Journal Of Clinical & Experimental Cardiology[JOURNAL]
Sun
200 papers
Transportation noise pollution and cardiovascular disease.
Münzel T, Sørensen M, Daiber A
Nat Rev Cardiol · 2021 Sep · PMID 33790462 · Publisher ↗
Epidemiological studies have found that transportation noise increases the risk of cardiovascular morbidity and mortality, with high-quality evidence for ischaemic heart disease. According to the WHO, ≥1.6 million health...
Epidemiological studies have found that transportation noise increases the risk of cardiovascular morbidity and mortality, with high-quality evidence for ischaemic heart disease. According to the WHO, ≥1.6 million healthy life-years are lost annually from traffic-related noise in Western Europe. Traffic noise at night causes fragmentation and shortening of sleep, elevation of stress hormone levels, and increased oxidative stress in the vasculature and the brain. These factors can promote vascular dysfunction, inflammation and hypertension, thereby elevating the risk of cardiovascular disease. In this Review, we focus on the indirect, non-auditory cardiovascular health effects of transportation noise. We provide an updated overview of epidemiological research on the effects of transportation noise on cardiovascular risk factors and disease, discuss the mechanistic insights from the latest clinical and experimental studies, and propose new risk markers to address noise-induced cardiovascular effects in the general population. We also explain, in detail, the potential effects of noise on alterations of gene networks, epigenetic pathways, gut microbiota, circadian rhythm, signal transduction along the neuronal-cardiovascular axis, oxidative stress, inflammation and metabolism. Lastly, we describe current and future noise-mitigation strategies and evaluate the status of the existing evidence on noise as a cardiovascular risk factor.
Use of Artificial Intelligence and Deep Neural Networks in Evaluation of Patients With Electrocardiographically Concealed Long QT Syndrome From the Surface 12-Lead Electrocardiogram.
Bos JM, Attia ZI, Albert DE … +3 more , Noseworthy PA, Friedman PA, Ackerman MJ
JAMA Cardiol · 2021 May · PMID 33566059 · Full text
IMPORTANCE: Long QT syndrome (LQTS) is characterized by prolongation of the QT interval and is associated with an increased risk of sudden cardiac death. However, although QT interval prolongation is the hallmark feature...
IMPORTANCE: Long QT syndrome (LQTS) is characterized by prolongation of the QT interval and is associated with an increased risk of sudden cardiac death. However, although QT interval prolongation is the hallmark feature of LQTS, approximately 40% of patients with genetically confirmed LQTS have a normal corrected QT (QTc) at rest. Distinguishing patients with LQTS from those with a normal QTc is important to correctly diagnose disease, implement simple LQTS preventive measures, and initiate prophylactic therapy if necessary. OBJECTIVE: To determine whether artificial intelligence (AI) using deep neural networks is better than the QTc alone in distinguishing patients with concealed LQTS from those with a normal QTc using a 12-lead electrocardiogram (ECG). DESIGN, SETTING, AND PARTICIPANTS: A diagnostic case-control study was performed using all available 12-lead ECGs from 2059 patients presenting to a specialized genetic heart rhythm clinic. Patients were included if they had a definitive clinical and/or genetic diagnosis of type 1, 2, or 3 LQTS (LQT1, 2, or 3) or were seen because of an initial suspicion for LQTS but were discharged without this diagnosis. A multilayer convolutional neural network was used to classify patients based on a 10-second, 12-lead ECG, AI-enhanced ECG (AI-ECG). The convolutional neural network was trained using 60% of the patients, validated in 10% of the patients, and tested on the remaining patients (30%). The study was conducted from January 1, 1999, to December 31, 2018. MAIN OUTCOMES AND MEASURES: The goal of the study was to test the ability of the convolutional neural network to distinguish patients with LQTS from those who were evaluated for LQTS but discharged without this diagnosis, especially among patients with genetically confirmed LQTS but a normal QTc value at rest (referred to as genotype positive/phenotype negative LQTS, normal QT interval LQTS, or concealed LQTS). RESULTS: Of the 2059 patients included, 1180 were men (57%); mean (SD) age at first ECG was 21.6 (15.6) years. All 12-lead ECGs from 967 patients with LQTS and 1092 who were evaluated for LQTS but discharged without this diagnosis were included for AI-ECG analysis. Based on the ECG-derived QTc alone, patients were classified with an area under the curve (AUC) value of 0.824 (95% CI, 0.79-0.858); using AI-ECG, the AUC was 0.900 (95% CI, 0.876-0.925). Furthermore, in the subset of patients who had a normal resting QTc (<450 milliseconds), the QTc alone distinguished those with LQTS from those without LQTS with an AUC of 0.741 (95% CI, 0.689-0.794), whereas the AI-ECG increased this discrimination to an AUC of 0.863 (95% CI, 0.824-0.903). In addition, the AI-ECG was able to distinguish the 3 main genotypic subgroups (LQT1, LQT2, and LQT3) with an AUC of 0.921 (95% CI, 0.890-0.951) for LQT1 compared with LQT2 and 3, 0.944 (95% CI, 0.918-0.970) for LQT2 compared with LQT1 and 3, and 0.863 (95% CI, 0.792-0.934) for LQT3 compared with LQT1 and 2. CONCLUSIONS AND RELEVANCE: In this study, the AI-ECG was found to distinguish patients with electrocardiographically concealed LQTS from those discharged without a diagnosis of LQTS and provide a nearly 80% accurate pregenetic test anticipation of LQTS genotype status. This model may aid in the detection of LQTS in patients presenting to an arrhythmia clinic and, with validation, may be the stepping stone to similar tools to be developed for use in the general population.
