A 68-year-old patient with triple vessel coronary artery disease was scheduled for elective coronary artery bypass grafting. Three days after the uneventful surgery, the patient went into cardiogenic shock, which was deemed to be caused by a dynamic left ventricular outflow tract obstruction and high-grade mitral regurgitation, which both had not been present before surgery. On an emergency basis, surgical transvalvular septal myectomy and mitral valve replacement were performed. After initial extra corporeal membrane oxygenation (ECMO) therapy and a prolonged (intensive care unit) ICU stay the patient finally recovered and is well one and a half years after surgery.
{"title":"Life Threatening Reactive Left Ventricular Hypertrophy Due to Increased Blood Flow after Coronary Artery Bypass Grafting","authors":"R. Balan, Christian Flora, D. Elsner, P. Massoudy","doi":"10.3390/hearts2010001","DOIUrl":"https://doi.org/10.3390/hearts2010001","url":null,"abstract":"A 68-year-old patient with triple vessel coronary artery disease was scheduled for elective coronary artery bypass grafting. Three days after the uneventful surgery, the patient went into cardiogenic shock, which was deemed to be caused by a dynamic left ventricular outflow tract obstruction and high-grade mitral regurgitation, which both had not been present before surgery. On an emergency basis, surgical transvalvular septal myectomy and mitral valve replacement were performed. After initial extra corporeal membrane oxygenation (ECMO) therapy and a prolonged (intensive care unit) ICU stay the patient finally recovered and is well one and a half years after surgery.","PeriodicalId":93563,"journal":{"name":"Hearts (Basel, Switzerland)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/hearts2010001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47494944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cardiovascular imaging techniques, including echocardiography, nuclear cardiology, multi-slice computed tomography, and cardiac magnetic resonance, have wide applications in cardiac resynchronization therapy (CRT). Our aim was to provide an update of cardiovascular imaging applications before, during, and after implantation of a CRT device. Before CRT implantation, cardiovascular imaging techniques may integrate current clinical and electrocardiographic selection criteria in the identification of patients who may most likely benefit from CRT. Assessment of myocardial viability by ultrasound, nuclear cardiology, or cardiac magnetic resonance may guide optimal left ventricular (LV) lead positioning and help to predict LV function improvement by CRT. During implantation, echocardiographic techniques may guide in the identification of the best site of LV pacing. After CRT implantation, cardiovascular imaging plays an important role in the assessment of CRT response, which can be defined according to LV reverse remodeling, function and dyssynchrony indices. Furthermore, imaging techniques may be used for CRT programming optimization during follow-up, especially in patients who turn out to be non-responders. However, in the clinical settings, the use of proposed functional indices for different imaging techniques is still debated, due to their suboptimal feasibility and reproducibility. Moreover, identifying CRT responders before implantation and turning non-responders into responders at follow-up remain challenging issues.
{"title":"Cardiovascular Imaging Applications in Clinical Management of Patients Treated with Cardiac Resynchronization Therapy","authors":"C. Valzania, F. Gadler, E. Maret, M. Eriksson","doi":"10.3390/hearts1030017","DOIUrl":"https://doi.org/10.3390/hearts1030017","url":null,"abstract":"Cardiovascular imaging techniques, including echocardiography, nuclear cardiology, multi-slice computed tomography, and cardiac magnetic resonance, have wide applications in cardiac resynchronization therapy (CRT). Our aim was to provide an update of cardiovascular imaging applications before, during, and after implantation of a CRT device. Before CRT implantation, cardiovascular imaging techniques may integrate current clinical and electrocardiographic selection criteria in the identification of patients who may most likely benefit from CRT. Assessment of myocardial viability by ultrasound, nuclear cardiology, or cardiac magnetic resonance may guide optimal left ventricular (LV) lead positioning and help to predict LV function improvement by CRT. During implantation, echocardiographic techniques may guide in the identification of the best site of LV pacing. After CRT implantation, cardiovascular imaging plays an important role in the assessment of CRT response, which can be defined according to LV reverse remodeling, function and dyssynchrony indices. Furthermore, imaging techniques may be used for CRT programming optimization during follow-up, especially in patients who turn out to be non-responders. However, in the clinical settings, the use of proposed functional indices for different imaging techniques is still debated, due to their suboptimal feasibility and reproducibility. Moreover, identifying CRT responders before implantation and turning non-responders into responders at follow-up remain challenging issues.","PeriodicalId":93563,"journal":{"name":"Hearts (Basel, Switzerland)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/hearts1030017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44052126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aortic dissection (AD) causes more deaths each year in the United Kingdom than road traffic collisions. Yet the incidence of AD is not known. The management of acute type B AD (TBAD) is changing, with the greater use of thoracic aortic stent grafts (TEVAR) in treatment and fewer open surgical procedures performed. The study’s aim is to review the worldwide, English language published, literature on acute TBAD incidence and treatment, to report on its strengths and limitations, and better understand changes in incidence over time and between countries. Thirty-one studies were identified that focus on the epidemiology and treatment of TBAD. Eight of these studies report the incidence of acute TBAD as between of 0.5–6.3 per 100,000 person years. Hospital admissions for aortic dissection are reported to be increasing in six studies and stable in one study. The proportion of patients with TBAD operated on varies between studies (range 13% to 76%). Studies identify patient age (median 51–77 years), gender (range 48%–81% male) and prevalence of cardio-vascular risk factors, specifically hypertension, in the populations studied as independent factors influencing aortic dissection incidence. Treatment of acute TBAD remains largely conservative with analgesia, hypertension control and serial cross-sectional imaging (range 24%–87% TBAD medically treated). The use of TEVAR to treat acute AD is increasing worldwide (range 13%–76% TBAD treated with TEVAR). The incidence of TBAD is under-reported due to out of hospital deaths, variable clinical presentation (miss-diagnosis) and coding errors. Importantly for research, the single International Classification of Diseases (ICD) code for aortic dissection, I17.0, does not distinguish between acute, chronic, type A or type B dissection types. Similarly, the OPCS Classification of Interventions and Procedures version 4 (OPCS-4) codes for TEVAR, L27.4 and L28.4, do not distinguish between acute and chronic AD presentation, unlike the codes for open thoracic aortic replacement. Standardised reporting of aortic dissection type, and the urgency of both the initial presentation (acute or chronic) and treatment (emergency, urgent or planned) in future studies would allow more meaningful comparisons between populations.
{"title":"Review of Studies Reporting the Incidence of Acute Type B Aortic Dissection","authors":"M. Brooks","doi":"10.3390/hearts1030016","DOIUrl":"https://doi.org/10.3390/hearts1030016","url":null,"abstract":"Aortic dissection (AD) causes more deaths each year in the United Kingdom than road traffic collisions. Yet the incidence of AD is not known. The management of acute type B AD (TBAD) is changing, with the greater use of thoracic aortic stent grafts (TEVAR) in treatment and fewer open surgical procedures performed. The study’s aim is to review the worldwide, English language published, literature on acute TBAD incidence and treatment, to report on its strengths and limitations, and better understand changes in incidence over time and between countries. Thirty-one studies were identified that focus on the epidemiology and treatment of TBAD. Eight of these studies report the incidence of acute TBAD as between of 0.5–6.3 per 100,000 person years. Hospital admissions for aortic dissection are reported to be increasing in six studies and stable in one study. The proportion of patients with TBAD operated on varies between studies (range 13% to 76%). Studies identify patient age (median 51–77 years), gender (range 48%–81% male) and prevalence of cardio-vascular risk factors, specifically hypertension, in the populations studied as independent factors influencing aortic dissection incidence. Treatment of acute TBAD remains largely conservative with analgesia, hypertension control and serial cross-sectional imaging (range 24%–87% TBAD medically treated). The use of TEVAR to treat acute AD is increasing worldwide (range 13%–76% TBAD treated with TEVAR). The incidence of TBAD is under-reported due to out of hospital deaths, variable clinical presentation (miss-diagnosis) and coding errors. Importantly for research, the single International Classification of Diseases (ICD) code for aortic dissection, I17.0, does not distinguish between acute, chronic, type A or type B dissection types. Similarly, the OPCS Classification of Interventions and Procedures version 4 (OPCS-4) codes for TEVAR, L27.4 and L28.4, do not distinguish between acute and chronic AD presentation, unlike the codes for open thoracic aortic replacement. Standardised reporting of aortic dissection type, and the urgency of both the initial presentation (acute or chronic) and treatment (emergency, urgent or planned) in future studies would allow more meaningful comparisons between populations.","PeriodicalId":93563,"journal":{"name":"Hearts (Basel, Switzerland)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/hearts1030016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48351252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cardiac injury manifested as either systolic or diastolic dysfunction is considered an important preceding stage that leads to or is associated with eventual heart failure (HF) [...]
