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Pubblicazioni recenti - cardiac amyloidosis
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Practical recommendations for the diagnosis and management of transthyretin cardiac amyloidosis.
Heart Fail Rev2021 Jan;():. doi: 10.1007/s10741-020-10062-w.
Bistola Vasiliki, Parissis John, Foukarakis Emmanouil, Valsamaki Pipitsa N, Anastasakis Aris, Koutsis Georgios, Efthimiadis Georgios, Kastritis Efstathios,
Abstract
Cardiac amyloidosis (CA) is an infiltrative restrictive cardiomyopathy caused by accumulation in the heart interstitium of amyloid fibrils formed by misfolded proteins. Most common CA types are light chain amyloidosis (AL) caused by monoclonal immunoglobulin light chains and transthyretin amyloidosis (ATTR) caused by either mutated or wild-type transthyretin aggregates. Previously considered a rare disease, CA is increasingly recognized among patients who may be misdiagnosed as undifferentiated heart failure with preserved ejection fraction (HFPEF), paradoxical low-flow/low-gradient aortic stenosis, or otherwise unexplained left ventricular hypertrophy. Progress in diagnosis has been due to the refinement of cardiac echocardiographic techniques (speckle tracking imaging) and magnetic resonance (T1 mapping) and mostly due to the advent of bone scintigraphy that has enabled noninvasive diagnosis of ATTR, limiting the need for endomyocardial biopsy. Importantly, proper management of CA starts from early recognition of suspected cases among high prevalence populations, followed by advanced diagnostic evaluation to confirm diagnosis and typing, preferentially in experienced amyloidosis centers. Differentiating ATTR from other types of amyloidosis, especially AL, is critical. Emerging targeted ATTR therapies offer the potential to improve outcomes of these patients previously treated only palliatively.
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Conversion of technetium-pyrophosphate scintigraphy in a patient with hereditary ATTR amyloidosis: importance of repeat scanning.
Eur Heart J Case Rep2020 Dec;4(6):1-2. doi: 10.1093/ehjcr/ytaa386.
Hussain Muzna, Sperry Brett W, Hanna Mazen, Jaber Wael A,
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Cardiac Amyloidosis for the Primary Care Provider: A Practical Review to Promote Earlier Recognition of Disease.
Am J Med2021 Jan;():. doi: S0002-9343(21)00016-4.
Zhang Kathleen W, Vallabhaneni Srilakshmi, Alvarez-Cardona Jose A, Krone Ronald J, Mitchell Joshua D, Lenihan Daniel J,
Abstract
Cardiac amyloidosis is increasingly recognized as an underdiagnosed cause of heart failure. Diagnostic delays of up to three years from symptom onset may occur, and patients may be evaluated by more than five specialists prior to receiving the correct diagnosis. Newly available therapies improve clinical outcomes by preventing amyloid fibril deposition and are usually more effective in early stages of disease, making early diagnosis essential. Better awareness among primary care providers of the clinical presentation and modern treatment landscape is essential to improve timely diagnosis and early treatment of this disease. In this review, we provide practical guidance on the epidemiology, clinical manifestations, diagnostic evaluation, and treatment of transthyretin and light chain cardiac amyloidosis to promote earlier disease recognition among primary care providers.
Copyright © 2021. Published by Elsevier Inc.
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Disrupting the DREAM transcriptional repressor complex induces apolipoprotein overexpression and systemic amyloidosis in mice.
J Clin Invest2021 Jan;():. doi: 10.1172/JCI140903.
Perampalam Pirunthan, Hassan Haider M, Lilly Grace E, Passos Daniel T, Torchia Joseph, Kiser Patti K, Bozovic Andrea, Kulasingam Vathany, Dick Frederick A,
Abstract
DREAM is a transcriptional repressor complex that regulates cell proliferation and its loss causes neonatal lethality in mice. To investigate DREAM function in adult mice, we utilized an assembly defective p107 protein and conditional deletion of its redundant family member p130. In the absence of DREAM assembly, mice displayed shortened survival characterized by systemic amyloidosis, but no evidence of excessive cellular proliferation. Amyloid deposits were found in the heart, liver, spleen, and kidneys, but not the brain or bone marrow. Using laser capture microdissection followed by mass spectrometry, we identified apolipoproteins as the most abundant components of amyloids. Intriguingly, apoA-IV was the most detected amyloidogenic protein in amyloid deposits, suggesting AApoAIV amyloidosis. AApoAIV is a recently described form whereby wildtype apoA-IV has been shown to predominate in amyloid plaques. We determined that DREAM directly regulates Apoa4 by chromatin immunoprecipitation and that the histone variant H2AZ is reduced from the Apoa4 gene body in DREAM's absence, leading to overexpression. Collectively, we describe a mechanism by which epigenetic misregulation causes apolipoprotein overexpression and amyloidosis, potentially explaining the origins of non-genetic amyloid subtypes.