[Echocardiography in the Assessment of Postsystolic Shortening of the Left Ventricle Myocardium of the Heart].
Alekhin MN, Stepanova AI
Kardiologiia · 2021 Jan · PMID 33522475 · Publisher ↗
Echocardiography allows evaluating left ventricular (LV) myocardial contractility; however, the visual assessment of contractility is subjective and requires considerable experience. Modern technologies for assessment of...
Echocardiography allows evaluating left ventricular (LV) myocardial contractility; however, the visual assessment of contractility is subjective and requires considerable experience. Modern technologies for assessment of LV myocardial contractility, such as tissue Doppler and speckle-tracking echocardiography, provide quantitative estimation of various parameters of myocardial strain, including the LV postsystolic shortening. Several studies have demonstrated the value of postsystolic shortening for evaluation of myocardial ischemia and "ischemic memory" in patients with cardiovascular diseases. This review analyzes experimental and clinical studies that addressed LV postsystolic shortening.
The Role of Neprilysin Inhibitors in the Treatment of Heart Failure with Preserved Ejection Fraction.
Ovchinnikov AG, Gvozdeva AD, Blankova ZN … +2 more , Borisov AA, Ageev FT
Kardiologiia · 2020 Dec · PMID 33487158 · Publisher ↗
Clinical and hemodynamic aggravation of heart failure with preserved ejection fraction (HFpEF) is largely due to progression of left ventricular (LV) diastolic dysfunction. The key role in the normal maintenance of diast...
Clinical and hemodynamic aggravation of heart failure with preserved ejection fraction (HFpEF) is largely due to progression of left ventricular (LV) diastolic dysfunction. The key role in the normal maintenance of diastolic function is played by a high level of activity of the intracellular signaling axis, cyclic guanosine-monophosphate-protein kinase G, the activity of which is significantly reduced in HFpEF. The activity of this axis can be increased by increasing the bioavailability of natriuretic peptides by blocking the enzyme neutral endopeptidase (neprilisin), which is responsible for the destruction of natriuretic peptides.This review presents experimental and clinical data on the use of neprilysin inhibitors in HFpEF and addresses prospects of this treatment.
Effectiveness of Systematic Echocardiographic Screening for Rheumatic Heart Disease in Nepalese Schoolchildren: A Cluster Randomized Clinical Trial.
Karki P, Uranw S, Bastola S … +12 more , Mahato R, Shrestha NR, Sherpa K, Dhungana S, Odutayo A, Gurung K, Pandey N, Agrawal K, Shah P, Rothenbühler M, Jüni P, Pilgrim T
JAMA Cardiol · 2021 Apr · PMID 33471029 · Full text
IMPORTANCE: Echocardiographic screening allows for early detection of subclinical stages of rheumatic heart disease among children in endemic regions. OBJECTIVE: To investigate the effectiveness of systematic echocardiog...
IMPORTANCE: Echocardiographic screening allows for early detection of subclinical stages of rheumatic heart disease among children in endemic regions. OBJECTIVE: To investigate the effectiveness of systematic echocardiographic screening in combination with secondary antibiotic prophylaxis on the prevalence of rheumatic heart disease. DESIGN, SETTING, AND PARTICIPANTS: This cluster randomized clinical trial included students 9 to 16 years of age attending public and private schools in urban and rural areas of the Sunsari district in Nepal that had been randomly selected on November 17, 2012. Echocardiographic follow-up was performed between January 7, 2016, and January 3, 2019. INTERVENTIONS: In the experimental group, children underwent systematic echocardiographic screening followed by secondary antibiotic prophylaxis in case they had echocardiographic evidence of latent rheumatic heart disease. In the control group, children underwent no echocardiographic screening. MAIN OUTCOMES AND MEASURES: Prevalence of the composite of definite or borderline rheumatic heart disease according to the World Heart Federation criteria in experimental and control schools as assessed 4 years after intervention. RESULTS: A total of 35 schools were randomized to the experimental group (n = 19) or the control group (n = 16). After a median of 4.3 years (interquartile range [IQR], 4.0-4.5 years), 17 of 19 schools in the experimental group (2648 children; median age at follow-up, 12.1 years; IQR, 10.3-12.5 years; 1308 [49.4%] male) and 15 of 16 schools in the control group (1325 children; median age at follow-up, 10.6 years; IQR, 10.0-12.5 years; 682 [51.5%] male) underwent echocardiographic follow-up. The prevalence of definite or borderline rheumatic heart disease was 10.8 per 1000 children (95% CI, 4.7-24.7) in the control group and 3.8 per 1000 children (95% CI, 1.5-9.8) in the experimental group (odds ratio, 0.34; 95% CI, 0.11-1.07; P = .06). The prevalence in the experimental group at baseline had been 12.9 per 1000 children (95% CI, 9.2-18.1). In the experimental group, the odds ratio of definite or borderline rheumatic heart disease at follow-up vs baseline was 0.29 (95% CI, 0.13-0.65; P = .008). CONCLUSIONS AND RELEVANCE: School-based echocardiographic screening in combination with secondary antibiotic prophylaxis in children with evidence of latent rheumatic heart disease may be an effective strategy to reduce the prevalence of definite or borderline rheumatic heart disease in endemic regions. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT01550068.
DGK and DZHK position paper on genome editing: basic science applications and future perspective.
