Risk Of Myocardial Infarction Research Articles

3D Printed Interdigitated Electrodes for Cardiac Biomarker Detection.

The identification of biomarkers has significant benefits for early disease diagnosis and treatment. Hence, there is an increasing demand for low-cost, disposable point-of-care diagnostic devices for rapid and specific biomarker detection, with good sensitivity and range. Interdigitated electrodes (IDEs) are among the most widely used transducers, especially in chemical and biological sensors, because of their high sensitivity, low cost, and straightforward manufacturing procedure. In this work, a simple 3D printed IDE structure has been developed for cardiac troponin I detection to indicate the risk of acute myocardial infarction (AMI). IDEs have been fabricated using 3D printing technique and the electrically conductive composite polylactic acid (PLA) filament being utilized for the fabrication of electrodes. The demonstrated cardiac troponin I sensor has a calculated quantification limit and detection limit of 0.233 ng ml-1 and 76.97 pg ml-1, respectively which are clinically significant ranges for AMI identification. Electrochemical analytical techniques, such as electrochemical impedance spectroscopy (EIS) and cyclic voltammetry (CV), were carried out for the detection of analyte concentration. Furthermore, using this fabrication methodology IDEs can be fabricated for under US$ 0.4 which can be utilized to detect several other biomarkers.

Myocardial infarction & C-reactive protein levels among Mexican adults with arthritis: Findings from the Mexican Health and Aging Study

BackgroundStudies of adult populations in high-income countries have found an association between arthritis and myocardial infarction (MI) due to high levels of systemic inflammation. Our objectives were to examine the association between arthritis and MI among Mexican adults and to assess the mediating effect of C-reactive protein (CRP) on this association. MethodsData came from the 2012, 2015, and 2018 observation waves of the Mexican Health and Aging Study. Our sample included 11,707 participants aged 50 and older with no prior MI before 2012. We used self-reported information for arthritis, joint pain, medication use, and limitations to daily activities in 2012. Logistic regression was used to model the association between arthritis and self-reported MI in 2015 or 2018. We used a sub-sample of 1602 participants to assess the mediating effect of CRP. ResultsIn the full sample, participants with arthritis that limited their daily activities had higher odds of MI than participants with no arthritis (OR = 1.40; 95 % CI = 1.04–1.88). In the sub-sample, arthritis that limited daily activities was associated with higher mean CRP (5.2 mg/dL; 95 % CI = 4.10–6.21) than arthritis with no limitations (3.5 mg/dL; 95 % CI = 2.93–4.01). However, CRP levels had a small mediating effect, and the relationship between arthritis with physical limitations and MI remained statistically significant. ConclusionMexican adults with arthritis that limits their daily activities are at an increased risk for MI. Continued research is needed to identify factors that contribute to this increased risk.

Long-term risk factors of recurrent stroke, myocardial infarction and death in patients leaving hospital with a diagnosis of ischemic stroke or TIA

Objectives. The prevalence of patients with prior stroke is increasing globally. Accordingly, there is a need for up-to-date evidence of patient-related prognostic factors for stroke recurrence, post stroke myocardial infarction (MI) and death based on long-term follow-up of stroke survivors. For this purpose, the RIALTO study was established in 2004. Design. A prospective cohort study in which patients diagnosed with ischemic stroke (IS) or transient ischemic attack (TIA) in three Copenhagen hospitals were included. Data were collected from medical records and by structured interview. Data on first stroke recurrence, first MI and all-cause death were extracted from the Danish National Patient Registry and the Danish Civil Registration System. Results. We included 1215 patients discharged after IS or TIA who were followed up by register data from April 2004 to end of 2018 giving a median follow-up of 3.5–6.9 years depending on the outcome. At the end of follow-up 406 (33%) patients had been admitted with a recurrent stroke, 100 (8%) had a MI and 822 (68%) had died. Long-term prognostic predictors included body mass index, diabetes, antihypertensive and lipid lowering treatment, smoking, a sedentary lifestyle as well as poor self-rated health and psychosocial problems. Conclusions. Long-term risk of recurrent stroke and MI remain high in patients discharged with IS or TIA despite substantial improvements in tertiary preventive care in recent decades. Continued attention to the patient risk profile among patients surviving the early phase of stroke, including comorbidities, lifestyle, and psychosocial challenges, is warranted.