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Orthopaedic Manifestations of Amyloidosis.
J Am Acad Orthop Surg2021 Jan;():. doi: 10.5435/JAAOS-D-20-01146.
Zhang Dafang, Makhni Melvin C, Kang James D, Blazar Philip,
Abstract
Amyloidosis is a disorder of misfolded proteins in human tissues, which can result in morbid cardiac and neurological disease. Historically, the utility of tissue biopsy during orthopaedic procedures to detect amyloidosis has been limited because no disease-modifying therapies were available; however, new drug therapies have recently emerged for the treatment of amyloidosis. Although these novel pharmaceuticals show promise for slowing disease progression, they are primarily effective in the early stages of amyloidosis, underscoring the importance of early diagnosis. Common orthopaedic manifestations of amyloidosis include carpal tunnel syndrome, trigger finger, spontaneous distal biceps tendon rupture, rotator cuff disease, and lumbar spinal stenosis. Carpal tunnel syndrome is frequently the earliest manifestation of amyloidosis, on average preceding a formal diagnosis of amyloidosis by over four years. By recognizing the constellation of musculoskeletal symptoms in the patient with amyloidosis, orthopaedic surgeons can play an active role in patient referral, early detection of systemic disease, and prompt initiation of disease-modifying treatment. There may be a role for selective biopsy for amyloid deposition in at-risk patients during routine orthopaedic procedures.
Copyright © 2021 by the American Academy of Orthopaedic Surgeons.
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Cardiac amyloidosis mimicking acute coronary syndrome: a case report and literature review.
Eur Heart J Case Rep2020 Dec;4(6):1-7. doi: 10.1093/ehjcr/ytaa325.
Nguyen Huan T, Nguyen Chuyen T H,
Abstract
Background:
Cardiac amyloidosis, a progressive cardiac disease, results from the accumulation of undegraded proteinaceous substrates in the extracellular matrix of the heart. It may present as acute coronary syndrome (ACS); therefore, a clear distinction remains challenging in clinical practice. We describe a case of cardiac amyloidosis mimicking ACS.
Case summary:
A 72-year-old man experienced chest discomfort for 2 days. He gradually developed dyspnoea during the preceding month. Electrocardiogram (ECG) showed sinus rhythm with right bundle branch block and low voltage. Echocardiography revealed concentric left ventricular thickening, biatrial dilation, and preserved ejection fraction with predominantly left ventricular basal hypokinesis. Serial testing of the cardiac biomarkers showed persistently increased high-sensitive cardiac troponin T levels and normal serum creatine kinase myocardial band levels. He was diagnosed with ACS with haemodynamic stability. However, coronary angiography demonstrated non-obstructive coronary arteries. Furthermore, significant macroglossia and periorbital purpura were noticed. Laboratory investigations revealed elevated serum immunoglobulin free light chain (FLC) kappa and lambda levels with an increased FLC ratio. Histological analysis of the biopsied abdominal skin confirmed amyloidosis.
Discussion:
Cardiac amyloidosis often presents as restrictive cardiomyopathy. The usual symptoms include dyspnoea and peripheral oedema. Chest pain may manifest rarely, leading to misdiagnosis as coronary artery disease. Some findings suggestive of cardiac amyloidosis include clinical signs such as amyloid deposits, dyspnoea, low ECG voltage, and basal-predominant hypokinesis with relative apical sparing in echocardiography. Serum FLC test and abdominal skin biopsy can confirm the diagnosis of amyloidosis when a myocardial biopsy is not feasible.
