| 1. |
- Henein, Michael Y., et al.
(författare)
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Biomarkers predict in-hospital major adverse cardiac events in covid-19 patients : A multicenter international study
- 2021
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Ingår i: Journal of Clinical Medicine. - : MDPI. - 2077-0383. ; 10:24
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Tidskriftsartikel (refereegranskat)abstract
- Background: The COVID-19 pandemic carries a high burden of morbidity and mortality worldwide. We aimed to identify possible predictors of in-hospital major cardiovascular (CV) events in COVID-19.Methods: We retrospectively included patients hospitalized for COVID-19 from 10 centers. Clinical, biochemical, electrocardiographic, and imaging data at admission and medications were collected. Primary endpoint was a composite of in-hospital CV death, acute heart failure (AHF), acute myocarditis, arrhythmias, acute coronary syndromes (ACS), cardiocirculatory arrest, and pulmonary embolism (PE).Results: Of the 748 patients included, 141(19%) reached the set endpoint: 49 (7%) CV death, 15 (2%) acute myocarditis, 32 (4%) sustained-supraventricular or ventricular arrhythmias, 14 (2%) cardiocirculatory arrest, 8 (1%) ACS, 41 (5%) AHF, and 39 (5%) PE. Patients with CV events had higher age, body temperature, creatinine, high-sensitivity troponin, white blood cells, and platelet counts at admission and were more likely to have systemic hypertension, renal failure (creatinine ≥ 1.25 mg/dL), chronic obstructive pulmonary disease, atrial fibrillation, and cardiomyopathy. On univariate and multivariate analysis, troponin and renal failure were associated with the composite endpoint. Kaplan–Meier analysis showed a clear divergence of in-hospital composite event-free survival stratified according to median troponin value and the presence of renal failure (Log rank p < 0.001).Conclusions: Our findings, derived from a multicenter data collection study, suggest the routine use of biomarkers, such as cardiac troponin and serum creatinine, for in-hospital prediction of CV events in patients with COVID-19.
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| 2. |
- Henein, Michael Y., et al.
(författare)
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Coronary Atherosclerosis Imaging
- 2020
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Ingår i: Diagnostics (Basel). - : MDPI. - 2075-4418. ; 10:2
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Forskningsöversikt (refereegranskat)abstract
- Identifying patients at increased risk of coronary artery disease, before the atherosclerotic complications become clinically evident, is the aim of cardiovascular prevention. Imaging techniques provide direct assessment of coronary atherosclerotic burden and pathological characteristics of atherosclerotic lesions which may predict the progression of disease. Atherosclerosis imaging has been traditionally based on the evaluation of coronary luminal narrowing and stenosis. However, the degree of arterial obstruction is a poor predictor of subsequent acute events. More recent techniques focus on the high-resolution visualization of the arterial wall and the coronary plaques. Most acute coronary events are triggered by plaque rupture or erosion. Hence, atherosclerotic plaque imaging has generally focused on the detection of vulnerable plaque prone to rupture. However, atherosclerosis is a dynamic process and the plaque morphology and composition may change over time. Most vulnerable plaques undergo progressive transformation from high-risk to more stable and heavily calcified lesions, while others undergo subclinical rupture and healing. Although extensive plaque calcification is often associated with stable atherosclerosis, the extent of coronary artery calcification strongly correlates with the degree of atherosclerosis and with the rate of future cardiac events. Inflammation has a central role in atherogenesis, from plaque formation to rupture, hence in the development of acute coronary events. Morphologic plaque assessment, both invasive and non-invasive, gives limited information as to the current activity of the atherosclerotic disease. The addition of nuclear imaging, based on radioactive tracers targeted to the inflammatory components of the plaques, provides a highly sensitive assessment of coronary disease activity, thus distinguishing those patients who have stable disease from those with active plaque inflammation.
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| 3. |
- Henein, Michael Y., et al.