Exacerbation History and Risk of Myocardial Infarction and Pulmonary Embolism in COPD

Acute exacerbations of COPD (AECOPDs) are increasingly recognized as episodes of heightened risk of cardiovascular events. It is not known whether exacerbation history is differentially associated with future myocardial infarction (MI) or pulmonary embolism (PE). Is the number and severity of AECOPDs associated with increased risk of MI or PE in a real-life cohort of patients with COPD? We identified a cohort of 66,422 patients (≥ 30 years of age) with a primary diagnosis of COPD in the Swedish National Airway Register from January 2014 to June 2022, with complete data on lung function. Patients were classified by moderate (prescription of oral corticosteroids) and severe (hospitalization) exacerbations the year before index date and were followed until December 2022 for hospitalization or death from MI or PE, corresponding to > 265,000 patient-years, with a maximum follow-up time of 9 years. Competing risk regression, according to the Fine-Gray model, was used to calculate subdistribution hazard ratios with 95%CIs. Compared with no AECOPDs in the baseline period, AECOPD number and severity were associated with increased long-term risk of both MI and PE in a gradual fashion, ranging from a subdistribution hazard ratio of 1.10 (95%CI, 0.97-1.24) and 1.33 (95%CI, 1.11-1.60), respectively, for one moderate exacerbation, to 1.82 (95%CI, 1.36-2.44) and 2.62 (95%CI, 1.77-3.89), respectively, for two or more severe exacerbations. In a time-restricted follow-up sensitivity analysis, the associations were stronger during the first year of follow-up and diminished over time. The risk of MI and PE increases with the frequency and severity of AECOPD in this large, real-life cohort of patients with COPD.

Role of GLP-1 Receptor Agonist in Diabetic Cardio-renal Disorder: Recent Updates of Clinical and Pre-clinical Evidence.

Cardiovascular complications and renal disease is the growing cause of mortality in patients with diabetes. The subversive complications of diabetes such as hyperglycemia, hyperlipidemia and insulin resistance lead to an increase in the risk of myocardial infarction (MI), stroke, heart failure (HF) as well as chronic kidney disease (CKD). Among the commercially available anti-hyperglycemic agents, incretin-based medications appear to be safe and effective in the treatment of type 2 diabetes mellitus (T2DM) and associated cardiovascular and renal disease. Glucagon-like peptide 1 receptor agonists (GLP-1RAs) have been shown to be fruitful in reducing HbA1c, blood glucose, lipid profile, and body weight in diabetic patients. Several preclinical and clinical studies revealed the safety, efficacy, and preventive advantages of GLP-1RAs against diabetes- induced cardiovascular and kidney disease. Data from cardio-renal outcome trials had highlighted that GLP-1RAs protected people with established CKD from significant cardiovascular disease, lowered the likelihood of hospitalization for heart failure (HHF), and lowered all-cause mortality. They also had a positive effect on people with end-stage renal disease (ESRD) and CKD. Beside clinical outcomes, GLP-1RAs reduced oxidative stress, inflammation, fibrosis, and improved lipid profile pre-clinically in diabetic models of cardiomyopathy and nephropathy that demonstrated the cardio-protective and reno-protective effect of GLP-1RAs. In this review, we have focused on the recent clinical and preclinical outcomes of GLP-1RAs as cardio-protective and reno-protective agents as GLP-1RAs medications have been demonstrated to be more effective in treating T2DM and diabetes-induced cardiovascular and renal disease than currently available treatments in clinics, without inducing hypoglycemia or weight gain.