Brandes RP, Dueck A, Engelhardt S … +10 more , Kaulich M, Kupatt C, De Angelis MT, Leisegang MS, le Noble F, Moretti A, Müller OJ, Skryabin BV, Thum T, Wurst W
Basic Res Cardiol · 2021 Jan · PMID 33449167 · Full text
For a long time, gene editing had been a scientific concept, which was limited to a few applications. With recent developments, following the discovery of TALEN zinc-finger endonucleases and in particular the CRISPR/Cas...
For a long time, gene editing had been a scientific concept, which was limited to a few applications. With recent developments, following the discovery of TALEN zinc-finger endonucleases and in particular the CRISPR/Cas system, gene editing has become a technique applicable in most laboratories. The current gain- and loss-of function models in basic science are revolutionary as they allow unbiased screens of unprecedented depth and complexity and rapid development of transgenic animals. Modifications of CRISPR/Cas have been developed to precisely interrogate epigenetic regulation or to visualize DNA complexes. Moreover, gene editing as a clinical treatment option is rapidly developing with first trials on the way. This article reviews the most recent progress in the field, covering expert opinions gathered during joint conferences on genome editing of the German Cardiac Society (DGK) and the German Center for Cardiovascular Research (DZHK). Particularly focusing on the translational aspect and the combination of cellular and animal applications, the authors aim to provide direction for the development of the field and the most frequent applications with their problems.
Cellular and molecular pathobiology of heart failure with preserved ejection fraction.
Mishra S, Kass DA
Nat Rev Cardiol · 2021 Jun · PMID 33432192 · Full text
Heart failure with preserved ejection fraction (HFpEF) affects half of all patients with heart failure worldwide, is increasing in prevalence, confers substantial morbidity and mortality, and has very few effective treat...
Heart failure with preserved ejection fraction (HFpEF) affects half of all patients with heart failure worldwide, is increasing in prevalence, confers substantial morbidity and mortality, and has very few effective treatments. HFpEF is arguably the greatest unmet medical need in cardiovascular disease. Although HFpEF was initially considered to be a haemodynamic disorder characterized by hypertension, cardiac hypertrophy and diastolic dysfunction, the pandemics of obesity and diabetes mellitus have modified the HFpEF syndrome, which is now recognized to be a multisystem disorder involving the heart, lungs, kidneys, skeletal muscle, adipose tissue, vascular system, and immune and inflammatory signalling. This multiorgan involvement makes HFpEF difficult to model in experimental animals because the condition is not simply cardiac hypertrophy and hypertension with abnormal myocardial relaxation. However, new animal models involving both haemodynamic and metabolic disease, and increasing efforts to examine human pathophysiology, are revealing new signalling pathways and potential therapeutic targets. In this Review, we discuss the cellular and molecular pathobiology of HFpEF, with the major focus being on mechanisms relevant to the heart, because most research has focused on this organ. We also highlight the involvement of other important organ systems, including the lungs, kidneys and skeletal muscle, efforts to characterize patients with the use of systemic biomarkers, and ongoing therapeutic efforts. Our objective is to provide a roadmap of the signalling pathways and mechanisms of HFpEF that are being characterized and which might lead to more patient-specific therapies and improved clinical outcomes.
The Novel Desmin Variant p.Leu115Ile Is Associated With a Unique Form of Biventricular Arrhythmogenic Cardiomyopathy.
Protonotarios A, Brodehl A, Asimaki A … +15 more , Jager J, Quinn E, Stanasiuk C, Ratnavadivel S, Futema M, Akhtar MM, Gossios TD, Ashworth M, Savvatis K, Walhorn V, Anselmetti D, Elliott PM, Syrris P, Milting H, Lopes LR
Can J Cardiol · 2021 Jun · PMID 33290826 · Publisher ↗
BACKGROUND: Arrhythmogenic cardiomyopathy (AC) is a heritable myocardial disorder and a major cause of sudden cardiac death. It is typically caused by mutations in desmosomal genes. Desmin gene (DES) variants have been p...
BACKGROUND: Arrhythmogenic cardiomyopathy (AC) is a heritable myocardial disorder and a major cause of sudden cardiac death. It is typically caused by mutations in desmosomal genes. Desmin gene (DES) variants have been previously reported in AC but with insufficient evidence to support their pathogenicity. METHODS: We aimed to assess a large AC patient cohort for DES mutations and describe a unique phenotype associated with a recurring variant in three families. A cohort of 138 probands with a diagnosis of AC and no identifiable desmosomal gene mutations were prospectively screened by whole-exome sequencing. RESULTS: A single DES variant (p.Leu115Ile, c.343C>A) was identified in 3 index patients (2%). We assessed the clinical phenotypes within their families and confirmed cosegregation. One carrier required heart transplantation, 2 died suddenly, and 1 died of noncardiac causes. All cases had right- and left-ventricular (LV) involvement. LV late gadolinium enhancement was present in all, and circumferential subepicardial distribution was confirmed on histology. A significant burden of ventricular arrhythmias was noted. Desmin aggregates were not observed macroscopically, but analysis of the desmin filament formation in transfected cardiomyocytes derived from induced pluripotent stem cells, and SW13 cells revealed cytoplasmic aggregation of mutant desmin. Atomic force microscopy revealed that the mutant form accumulates into short protofilaments and small fibrous aggregates. CONCLUSIONS: DES p.Leu115Ile leads to disruption of the desmin filament network and causes a malignant biventricular form of AC, characterized by LV dysfunction and a circumferential subepicardial distribution of myocardial fibrosis.