(författare)
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Diabetes and coronary circulation : from pathology to imaging
- 2021
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Ingår i: Diabetes and cardiovascular disease. - Amsterdam : Elsevier. - 9780128174289 ; , s. 227-267
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Bokkapitel (refereegranskat)abstract
- Coronary artery disease (CAD) is the leading cause of mortality and morbidity among patients with diabetes mellitus. Despite the large fall in CAD mortality in the general population over the last four decades, the overall risk of CAD in people with diabetes did not change significantly. Compared to the general population, diabetics have a higher prevalence, extent, and severity of CAD and a higher risk of mortality due to myocardial infarction and to a lesser extent to stroke. Also, cardiovascular disease has been shown to develop earlier in individuals with diabetes and is followed by worse event-related survival than in nondiabetics. Although most data on the relationship between diabetes and CAD refer to type 2 diabetes, cardiovascular disease remains the leading cause of mortality even in patients with type 1 diabetes. Chronic hyperglycemia and insulin resistance have a key role in inducing coronary atherosclerosis by promoting inflammation and endothelial dysfunction. In diabetic patients, once the coronary atherogenesis has started, the progression from early lesions to plaque rupture or erosion follows the same pathological pathway as in the general population. Although the risk of CAD has been traditionally associated with coronary stenosis severity, more recent research has led to a paradigm shift, with more emphasis on total coronary plaque burden. Both clinical and postmortem studies have shown that diabetics have significantly greater total plaque burden compared to nondiabetics. Direct, invasive, and noninvasive visualization of atherosclerotic lesions allows accurate evaluation of the extent of disease and degree of plaque calcification. However, imaging of the presence and extent of plaque inflammatory activity, using positron emission tomography or cardiac magnetic resonance, may serve in identifying individuals with a more severe atherosclerotic disease who may benefit from intensive treatment.
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| 4. |
- Henein, Michael Y., et al.
(författare)
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The Impact of Mental Stress on Cardiovascular Health - Part II
- 2022
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Ingår i: Journal of Clinical Medicine. - : MDPI. - 2077-0383. ; 11:15
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Forskningsöversikt (refereegranskat)abstract
- Endothelial dysfunction is one of the earliest manifestations of atherosclerosis, contributing to its development and progression. Mental stress induces endothelial dysfunction through increased activity of the sympathetic nervous system, release of corticotropin-releasing hormone from the hypothalamus, inhibition of nitric oxide (NO) synthesis by cortisol, and increased levels of pro-inflammatory cytokines. Mental-stress-induced increased output of the sympathetic nervous system and concomitant withdrawal of the parasympathetic inflammatory reflex results in systemic inflammation and activation of a neural–hematopoietic–arterial axis. This includes the brainstem and subcortical regions network, bone marrow activation, release of leukocytes into the circulation and their migration to the arterial wall and atherosclerotic plaques. Low-grade, sterile inflammation is involved in all steps of atherogenesis, from coronary plaque formation to destabilisation and rupture. Increased sympathetic tone may cause arterial smooth-muscle-cell proliferation, resulting in vascular hypertrophy, thus contributing to the development of hypertension. Emotional events also cause instability of cardiac repolarisation due to brain lateralised imbalance of cardiac autonomic nervous stimulation, which may lead to asymmetric repolarisation and arrhythmia. Acute emotional stress can also provoke severe catecholamine release, leading to direct myocyte injury due to calcium overload, known as myocytolysis, coronary microvascular vasoconstriction, and an increase in left ventricular afterload. These changes can trigger a heart failure syndrome mimicking acute myocardial infarction, characterised by transient left ventricular dysfunction and apical ballooning, known as stress (Takotsubo) cardiomyopathy. Women are more prone than men to develop mental-stress-induced myocardial ischemia (MSIMI), probably reflecting gender differences in brain activation patterns during mental stress. Although guidelines on CV prevention recognise psychosocial factors as risk modifiers to improve risk prediction and decision making, the evidence that their assessment and treatment will prevent CAD needs further evaluation.
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| 5. |
- Henein, Michael Y., et al.