Differing genetic variants associated with liver fat and their contrasting relationships with cardiovascular diseases and cancer

The mechanisms underlying the association of steatotic liver disease with cardiovascular and cancer outcomes are poorly understood. We aimed to use MRI-derived measures of liver fat and genetics to investigate causal mechanisms that link higher liver fat to various health outcomes. We conducted a genome-wide association study on 37,358 UK Biobank participants to identify genetic variants associated with liver fat measured from MRI scans. We used a Mendelian randomisation approach to investigate the causal effect of liver fat on health outcomes independent of BMI, alcohol consumption and lipids using data from published genome-wide association studies and FinnGen. We identified 13 genetic variants associated with liver fat that had differing effects on the risks of health outcomes. Genetic variants associated with impaired hepatic triglyceride export showed liver fat-increasing alleles to be correlated with a reduced risk of coronary artery disease and myocardial infarction but an elevated risk of type 2 diabetes, while variants associated with enhanced de novo lipogenesis showed liver fat-increasing alleles to be linked to a higher risk of myocardial infarction and coronary artery disease. Genetically higher liver fat content increased the risk of non-alcohol-related cirrhosis, hepatocellular carcinoma, and intrahepatic bile duct and gallbladder cancers, exhibiting a dose-dependent relationship, irrespective of the mechanism. This study provides fresh insight into the heterogeneous effect of liver fat on health outcomes. It challenges the notion that liver fat per se is an independent risk factor for cardiovascular disease, underscoring the dependency of this association on the specific mechanisms that drive fat accumulation in the liver. However, excess liver fat, regardless of the underlying mechanism, appears to be causally linked to cirrhosis and cancers in a dose-dependent manner. This research advances our understanding of the heterogeneity in mechanisms influencing liver fat accumulation, providing new insights into how liver fat accumulation may impact various health outcomes. The findings challenge the notion that liver fat is an independent risk factor for cardiovascular disease and highlight the mechanistic effect of some genetic variants on fat accumulation and the development of cardiovascular diseases. This study is of particular importance for healthcare professionals including physicians and researchers, as well as patients, as it allows for more targeted and personalised treatment by understanding the relationship between liver fat and various health outcomes. The findings emphasise the need for a personalised management approach and a reshaping of risk assessment criteria. It also provides room for prioritising a clinical intervention aimed at reducing liver fat content (likely via intentional weight loss) that could help protect against liver-related fibrosis and cancer.

Increased risk of developing cerebro-cardiovascular diseases in police officers: a nationwide retrospective cohort study

BackgroundPolice officers face an increased risk of developing cerebro-cardiovascular diseases (CVD). However, current literature lacks population-based cohort studies specifically focusing on this association. This study aimed to investigate the association between police officers and the risk of developing CVD compared with education officers, while accounting for socioeconomic and demographic factors.MethodsWe used the Korean National Health Insurance Service data spanning from 2009 to 2020. In this population-based retrospective matched cohort study, we identified age, sex, and calendar years of job-enrollment–matched education officers for each police officer. This study evaluated the CVD occurrence, including acute myocardial infarction, ischemic stroke, and hemorrhagic stroke. Using multivariable Cox regression analysis, we determined the risk of developing CVD, expressed as a hazard ratio (HR) and 95% confidence interval (CI).ResultsAmong 104,134 police officers and 104,134 education officers, 4,391(42.2%) cases and 3,631(34.9%) cases of CVD occurred, respectively. The mean ± standard deviation age was 38.4 ± 9.4 years in police officers and 38.6 ± 9.5 years in education officers. The proportion of men was 84.8 % in both groups. Police officers were significantly associated with a higher risk of developing CVD compared with education officers, with an adjusted HR of 1.15 (95% CI, 1.09–1.22). In addition, police officers had significantly higher risks for acute myocardial infarction (adjusted HR, 1.16; 95% CI, 1.06–1.26) and ischemic stroke (adjusted HR, 1.17; 95% CI, 1.09–1.25).ConclusionsThe findings of our study highlight a significant increase in the risk of developing CVD among police officers, particularly among those aged 45 years and older and those with uncontrolled blood pressure compared to their education officer counterparts. Future cohort studies are required to confirm this association.

