Summary Background Acute exposure to air pollution has been linked to myocardial infarction, but its effect on heart failure is uncertain. We did a systematic review and meta-analysis to assess the ...association between air pollution and acute decompensated heart failure including hospitalisation and heart failure mortality. Methods Five databases were searched for studies investigating the association between daily increases in gaseous (carbon monoxide, sulphur dioxide, nitrogen dioxide, ozone) and particulate (diameter <2·5 μm PM2·5 or <10 μm PM10 ) air pollutants, and heart failure hospitalisations or heart failure mortality. We used a random-effects model to derive overall risk estimates per pollutant. Findings Of 1146 identified articles, 195 were reviewed in-depth with 35 satisfying inclusion criteria. Heart failure hospitalisation or death was associated with increases in carbon monoxide (3·52% per 1 part per million; 95% CI 2·52–4·54), sulphur dioxide (2·36% per 10 parts per billion; 1·35–3·38), and nitrogen dioxide (1·70% per 10 parts per billion; 1·25–2·16), but not ozone (0·46% per 10 parts per billion; −0·10 to 1·02) concentrations. Increases in particulate matter concentration were associated with heart failure hospitalisation or death (PM2·5 2·12% per 10 μg/m3 , 95% CI 1·42–2·82; PM10 1·63% per 10 μg/m3 , 95% CI 1·20–2·07). Strongest associations were seen on the day of exposure, with more persistent effects for PM2·5 . In the USA, we estimate that a mean reduction in PM2·5 of 3·9 μg/m3 would prevent 7978 heart failure hospitalisations and save a third of a billion US dollars a year. Interpretation Air pollution has a close temporal association with heart failure hospitalisation and heart failure mortality. Although more studies from developing nations are required, air pollution is a pervasive public health issue with major cardiovascular and health economic consequences, and it should remain a key target for global health policy. Funding British Heart Foundation.
Objective To review the evidence for the short term association between air pollution and stroke.Design Systematic review and meta-analysis of observational studiesData sources Medline, Embase, ...Global Health, Cumulative Index to Nursing and Allied Health Literature (CINAHL), and Web of Science searched to January 2014 with no language restrictions.Eligibility criteria Studies investigating the short term associations (up to lag of seven days) between daily increases in gaseous pollutants (carbon monoxide, sulphur dioxide, nitrogen dioxide, ozone) and particulate matter (<2.5 µm or <10 µm diameter (PM2.5 and PM10)), and admission to hospital for stroke or mortality.Main outcome measures Admission to hospital and mortality from stroke.Results From 2748 articles, 238 were reviewed in depth with 103 satisfying our inclusion criteria and 94 contributing to our meta-estimates. This provided a total of 6.2 million events across 28 countries. Admission to hospital for stroke or mortality from stroke was associated with an increase in concentrations of carbon monoxide (relative risk 1.015 per 1 ppm, 95% confidence interval 1.004 to 1.026), sulphur dioxide (1.019 per 10 ppb, 1.011 to 1.027), and nitrogen dioxide (1.014 per 10 ppb, 1.009 to 1.019). Increases in PM2.5 and PM10 concentration were also associated with admission and mortality (1.011 per 10 μg/m3 (1.011 to 1.012) and 1.003 per 10 µg/m3 (1.002 to 1.004), respectively). The weakest association was seen with ozone (1.001 per 10 ppb, 1.000 to 1.002). Strongest associations were observed on the day of exposure with more persistent effects observed for PM2·5.Conclusion Gaseous and particulate air pollutants have a marked and close temporal association with admissions to hospital for stroke or mortality from stroke. Public and environmental health policies to reduce air pollution could reduce the burden of stroke.Systematic review registration PROSPERO-CRD42014009225.