(författare)
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The Role of Inflammation in Cardiovascular Disease
- 2022
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Ingår i: International Journal of Molecular Sciences. - : MDPI. - 1661-6596 .- 1422-0067. ; 23:21
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Forskningsöversikt (refereegranskat)abstract
- Atherosclerosis is a chronic inflammatory disease, in which the immune system has a prominent role in its development and progression. Inflammation-induced endothelial dysfunction results in an increased permeability to lipoproteins and their subendothelial accumulation, leukocyte recruitment, and platelets activation. Recruited monocytes differentiate into macrophages which develop pro- or anti-inflammatory properties according to their microenvironment. Atheroma progression or healing is determined by the balance between these functional phenotypes. Macrophages and smooth muscle cells secrete inflammatory cytokines including interleukins IL-1β, IL-12, and IL-6. Within the arterial wall, low-density lipoprotein cholesterol undergoes an oxidation. Additionally, triglyceride-rich lipoproteins and remnant lipoproteins exert pro-inflammatory effects. Macrophages catabolize the oxidized lipoproteins and coalesce into a lipid-rich necrotic core, encapsulated by a collagen fibrous cap, leading to the formation of fibro-atheroma. In the conditions of chronic inflammation, macrophages exert a catabolic effect on the fibrous cap, resulting in a thin-cap fibro-atheroma which makes the plaque vulnerable. However, their morphology may change over time, shifting from high-risk lesions to more stable calcified plaques. In addition to conventional cardiovascular risk factors, an exposure to acute and chronic psychological stress may increase the risk of cardiovascular disease through inflammation mediated by an increased sympathetic output which results in the release of inflammatory cytokines. Inflammation is also the link between ageing and cardiovascular disease through increased clones of leukocytes in peripheral blood. Anti-inflammatory interventions specifically blocking the cytokine pathways reduce the risk of myocardial infarction and stroke, although they increase the risk of infections.
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| 6. |
- Shenouda, Rafik B., et al.
(författare)
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The relationship between carotid and coronary calcification in patients with coronary artery disease
- 2021
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Ingår i: Clinical Physiology and Functional Imaging. - : John Wiley & Sons. - 1475-0961 .- 1475-097X. ; 41:3, s. 271-280
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Tidskriftsartikel (refereegranskat)abstract
- Background: Atherosclerosis is a multi-system pathology with heterogeneous involvement. We aimed to investigate the relationship between the presence and severity of carotid and coronary calcification in a group of patients with coronary artery disease.Methods: Sixty-three patients presenting with unstable angina or positive stress test for myocardial ischaemia were enrolled in this study. All patients underwent CT scanning of the carotid and coronary arteries using the conventional protocol and Agatston scoring system. Risk factors for atherosclerosis were also analyzed for correlation with the extent of arterial calcification.Results: Total coronary artery calcium score (CAC) was several times higher than total carotid calcium score (1274 (1018) vs 6 (124), p = 0·0001, respectively). The left carotid calcium score correlated strongly with the right carotid calcium score (rho = 0·69, p < 0·0001). The total CAC score correlated modestly with the total carotid calcium score (rho = 0·34, p = 0·007), in particular with left carotid score (rho = 0·38, p = 0·002), but not with the right carotid score. The left coronary calcium score correlated with the right coronary calcium score (rho = 0·35, p = 0·004), left carotid calcium score (rho = 0·33, p = 0·007) and left carotid calcium score at the bifurcation (rho = 0·34, p = 0·006). While hypertension correlated with carotid calcium score, diabetes and dyslipidaemia correlated with left CAC score.Conclusion: In patients with coronary disease, the carotid calcification pattern appeared to be similar between the right and left system in contrast to that of the coronary arteries. CAC correlated only modestly with the carotid score, despite being significantly higher. Hypertension was related to carotid calcium score while diabetes and dyslipidaemia correlated with coronary calcification.
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| 7. |
- Vancheri, Federico, et al.