© The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology.
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A case report of an infiltrative cardiomyopathy in everyday practice: a specific cause that cannot be missed in the elderly.
Eur Heart J Case Rep2020 Dec;4(6):1-6. doi: 10.1093/ehjcr/ytaa382.
Chiou Andrew, Aman Edris, Kesarwani Manoj,
Abstract
Background :
Transthyretin amyloid cardiomyopathy (ATTR-CM) is a commonly misdiagnosed cardiac condition due to low disease awareness and perceived rarity, which frequently results in incorrect management and poor outcomes. Early and prompt diagnosis has become critical with emerging therapies that improve patient survival.
Case summary :
A 68-year-old woman presented to a tertiary care centre with acute decompensated heart failure following recurrent hospitalizations for the same issue over the past several months. Transthoracic echocardiography revealed severe concentric left ventricular hypertrophy with grade III diastolic dysfunction. However, QRS voltage by 12-lead electrocardiogram (ECG) was discordant with the degree of left ventricular hypertrophy seen by echocardiography, and the patient had recurrent non-sustained ventricular tachycardia that necessitated implantable cardioverter-defibrillator implantation a few months prior. After aggressive diuresis, the patient completed cardiac magnetic resonance imaging that raised concern for cardiac amyloidosis. Subsequent serum and urine protein electrophoresis with associated immunofixation were within normal limits. Finally, ATTR-CM was confirmed by technetium-99m pyrophosphate scintigraphy with plans to initiate tafamidis after genetic testing.
Discussion :
Patients >60?years of age with diastolic heart failure phenotypically similar to hypertrophic cardiomyopathy and/or hypertensive heart disease should always be evaluated for ATTR-CM. Features that increase suspicion include discordance between left ventricular wall thickness and ECG voltage, and signs/symptoms of a primary peripheral and autonomic neuropathy. Useful non-invasive diagnostic testing has also made the diagnosis of ATTR-CM inexpensive and possible without the need for an endomyocardial biopsy. Unfortunately, this patient's diagnosis of ATTR-CM came late in her disease course, which delayed the onset of definitive therapy.
© The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology.
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Tip of the iceberg: a tertiary care centre retrospective study of left ventricular hypertrophy aetiologies.
Open Heart2021 Jan;8(1):. doi: e001462.
Beneyto Maxime, Cariou Eve, Brunel Jérémy, Scripcariu Alex, Delasnerie Hubert, Brun Stéphanie, Lavie-Badie Yoan, Dupin Deguine Delphine, Galinier Michel, Carrié Didier, Lairez Olivier,
Abstract
AIMS:
To phenotype patients referred to a tertiary centre for the exploration of a left ventricular hypertrophy (LVH) starting from 12?mm of left ventricular wall thickness (LVWT).
METHODS AND RESULTS:
Consecutive patients referred for aetiological workup of LVH, beginning at 12?mm of LVWT were retrospectively included in this tertiary single-centred observational study. Patients presenting with severe aortic stenosis were excluded. Aetiological workup was reviewed for each subject and aetiologies were adjudicated by expert consensus.Among 591 patients referred for LVH aetiological workup, 41% had a maximal LVWT below 15?mm. LVH aetiologies were led by cardiac amyloidosis (CA, 34.3%), followed by sarcomeric hypertrophic cardiomyopathy (S-HCM, 32.1%), hypertensive cardiomyopathy (21.7%), unknown aetiology (7.6%) and other (4.2%), including Anderson-Fabry's disease (1.7%). CA and S-HCM affected over 50% of patients with mild LVH (12-14?mm); the prevalence of these aetiologies rose with LVH severity. Among patients with Anderson-Fabry's disease, 4 (40%) had a maximal LVWT <15?mm.
CONCLUSIONS:
Mild LVH (ie, 12-14 mm) conceals multiple aetiologies that can lead to specific treatment, cascade family screening and specific follow-up. Overall, CA is nowadays the leading cause of LVH in tertiary centers.
© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.
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Left ventricular fibrosis and hypertrophy are associated with mortality in heart failure with preserved ejection fraction.
Sci Rep2021 Jan;11(1):617. doi: 10.1038/s41598-020-79729-6.
