 3 large cohorts in the
U
nited
S
tates (Atherosclerosis Risk in Communities [
ARIC
] study, the Cardiovascular Health Study [
CHS
], and the Framingham Heart Study [
FHS
]), including 18 556 men and women aged 46 to 94 years (19%
A
frican
A
mericans, 81% whites) were pooled to derive predictive models for
AF
using clinical variables. Validation of the derived models was performed in 7672 participants from the Age, Gene and Environment—Reykjavik study (
AGES
) and the Rotterdam Study (
RS
). The analysis included 1186 incident
AF
cases in the derivation cohorts and 585 in the validation cohorts. A simple 5‐year predictive model including the variables age, race, height, weight, systolic and diastolic blood pressure, current smoking, use of antihypertensive medication, diabetes, and history of myocardial infarction and heart failure had good discrimination (C‐statistic, 0.765; 95%
CI
, 0.748 to 0.781). Addition of variables from the electrocardiogram did not improve the overall model discrimination (C‐statistic, 0.767; 95%
CI
, 0.750 to 0.783; categorical net reclassification improvement, −0.0032; 95%
CI
, −0.0178 to 0.0113). In the validation cohorts, discrimination was acceptable (
AGES
C‐statistic, 0.664; 95%
CI
, 0.632 to 0.697 and
RS
C‐statistic, 0.705; 95%
CI
, 0.664 to 0.747) and calibration was adequate.
Conclusion
A risk model including variables readily available in primary care settings adequately predicted
AF
in diverse populations from the
U
nited
S
tates and
E
urope.
Tập 2 Số 2 - 2013
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
Risk Profiles for Aortic Dissection and Ruptured or Surgically Treated Aneurysms: A Prospective Cohort Study
Background
Community screening to guide preventive interventions for acute aortic disease has been recommended in high‐risk individuals. We sought to prospectively assess risk factors in the general population for aortic dissection (
AD
) and severe aneurysmal disease in the thoracic and abdominal aorta.
Methods and Results
We studied the incidence of
AD
and ruptured or surgically treated aneurysms in the abdominal (
AAA
) or thoracic aorta (
TAA
) in 30 412 individuals without diagnosis of aortic disease at baseline from a contemporary, prospective cohort of middle‐aged individuals, the Malmö Diet and Cancer study. During up to 20 years of follow‐up (median 16 years), the incidence rate per 100 000 patient‐years at risk was 15 (95%
CI
11.7 to 18.9) for
AD
, 27 (95%
CI
22.5 to 32.1) for
AAA
, and 9 (95%
CI
6.8 to 12.6) for
TAA
. The acute and in‐hospital mortality was 39% for
AD
, 34% for ruptured
AAA
, and 41% for ruptured
TAA
. Hypertension was present in 86% of individuals who subsequently developed
AD
, was strongly associated with incident
AD
(hazard ratio [
HR
] 2.64, 95%
CI
1.33 to 5.25), and conferred a population‐attributable risk of 54%. Hypertension was also a risk factor for
AAA
with a smaller effect. Smoking (
HR
5.07, 95%
CI
3.52 to 7.29) and high apolipoprotein B/A1 ratio (
HR
2.48, 95%
CI
1.73 to 3.54) were strongly associated with
AAA
and conferred a population‐attributable risk of 47% and 25%, respectively. Smoking was also a risk factor for
AD
and
TAA
with smaller effects.
Conclusions
This large prospective study identified distinct risk factor profiles for different aortic diseases in the general population. Hypertension accounted for more than half of the population risk for
AD
, and smoking for half of the population risk of
AAA
.
Tập 4 Số 1 - 2015
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
MicroRNA‐33 Deficiency Reduces the Progression of Atherosclerotic Plaque in ApoE −/− Mice
Background
Cholesterol efflux from cells to apolipoprotein A‐I (apoA‐I) acceptors via the
ATP
‐binding cassette transporters
ABCA
1 and
ABCG
1 is thought to be central in the antiatherogenic mechanism. Micro
RNA
(miR)‐33 is known to target
ABCA
1 and
ABCG
1 in vivo.
Methods and Results
We assessed the impact of the genetic loss of miR‐33 in a mouse model of atherosclerosis. MiR‐33 and apoE double‐knockout mice (miR‐33
−/−
Apoe
−/−
) showed an increase in circulating
HDL‐C
levels with enhanced cholesterol efflux capacity compared with miR‐33
+/+
Apoe
−/−
mice. Peritoneal macrophages from miR‐33
−/−
Apoe
−/−
mice showed enhanced cholesterol efflux to apoA‐I and
HDL‐C
compared with miR‐33
+/+
Apoe
−/−
macrophages. Consistent with these results, miR‐33
−/−
Apoe
−/−
mice showed reductions in plaque size and lipid content. To elucidate the roles of miR‐33 in blood cells, bone marrow transplantation was performed in these mice. Mice transplanted with miR‐33
−/−
Apoe
−/−
bone marrow showed a significant reduction in lipid content in atherosclerotic plaque compared with mice transplanted with miR‐33
+/+
Apoe
−/−
bone marrow, without an elevation of
HDL‐C
. Some of the validated targets of miR‐33 such as
RIP
140 (
NRIP
1) and
CROT
were upregulated in miR‐33
−/−
Apoe
−/−
mice compared with miR‐33
+/+
Apoe
−/−
mice, whereas
CPT
1a and
AMPK
α were not.
Conclusions
These data demonstrate that miR‐33 deficiency serves to raise
HDL‐C
, increase cholesterol efflux from macrophages via
ABCA
1 and
ABCG
1, and prevent the progression of atherosclerosis. Many genes are altered in miR‐33‐deficient mice, and detailed experiments are required to establish miR‐33 targeting therapy in humans.
Tập 1 Số 6 - 2012
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