Impact of Obstructive Sleep Apnea on Diabetic Retinopathy Progression and Systemic Complications

PurposeEvaluate the risk of diabetic retinopathy progression and systemic vascular events, including death, in patients with non-proliferative diabetic retinopathy (NPDR) with obstructive sleep apnea (OSA). DesignRetrospective cohort study. MethodsElectronic chart query using TriNetX (Cambridge, MA, USA), an electronic health records network comprising data from over 124 million patients. Patients with NPDR with and without OSA were identified. Patients were excluded if they had history of proliferative disease (PDR), diabetic macular edema (DME), or prior ocular intervention (intravitreal injection, laser, or pars plana vitrectomy). Propensity score matching was performed to control for baseline demographics and comorbidities. Rate of progressing to vision threatening complications (VTCs), need for ocular intervention, and systemic events was measured at 1, 3, and 5 years. Results11,931 patients in each group were analyzed after propensity score matching. There was elevated risk of PDR in the OSA cohort at 1 (RR: 1.34, P<0.001), 3 (RR: 1.31, P<0.001), and 5 years (RR: 1.28, P<0.001). There was elevated risk of DME in the OSA group at all timepoints: 1 (RR: 1.31, P<0.001), 3 (RR: 1.19, P<0.001), and 5 years (RR: 1.18, P<0.001). With respect to ocular interventions, there was an increased risk of intravitreal injection in OSA patients at 1 (RR: 1.59, P<0.001), 3 (RR: 1.58, P<0.001), and 5 years (RR: 1.54, P<0.001), and similar trends were noted with laser photocoagulation, but not vitrectomy. Regardingsystemic events, NPDR patients with OSA had a greater risk of stroke (1 year RR: 1.80, P<0.001; 3 year RR: 1.56, P<0.001; 5 year RR: 1.49, P<0.001), myocardial infarction (1 year RR: 1.51, P<0.001; 3 year RR: 1.46, P<0.001; 5 year RR: 1.43, P<0.001), and death (1 year RR: 1.31, P<0.001; 3 year RR: 1.19, P<0.001; 5 year RR: 1.15, P<0.001). ConclusionsThere is an increased rate of DR progression to VTCs, need for ocular intervention, and systemic complications, including death, for patients with OSA. We emphasize the need for improved screening measures of patients with NPDR and potential OSA.

Metabolic syndrome-associated murine aortic wall stiffening is associated with premature elastic fibers aging.

Type 2 diabetes (T2D) constitutes a major public health problem, and despite prevention efforts, this pandemic disease is one of the deadliest diseases in the world. In 2022, 6.7 million patients with T2D died prematurely from vascular complications. Indeed, diabetes increases the risk of myocardial infarction or stroke eightfold. The identification of the molecular factors involved in the occurrence of cardiovascular complications and their prevention are therefore major axes. Our hypothesis is that factors brought into play during physiological aging appear prematurely with diabetes progression. Our study focused on the aging of the extracellular matrix (ECM), a major element in the maintenance of vascular homeostasis. We characterized the morphological and functional aspects of aorta, with a focus on the collagen and elastic fibers of diabetic mice aged from 6 mo to nondiabetic mice aged 6 mo and 20 mo. The comparison with the two nondiabetic models (young and old) highlighted an exacerbated activity of proteases, which could explain a disturbance in the collagen accumulation and an excessive degradation of elastic fibers. Moreover, the generation of circulating elastin-derived peptides reflects premature aging of the ECM. These extracellular elements contribute to the appearance of vascular rigidity, often the origin of pathologies such as hypertension and atherosclerosis. In conclusion, we show that diabetic mice aged 6 mo present the same characteristics of ECM wear as those observed in mice aged 20 mo. This accelerated aortic wall remodeling could then explain the early onset of cardiovascular diseases and, therefore, the premature death of patients with T2D.NEW & NOTEWORTHY Aortic elastic fibers of young (6-mo old) individuals with diabetes degrade prematurely and exhibit an appearance like that found in aged (20-mo old) nondiabetic mice. Exacerbated elastolysis and elastin-derived peptide production are characteristic elements, contributing to early aortic wall rigidity and hypertension development. Therefore, limiting this early aging could be a judicious therapeutic approach to reduce cardiovascular complications and premature death in patients with diabetes.