Reduced reticulum-mitochondria Ca transfer is an early and reversible trigger of mitochondrial dysfunctions in diabetic cardiomyopathy.
Dia M, Gomez L, Thibault H … +15 more , Tessier N, Leon C, Chouabe C, Ducreux S, Gallo-Bona N, Tubbs E, Bendridi N, Chanon S, Leray A, Belmudes L, Couté Y, Kurdi M, Ovize M, Rieusset J, Paillard M
Basic Res Cardiol · 2020 Nov · PMID 33258101 · Full text
Type 2 diabetic cardiomyopathy features Ca signaling abnormalities, notably an altered mitochondrial Ca handling. We here aimed to study if it might be due to a dysregulation of either the whole Ca homeostasis, the retic...
Type 2 diabetic cardiomyopathy features Ca signaling abnormalities, notably an altered mitochondrial Ca handling. We here aimed to study if it might be due to a dysregulation of either the whole Ca homeostasis, the reticulum-mitochondrial Ca coupling, and/or the mitochondrial Ca entry through the uniporter. Following a 16-week high-fat high-sucrose diet (HFHSD), mice developed cardiac insulin resistance, fibrosis, hypertrophy, lipid accumulation, and diastolic dysfunction when compared to standard diet. Ultrastructural and proteomic analyses of cardiac reticulum-mitochondria interface revealed tighter interactions not compatible with Ca transport in HFHSD cardiomyocytes. Intramyocardial adenoviral injections of Ca sensors were performed to measure Ca fluxes in freshly isolated adult cardiomyocytes and to analyze the direct effects of in vivo type 2 diabetes on cardiomyocyte function. HFHSD resulted in a decreased IP3R-VDAC interaction and a reduced IP3-stimulated Ca transfer to mitochondria, with no changes in reticular Ca level, cytosolic Ca transients, and mitochondrial Ca uniporter function. Disruption of organelle Ca exchange was associated with decreased mitochondrial bioenergetics and reduced cell contraction, which was rescued by an adenovirus-mediated expression of a reticulum-mitochondria linker. An 8-week diet reversal was able to restore cardiac insulin signaling, Ca transfer, and cardiac function in HFHSD mice. Therefore, our study demonstrates that the reticulum-mitochondria Ca miscoupling may play an early and reversible role in the development of diabetic cardiomyopathy by disrupting primarily the mitochondrial bioenergetics. A diet reversal, by counteracting the MAM-induced mitochondrial Ca dysfunction, might contribute to restore normal cardiac function and prevent the exacerbation of diabetic cardiomyopathy.
Mouse models of atherosclerosis and their suitability for the study of myocardial infarction.
Golforoush P, Yellon DM, Davidson SM
Basic Res Cardiol · 2020 Nov · PMID 33258000 · Full text
Atherosclerotic plaques impair vascular function and can lead to arterial obstruction and tissue ischaemia. Rupture of an atherosclerotic plaque within a coronary artery can result in an acute myocardial infarction, whic...
Atherosclerotic plaques impair vascular function and can lead to arterial obstruction and tissue ischaemia. Rupture of an atherosclerotic plaque within a coronary artery can result in an acute myocardial infarction, which is responsible for significant morbidity and mortality worldwide. Prompt reperfusion can salvage some of the ischaemic territory, but ischaemia and reperfusion (IR) still causes substantial injury and is, therefore, a therapeutic target for further infarct limitation. Numerous cardioprotective strategies have been identified that can limit IR injury in animal models, but none have yet been translated effectively to patients. This disconnect prompts an urgent re-examination of the experimental models used to study IR. Since coronary atherosclerosis is the most prevalent morbidity in this patient population, and impairs coronary vessel function, it is potentially a major confounder in cardioprotective studies. Surprisingly, most studies suggest that atherosclerosis does not have a major impact on cardioprotection in mouse models. However, a major limitation of atherosclerotic animal models is that the plaques usually manifest in the aorta and proximal great vessels, and rarely in the coronary vessels. In this review, we examine the commonly used mouse models of atherosclerosis and their effect on coronary artery function and infarct size. We conclude that none of the commonly used strains of mice are ideal for this purpose; however, more recently developed mouse models of atherosclerosis fulfil the requirement for coronary artery lesions, plaque rupture and lipoprotein patterns resembling the human profile, and may enable the identification of therapeutic interventions more applicable in the clinical setting.
Association of Circulating Monocyte Chemoattractant Protein-1 Levels With Cardiovascular Mortality: A Meta-analysis of Population-Based Studies.
Georgakis MK, de Lemos JA, Ayers C … +24 more , Wang B, Björkbacka H, Pana TA, Thorand B, Sun C, Fani L, Malik R, Dupuis J, Engström G, Orho-Melander M, Melander O, Boekholdt SM, Zierer A, Elhadad MA, Koenig W, Herder C, Hoogeveen RC, Kavousi M, Ballantyne CM, Peters A, Myint PK, Nilsson J, Benjamin EJ, Dichgans M
JAMA Cardiol · 2021 May · PMID 33146689 · Full text
IMPORTANCE: Human genetics and studies in experimental models support a key role of monocyte-chemoattractant protein-1 (MCP-1) in atherosclerosis. Yet, the associations of circulating MCP-1 levels with risk of coronary h...
