Reduction Of Acute Coronary Events Research Articles

Reduction in acute coronary events without excess out of hospital cardiac arrest during the COVID-19 lockdown of 2020 in new South Wales, Australia

Abstract Background The COVID-19 pandemic has seen a significant reduction in reported ACS cases, raising concerns of avoidance behaviour contributing to increased OHCA incidence; exploring this phenomenon can help identify potential mediating factors for these changes and better understand its impact on cardiovascular health. Purpose Australia's successful COVID-19 lockdown provides a unique opportunity to study whether it affected the incidence of ACS and OHCAs, shedding light on the impact of pandemic-related behavioural modifications on cardiovascular health. Method Using data from the NSW Government database for ACS and NSW Ambulance dispatch data for OHCA, along with climate, traffic, and air quality data, we estimated the excess number of cases using an interrupted time-series analysis that adjusted for seasonal variations, day of the week and temperature. As a sensitivity analysis, we also conducted a two-stage time series analysis for the excess OHCA. Results During COVID-19’s first lockdown period (15th March to 1st July 2020), there were reductions in both ACS (-1259 [95% CI -1530, -989]) and OHCA (-69[-235, -92]) (Fig1). In this period there was a clear changes in anthropogenic activities with reductions in traffic (5670±1380 in 2020 versus 9150±1220 in 2018 and 8640±2370 in 2019) and flights (207±169 versus 884±152 and 902±103).These reductions were accompanied with improvement in PM2.5 (5.1±2.1μg/m3 versus 9.0±3.2 in 2018 and 8.2±3.2 in 2019), PM10 (13.3±5.4μg/m3 versus 20.9±8.6 and 17.7±6.0), and NO2 (7.4±2.7 ppb versus 8.4±3.3 and 9.0±2.8) (Fig2). Conclusion During the first COVID-19 lockdown in NSW, there was a significant reduction in the number of ACS cases without any associated excess in OHCA. This may be caused, at least partly, by the improved air quality from the behavioural changes.Excess ACS (STEMI & NSTEMI) and OHCAChanges in Traffic and Flights Activitie

Reduction in Acute Coronary Events Without Excess Out of Hospital Cardiac Arrest During the COVID-19 Lockdown of 2020 in New South Wales, Australia

Reduction in Acute Coronary Events Without Excess Out of Hospital Cardiac Arrest During the COVID-19 Lockdown of 2020 in New South Wales, Australia

Will the hidden specter of acute coronary syndrome (ACS) and ST-segment elevation myocardial infarction (STEMI) emerge from the avalanche of COVID-19?

There has been a huge impact of the COVID-19 pandemic on global healthcare systems. Advisories across the world have appealed to people to stay at home and observe social distancing to slow down the pandemic. However it is important to realize as to how this is affecting acute cardiovascular care. Recent studies from Europe and USA have reported > 50% reduction in hospital admissions for ACS and declining rates of coronary interventions. The possible reasons for this noticeable reduction in patients with ACS/STEMI during the COVID-19 pandemic are multi-factorial. On one hand, it is due to change in thresholds for referring patients of ACS/STEMI for cardiac catheterization, with fibrinolysis being acceptable for many stable STEMI patients and conservative management being preferred for NSTEMI patients. Theories abound on how “staying at home” strategy may have led to an reduction in acute coronary events due to healthier lifestyle, better compliance and reduced stress. Realistically however, a more disquieting reason would be a “pseudo-reduction” ie. the incidence of ACS/STEMI is actually the same, but these patients are staying away from hospitals due to fear of contracting the infection. Lockdown restrictions have also limited transport options for patients seeking to reach hospitals in time. Healthcare systems need to be prepared for an anticipated downstream deluge of such untreated patients who may present with sequelae like heart failure, reinfarction, arrhythmias, mechanical complications etc. Scientific societies should have proactive campaigns to alleviate patient concerns, and encourage them to seek timely medical attention despite the COVID-19 pandemic.