(författare)
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Coronary Artery Microcalcification : Imaging and Clinical Implications
- 2019
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Ingår i: Diagnostics (Basel). - : MDPI. - 2075-4418. ; 9:4
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Forskningsöversikt (refereegranskat)abstract
- Strategies to prevent acute coronary and cerebrovascular events are based on accurate identification of patients at increased cardiovascular (CV) risk who may benefit from intensive preventive measures. The majority of acute CV events are precipitated by the rupture of the thin cap overlying the necrotic core of an atherosclerotic plaque. Hence, identification of vulnerable coronary lesions is essential for CV prevention. Atherosclerosis is a highly dynamic process involving cell migration, apoptosis, inflammation, osteogenesis, and intimal calcification, progressing from early lesions to advanced plaques. Coronary artery calcification (CAC) is a marker of coronary atherosclerosis, correlates with clinically significant coronary artery disease (CAD), predicts future CV events and improves the risk prediction of conventional risk factors. The relative importance of coronary calcification, whether it has a protective effect as a stabilizing force of high-risk atherosclerotic plaque has been debated until recently. The extent of calcium in coronary arteries has different clinical implications. Extensive plaque calcification is often a feature of advanced and stable atherosclerosis, which only rarely results in rupture. These macroscopic vascular calcifications can be detected by computed tomography (CT). The resulting CAC scoring, although a good marker of overall coronary plaque burden, is not useful to identify vulnerable lesions prone to rupture. Unlike macrocalcifications, spotty microcalcifications assessed by intravascular ultrasound or optical coherence tomography strongly correlate with plaque instability. However, they are below the resolution of CT due to limited spatial resolution. Microcalcifications develop in the earliest stages of coronary intimal calcification and directly contribute to plaque rupture producing local mechanical stress on the plaque surface. They result from a healing response to intense local macrophage inflammatory activity. Most of them show a progressive calcification transforming the early stage high-risk microcalcification into the stable end-stage macroscopic calcification. In recent years, new developments in noninvasive cardiovascular imaging technology have shifted the study of vulnerable plaques from morphology to the assessment of disease activity of the atherosclerotic lesions. Increased disease activity, detected by positron emission tomography (PET) and magnetic resonance (MR), has been shown to be associated with more microcalcification, larger necrotic core and greater rates of events. In this context, the paradox of increased coronary artery calcification observed in statin trials, despite reduced CV events, can be explained by the reduction of coronary inflammation induced by statin which results in more stable macrocalcification.
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| 8. |
- Vancheri, Federico, et al.
(författare)
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Coronary microcalcification
- 2022. - 1
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Ingår i: Cardiovascular calcification. - Cham : Springer. - 9783030815158 - 9783030815141 ; , s. 139-175
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Bokkapitel (refereegranskat)abstract
- Although the assessment of myocardial ischemia has been traditionally based on angiographic evaluation of epicardial coronary artery stenosis, it is recognized that the severity of coronary obstruction has a limited prognostic value of subsequent coronary syndromes. Indeed, many patients with clinical features of myocardial ischemia do not have flow-limiting coronary lesions on angiography. However, the absence of angiographic obstructive lesions does not exclude coronary artery structural or functional abnormalities. Such discordance between coronary stenosis and coronary syndromes is due to the complex nature of atherosclerosis, which is no longer considered just a simple lipid-storage disease but includes inflammation, endothelial dysfunction, arterial wall shear stress, immunological activity, arterial remodeling and calcification. Since arterial endothelium regulates vascular permeability and the arterial tone and flow, inflammation-induced endothelial dysfunction has a central role in the initiation and progression of atherosclerosis. Although the endothelium of the entire vasculature is exposed to inflammation, atherosclerotic plaques develop near arterial bifurcation or curved segments. This focal localization is determined by the effect of wall shear stress (WSS). In the presence of cardiovascular risk factors, WSS induces endothelial inflammation and has an essential role in the development and progression of atherosclerotic plaques. Endothelial damage results in increased permeability and subendothelial retention of small and dense low-density lipoprotein cholesterol. Lipid accumulation promotes migration of macrophages which catabolize the lipoproteins within the arterial wall and coalesce into a necrotic core. Also, vascular smooth muscle cells migrate into the intima forming a fibrous cap, mostly collagen. If the inflammation persists, macrophages exert a catabolic effect resulting in the dissolution of collagen, producing a thin-cap fibro-atheroma (TCFA) which makes the plaque unstable. Inflammation also stimulates the aggregation of small crystals of hydroxyapatite giving rise to microcalcification, less than 50 microns in diameter, embedded in the fibrous cap. Microcalcifications exert a mechanical stress within the fibrous cap and may predispose to plaque rupture. The majority of microcalcifications merge into larger layers of calcium which stabilize the plaque. The morphology of atherosclerotic plaques may change over time, undergoing progressive transformation from high-risk to more stable lesions, or subclinical rupture and healing. Such changes in plaque stability are not simply related to local vascular factors but may reflect more systemic factors, such as inflammatory state and blood thrombogenicity. Direct visualization of plaque morphology and extent of atherosclerosis is currently achieved by angiography, non-contrast computed tomography (CT) with measurement of coronary artery calcium (CAC) score, contrast enhanced computed tomographic coronary angiography (CTCA), cardiac magnetic resonance (CMR), intravascular ultrasound (IVUS), optical coherence tomography (OCT), and near-infrared spectroscopy (NIRS). Among these, only OCT has the spatial resolution to visualize microcalcifications. Metabolic imaging that could assess disease activity and distinguish between patients with stable disease from those with increased inflammatory activity, is based on positron emission tomography (PET) which may incorporate CT or CMR to provide simultaneous disease activity and morphological information.