IMPORTANCE: Human genetics and studies in experimental models support a key role of monocyte-chemoattractant protein-1 (MCP-1) in atherosclerosis. Yet, the associations of circulating MCP-1 levels with risk of coronary heart disease and cardiovascular death in the general population remain largely unexplored. OBJECTIVE: To explore whether circulating levels of MCP-1 are associated with risk of incident coronary heart disease, myocardial infarction, and cardiovascular mortality in the general population. DATA SOURCES AND SELECTION: Population-based cohort studies, identified through a systematic review, that have examined associations of circulating MCP-1 levels with cardiovascular end points. DATA EXTRACTION AND SYNTHESIS: Using a prespecified harmonized analysis plan, study-specific summary data were obtained from Cox regression models after excluding individuals with overt cardiovascular disease at baseline. Derived hazard ratios (HRs) were synthesized using random-effects meta-analyses. MAIN OUTCOMES AND MEASURES: Incident coronary heart disease (myocardial infarction, coronary revascularization, and unstable angina), nonfatal myocardial infarction, and cardiovascular death (from cardiac or cerebrovascular causes). RESULTS: The meta-analysis included 7 cohort studies involving 21 401 individuals (mean [SD] age, 53.7 [10.2] years; 10 012 men [46.8%]). Mean (SD) follow-up was 15.3 (4.5) years (326 392 person-years at risk). In models adjusting for age, sex, and race/ethnicity, higher MCP-1 levels at baseline were associated with increased risk of coronary heart disease (HR per 1-SD increment in MCP-1 levels: 1.06 [95% CI, 1.01-1.11]; P = .01), nonfatal myocardial infarction (HR, 1.07 [95% CI, 1.01-1.13]; P = .02), and cardiovascular death (HR, 1.12 [95% CI, 1.05-1.20]; P < .001). In analyses comparing MCP-1 quartiles, these associations followed dose-response patterns. After additionally adjusting for vascular risk factors, the risk estimates were attenuated, but the associations of MCP-1 levels with cardiovascular death remained statistically significant, as did the association of MCP-1 levels in the upper quartile with coronary heart disease. There was no significant heterogeneity; the results did not change in sensitivity analyses excluding events occurring in the first 5 years after MCP-1 measurement, and the risk estimates were stable after additional adjustments for circulating levels of interleukin-6 and high-sensitivity C-reactive protein. CONCLUSIONS AND RELEVANCE: Higher circulating MCP-1 levels are associated with higher long-term cardiovascular mortality in community-dwelling individuals free of overt cardiovascular disease. These findings provide further support for a key role of MCP-1-signaling in cardiovascular disease.
Myocarditis and inflammatory cardiomyopathy: current evidence and future directions.
Tschöpe C, Ammirati E, Bozkurt B … +16 more , Caforio ALP, Cooper LT, Felix SB, Hare JM, Heidecker B, Heymans S, Hübner N, Kelle S, Klingel K, Maatz H, Parwani AS, Spillmann F, Starling RC, Tsutsui H, Seferovic P, Van Linthout S
Nat Rev Cardiol · 2021 Mar · PMID 33046850 · Full text
Inflammatory cardiomyopathy, characterized by inflammatory cell infiltration into the myocardium and a high risk of deteriorating cardiac function, has a heterogeneous aetiology. Inflammatory cardiomyopathy is predominan...
Inflammatory cardiomyopathy, characterized by inflammatory cell infiltration into the myocardium and a high risk of deteriorating cardiac function, has a heterogeneous aetiology. Inflammatory cardiomyopathy is predominantly mediated by viral infection, but can also be induced by bacterial, protozoal or fungal infections as well as a wide variety of toxic substances and drugs and systemic immune-mediated diseases. Despite extensive research, inflammatory cardiomyopathy complicated by left ventricular dysfunction, heart failure or arrhythmia is associated with a poor prognosis. At present, the reason why some patients recover without residual myocardial injury whereas others develop dilated cardiomyopathy is unclear. The relative roles of the pathogen, host genomics and environmental factors in disease progression and healing are still under discussion, including which viruses are active inducers and which are only bystanders. As a consequence, treatment strategies are not well established. In this Review, we summarize and evaluate the available evidence on the pathogenesis, diagnosis and treatment of myocarditis and inflammatory cardiomyopathy, with a special focus on virus-induced and virus-associated myocarditis. Furthermore, we identify knowledge gaps, appraise the available experimental models and propose future directions for the field. The current knowledge and open questions regarding the cardiovascular effects associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are also discussed. This Review is the result of scientific cooperation of members of the Heart Failure Association of the ESC, the Heart Failure Society of America and the Japanese Heart Failure Society.
Carotid Plaque Morphology is Similar in Patients with Reduced and Normal Renal Function.
Heijl C, Kahn F, Edsfeldt A … +3 more , Tengryd C, Nilsson J, Goncalves I
Clin Med Insights Cardiol · 2020 · PMID 32922111 · Full text
BACKGROUND: Chronic Kidney Disease (CKD) is associated with an increased risk for cardiovascular events such as stroke. However, it is still unclear if decreased kidney function is associated with a vulnerable atheroscle...
BACKGROUND: Chronic Kidney Disease (CKD) is associated with an increased risk for cardiovascular events such as stroke. However, it is still unclear if decreased kidney function is associated with a vulnerable atherosclerotic plaque phenotype. To explore if renal function was associated with carotid plaque vulnerability we analyzed carotid plaques obtained at surgery from the Carotid Plaque Imaging Project (CPIP). METHODS: Patients were enrolled through the CPIP cohort. The indication for surgery was plaques with stenosis >70%, associated with ipsilateral symptoms or plaques with stenosis >80% not associated with symptoms. Transversal sections from the most stenotic plaque region were analyzed for connective tissue, calcium, lipids, macrophages, intraplaque hemorrhage, and smooth muscle cells. Homogenates were analyzed for collagen and elastin. RESULTS: Carotid endarterectomy specimens from 379 patients were obtained. The median GFR was 73 ml/min/1.73 m. Plaque characteristics showed no significant association with eGFR, neither when eGFR was divided in CKD groups nor when eGFR was handled as a continuous variable and adjusting for other known risk factors (ie, age, diabetes, hypertension, and smoking). CONCLUSIONS: The higher risk of cardiovascular disease such as stroke in CKD is not associated with increased plaque vulnerability and other factors have to be sought.