Associations of uric acid with the risk of cardiovascular disease and all-cause mortality among individuals with chronic kidney disease: the Kailuan Study

Abstract Aims The relationship between uric acid (UA) concentrations and the risk of cardiovascular disease (CVD), especially for subtypes of CVD among individuals with chronic kidney disease (CKD), is not well understood. This study aimed to investigate whether UA concentration was associated with subtypes of CVD and all-cause mortality among individuals with CKD. Methods and results A total of 27 707 individuals with CKD, free of CVD at recruitment from the Kailuan Study, were included. Cox proportional hazards regression models were used to compute hazard ratios (HRs) and 95% confidence intervals (CIs). Over a median follow-up of 11–12 years, we documented 674 myocardial infarctions, 1197 heart failures, 2406 strokes, and 5676 total deaths. Among participants with CKD, compared with those in the lowest tertile of UA, the HRs (95% CIs) of participants in the highest UA tertile were 1.38 (1.13–1.67) for myocardial infarction, 1.60 (1.38–1.85) for heart failure, 1.01 (0.91–1.12) for stroke, and 1.29 (1.21–1.38) for all-cause mortality. Subgroup analyses showed that the associations between UA and heart failure and all-cause mortality were stronger in individuals with estimated glomerular filtration rate &amp;lt;45 mL/min/1.73 m2 compared to their counterparts (Pinteraction &amp;lt; 0.05). Additionally, the association between UA and all-cause mortality was stronger among individuals without diabetes than those with diabetes (Pinteraction &amp;lt; 0.05). Conclusion In individuals with CKD, a higher concentration of UA was associated with a higher risk of myocardial infarction, heart failure, and all-cause mortality, following a dose–response relationship. Our data underscore the importance of UA screening among individuals with CKD for CVD and premature death prevention.

Advancing non-ST-elevation myocardial infarction risk assessment with artificial intelligence-based algorithms

Advancing non-ST-elevation myocardial infarction risk assessment with artificial intelligence-based algorithms

Impact of Obstructive Sleep Apnea and Sympathetic Nervous System on Cardiac Health: A Comprehensive Review.

A prevalent condition linked to an elevated risk of cardiovascular disease is sleep apnea. This review examines the connections between cardiac risk, the sympathetic nervous system, and sleep apnea. The increased risk of hypertension, arrhythmias, myocardial infarction, and heart failure was highlighted in the pathophysiology of sleep apnea and its effect on sympathetic activation. It is also important to consider potential processes such as oxidative stress, inflammation, endothelial dysfunction, and autonomic imbalance that may relate sleep apnea-induced sympathetic activation to cardiac risk. With implications for creating innovative diagnostic and treatment approaches to lessen the cardiovascular effects of sleep apnea, the goal of this investigation is to improve the understanding of the intricate link between sympathetic activity, cardiac risk, and sleep apnea. This study aimed to clarify the complex relationship between cardiovascular health and sleep apnea by synthesizing the available research and highlighting the crucial role played by the sympathetic nervous system in moderating this relationship. Our thorough investigation may have important therapeutic ramifications that will direct the creation of focused therapies to enhance cardiovascular outcomes in sleep apnea sufferers.

MODERN VIEW ON RADIOFREQUENCY DENERVATION OF RENAL ARTERIES

Today, arterial hypertension is one of the most important health problems. It is also the main cause of cardiovascular complications and death. Despite significant success of modern antihypertensive pharmacotherapy, 10 % of the entire patient population with high blood pressure have extremely low sensitivity to core drugs aimed at BP correction. According to large clinical studies, the risk of myocardial infarction, stroke and other adverse cardiovascular outcomes in individuals with resistant hypertension is several times higher than in patients with controlled blood pressure. The purpose of this work is to analyze scientific literature on the history of development, effectiveness and safety of catheter radiofrequency denervation of renal arteries in patients with resistant arterial hypertension. The authors used articles from Pubmed, eLIBRARY, etc. for their analysis. The results of clinical studies show that patients with resistant arterial hypertension, in contrast to patients with controlled blood pressure, have more pronounced sympathetic activity. Hyperactivity of this part of the nervous system may be one of the main pathogenetic factors causing development of resistance to pharmacotherapy. Thus, radiofrequency renal denervation, modulating the tone of the sympathetic nervous system, is of particular interest.