P653PCSK-9 inhibitors and acute coronary syndrome in hyperlipidemic patients: a systematic review and meta-analysis

Abstract Introduction Hyperlipidemia has been associated with several adverse cardiac and cerebrovascular events. Treatment with statins has proven to reduce the risk of cardiovascular events, however not all patients could reach adequate low-density lipoprotein targets or tolerate statin therapy. This has led to a recent increase in the use of PCSK-9 inhibitors for management of uncontrolled hyperlipidemia. Purpose Effect of PCSK-9 inhibitors on the reduction of acute coronary events in patients with hyperlipidemia. Methods A systematic search of electronic databases for published phase 2 or 3 randomized controlled trials involving hyperlipidemic adults on PCSK-9 inhibitors was conducted. Trials involving evolocumab or alirocumab were included in the analysis. The end points of myocardial infarction and unstable angina were computed together as the composite outcome of acute coronary events. Meta-analysis using a random effects model, with dichotomous outcomes expressed as odds ratios (OR) with 95% confidence intervals (CI), was performed. Results Thirty randomized controlled trials comprising 62,961 patients were included in the meta-analysis, including the recently published ODYSSEY OUTCOMES trial with 18,942 patients. Analysis was stratified according to PCSK-9 inhibitor, either evolocumab or alirocumab. In the stratified analysis, evolocumab was associated with a significantly lower rate of acute coronary events with an OR: 0.79 (95% CI, 0.72–0.87; P<0.001). In contrast, alirocumab was not associated with a significantly lower rate of acute coronary events with an OR: 0.71 (95% CI, 0.47–1.10; P=0.12). For the combined group, compared with no PCSK-9 inhibitor therapy, PCSK9 inhibitor therapy was associated with a significantly lower rate of acute coronary events (4.3% versus 5.8%; OR: 0.81 (95% CI, 0.75–0.87; P<0.001). The modest reduction of risk of acute coronary events of 1.5% translates into a number needed to treat of 67. Neither publication bias, nor significant heterogeneity was observed in the analysis. Acute coronary events Conclusions PCSK-9 inhibitor therapy significantly reduces the risk of acute coronary syndrome when compared to the usual standard of care in adults with uncontrolled hyperlipidemia.

Impact of Scotland’s Comprehensive, Smoke-Free Legislation on Stroke

BackgroundPrevious studies have reported a reduction in acute coronary events following smoke-free legislation. Evidence is lacking on whether stroke is also reduced. The aim was to determine whether the incidence of stroke, overall and by sub-type, fell following introduction of smoke-free legislation across Scotland on 26 March 2006.Methods and FindingsA negative binomial regression model was used to determine whether the introduction of smoke-free legislation resulted in a step and/or slope change in stroke incidence. The model was adjusted for age-group, sex, socioeconomic deprivation quintile, urban/rural residence and month. Interaction tests were also performed. Routine hospital administrative data and death certificates were used to identify all hospital admissions and pre-hospital deaths due to stroke (ICD10 codes I61, I63 and I64) in Scotland between 2000 and 2010 inclusive. Prior to the legislation, rates of all stroke, intracerebral haemorrhage and unspecified stroke were decreasing, whilst cerebral infarction was increasing at 0.97% per annum. Following the legislation, there was a dramatic fall in cerebral infarctions that persisted for around 20 months. No visible effect was observed for other types of stroke. The model confirmed an 8.90% (95% CI 4.85, 12.77, p<0.001) stepwise reduction in cerebral infarction at the time the legislation was implemented, after adjustment for potential confounders.ConclusionsFollowing introduction of national, comprehensive smoke-free legislation there was a selective reduction in cerebral infarction that was not apparent in other types of stroke.

Meta-analysis of before and after studies shows a 10% reduction in acute coronary events after introduction of comprehensive smoke-free legislation

Commentary on: Mackay DF, Irfan MO, Haw S, et al. Meta-analysis of the effect of comprehensive smoke-free legislation on acute coronary events. Heart 2010;96:1525–30.[OpenUrl][1][Abstract/FREE Full Text][2] That tobacco (active and passive smoking) is the leading cause of cardiovascular disease (CVD) is no longer subject to debate. However, as opposed to some other CVD risk factors, we do know what works for tobacco control. From an individual and societal perspective, smoke-free environments have proven to be one of the most effective measures to prevent CVD (and other chronic diseases). Smoke-free environments decrease smoking prevalence, heart disease mortality and lung cancer incidence.1 Globally, as of November 2010, 169 nations had signed the World Health Organization Framework Convention on Tobacco Control and, partially stimulated by it, as of January 2011, 55 countries had some sort of smoke-free law, 37 of which include both bars and restaurants. … [1]: {openurl}?query=rft.jtitle%253DHeart%26rft_id%253Dinfo%253Adoi%252F10.1136%252Fhrt.2010.199026%26rft_id%253Dinfo%253Apmid%252F20736203%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [2]: /lookup/ijlink?linkType=ABST&journalCode=heartjnl&resid=96/19/1525&atom=%2Febnurs%2F14%2F2%2F46.atom