The development of engineered nanomaterials is growing exponentially, despite concerns over their potential similarities to environmental nanoparticles that are associated with significant ...cardiorespiratory morbidity and mortality. The mechanisms through which inhalation of nanoparticles could trigger acute cardiovascular events are emerging, but a fundamental unanswered question remains: Do inhaled nanoparticles translocate from the lung in man and directly contribute to the pathogenesis of cardiovascular disease? In complementary clinical and experimental studies, we used gold nanoparticles to evaluate particle translocation, permitting detection by high-resolution inductively coupled mass spectrometry and Raman microscopy. Healthy volunteers were exposed to nanoparticles by acute inhalation, followed by repeated sampling of blood and urine. Gold was detected in the blood and urine within 15 min to 24 h after exposure, and was still present 3 months after exposure. Levels were greater following inhalation of 5 nm (primary diameter) particles compared to 30 nm particles. Studies in mice demonstrated the accumulation in the blood and liver following pulmonary exposure to a broader size range of gold nanoparticles (2–200 nm primary diameter), with translocation markedly greater for particles <10 nm diameter. Gold nanoparticles preferentially accumulated in inflammation-rich vascular lesions of fat-fed apolipoproteinE-deficient mice. Furthermore, following inhalation, gold particles could be detected in surgical specimens of carotid artery disease from patients at risk of stroke. Translocation of inhaled nanoparticles into the systemic circulation and accumulation at sites of vascular inflammation provides a direct mechanism that can explain the link between environmental nanoparticles and cardiovascular disease and has major implications for risk management in the use of engineered nanomaterials.
Air pollution, especially airborne particulate matter (PM), is associated with an increase in both morbidity and mortality from cardiovascular disease, although the underlying mechanisms remain ...incompletely established. The one consistent observation that links the pulmonary and cardiovascular effects of inhaled PM is oxidative stress. This article examines the evidence for the role of oxidative stress in the cardiovascular effects of air pollution, beginning with observations from epidemiological and controlled exposure studies and then exploring potential mechanistic pathways involving free radical generation from PM itself, to effects of PM on cell cultures, isolated organs, healthy animals and animal models of disease. Particular emphasis is placed on the vascular and atherosclerotic effects of urban air pollution and diesel exhaust emissions as rich sources of environmental ultrafine particles.
Immediate assessment of coronary microcirculation during treatment of ST elevation myocardial infarction (STEMI) may facilitate patient stratification for targeted treatment algorithms. Use of ...pressure-wire to measure the index of microcirculatory resistance (IMR) is possible but has inevitable practical restrictions. We aimed to develop and validate angiography-derived index of microcirculatory resistance (IMR
angio
) as a novel and pressure-wire-free index to facilitate assessment of the coronary microcirculation. 45 STEMI patients treated with primary percutaneous coronary intervention (pPCI) were enrolled. Immediately before stenting and at completion of pPCI, IMR was measured within the infarct related artery (IRA). At the same time points, 2 angiographic views were acquired during hyperaemia to measure quantitative flow ratio (QFR) from which IMR
angio
was derived. In a subset of 15 patients both IMR and IMR
angio
were also measured in the non-IRA. Patients underwent cardiovascular magnetic resonance imaging (CMR) at 48 h for assessment of microvascular obstruction (MVO). IMR
angio
and IMR were significantly correlated (ρ: 0.85, p < 0.001). Both IMR and IMR
angio
were higher in the IRA rather than in the non-IRA (p = 0.01 and p = 0.006, respectively) and were higher in patients with evidence of clinically significant MVO (> 1.55% of left ventricular mass) (p = 0.03 and p = 0.005, respectively). Post-pPCI IMR
angio
presented and area under the curve (AUC) of 0.96 (CI95% 0.92–1.00, p < 0.001) for prediction of post-pPCI IMR > 40U and of 0.81 (CI95% 0.65–0.97, p < 0.001) for MVO > 1.55%. IMR
angio
is a promising tool for the assessment of coronary microcirculation. Assessment of IMR without the use of a pressure-wire may enable more rapid, convenient and cost-effective assessment of coronary microvascular function.
This study aimed to compare the value of the index of microcirculatory resistance (IMR) and microvascular obstruction (MVO) measured by cardiac magnetic resonance (CMR) in patients treated for and ...recovering from ST-segment elevation myocardial infarction.
IMR can identify patients with microvascular dysfunction acutely after primary percutaneous coronary intervention (pPCI), and a threshold of >40 has been shown to be associated with an adverse clinical outcome. Similarly, MVO is recognized as an adverse feature in patients with ST-segment elevation myocardial infarction. Even though both IMR and MVO reflect coronary microvascular status, the interaction between these 2 parameters is uncertain.