Evaluation of Stress Cardiac Magnetic Resonance Imaging in Risk Reclassification of Patients With Suspected Coronary Artery Disease.
Antiochos P, Ge Y, Steel K … +20 more , Chen YY, Bingham S, Abdullah S, Mikolich JR, Arai AE, Bandettini WP, Patel AR, Farzaneh-Far A, Heitner JF, Shenoy C, Leung SW, Gonzalez JA, Shah DJ, Raman SV, Ferrari VA, Schulz-Menger J, Stuber M, Simonetti OP, Murthy VL, Kwong RY
JAMA Cardiol · 2020 Dec · PMID 32745166 · Full text
IMPORTANCE: The role of stress cardiac magnetic resonance (CMR) imaging in clinical decision-making by reclassification of risk across American College of Cardiology/American Heart Association guideline-recommended categ...
IMPORTANCE: The role of stress cardiac magnetic resonance (CMR) imaging in clinical decision-making by reclassification of risk across American College of Cardiology/American Heart Association guideline-recommended categories has not been established. OBJECTIVE: To examine the utility of stress CMR imaging for risk reclassification in patients without a history of coronary artery disease (CAD) who presented with suspected myocardial ischemia. DESIGN, SETTING, AND PARTICIPANTS: A retrospective, multicenter cohort study with median follow-up of 5.4 years (interquartile range, 4.6-6.9) was conducted at 13 centers across 11 US states. Participants included 1698 consecutive patients aged 35 to 85 years with 2 or more coronary risk factors but no history of CAD who presented with suspected myocardial ischemia to undergo stress CMR imaging. The study was conducted from February 18, 2019, to March 1, 2020. MAIN OUTCOMES AND MEASURES: Cardiovascular (CV) death and nonfatal myocardial infarction (MI). Major adverse CV events (MACE) including CV death, nonfatal MI, hospitalization for heart failure or unstable angina, and late, unplanned coronary artery bypass graft surgery. RESULTS: Of the 1698 patients, 873 were men (51.4%); mean (SD) age was 62 (11) years, accounting for 67 CV death/nonfatal MIs and 190 MACE. Clinical models of pretest risk were constructed and patients were categorized using guideline-based categories of low (<1% per year), intermediate (1%-3% per year), and high (>3% year) risk. Stress CMR imaging provided risk reclassification across all baseline models. For CV death/nonfatal MI, adding stress CMR-assessed left ventricular ejection fraction, presence of ischemia, and late gadolinium enhancement to a model incorporating the validated CAD Consortium score, hypertension, smoking, and diabetes provided significant net reclassification improvement of 0.266 (95% CI, 0.091-0.441) and C statistic improvement of 0.086 (95% CI, 0.022-0.149). Stress CMR imaging reclassified 60.3% of patients in the intermediate pretest risk category (52.4% reclassified as low risk and 7.9% as high risk) with corresponding changes in the observed event rates of 0.6% per year for low posttest risk and 4.9% per year for high posttest risk. For MACE, stress CMR imaging further provided significant net reclassification improvement (0.361; 95% CI, 0.255-0.468) and C statistic improvement (0.092; 95% CI, 0.054-0.131), and reclassified 59.9% of patients in the intermediate pretest risk group (48.7% reclassified as low risk and 11.2% as high risk). CONCLUSIONS AND RELEVANCE: In this multicenter cohort of patients with no history of CAD presenting with suspected myocardial ischemia, stress CMR imaging reclassified patient risk across guideline-based risk categories, beyond clinical risk factors. The findings of this study support the value of stress CMR imaging for clinical decision-making, especially in patients at intermediate risk for CV death and nonfatal MI.
Deficiency of Nucleotide-binding oligomerization domain-containing proteins (NOD) 1 and 2 reduces atherosclerosis.
Vlacil AK, Schuett J, Ruppert V … +11 more , Soufi M, Oberoi R, Shahin K, Wächter C, Tschernig T, Lei Y, Liu F, Tietge UJF, Schieffer B, Schuett H, Grote K
Basic Res Cardiol · 2020 Jun · PMID 32588196 · Full text
Atherosclerosis is crucially fueled by inflammatory pathways including pattern recognition receptor (PRR)-related signaling of the innate immune system. Currently, the impact of the cytoplasmic PRRs nucleotide-binding ol...