Garg Pankaj, Assadi Hosamadin, Jones Rachel, Chan Wei Bin, Metherall Peter, Thomas Richard, van der Geest Rob, Swift Andrew J, Al-Mohammad Abdallah,
Abstract
Cardiac magnetic resonance (CMR) is emerging as an important tool in the assessment of heart failure with preserved ejection fraction (HFpEF). This study sought to investigate the prognostic value of multiparametric CMR, including left and right heart volumetric assessment, native T1-mapping and LGE in HFpEF. In this retrospective study, we identified patients with HFpEF who have undergone CMR. CMR protocol included: cines, native T1-mapping and late gadolinium enhancement (LGE). The mean follow-up period was 3.2?±?2.4 years. We identified 86 patients with HFpEF who had CMR. Of the 86 patients (85% hypertensive; 61% males; 14% cardiac amyloidosis), 27 (31%) patients died during the follow up period. From all the CMR metrics, LV mass (area under curve [AUC] 0.66, SE 0.07, 95% CI 0.54-0.76, p?=?0.02), LGE fibrosis (AUC 0.59, SE 0.15, 95% CI 0.41-0.75, p?=?0.03) and native T1-values (AUC 0.76, SE 0.09, 95% CI 0.58-0.88, p??133.24 g (hazard ratio [HR] 1.58, 95% CI 1.1-2.2, p??34.86% (HR 1.77, 95% CI 1.1-2.8, p?=?0.01) and native T1?>?1056.42 ms (HR 2.36, 95% CI 0.9-6.4, p?=?0.07). In multivariate cox regression, CMR score model comprising these three variables independently predicted mortality in HFpEF when compared to NTproBNP (HR 4 vs HR 1.65). In non-amyloid HFpEF cases, only native T1?>?1056.42 ms demonstrated higher mortality (AUC 0.833, p?
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Epigenomic Profiles of African American Val122Ile Carriers Reveals Putatively Dysregulated Amyloid Mechanisms.
Circ Genom Precis Med2021 Jan;():. doi: 10.1161/CIRCGEN.120.003011.
Pathak Gita A, Wendt Frank R, De Lillo Antonella, Nunez Yaira Z, Goswami Aranyak, De Angelis Flavio, Fuciarelli Maria, Kranzler Henry R, Gelernter Joel, Polimanti Renato,
Abstract
- The Val122Ile mutation in () gene causes a rare, difficult to diagnose hereditary form of cardiac amyloidosis. This mutation is most common in the United States and mainly present in people of African descent. The carriers have an increased risk of congestive heart failure, peripheral edema, and several other non-cardiac phenotypes such as carpal tunnel syndrome, and arthroplasty which are top reasons for ambulatory/outpatient surgeries in the country. - We conducted first-ever epigenome-wide association study using the Illumina's EPIC array, in Val122Ile carriers of African descent for heart disease (HD) and multiple outpatient surgeries (OS) - an early disease indicator. Differential methylation across genome wide CpG sites was tested between carriers with and without HD and OS. Significant CpG sites were investigated for cis-mQTLs loci, followed by gene ontology and protein-protein interaction (PPI) network. We also investigated the significant CpG sites in a secondary cohort of carriers for replication. - Five differentially methylated sites (p?2.1e-08) in genes - , , , , and an intergenic site near RP11-550A5.2, and one differentially methylated region containing and (p=1.1e-12) were associated with HD. For OS, we observe four sites - two sites in and , and other two in intergenic regions (p?1.8e-07) and three regions overlapping , , and (p?3.9e-07). Functional protein-interaction module analysis identified (p=0.001) for HD. Six cis-mQTLs were associated with one of the significant CpG sites (; p=4.1e-24). We replicated two CpG sites (cg18546846 and cg06641417; p<0.05) in an external cohort of biopsy- confirmed cases of TTR amyloidosis. The genes identified are involved in transport and clearance of amyloid deposits (, , ); cardiac fibrosis (); and muscle tissue regulation (, ). - These findings highlight the link between a complex amyloid circuit and diverse symptoms of Val122Ile.
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Incidental detection of ATTR cardiac amyloidosis.
J Nucl Cardiol2021 Jan;():. doi: 10.1007/s12350-020-02467-9.