A total of 110 patients treated with pPCI were included, and IMR was measured immediately at completion of pPCI. Infarct size (IS) as a percentage of left ventricular mass was quantified at 48 h (38.4 ± 12.0 h) and 6 months (194.0 ± 20.0 days) using CMR. MVO was identified and quantified at 48 h by CMR.
Overall, a discordance between IMR and MVO was observed in 36.7% of cases, with 31 patients having MVO and IMR ≤40. Compared with patients with MVO and IMR ≤40, patients with both MVO and IMR >40 had an 11.9-fold increased risk of final IS >25% at 6 months (p = 0.001). Patients with MVO and IMR ≤40 had a significantly smaller IS at 6 months (p = 0.001), with significant regression in IS over time (34.4% interquartile range (IQR): 27.3% to 41.0% vs. 22.3% IQR: 16.0% to 30.0%; p = 0.001).
Discordant prognostic information was obtained from IMR and MVO in nearly one-third of cases; however, IMR can be helpful in grading the degree and severity of MVO.
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High-sensitivity cardiac troponin I (cTnI) assays hold promise in detecting the transition from hypertrophy to heart failure in aortic stenosis. We sought to investigate the mechanism for troponin ...release in patients with aortic stenosis and whether plasma cTnI concentrations are associated with long-term outcome.
Plasma cTnI concentrations were measured in two patient cohorts using a high-sensitivity assay. First, in the Mechanism Cohort, 122 patients with aortic stenosis (median age 71, 67% male, aortic valve area 1.0 ± 0.4 cm(2)) underwent cardiovascular magnetic resonance and echocardiography to assess left ventricular (LV) myocardial mass, function, and fibrosis. The indexed LV mass and measures of replacement fibrosis (late gadolinium enhancement) were associated with cTnI concentrations independent of age, sex, coronary artery disease, aortic stenosis severity, and diastolic function. In the separate Outcome Cohort, 131 patients originally recruited into the Scottish Aortic Stenosis and Lipid Lowering Trial, Impact of REgression (SALTIRE) study, had long-term follow-up for the occurrence of aortic valve replacement (AVR) and cardiovascular deaths. Over a median follow-up of 10.6 years (1178 patient-years), 24 patients died from a cardiovascular cause and 60 patients had an AVR. Plasma cTnI concentrations were associated with AVR or cardiovascular death HR 1.77 (95% CI, 1.22 to 2.55) independent of age, sex, systolic ejection fraction, and aortic stenosis severity.
In patients with aortic stenosis, plasma cTnI concentration is associated with advanced hypertrophy and replacement myocardial fibrosis as well as AVR or cardiovascular death.
Exposure to air pollution is an important risk factor for cardiovascular morbidity and mortality, and is associated with increased blood pressure, reduced heart rate variability, endothelial ...dysfunction and myocardial ischaemia. Our objectives were to assess the cardiovascular effects of reducing air pollution exposure by wearing a facemask.
In an open-label cross-over randomised controlled trial, 15 healthy volunteers (median age 28 years) walked on a predefined city centre route in Beijing in the presence and absence of a highly efficient facemask. Personal exposure to ambient air pollution and exercise was assessed continuously using portable real-time monitors and global positional system tracking respectively. Cardiovascular effects were assessed by continuous 12-lead electrocardiographic and ambulatory blood pressure monitoring.
Ambient exposure (PM2.5 86 +/- 61 vs 140 +/- 113 mug/m3; particle number 2.4 +/- 0.4 vs 2.3 +/- 0.4 x 104 particles/cm3), temperature (29 +/- 1 vs 28 +/- 3 degrees C) and relative humidity (63 +/- 10 vs 64 +/- 19%) were similar (P > 0.05 for all) on both study days. During the 2-hour city walk, systolic blood pressure was lower (114 +/- 10 vs 121 +/- 11 mmHg, P < 0.01) when subjects wore a facemask, although heart rate was similar (91 +/- 11 vs 88 +/- 11/min; P > 0.05). Over the 24-hour period heart rate variability increased (SDNN 65.6 +/- 11.5 vs 61.2 +/- 11.4 ms, P < 0.05; LF-power 919 +/- 352 vs 816 +/- 340 ms2, P < 0.05) when subjects wore the facemask.
Wearing a facemask appears to abrogate the adverse effects of air pollution on blood pressure and heart rate variability. This simple intervention has the potential to protect susceptible individuals and prevent cardiovascular events in cities with high concentrations of ambient air pollution.