Effects of Italian Smoking Regulation on Rates of Hospital Admission for Acute Coronary Events: A Country-Wide Study

BackgroundSeveral studies have reported a reduction in acute coronary events (ACEs) in the general population after the enforcement of smoking regulations, although there is uncertainty concerning the magnitude of the effect of such interventions. We conducted a country-wide evaluation of the health effects of the introduction of a smoking ban in public places, using data on hospital admissions for ACEs from the Italian population after the implementation of a national smoking regulation in January 2005.Methods and FindingsRates of admission for ACEs in the 20 Italian regions from January 2002 to November 2006 were analysed using mixed-effect regression models that allowed for long-term trends and seasonality. Standard methods for interrupted time-series were adopted to assess the immediate and gradual effects of the smoking ban. Effect modification by age was investigated, with the assumption that exposure to passive smoking in public places would be greater among young people. In total, 936,519 hospital admissions for ACEs occurred in the Italian population during the study period. A 4% reduction in hospital admissions for ACEs among persons aged less than 70 years was evident after the introduction of the ban (Rate Ratio [RR], 0.96; 95% Confidence Interval [CI], 0.95–0.98). No effect was found among persons aged at least 70 years (RR 1.00; 95% CI 0.99–1.02). Effect modification by age was further suggested by analyses using narrower age categories.ConclusionsSmoke-free policies can constitute a simple and inexpensive intervention for the prevention of cardiovascular diseases and thus should be included in prevention programmes.

Die Geschichte des Rauchens – wie Nichtrauchen wieder gesellschaftsfähig wird

After the invention of the cigarette 1881 the health consequences of active smoking were fully known only in 1964. Since 1986 research findings allow increasingly stronger conclusions about the impact of passive smoking on health, especially for lung cancer, cardiovascular and respiratory disease in adults and children and the sudden infant death syndrome. On the basis of current consumption patterns, approximately 450 million adults will be killed by smoking between 2000 and 2050. At least half of these adults will die between age 30 and 69. Cancer and total deaths due to smoking have fallen so far only in men in high-income countries but will rise globally unless current smokers stop smoking before or during middle age. Higher taxes, regulations on smoking, including 100 % smoke free indoor spaces, and information for consumers could avoid smoking-associated deaths. Irland was 2004 the first country worldwide introducing smoke free bars and restaurants with positive effects on compliance, health of employees and business. In the first year after the introduction these policies have resulted in a 10 - 20 % reduction of acute coronary events. In Switzerland smoke free regulations have been accepted by popular vote first in the canton of Ticino in 2006 and since then in 15 more cantons. The smoking rate dropped from 33 to 27 % since 2001.

Effect of the Italian Smoking Ban on Population Rates of Acute Coronary Events

Several countries in the world have not yet prohibited smoking in public places. Few studies have been conducted on the effects of smoking bans on cardiac health. We evaluated changes in the frequency of acute coronary events in Rome, Italy, after the introduction of legislation that banned smoking in all indoor public places in January 2005. We analyzed acute coronary events (out-of-hospital deaths and hospital admissions) between 2000 and 2005 in city residents 35 to 84 years of age. We computed annual standardized rates and estimated rate ratios by comparing the data from prelegislation (2000-2004) and postlegislation (2005) periods. We took into account several time-related potential confounders, including particulate matter (PM10) air pollution, temperature, influenza epidemics, time trends, and total hospitalization rates. The reduction in acute coronary events was statistically significant in 35- to 64-year-olds (11.2%, 95% CI 6.9% to 15.3%) and in 65- to 74-year-olds (7.9%, 95% CI 3.4% to 12.2%) after the smoking ban. No evidence was found of an effect among the very elderly. The reduction tended to be greater in men and among lower socioeconomic groups. We found a statistically significant reduction in acute coronary events in the adult population after the smoking ban. The size of the effect was consistent with the pollution reduction observed in indoor public places and with the known health effects of passive smoking. The results affirm that public interventions that prohibit smoking can have enormous public health implications.