Quaggin-Smith Jessica A, Wehbe Ramsey M, Holly Thomas A,
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A Cardiac Amyloidosis Presentation: Atrial Mass Versus Thrombus.
Cureus2020 Dec;12(12):e11944. doi: 10.7759/cureus.11944.
Nanda Saheba, Gyftopoulos Alex, Hardy Naomi, Burke Allen P, Chow Robert Td,
Abstract
Cardiac neoplasms are a rare finding of which a cardiac myxoma is the most commonly encountered. Therefore, a density identified in the left atrium commonly leads to the presumptive diagnosis of an atrial myxoma. However, other pathologies, such as atrial thrombi, can mimic in clinical presentation and appearance to a myxoma. Clinically, these pathologies may lead to obstructive symptoms such as syncope, palpitations, or sudden cardiac death. At present, echocardiography, magnetic resonance imaging, or computed tomography can be used to identify such masses, but fall short of identifying the primary cause. The management of atrial thrombi is not yet fully understood and definite recommendations have not been established. We present a case of an 87-year-old man complaining of syncopal episodes found to be secondary to an incidental intracardiac density resulting from age-related amyloidosis.
Copyright © 2020, Nanda et al.
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AL Amyloidosis: Unfolding a Complex Disease.
J Adv Pract Oncol;10(8):813-825. doi: 10.6004/jadpro.2019.10.8.4.
Lu Rebecca, Richards Tiffany A,
Abstract
Light chain (AL) amyloidosis is a rare plasma cell dyscrasia. An estimated 12,000 people live with the disease in the United States. AL amyloidosis occurs from the misfolding of proteins that deposit in organs (heart, kidneys, digestive tract, tongue, lungs, and nervous system), leading to progressive organ damage and impairment of quality of life. The treatment of AL amyloidosis has improved greatly over the past several years, with new treatments currently in development. This article will focus on the pathophysiology, diagnosis, and treatment of AL amyloidosis.
© 2019 Harborside?.
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Wild type transthyretin amyloidosis, a reason not to be forgotten for heart failure of preserved ejection fraction in the elderly.
J Geriatr Cardiol2020 Dec;17(12):793-796. doi: 10.11909/j.issn.1671-5411.2020.12.010.
Tian Zhuang, Ren Chao, Huo Li, Li Xiao, Wang Yi-Ning, Huang Lun, Tian Ran, Zhang Shu-Yang,
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Tafamidis Should Be Accessible for All Patients With Transthyretin Amyloid Cardiomyopathy.
JACC Heart Fail -
[Cardiac amyloidosis].
Ann Pathol2021 Jan;():. doi: S0242-6498(20)30276-5.
Poullot Elsa, Oghina Silvia, Kalsoum Sarah, Damy Thibaud,
Abstract
Different types of amyloid deposits involve the heart. Transthyretin and light chain amyloidosis are the most frequent. Diagnostic performance, typing and treatments have improved in the last decade, and prognosis of cardiac amyloidosis is now significantly better thanks to targeted therapies. In this article, we will describe the clinical manifestations of cardiac amyloidosis, the diagnostic approach and detail the characteristics and specific treatments of the most frequent types of cardiac amyloidosis. We will focus on the histopathological aspects, especially on the importance of amyloid typing.
Copyright © 2020 Elsevier Masson SAS. All rights reserved.
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If not now, when? Enhancing cardiologists' psychological well-being as a COVID-19 gain.
Heart2021 Jan;():. doi: heartjnl-2020-318852.
Patel Rishi K, Sweeney Mark D, Baker Christopher S R, Greenberg Neil, Piper Susan E, Shergill Sukhi S, Tracy Derek K, Plymen Carla M,
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Musculoskeletal pathology as an early warning sign of systemic amyloidosis: a systematic review of amyloid deposition and orthopedic surgery.
BMC Musculoskelet Disord2021 Jan;22(1):51. doi: 10.1186/s12891-020-03912-z.
Wininger Austin E, Phelps Brian M, Le Jessica T, Harris Joshua D, Trachtenberg Barry H, Liberman Shari R,
Abstract
BACKGROUND:
Transthyretin and immunoglobulin light-chain amyloidoses cause amyloid deposition throughout various organ systems. Recent evidence suggests that soft tissue amyloid deposits may lead to orthopedic conditions before cardiac manifestations occur. Pharmacologic treatments reduce further amyloid deposits in these patients. Thus, early diagnosis improves long term survival.