Association between Smoking Habit Changes and the Risk of Myocardial Infarction in Ischemic Stroke Patients: a Nationwide cohort study.

Smoking is a well-known risk factor for cardiovascular diseases, including myocardial infarction (MI) and ischemic stroke (IS). While the relationship between smoking and the risk of cardiovascular diseases is established, the impact of changing smoking habits post-IS on the risk of subsequent MI remains unclear. This study aims to elucidate the effects of alterations in smoking behavior following an IS diagnosis on the likelihood of experiencing an MI. Utilizing data from the Korean National Health Insurance Services Database, this nationwide population-based cohort study included 199,051 participants diagnosed with IS between January 2010 and December 2016. Smoking status was categorized based on changes in smoking habits before and after IS diagnosis. The association between changes in smoking behavior and the risk of subsequent MI was analyzed using multivariable Cox proportional hazard regression models. During a median follow-up of 4.17 person-years, a total of 5,734 (2.88%) patients were diagnosed with MI after IS. Smoking quitters (2.93%) or former smokers (2.47%) have a similar or lower rate of MI than the average, even if they have smoked cigarettes, while sustained smokers (3.46%) or new smokers (3.81%) have much higher rates of MI. Among sustained and new smokers, the risk of incident MI were significantly higher than never smokers (new smoker adjusted HR [aHR]: 1.496, 95% CI 1.262-1.774; sustained smoker aHR 1.494, 95% CI 1.361-1.641). Also, among the study participants, approximately two-thirds continued smoking after their IS diagnosis. Changing smoking habits after an IS diagnosis significantly influences the risk of subsequent MI. Specifically, continuing or starting to smoke after an IS diagnosis is associated with a higher risk of MI. These results underscore the importance of targeted smoking cessation interventions for stroke patients to reduce the risk of subsequent myocardial infarction.

Sex differences in coronary atherosclerotic plaque activity using 18F-sodium fluoride positron emission tomography.

There are sex differences in the extent, severity, and outcomes of coronary artery disease. We aimed to assess the influence of sex on coronary atherosclerotic plaque activity measured using coronary 18F-sodium fluoride (18F-NaF) positron emission tomography (PET), and to determine whether 18F-NaF PET has prognostic value in both women and men. In a post-hoc analysis of observational cohort studies of patients with coronary atherosclerosis who had undergone 18F-NaF PET CT angiography, we compared the coronary microcalcification activity (CMA) in women and men. Baseline 18F-NaF PET CT angiography was available in 999 participants (151 (15%) women) with 4282 patient-years of follow-up. Compared to men, women had lower coronary calcium scores (116 [interquartile range, 27-434] versus 205 [51-571] Agatston units; p = 0.002) and CMA values (0.0 [0.0-1.12] versus 0.53 [0.0-2.54], p = 0.01). Following matching for plaque burden by coronary calcium scores and clinical comorbidities, there was no sex-related difference in CMA values (0.0 [0.0-1.12] versus 0.0 [0.0-1.23], p = 0.21) and similar proportions of women and men had no 18F-NaF uptake (53.0% (n = 80) and 48.3% (n = 73); p = 0.42), or CMA values > 1.56 (21.8% (n = 33) and 21.8% (n = 33); p = 1.00). Over a median follow-up of 4.5 [4.0-6.0] years, myocardial infarction occurred in 6.6% of women (n = 10) and 7.8% of men (n = 66). Coronary microcalcification activity greater than 0 was associated with a similarly increased risk of myocardial infarction in both women (HR: 3.83; 95% CI:1.10-18.49; p = 0.04) and men (HR: 5.29; 95% CI:2.28-12.28; p < 0.001). Although men present with more coronary atherosclerotic plaque than women, increased plaque activity is a strong predictor of future myocardial infarction regardless of sex.

Rare damaging CCR2 variants are associated with lower lifetime cardiovascular risk.