Atorvastatin reduces the expression of cyclooxygenase-2 in a rabbit model of atherosclerosis and in cultured vascular smooth muscle cells

Inflammation is involved in the genesis and rupture of atherosclerotic plaques. We assessed the effect of atorvastatin (ATV) on the expression of cyclooxygenase-2 (COX-2) and other proinflammatory molecules in a rabbit model of atherosclerosis. Fourteen animals underwent injury of femoral arteries and 2 weeks of atherogenic diet. Afterwards, they were randomized to receive either 5 mg/kg per day of ATV ( n=8) or no treatment (NT, n=6) during 4 weeks, and were finally killed. ATV reduced lipid levels, neointimal size (0.13 (0.03–0.29) mm 2 vs 0.65 (0.14–1.81) mm 2, P=0.005) and the percentage of neointimal area positive for macrophages (1% (0–3) vs 19% (5–32), P=0.001), COX-2 (32% (23–39) vs 60% (37–81) P=0.019), interleukin-8 (IL-8) (23% (3–63) vs 63% (25–88) P=0.015), and metalloproteinase-3 (19% (12–34) vs 42% (27–93), P=0.010), without significant differences in COX-1 expression (immunohistochemistry). In situ hybridization confirmed a decreased expression of COX-2 mRNA (22% (5–40) vs 43% (34–59) P=0.038). The activity of nuclear factor-κB, which controls many proinflammatory genes including COX-2, was reduced in atherosclerotic lesions (3538 (2663–5094) vs 8696 (5429–11 312)) positive nuclei per mm 2, P=0.001) and circulating mononuclear cells (2966 vs 17 130 arbitrary units). In cultured vascular smooth muscle cells, ATV reduced the expression of COX-2 mRNA induced by IL-1β and TNF-α without affecting COX-1 expression. In conclusion, ATV, besides decreasing a number of inflammatory mediators in the atherosclerotic lesion, significantly downregulates COX-2 both in vivo and in vitro. These anti-inflammatory actions could partially account for the reduction of acute coronary events achieved by statins.

Mechanisms modifying atherosclerotic disease — from lipids to vascular biology

Recent clinical trials of three statins, pravastain, simvastatin and lovastatin, have demonstrated a major reduction in acute coronary events typically precipitated by plaque rupture. However, angiographic studies with several statins have shown that they do not appear to greatly affect the size of pre-existing plaques. These findings strongly suggest that the demonstrated protective effect of these statins is mediated through changes in plaque composition rather than size, highlighting the greater importance of composition than size in determining clinical outcome. Atherosclerotic plaques are composed of a thrombogenic lipid-rich core protected by a fibrous cap comprising smooth muscle cells (SMCs) and inflammatory cells, predominantly macrophages. SMCs are the only cell type in the atherosclerotic plaque capable of synthesizing a strong fibrous cap. Their survival is therefore crucial to plaque stability. In contrast, inflammatory cells such as macrophages increase the risk of plaque rupture by a number of mechanisms. Thus, in atherosclerosis, there is a balance between the influence of inflammatory cells tending towards plaque instability and the reparative influence of SMCs tending to plaque stability. The implication of the successful outcome studies is that the statins tested may beneficially influence this balance either by decreasing inflammation or promoting repair or both. However, because statins do not have a uniform effect on all the biological processes contributing to plaque rupture and subsequent thrombosis, the potential benefit from treating with a statin cannot necessarily be presumed or predicted from its lipid lowering potency alone. Therefore prescription of statins to prevent cardiovascular events should be based on the evidence of outcome trials.

Atherosclerotic plaque rupture: emerging insights and opportunities

Reduction in acute coronary events requires interventions that affect the mechanisms leading to formation of atherosclerotic lesions, as well as the molecular events that precipitate acute myocardial infarction. Data from clinical trials indicate that it is the vulnerability of atherosclerotic plaque to rupture, rather than the degree of atherosclerosis, that is the primary determinant of thrombosis-mediated acute coronary events. The characteristics of a plaque that is vulnerable to rupture include a thin fibrous cap separating the circulation from procoagulants in the plaque’s lipid core; increased numbers of inflammatory cells (e.g., macrophages and T cells); and a relative paucity of vascular smooth muscle cells (VSMC). Plaque stability reflects various dynamic factors: interaction of inflammatory cells, VSMC production of the extracellular matrix that is the bulwark of the fibrous cap, inhibition of this process by certain cytokines, and increased degradation of the matrix by matrix metalloproteinases. There is growing interest in the concept that intervention in the inflammatory processes of atherogenesis might reduce lesion formation and/or progression. There has also been substantial progress in understanding the transcriptional regulation of proteins that are critically involved in atherogenesis. Recently, peroxisomal proliferator–activated receptors (PPARs) have been identified as a potential link between insulin resistance and atherosclerosis. This concept is supported by the discovery through drug screening of thiazolidinediones (troglitazone, rosiglitazone), compounds that are not only ligands for PPARγ, a nuclear receptor involved in adipogenesis, but also are antidiabetic agents.