Atherosclerosis is crucially fueled by inflammatory pathways including pattern recognition receptor (PRR)-related signaling of the innate immune system. Currently, the impact of the cytoplasmic PRRs nucleotide-binding oligomerization domain-containing protein (NOD) 1 and 2 is incompletely characterized. We, therefore, generated Nod1/Nod2 double knockout mice on a low-density lipoprotein receptor (Ldlr)-deficient background (= LdlrNod1/2) which were subsequently analyzed regarding experimental atherosclerosis, lipid metabolism, insulin resistance and gut microbiota composition. Compared to Ldlr mice, LdlrNod1/2 mice showed reduced plasma lipids and increased hepatic expression of the scavenger receptor LDL receptor-related protein 1 after feeding a high-fat diet for 12 weeks. Furthermore, intestinal cholesterol and its bacterial degradation product coprostanol were elevated in LdlrNod1/2 mice, correlating with the increased abundance of Eubacterium coprostanoligenes as assessed by 3rd generation sequencing of the gut microbiota. Atherosclerotic plaques of LdlrNod1/2 mice exhibited less lipid deposition and macrophage accumulation. Moreover, macrophages from LdlrNod1/2 mice showed higher expression of the cholesterol efflux transporters Abca1 and Abcg1 and accordingly reduced foam cell formation. Deficiency of Nod1 and Nod2 led to reduced plaque lipid deposition and inflammatory cell infiltration in atherosclerotic plaques. This might be explained by diminished plasma lipid levels and foam cell formation due to altered expression of key regulators of the hepatic cholesterol pathway as well as differential intestinal cholesterol metabolism and microbiota composition.
Myocardial Deformation in the Systemic Right Ventricle: Strain Imaging Improves Prediction of the Failing Heart.
Woudstra OI, van Dissel AC, van der Bom T … +8 more , de Bruin-Bon RHACM, van Melle JP, van Dijk APJ, Vliegen HW, Mulder BJM, Tanck MWT, Meijboom FJ, Bouma BJ
Can J Cardiol · 2020 Sep · PMID 32553818 · Publisher ↗
BACKGROUND: Predicting heart failure events in patients with a systemic right ventricle (sRV) due to transposition of the great arteries (TGA) is important for timely intensification of follow-up. This study assessed the...
BACKGROUND: Predicting heart failure events in patients with a systemic right ventricle (sRV) due to transposition of the great arteries (TGA) is important for timely intensification of follow-up. This study assessed the value of strain compared with currently used parameters as predictor for heart failure-free survival in patients with sRV. METHODS: In participants of a multicentre trial, speckle-tracking echocardiography (STE) was performed to assess global longitudinal strain (GLS), mechanical dispersion (MD), and postsystolic shortening (PSS). Cox regression was used to determine the association of STE parameters with the combined end point of progression of heart failure and death, compared with cardiovascular magnetic resonance (CMR) and computed tomography (CT) derived parameters. RESULTS: Echocardiograms of 60 patients were analyzed (mean age 34 ± 11 years, 65% male, 35% congenitally corrected TGA). Mean GLS was -13.5 ± 2.9%, median MD was 49 (interquartile range [IQR] 30-76) ms, and 14 patients (23%) had PSS. During a median 8 (IQR 7-9) years, 15 patients (25%) met the end point. GLS, MD, and PSS were all associated with heart failure-free survival in univariable analysis. After correction for age, only GLS (optimal cutoff > -10.5%) and CMR/CT-derived sRV ejection fraction (optimal cutoff < 30%) remained associated with heart failure-free survival: hazard ratio (HR) 8.27, 95% confidence interval (CI) 2.50-27.41 (P < 0.001), and HR 4.34, 95% CI 1.48-12.74 (P = 0.007), respectively). Combining GLS and ejection fraction improved prediction, with patients with both GLS > -10.5% and sRV ejection fraction < 30% at highest risk (HR 19.69, 95% CI 4.90-79.13; P < 0.001). CONCLUSIONS: The predictive value of GLS was similar to that of CMR/CT-derived ejection fraction. The combination of GLS and ejection fraction identified patients at highest risk of heart failure and death. Easily available STE parameters can be used to guide follow-up intensity and can be integrated into future risk prediction scores.
A Critical Comparison of Canadian and International Guidelines Recommendations for Antiplatelet Therapy in Coronary Artery Disease.
Marquis-Gravel G, Mehta SR, Valgimigli M … +9 more , Levine GN, Neumann FJ, Granger CB, Costa F, Lordkipanidzé M, Roffi M, Robinson SD, Cantor WJ, Tanguay JF
Can J Cardiol · 2020 Aug · PMID 32553812 · Publisher ↗
Antiplatelet therapy for patients with coronary artery disease has evolved dramatically over the last decade. P2Y12 inhibitors offering more potent and consistent platelet inhibition than clopidogrel are now widely avail...
Antiplatelet therapy for patients with coronary artery disease has evolved dramatically over the last decade. P2Y12 inhibitors offering more potent and consistent platelet inhibition than clopidogrel are now widely available, dual antiplatelet therapy (DAPT) duration can be tailored to individual ischemic and bleeding risks, and strategies to personalize antiplatelet therapy have been developed when concomitant oral anticoagulation (OAC) is indicated. Scientific societies from Canada, the United States, and Europe have all published updated recommendations addressing antiplatelet therapy in the recent years. The purpose of this review is to put the Canadian guidelines into perspective vis-à-vis international recommendations by highlighting similarities and critically analyzing differences. We focus on 3 major topics relevant for clinical practice: DAPT duration following drug-eluting stent implantation, DAPT following percutaneous coronary intervention in patients with concomitant indications for OAC, and DAPT management for noncardiac surgery following drug-eluting stent implantation. Although guidelines broadly agree on the majority of recommendations, the justifications for major differences were contrasted in the manuscript. Unanswered questions remain, including the place of aspirin in secondary prevention of coronary artery disease in the contemporary era, aspirin-free strategies early after percutaneous coronary intervention, and the safe minimal duration of DAPT with newer generation stents.
Prediction for Contrast Volume in Transcatheter Aortic Valve Replacement - Important but Modifiable?