QUESTIONS/PURPOSES:
The primary purpose of this systematic review was to characterize the association between amyloid deposition and musculoskeletal pathology in patients with common orthopedic conditions. A secondary purpose was to determine the relationship between amyloid positive biopsy in musculoskeletal tissue and the eventual diagnosis of systemic amyloidosis.
METHODS:
We performed a systematic review using PRISMA guidelines. Inclusion criteria were level I-IV evidence articles that analyzed light-chain or transthyretin amyloid deposits in common orthopedic surgeries. Study methodological quality, risk of bias, and recommendation strength were assessed using MINORS, ROBINS-I, and SORT.
RESULTS:
This systematic review included 24 studies for final analysis (3606 subjects). Amyloid deposition was reported in five musculoskeletal pathologies, including carpal tunnel syndrome (transverse carpal ligament and flexor tenosynovium), hip and knee osteoarthritis (synovium and articular cartilage), lumbar spinal stenosis (ligamentum flavum), and rotator cuff tears (tendon). A majority of studies reported a mean age greater than 70 for patients with TTR or AL positive amyloid.
CONCLUSIONS:
This systematic review has shown the presence of amyloid deposition detected at the time of common orthopedic surgeries, especially in patients ?70?years old. Subtyping of the amyloid has been shown to enable diagnosis of systemic light-chain or transthyretin amyloidosis prior to cardiac manifestations.
LEVEL OF EVIDENCE:
Level IV.
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Nerve ultrasonography features in hereditary transthyretin amyloidosis with V30M mutation and polyneuropathy.
Neurol Sci2021 Jan;():. doi: 10.1007/s10072-020-05033-w.
Salvalaggio Alessandro, Coraci Daniele, Cacciavillani Mario, Padua Luca, Briani Chiara,
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Patient-reported burden of hereditary transthyretin amyloidosis on functioning and well-being.
J Patient Rep Outcomes2021 Jan;5(1):3. doi: 10.1186/s41687-020-00273-y.
Lovley Andrew, Raymond Kimberly, Guthrie Spencer D, Pollock Michael, Sanchorawala Vaishali, White Michelle K,
Abstract
BACKGROUND:
Hereditary transthyretin (hATTR) amyloidosis is a rare, systemic, progressive, and life-threatening disease in which transthyretin proteins misfold and aggregate as insoluble amyloid deposits, disrupting nervous, cardiac, gastrointestinal, and other organ tissues. There are limited available data about the experience of patients living with hATTR amyloidosis. This study used a qualitative, non-interventional design to explore the humanistic burden of hATTR amyloidosis from the patient's perspective.
RESULTS:
Fourteen adults with hATTR amyloidosis, recruited from a patient advocacy group or an academic clinical center, participated in individual semi-structured interviews either in person or by telephone. Patients were asked to describe their experiences living with the condition, including symptoms and disease-related impacts on functioning and well-being, work, and activities of daily living (ADLs). Interviews were transcribed verbatim and analyzed for key concepts using a grounded theory approach. Patients described many symptoms of hATTR amyloidosis, particularly those associated with peripheral neuropathy such as pain, numbness, weakness, and paresthesia. Symptoms of autonomic neuropathy, such as gastrointestinal dysfunction, and symptoms related to cardiac dysfunction were also common. Worsening symptoms, especially those impacting patients' ability to walk or use their hands, often led to a loss of autonomy and an inability to work or perform ADLs. Disease-related disability also interfered with patients' participation in social activities, and contributed to feelings of fear, frustration, or sadness.
CONCLUSIONS:
The impacts of hATTR amyloidosis were profound for the patients interviewed for this study. They described a sense of loss as their condition progressed and impacted them physically, emotionally, and socially. Patients' reports of symptoms and impacts of hATTR amyloidosis illustrate the complex and varied manifestations of this disease. The progression of symptoms and increasing impacts of hATTR amyloidosis also highlight the need for an earlier diagnosis and effective clinical intervention to preserve patients' functioning and well-being.
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