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| 9. |
- Vancheri, Federico, et al.
(författare)
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Coronary Microvascular Dysfunction
- 2020
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Ingår i: Journal of Clinical Medicine. - : MDPI. - 2077-0383. ; 9:9
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Forskningsöversikt (refereegranskat)abstract
- Many patients with chest pain undergoing coronary angiography do not show significant obstructive coronary lesions. A substantial proportion of these patients have abnormalities in the function and structure of coronary microcirculation due to endothelial and smooth muscle cell dysfunction. The coronary microcirculation has a fundamental role in the regulation of coronary blood flow in response to cardiac oxygen requirements. Impairment of this mechanism, defined as coronary microvascular dysfunction (CMD), carries an increased risk of adverse cardiovascular clinical outcomes. Coronary endothelial dysfunction accounts for approximately two-thirds of clinical conditions presenting with symptoms and signs of myocardial ischemia without obstructive coronary disease, termed "ischemia with non-obstructive coronary artery disease" (INOCA) and for a small proportion of "myocardial infarction with non-obstructive coronary artery disease" (MINOCA). More frequently, the clinical presentation of INOCA is microvascular angina due to CMD, while some patients present vasospastic angina due to epicardial spasm, and mixed epicardial and microvascular forms. CMD may be associated with focal and diffuse epicardial coronary atherosclerosis, which may reinforce each other. Both INOCA and MINOCA are more common in females. Clinical classification of CMD includes the association with conditions in which atherosclerosis has limited relevance, with non-obstructive atherosclerosis, and with obstructive atherosclerosis. Several studies already exist which support the evidence that CMD is part of systemic microvascular disease involving multiple organs, such as brain and kidney. Moreover, CMD is strongly associated with the development of heart failure with preserved ejection fraction (HFpEF), diabetes, hypertensive heart disease, and also chronic inflammatory and autoimmune diseases. Since coronary microcirculation is not visible on invasive angiography or computed tomographic coronary angiography (CTCA), the diagnosis of CMD is usually based on functional assessment of microcirculation, which can be performed by both invasive and non-invasive methods, including the assessment of delayed flow of contrast during angiography, measurement of coronary flow reserve (CFR) and index of microvascular resistance (IMR), evaluation of angina induced by intracoronary acetylcholine infusion, and assessment of myocardial perfusion by positron emission tomography (PET) and magnetic resonance (CMR).
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| 10. |
- Vancheri, Federico, et al.
(författare)
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Effect of Age on Left Ventricular Global Dyssynchrony in Asymptomatic Individuals : A Population Study
- 2016
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Ingår i: Echocardiography. - : Wiley-Blackwell. - 0742-2822 .- 1540-8175. ; 33:7, s. 977-983
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Tidskriftsartikel (refereegranskat)abstract
- Background and Aim: Left ventricular (LV) segmental dyssynchrony is common in patients with heart failure or myocardial activation abnormalities and is associated with increased cardiovascular risk. Total isovolumic time (t-IVT) and Tei index are sensitive indexes of global ventricular dyssynchrony. The aim of this study was to investigate the effect of age on t-IVT and Tei index. Methods: We evaluated 410 individuals with no evidence for coronary heart disease or activation abnormalities. T-IVT was calculated as 60 - (total ejection time + total filling time) and Tei index as t-IVT/total ejection time. The relationship between age, LV systolic and diastolic function parameters as well as t-IVT and Tei index was studied. Results: Ejection fraction and stroke volume did not change with age, whereas early diastolic filling velocity fell and atrial systolic velocity increased, reducing the E/A ratio. Isovolumic contraction time (IVCT) and isovolumic relaxation time (IVRT) lengthened. With every 10 years of age, total LV ejection time shortened by 1.5 sec/min and total filling time by 2.1 sec/min. T-IVT and Tei index increased with age and strongly correlated with IVCT and E/A, but not with ejection fraction or QRS duration. Conclusion: Normal aging is associated with worsening of LV global dyssynchrony shown by prolongation of isovolumic times resulting in shortening of filling and ejection times. Age also affects diastolic function as shown by E/A but not systolic function parameters, ejection fraction or stroke volume. Worsening of global dyssynchrony correlates with that of diastolic function but not with QRS duration.
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