To investigate the diagnostic accuracy of (1) hyperaemic angiography-derived index of microcirculatory resistance (IMR
angio
) in defining coronary microvascular dysfunction (CMD) across patients ...with acute coronary syndromes (ST-elevation myocardial infarction STEMI; non-ST elevation acute coronary syndrome NSTE-ACS) and stable chronic coronary syndrome CCS) and (2) the accuracy of non-hyperaemic IMR
angio
(NH-IMR
angio
) to detect CMD in STEMI. 145 patients (STEMI = 66; NSTEMI = 43; CCS = 36) were enrolled. 246 pressure-wire IMR measurements were made in 189 coronary vessels. IMR
angio
and NH-IMR
angio
was derived using quantitative flow ratio. In patients with STEMI, cardiac magnetic resonance was performed to quantify microvascular obstruction (MVO). IMR
angio
was correlated with IMR (overall rho = 0.78, p < 0.0001; STEMI, rho = 0.85 p < 0.0001; NSTE-ACS and rho = 0.72, p < 0.0001; CCS, rho = 0.70, p < 0.0001) and demonstrated good diagnostic performance in predicting high IMR (STEMI AUC
ROC
= 0.93 0.88–0.98; NSTE-ACS AUC
ROC
= 0.77 0.63–0.92; CCS AUC
ROC
= 0.88 0.79–0.97). Agreement between the two indices was evident on Bland Altman analysis. In STEMI, NH-IMR
angio
was also well correlated with IMR (rho = 0.64, p < 0.0001), with good diagnostic accuracy in predicting high invasive IMR (AUC
ROC
= 0.82 0.74–0.90). Both IMR
angio
(AUC
ROC
= 0.74 0.59–0.89) and NH-IMR
angio
(AUC
ROC
= 0.76 0.54–0.87) were significantly associated with MVO in STEMI. In conclusions, IMR
angio
is a valid alternative to invasive IMR to detect CMD in patients with acute and stable coronary syndromes, whilst NH-IMR
angio
has a good diagnostic accuracy in STEMI where it could become a user-friendly diagnostic tool as it is adenosine-free.
Myocardial recovery after primary percutaneous coronary intervention in acute myocardial infarction is variable and the extent and severity of injury are difficult to predict. We sought to ...investigate the role of cardiovascular magnetic resonance T1 mapping in the determination of myocardial injury very early after treatment of ST-segment elevation myocardial infarction (STEMI).
STEMI patients underwent 3 T cardiovascular magnetic resonance (CMR), within 3 h of primary percutaneous intervention (PPCI). T1 mapping determined the extent (area-at-risk as %left ventricle, AAR) and severity (average T1 values of AAR) of acute myocardial injury, and related these to late gadolinium enhancement (LGE), and microvascular obstruction (MVO). The characteristics of myocardial injury within 3 h was compared with changes at 24-h to predict final infarct size.
Forty patients were included in this study. Patients with average T1 values of AAR ≥1400 ms within 3 h of PPCI had larger LGE at 24-h (33% ±14 vs. 18% ±10, P = 0.003) and at 6-months (27% ±9 vs. 12% ±9; P < 0.001), higher incidence and larger extent of MVO (85% vs. 40%, P = 0.016) & 4.0 (0.5-9.5)% vs. 0 (0-3.0)%, P = 0.025. The average T1 value was an independent predictor of acute LGE (β 0.61, 95%CI 0.13 to 1.09; P = 0.015), extent of MVO (β 0.22, 95%CI 0.03 to 0.41, P = 0.028) and final infarct size (β 0.63, 95%CI 0.21 to 1.05; P = 0.005). Receiver-operating-characteristic analysis showed that T1 value of AAR obtained within 3-h, but not at 24-h, predicted large infarct size (LGE > 9.5%) with 100% positive predictive value at the optimal cut-off of 1400 ms (area-under-the-curve, AUC 0.88, P = 0.006).
Hyper-acute T1 values of the AAR (within 3 h post PPCI, but not 24 h) predict a larger extent of MVO and infarct size at both 24 h and 6 months follow-up. Delayed CMR scanning for 24 h could not substitute the significant value of hyper-acute average T1 in determining infarct characteristics.
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