Previous work has shown a role of CCL2, a key chemokine governing monocyte trafficking, in atherosclerosis. However, it remains unknown whether targeting CCR2, the cognate receptor of CCL2, provides protection against human atherosclerotic cardiovascular disease. Computationally predicted damaging or loss-of-function (REVEL>0.5) variants within CCR2 were detected in whole-exome-sequencing data from 454,775 UK Biobank participants and tested for association with cardiovascular endpoints in gene-burden tests. Given the key role of CCR2 in monocyte mobilization, variants associated with lower monocyte count were prioritized for experimental validation. The response to CCL2 of human cells transfected with these variants was tested in migration and cAMP assays. Validated damaging variants were tested for association with cardiovascular endpoints, atherosclerosis burden, and vascular risk factors. Significant associations were replicated in six independent datasets (n=1,062,595). Carriers of 45 predicted damaging or loss-of-function CCR2 variants (n=787 individuals) were at lower risk of myocardial infarction and coronary artery disease. One of these variants (M249K, n=585, 0.15% of European ancestry individuals) was associated with lower monocyte count and with both decreased downstream signaling and chemoattraction in response to CCL2. While M249K showed no association with conventional vascular risk factors, it was consistently associated with a lower risk of myocardial infarction (Odds Ratio [OR]: 0.66 95% Confidence Interval [CI]: 0.54-0.81, p=6.1×10-5) and coronary artery disease (OR: 0.74 95%CI: 0.63-0.87, p=2.9×10-4) in the UK Biobank and in six replication cohorts. In a phenome-wide association study, there was no evidence of a higher risk of infections among M249K carriers. Carriers of an experimentally confirmed damaging CCR2 variant are at a lower lifetime risk of myocardial infarction and coronary artery disease without carrying a higher risk of infections. Our findings provide genetic support for the translational potential of CCR2-targeting as an atheroprotective approach.

Myocardial Bridging Increases the Risk of Adverse Cardiovascular Events in Patients without Coronary Atherosclerosis.

Background: Myocardial bridging (MB) is a congenital coronary anomaly and an important cause of chest pain. The long-term effects of MB on cardiovascular events remain elusive. Methods: We used the National Health Insurance Research Database of Taiwan to conduct an analysis. All patients who had undergone coronary angiography were considered for inclusion. The primary endpoint was a composite of nonfatal myocardial infarction, nonfatal ischemic stroke, and cardiovascular death. Results: We identified 10,749 patients from 2008 to 2018 and matched them with an equal number of controls by propensity-score matching. The mean follow-up period was 5.78 years. In patients without coronary artery disease, MB increased the risk of the composite endpoint (hazard ratio [HR]: 1.57, 95% confidence interval [CI]: 1.44-1.72, p < 0.001), which was driven by increased risks of nonfatal myocardial infarction and cardiovascular death. In patients with significant coronary artery disease, MB did not increase the risk of major adverse cardiovascular events. MB was identical to insignificant coronary artery disease from the viewpoint of clinical outcomes. Conclusions: The presence of MB significantly increases cardiovascular risks in patients with normal coronary vessels. Atherosclerotic coronary artery disease mitigates the effect of MB on cardiovascular outcomes. MB can be considered an insignificant coronary artery disease equivalent.

Influenza Infection and Acute Myocardial Infarction

BackgroundAcute respiratory infections can trigger acute myocardial infarction. We aimed to quantify the association between laboratory-confirmed influenza infection and acute myocardial infarction, particularly in patients with and without known coronary artery disease.MethodsThis observational, registry-based, self-controlled case series study evaluated the association between laboratory-confirmed influenza infection and occurrence of acute myocardial infarction. Laboratory records on respiratory virus polymerase chain reaction (PCR) testing from 16 laboratories across the Netherlands were linked to national mortality, hospitalization, medication, and administrative registries. Influenza infection was defined as a positive PCR test result. Acute myocardial infarction was defined as a registered diagnostic code for either acute myocardial infarction hospitalization or death. Using a self-controlled case series method, we then compared the incidence of acute myocardial infarction during the risk period (days 1 to 7 after influenza infection) versus the control period (1 year before and 51 weeks after the risk period).ResultsBetween 2008 and 2019, we identified 158,777 PCR tests for influenza in the study population; 26,221 were positive for influenza, constituting 23,405 unique influenza illness episodes. A total of 406 episodes were identified with acute myocardial infarction occurring within 1 year before and 1 year after confirmed influenza infection and were included in analysis. Twenty-five cases of acute myocardial infarction occurred during the risk period versus 394 during the control period. The adjusted relative incidence of acute myocardial infarction during the risk period compared with the control period was 6.16 (95% confidence interval [CI], 4.11 to 9.24). The relative incidence of acute myocardial infarction in individuals without prior hospitalization for coronary artery disease was 16.60 (95% CI, 10.45 to 26.37) compared with 1.43 (95% CI, 0.53 to 3.84) for those with prior admission for coronary artery disease.ConclusionsInfluenza infection was associated with an increased risk of acute myocardial infarction, especially in individuals without a prior hospitalization for coronary artery disease. (Funded by the Dutch Research Council [NWO].)