Siller-Matula JM, Mamas MA
Cardiology · 2020 · PMID 32506061 · Publisher ↗
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Sex-Based Outcomes in Patients With a High Bleeding Risk After Percutaneous Coronary Intervention and 1-Month Dual Antiplatelet Therapy: A Secondary Analysis of the LEADERS FREE Randomized Clinical Trial.
Mehran R, Chandrasekhar J, Urban P … +7 more , Lang IM, Windhoevel U, Spaulding C, Copt S, Stoll HP, Morice MC, LEADERS FREE Investigators
JAMA Cardiol · 2020 Aug · PMID 32432718 · Full text
IMPORTANCE: Female sex has been identified as a risk factor for bleeding after percutaneous coronary intervention (PCI) and may have contributed to the underuse of drug-eluting stents in women. This risk may be further e...
IMPORTANCE: Female sex has been identified as a risk factor for bleeding after percutaneous coronary intervention (PCI) and may have contributed to the underuse of drug-eluting stents in women. This risk may be further enhanced among patients with a high bleeding risk. OBJECTIVE: To assess the 2-year outcomes by sex in patients with a high bleeding risk who were enrolled in the LEADERS FREE trial. DESIGN, SETTING, AND PARTICIPANTS: This cohort study is a prespecified, sex-based secondary analysis of the LEADERS FREE double-blind, randomized clinical trial that was conducted at 68 sites in 20 countries from December 2012 to May 2014. Patients with a high bleeding risk who underwent PCI and met the trial eligibility criteria were enrolled at the participating sites and followed up for up to 2 years. INTERVENTIONS: Patients were randomized 1:1 to either a bare-metal stent or a polymer-free, biolimus A9-eluting drug-coated stent with 1-month of dual antiplatelet therapy. MAIN OUTCOMES AND MEASURES: The primary safety end point was a composite of cardiac death, myocardial infarction, or stent thrombosis. The primary efficacy end point was clinically driven target lesion revascularization. Bleeding was assessed using the Bleeding Academic Research Consortium (BARC) scale, and the source of bleeding was recorded. RESULTS: A total of 2432 patients with a high bleeding risk were included in the study. Of these patients, the mean (SD) age was 75 (9) years, and 1694 (69.7%) were men and 738 (30.3%) were women. Women and men had similar incidence of the 2-year primary safety (14.7% vs 13.6%; P = .37) and efficacy (9.2% vs 9.5%; P = .70) end points. The drug-coated stent was found to be superior to the bare-metal stent in both sexes, with lower target lesion revascularization (women: 6.3% vs 12.1%; men: 7.0% vs 12.0%; P for interaction = .70) and similar rates of the primary safety end point (women: 12.4% vs 17.0%; men: 12.6% vs 14.5%; P for interaction = .40). Overall, 2-year BARC types 3 to 5 major bleeding (10.2% vs 8.6%; P = .14) was not statistically different between the sexes, but women experienced greater BARC types 3 to 5 major bleeding within the first 30 days (5.1% vs 2.4%; P = .007) and greater vascular access site major bleeding than men (2.2% vs 0.5%; P < .001). In both sexes, vascular (women: hazard ratio [HR], 3.45 [95% CI, 1.51-7.87]; men: HR, 4.14 [95% CI, 1.33-12.95]) and nonvascular major bleeding (women: HR, 3.76 [95% CI, 2.17- 6.53]; men: HR, 4.62 [95% CI, 3.23-6.61]) were associated with greater 2-year mortality. CONCLUSIONS AND RELEVANCE: This study found no sex differences in the ischemic outcomes of patients with a high bleeding risk after PCI, but women appeared to demonstrate greater early bleeding and major bleeding from the vascular access site. Both women and men with major bleeding seemed to experience worse 2-year mortality, suggesting that bleeding avoidance strategies should be uniformly adopted for all patients, with close attention dedicated to women to avoid denying them the benefits of PCI. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02843633.
Non-hyperaemic coronary pressure measurements to guide coronary interventions.
van de Hoef TP, Lee JM, Echavarria-Pinto M … +6 more , Koo BK, Matsuo H, Patel MR, Davies JE, Escaned J, Piek JJ
Nat Rev Cardiol · 2020 Oct · PMID 32409779 · Publisher ↗
Evidence supporting the use of coronary physiology as an adjunct to coronary angiography to guide percutaneous coronary interventions has accumulated over the past 25 years. The fractional flow reserve has dominated this...
Evidence supporting the use of coronary physiology as an adjunct to coronary angiography to guide percutaneous coronary interventions has accumulated over the past 25 years. The fractional flow reserve has dominated this evolving physiological guidance of coronary intervention and its use is supported by large clinical outcome trials. However, despite clinical practice guidelines advocating its use in most patients with coronary stenosis who are eligible for coronary intervention, the uptake of a physiology-guided approach remains limited. The use of non-hyperaemic coronary pressure measurements to guide coronary interventions was introduced in an attempt to simplify the routine application of coronary physiology-guided intervention in daily practice. Over the past decade, a large scientific effort has focused on the development of several non-hyperaemic pressure ratios. In this Review, we detail the basic principles of coronary physiology in non-hyperaemic conditions, the rationale for the use of non-hyperaemic coronary pressure measurements for stenosis evaluation, the current evidence base for the available non-hyperaemic coronary pressure ratios, the basis for the discordance between non-hyperaemic coronary pressure ratios and fractional flow reserve, and the potential advantages of these new parameters over fractional flow reserve.
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