心脏损伤表现为收缩或舒张功能障碍，被认为是导致或与最终心力衰竭(HF)相关的重要前期阶段[…]
{"title":"Preface to Hearts Special Issue “Nutrient Deficiency and Drug Induced Cardiac Injury and Dysfunction”","authors":"I. Mak, J. Kramer","doi":"10.3390/hearts1030015","DOIUrl":"https://doi.org/10.3390/hearts1030015","url":null,"abstract":"Cardiac injury manifested as either systolic or diastolic dysfunction is considered an important preceding stage that leads to or is associated with eventual heart failure (HF) [...]","PeriodicalId":93563,"journal":{"name":"Hearts (Basel, Switzerland)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/hearts1030015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42063466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vitamin A is a micronutrient and signaling molecule that regulates transcription, cellular differentiation, and organ homeostasis. Additionally, metabolites of Vitamin A are utilized as differentiation agents in the treatment of hematological cancers and skin disorders, necessitating further study into the effects of both nutrient deficiency and the exogenous delivery of Vitamin A and its metabolites on cardiovascular phenotypes. Though vitamin A/retinoids are well-known regulators of cardiac formation, recent evidence has emerged that supports their role as regulators of cardiac regeneration, postnatal cardiac function, and cardiovascular disease progression. We here review findings from genetic and pharmacological studies describing the regulation of both myocyte- and vascular-driven cardiac phenotypes by vitamin A signaling. We identify the relationship between retinoids and maladaptive processes during the pathological hypertrophy of the heart, with a focus on the activation of neurohormonal signaling and fetal transcription factors (Gata4, Tbx5). Finally, we assess how this information might be leveraged to develop novel therapeutic avenues.
{"title":"Vitamin A as a Transcriptional Regulator of Cardiovascular Disease","authors":"R. Leigh, Bogac L. Kaynak","doi":"10.3390/HEARTS1020013","DOIUrl":"https://doi.org/10.3390/HEARTS1020013","url":null,"abstract":"Vitamin A is a micronutrient and signaling molecule that regulates transcription, cellular differentiation, and organ homeostasis. Additionally, metabolites of Vitamin A are utilized as differentiation agents in the treatment of hematological cancers and skin disorders, necessitating further study into the effects of both nutrient deficiency and the exogenous delivery of Vitamin A and its metabolites on cardiovascular phenotypes. Though vitamin A/retinoids are well-known regulators of cardiac formation, recent evidence has emerged that supports their role as regulators of cardiac regeneration, postnatal cardiac function, and cardiovascular disease progression. We here review findings from genetic and pharmacological studies describing the regulation of both myocyte- and vascular-driven cardiac phenotypes by vitamin A signaling. We identify the relationship between retinoids and maladaptive processes during the pathological hypertrophy of the heart, with a focus on the activation of neurohormonal signaling and fetal transcription factors (Gata4, Tbx5). Finally, we assess how this information might be leveraged to develop novel therapeutic avenues.","PeriodicalId":93563,"journal":{"name":"Hearts (Basel, Switzerland)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/HEARTS1020013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44158873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J. Kramer, I. Mak, J. Chmielinska, C. Spurney, T. Phillips, W. Weglicki
Hypomagnesemia occurs clinically as a result of restricted dietary intake, Mg-wasting drug therapies, chronic disease status and may be a risk factor in patients with cardiovascular disorders. Dietary restriction of magnesium (Mg deficiency) in animal models produced a pro-inflammatory/pro-oxidant condition, involving hematopoietic, neuronal, cardiovascular, renal and other systems. In Mg-deficient rodents, early elevations in circulating levels of the neuropeptide, substance P (SP) may trigger subsequent deleterious inflammatory/oxidative/nitrosative stress events. Evidence also suggests that activity of neutral endopeptidase (NEP, neprilysin), the major SP-degrading enzyme, may be impaired during later stages of Mg deficiency, and this may sustain the neurogenic inflammatory response. In this article, experimental findings using substance P receptor blockade, NEP inhibition, and N-methyl-D-aspartate (NMDA) receptor blockade demonstrated the connection between hypomagnesemia, neurogenic inflammation, oxidative stress and enhanced cardiac dysfunction. Proof of concept concerning neurogenic inflammation is provided using an isolated perfused rat heart model exposed to acute reductions in perfusate magnesium concentrations.