Overview of Cochrane Systematic Reviews on Interventions for Rehabilitation in People with Ischemic Heart Disease: A Mapping Synthesis.

Objectives: This overview of Cochrane Systematic Reviews (CSRs) reports on current evidence and its certainty of the effectiveness of interventions for the rehabilitation of people with ischemic heart disease (IHD), included in the World Health Organization Rehabilitation Programme Package of Interventions for Rehabilitation. Methods: We included all the CSRs relevant to people with IHD. We used a mapping synthesis to group outcomes and comparisons of included CSRs, indicating the effectiveness of interventions for rehabilitation and the certainty of evidence. Results: The evidence map included a total of 13 CSRs. The effect of the interventions varied across comparisons, and the certainty of evidence was inconsistent, ranging from high to very low. We found the best evidence for exercise-based cardiac rehabilitation in the reduction of fatal and non-fatal myocardial infarction and all-cause hospital admission up to 12 months follow-up. Also, combined interventions (work-directed interventions, physical conditioning interventions, and psychological interventions) reduce the days needed for returning to work. Conclusions: The current effect and certainty of evidence for several comparisons investigated support the role of exercise-based cardiac rehabilitation in the management of people with IHD, specifically reducing the risk of fatal and non-fatal myocardial infarction and hospitalisation. However, our findings highlight the lack of high-certainty evidence about hard endpoints, particularly total mortality. Future research should prioritise these primary endpoints to enhance the credibility of cardiac rehabilitation.

Minor Genetic Overlap Among Rheumatoid Arthritis, Myocardial Infarction, and Myocardial Infarction Risk Determinants.

The aim of this study was to investigate whether a shared genetic susceptibility exists between individuals with rheumatoid arthritis (RA) and individuals with myocardial infarction (MI)-including major MI risk factors-and to quantify the degree of any such overlap. Genome-wide association study (GWAS) data for individuals with RA were constructed from a sample of 26,637 Swedish patients with RA and controls without RA. For patients with MI, GWAS data were obtained from a previously published meta-analysis. Genome-wide genetic correlation was estimated via linkage disequilibrium score regression. LAVA was employed to estimate local genetic correlations in ~2,500 nonoverlapping loci, including the major histocompatibility complex. The controls without RA were used for reference panel data. We also assessed stratified estimates of both genome-wide and local genetic correlation based on subsamples of individuals with seropositive RA and those with seronegative RA. Furthermore, genome-wide genetic correlation was estimated between RA and selected cardiovascular risk factors to elucidate pleiotropic relationships. Following quality control, our GWAS of patients with RA consisted of 25,826 individuas. Genome-wide genetic correlation between patients with RA and MI was estimated to 0.13 (95% confidence interval -0.03 to 0.29). Six regions exhibited significant local genetic correlation, though none harbored any known risk single-nucleotide polymorphisms for either of the two traits. Estimates were similar in both individuals with seropositive RA and those with seronegative RA. No statistically significant genetic correlations were observed between RA risk factors and any of the MI risk factors. Our findings indicate that genetic overlap between patients with RA and MI is minor. Furthermore, genetic overlap between RA and MI risk factors seem unlikely to provide a major contribution to the increased risk of MI observed in patients with RA.