Primary prevention of coronary heart disease: guidance from Framingham: a statement for healthcare professionals from the AHA Task Force on Risk Reduction. American Heart Association.

The Framingham Heart Study has contributed importantly to understanding of the causes of coronary heart disease (CHD), stroke, and other cardiovascular diseases. Framingham research has helped define the quantitative and additive nature of these causes or, as they are now called, “cardiovascular risk factors.”1 The National Cholesterol Education Program (NCEP)2 3 has made extensive use of Framingham data in developing its strategy for preventing CHD by controlling high cholesterol levels. The NCEP guidelines2 3 adjust the intensity of cholesterol-lowering therapy with absolute risk as determined by summation of risk factors. The National High Blood Pressure Education Program (NHBPEP) has set forth a parallel approach for blood pressure control. In contrast to the NCEP,2 however, earlier NHBPEP reports issued through the Joint National Committee4 did not match the intensity of therapy to absolute risk for CHD. “Normalization” of blood pressure is the essential goal of therapy regardless of risk status. Blood pressure–lowering therapy is carried out as much for prevention of stroke and other cardiovascular complications as for reduction of CHD risk. Nonetheless, risk assessment could be important for making decisions about type and intensity of therapy for hypertension. Thus, the most recent Joint National Committee report5 gives more attention to risk stratification for adjustment of therapy for hypertension. Although Framingham data have already been influential in the development of national guidelines for risk factor management, the opportunity may exist for both cholesterol and blood pressure programs to draw more extensively from Framingham results when formulating improved risk assessment guidelines and recommending more specific strategies for risk factor modification. The American Heart Association has previously used Framingham risk factor data to prepare charts for estimating CHD risk. Framingham investigators of the National Heart, Lung, and Blood Institute prepared the original charts and have now revised …

New insights into plaque stabilisation by lipid lowering.

Thrombosis on the substrate of a disrupted plaque causes most acute coronary events. The physical integrity of the plaque thus governs the most important clinical manifestations of atherosclerosis. Of particular importance is the extracellular matrix of the fibrous capsule overlying the thrombogenic core of the atheroma. Stable atheroma generally have thick fibrous caps, and smaller lipid cores than lesions that have ruptured. Accumulating evidence supports a key role for inflammation as another critical determinant of the stability of human atherosclerotic plaques. Plaques that rupture usually have more abundant leucocytic infiltrates than those considered stable. Inflammatory mediators such as cytokines can influence several biological processes that regulate the stability of the plaque's fibrous cap, and thus its resistance to rupture. For example, interferon-gamma produced by activated T lymphocytes within atheroma inhibits the production of interstitial forms of collagen by human vascular smooth muscle cells. Inflammatory cytokines such as interleukin-1, tumour necrosis factor (TNF) and CD-40 ligand (a cell surface homologue of TNFalpha) can also elicit the expression by macrophages and smooth muscle cells of proteolytic enzymes that can weaken the extracellular matrix. We have hypothesised that lipid lowering reduces stimuli for the inflammatory response within the complex atherosclerotic lesion. Recent studies in rabbits with experimentally produced atherosclerosis have indeed shown that lipid lowering can (i) reduce macrophage numbers, (ii) decrease expression of the collagenolytic enzyme MMP-1, and (iii) reinforce the plaque's fibrous skeleton by increasing the content of interstitial collagen. By reducing local inflammation, lipid lowering can thus stabilise the plaque's fibrous cap, rendering the atheroma less prone to rupture and to precipitate thrombotic complications. These observations provide a mechanistic basis for understanding the marked reduction in acute coronary events and cerebrovascular accidents observed in patients treated with agents that reduce plasma lipids.