{"title":"Experimental Hypomagnesemia Induces Neurogenic Inflammation and Cardiac Dysfunction","authors":"J. Kramer, I. Mak, J. Chmielinska, C. Spurney, T. Phillips, W. Weglicki","doi":"10.3390/hearts1020011","DOIUrl":"https://doi.org/10.3390/hearts1020011","url":null,"abstract":"Hypomagnesemia occurs clinically as a result of restricted dietary intake, Mg-wasting drug therapies, chronic disease status and may be a risk factor in patients with cardiovascular disorders. Dietary restriction of magnesium (Mg deficiency) in animal models produced a pro-inflammatory/pro-oxidant condition, involving hematopoietic, neuronal, cardiovascular, renal and other systems. In Mg-deficient rodents, early elevations in circulating levels of the neuropeptide, substance P (SP) may trigger subsequent deleterious inflammatory/oxidative/nitrosative stress events. Evidence also suggests that activity of neutral endopeptidase (NEP, neprilysin), the major SP-degrading enzyme, may be impaired during later stages of Mg deficiency, and this may sustain the neurogenic inflammatory response. In this article, experimental findings using substance P receptor blockade, NEP inhibition, and N-methyl-D-aspartate (NMDA) receptor blockade demonstrated the connection between hypomagnesemia, neurogenic inflammation, oxidative stress and enhanced cardiac dysfunction. Proof of concept concerning neurogenic inflammation is provided using an isolated perfused rat heart model exposed to acute reductions in perfusate magnesium concentrations.","PeriodicalId":93563,"journal":{"name":"Hearts (Basel, Switzerland)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/hearts1020011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43280425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. Schaffer, Takashi Ito, J. Azuma, C. J. Jong, J. Kramer
Taurine is a ubiquitous β-amino acid that plays an essential role in ensuring normal mitochondrial and myocardial function. In the mitochondria, taurine reacts with a tRNA forming a 5-taurinomethyluridine conjugate that primarily regulates the biosynthesis of the mitochondria encoded protein, ND6, which serves as a subunit of complex I of the respiratory chain. Impaired formation of the taurine conjugate reduces activity of complex I and plays a central role in the pathophysiology of the mitochondrial disease MELAS (myopathy, encephalopathy, lactic acidosis and stroke-like episodes). The restoration of mitochondrial levels of the taurine conjugate enhances electron flux through the respiratory chain, thereby preventing at least some of the symptoms of MELAS. Taurine therapy also diminishes the severity of congestive heart failure, an observation that led to its approval for the treatment of congestive heart failure in Japan. The review article discusses the role of defective calcium handling, reduced ATP generation, enhanced oxidative stress and apoptosis in the development of taurine-deficient cardiomyopathy. Some patients suffering from congestive heart failure are taurine-deficient, an observation supporting the hypothesis that low taurine levels contribute to the severity of heart failure. Thus, mishandling of taurine leads to mitochondrial dysfunction, which is involved in the development of both MELAS and congestive heart failure.
{"title":"Mechanisms Underlying Development of Taurine-Deficient Cardiomyopathy","authors":"S. Schaffer, Takashi Ito, J. Azuma, C. J. Jong, J. Kramer","doi":"10.3390/hearts1020010","DOIUrl":"https://doi.org/10.3390/hearts1020010","url":null,"abstract":"Taurine is a ubiquitous β-amino acid that plays an essential role in ensuring normal mitochondrial and myocardial function. In the mitochondria, taurine reacts with a tRNA forming a 5-taurinomethyluridine conjugate that primarily regulates the biosynthesis of the mitochondria encoded protein, ND6, which serves as a subunit of complex I of the respiratory chain. Impaired formation of the taurine conjugate reduces activity of complex I and plays a central role in the pathophysiology of the mitochondrial disease MELAS (myopathy, encephalopathy, lactic acidosis and stroke-like episodes). The restoration of mitochondrial levels of the taurine conjugate enhances electron flux through the respiratory chain, thereby preventing at least some of the symptoms of MELAS. Taurine therapy also diminishes the severity of congestive heart failure, an observation that led to its approval for the treatment of congestive heart failure in Japan. The review article discusses the role of defective calcium handling, reduced ATP generation, enhanced oxidative stress and apoptosis in the development of taurine-deficient cardiomyopathy. Some patients suffering from congestive heart failure are taurine-deficient, an observation supporting the hypothesis that low taurine levels contribute to the severity of heart failure. Thus, mishandling of taurine leads to mitochondrial dysfunction, which is involved in the development of both MELAS and congestive heart failure.","PeriodicalId":93563,"journal":{"name":"Hearts (Basel, Switzerland)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/hearts1020010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48843749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Intramural haematoma (IMH) of the aorta is one of the causes of acute aortic syndrome which often requires emergency or urgent life-saving surgery. In this review, we discuss the pathophysiology, epidemiology, clinical presentation, diagnostic imaging, surgery and clinical outcomes associated with IMH.
{"title":"A Review on the Surgical Management of Intramural Haematoma of the Aorta","authors":"J. Kho, M. Petrou","doi":"10.3390/hearts1020009","DOIUrl":"https://doi.org/10.3390/hearts1020009","url":null,"abstract":"Intramural haematoma (IMH) of the aorta is one of the causes of acute aortic syndrome which often requires emergency or urgent life-saving surgery. In this review, we discuss the pathophysiology, epidemiology, clinical presentation, diagnostic imaging, surgery and clinical outcomes associated with IMH.","PeriodicalId":93563,"journal":{"name":"Hearts (Basel, Switzerland)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/hearts1020009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44868163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Takayasu arteritis is a large vessel vasculitis which commonly affects the aorta and its major branches. Active arterial inflammation is characterised by the presence of T and B lymphocytes, natural killer cells, macrophages and occasional multinucleate giant cells. Uncontrolled vascular inflammation can progress to cause arterial stenosis, occlusion or aneurysmal dilatation. Medical treatment involves combination immunosuppression and more recently biologic therapies targeting TNF-α and IL-6. Due to the typical delays in diagnosis and accumulation of arterial injury, open and endovascular surgical intervention are important and potentially life-saving treatment options for Takayasu arteritis. Common indications for surgery include aortic coarctation and ascending aortic dilatation ± aortic valve regurgitation, renal artery stenosis, ischaemic heart disease, supra-aortic disease, mesenteric ischaemia, severe limb-threatening claudication and aneurysm repair. Surgical outcomes are markedly improved in patients with clinically inactive disease and those who receive adequate periprocedural immunosuppression. Decisions regarding surgical approaches are best made as part of a multi-disciplinary team.
{"title":"Intervention in Takayasu Aortitis: When, Where and How?","authors":"A. Porter, J. Mason","doi":"10.3390/hearts1020008","DOIUrl":"https://doi.org/10.3390/hearts1020008","url":null,"abstract":"Takayasu arteritis is a large vessel vasculitis which commonly affects the aorta and its major branches. Active arterial inflammation is characterised by the presence of T and B lymphocytes, natural killer cells, macrophages and occasional multinucleate giant cells. Uncontrolled vascular inflammation can progress to cause arterial stenosis, occlusion or aneurysmal dilatation. Medical treatment involves combination immunosuppression and more recently biologic therapies targeting TNF-α and IL-6. Due to the typical delays in diagnosis and accumulation of arterial injury, open and endovascular surgical intervention are important and potentially life-saving treatment options for Takayasu arteritis. Common indications for surgery include aortic coarctation and ascending aortic dilatation ± aortic valve regurgitation, renal artery stenosis, ischaemic heart disease, supra-aortic disease, mesenteric ischaemia, severe limb-threatening claudication and aneurysm repair. Surgical outcomes are markedly improved in patients with clinically inactive disease and those who receive adequate periprocedural immunosuppression. Decisions regarding surgical approaches are best made as part of a multi-disciplinary team.","PeriodicalId":93563,"journal":{"name":"Hearts (Basel, Switzerland)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/hearts1020008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41928594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J. Rodrigues Bento, J. Meester, I. Luyckx, A. Verstraeten, B. Loeys
Thoracic aortic aneurysms are prevalent in the Western population and are often caused by genetic defects. If undetected, aneurysms can dissect or rupture, which are events associated with a high mortality rate. Hitherto no cure exists other than elective surgery if aneurysm dimensions reach a certain threshold. In the past decades, genotype-phenotype associations have emerged that enable clinicians to start stratifying patients according to risk for dissection. Nonetheless, risk assessment is—to this day—confounded by the lack of full comprehension of underlying genetics and modifying genetic risk factors that complicate the yet established genotype-phenotype correlations. Further research that focuses on identifying these additional risk markers is crucial.
{"title":"The Role of Genetics in Risk Stratification of Thoracic Aortic Aneurysm Dissection","authors":"J. Rodrigues Bento, J. Meester, I. Luyckx, A. Verstraeten, B. Loeys","doi":"10.3390/hearts1020007","DOIUrl":"https://doi.org/10.3390/hearts1020007","url":null,"abstract":"Thoracic aortic aneurysms are prevalent in the Western population and are often caused by genetic defects. If undetected, aneurysms can dissect or rupture, which are events associated with a high mortality rate. Hitherto no cure exists other than elective surgery if aneurysm dimensions reach a certain threshold. In the past decades, genotype-phenotype associations have emerged that enable clinicians to start stratifying patients according to risk for dissection. Nonetheless, risk assessment is—to this day—confounded by the lack of full comprehension of underlying genetics and modifying genetic risk factors that complicate the yet established genotype-phenotype correlations. Further research that focuses on identifying these additional risk markers is crucial.","PeriodicalId":93563,"journal":{"name":"Hearts (Basel, Switzerland)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/hearts1020007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43162311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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