Patients with recurrent pericarditis were treated with the interleukin-1 trap rilonacept. Those who had a response were randomly assigned to receive continued rilonacept or placebo. Rilonacept led to ...a significantly lower risk of pericarditis recurrence than placebo.
The initial mechanism for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is the binding of the virus to the membrane-bound form of ACE2, which is mainly expressed in the lung. ...Since the heart and the vessels also express ACE2, they both could become targets of the virus. However, at present the extent and importance of this potential involvement are unknown. Cardiac troponin levels are significantly higher in patients with more severe infections, patients admitted to intensive care units or in those who have died. In the setting of COVID-19, myocardial injury, defined by an increased troponin level, occurs especially due to non-ischaemic myocardial processes, including severe respiratory infection with hypoxia, sepsis, systemic inflammation, pulmonary thrombosis and embolism, cardiac adrenergic hyperstimulation during cytokine storm syndrome, and myocarditis. At present, there are limited reports on definite diagnosis of myocarditis caused by SARS-CoV-2 in humans and limited demonstration of the virus in the myocardium. In conclusion, although the heart and the vessels are potential targets in COVID-19, there is currently limited evidence on the direct infection of the myocardium by SARS-CoV-2. Additional pathological studies and autopsy series will be very helpful to clarify the potentiality of COVID-19 to directly infect the myocardium and cause myocarditis.
A Randomized Trial of Colchicine for Acute Pericarditis Imazio, Massimo; Brucato, Antonio; Cemin, Roberto ...
New England journal of medicine/The New England journal of medicine,
10/2013, Volume:
369, Issue:
16
Journal Article
Peer reviewed
Open access
In a randomized trial, patients with acute pericarditis were assigned to either colchicine or placebo in addition to conventional antiinflammatory therapy. Colchicine significantly reduced the ...incidence of incessant or recurrent pericarditis.
Colchicine has been used for centuries to treat and prevent gouty attacks
1
and more recently has been recommended to treat and prevent serositis in patients with familial Mediterranean fever and recurrent pericarditis.
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,
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Preliminary data from nonrandomized trials have also supported the use of colchicine for the treatment and prevention of acute pericarditis.
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In a single-center, open-label, randomized trial, called the Colchicine for Acute Pericarditis (COPE) study, the addition of colchicine to conventional therapy with either aspirin or glucocorticoids halved the recurrence rate after an initial attack of acute pericarditis.
5
Our study, called the Investigation on Colchicine for Acute Pericarditis . . .
Abstract The term “post-cardiac injury syndromes” includes post-myocardial infarction pericarditis, post-pericardiotomy syndrome, and post-traumatic pericarditis (iatrogenic, i.e. after percutaneous ...coronary or intracardiac interventions, such as pacemaker lead insertion, radiofrequency ablation, or non-iatrogenic, i.e. following blunt or penetrating trauma). All these conditions represent different clinical conditions characterized by an initial cardiac injury involving the pericardium/myocardium and/or pleura and the subsequent inflammatory syndrome ranging from simple, uncomplicated pericarditis to more complicated cases with pleuropericarditis, cardiac tamponade or massive pleural effusion. The etiopathogenesis is presumed to be immune-mediated in predisposed individuals that develop autoreactive reactions following the initial traumatic event. Treatment is essentially based on empirical anti-inflammatory therapy and adjunctive colchicine, which has been shown to be safe and efficacious for the prevention of pericarditis.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Cardiac amyloidosis is a serious and progressive infiltrative disease that is caused by the deposition of amyloid fibrils at the cardiac level. It can be due to rare genetic variants in the ...hereditary forms or as a consequence of acquired conditions. Thanks to advances in imaging techniques and the possibility of achieving a non-invasive diagnosis, we now know that cardiac amyloidosis is a more frequent disease than traditionally considered. In this position paper the Working Group on Myocardial and Pericardial Disease proposes an invasive and non-invasive definition of cardiac amyloidosis, addresses clinical scenarios and situations to suspect the condition and proposes a diagnostic algorithm to aid diagnosis. Furthermore, we also review how to monitor and treat cardiac amyloidosis, in an attempt to bridge the gap between the latest advances in the field and clinical practice.
Cardiac amyloidosis is a serious and progressive infiltrative disease that is caused by the deposition of amyloid fibrils at the cardiac level. It can be due to rare genetic variants in the ...hereditary forms or as a consequence of acquired conditions. Thanks to advances in imaging techniques and the possibility of achieving a non‐invasive diagnosis, we now know that cardiac amyloidosis is a more frequent disease than traditionally considered. In this position paper the Working Group on Myocardial and Pericardial Disease proposes an invasive and non‐invasive definition of cardiac amyloidosis, addresses clinical scenarios and situations to suspect the condition and proposes a diagnostic algorithm to aid diagnosis. Furthermore, we also review how to monitor and treat cardiac amyloidosis, in an attempt to bridge the gap between the latest advances in the field and clinical practice.
Diagnosis and treatment of cardiac amyloidosis.
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Constrictive pericarditis (CP) is considered a rare, dreaded possible complication of acute pericarditis. Nevertheless, there is a lack of prospective studies that have evaluated the specific risk ...according to different etiologies. The aim of this study is to evaluate the risk of CP after acute pericarditis in a prospective cohort study with long-term follow-up.
From January 2000 to December 2008, 500 consecutive cases with a first episode of acute pericarditis (age, 51±16 years; 270 men) were prospectively studied to evaluate the evolution toward CP. Etiologies were viral/idiopathic in 416 cases (83.2%), connective tissue disease/pericardial injury syndromes in 36 cases (7.2%), neoplastic pericarditis in 25 cases (5.0%), tuberculosis in 20 cases (4.0%), and purulent in 3 cases (0.6%). During a median follow-up of 72 months (range, 24 to 120 months), CP developed in 9 of 500 patients (1.8%): 2 of 416 patients with idiopathic/viral pericarditis (0.48%) versus 7 of 84 patients with a nonviral/nonidiopathic etiology (8.3%). The incidence rate of CP was 0.76 cases per 1000 person-years for idiopathic/viral pericarditis, 4.40 cases per 1000 person-years for connective tissue disease/pericardial injury syndrome, 6.33 cases per 1000 person-years for neoplastic pericarditis, 31.65 cases for 1000 person-years for tuberculous pericarditis, and 52.74 cases per 1000 person-years for purulent pericarditis.
CP is a relatively rare complication of viral or idiopathic acute pericarditis (<0.5%) but, in contrast, is relatively frequent for specific etiologies, especially bacterial.
In this paper the Working Group on Myocardial and Pericardial Disease proposes a revised definition of dilated cardiomyopathy (DCM) in an attempt to bridge the gap between our recent understanding of ...the disease spectrum and its clinical presentation in relatives, which is key for early diagnosis and the institution of potential preventative measures. We also provide practical hints to identify subsets of the DCM syndrome where aetiology directed management has great clinical relevance.
Abstract Acute pericarditis is often accompanied by some degree of myocarditis. In clinical practice both pericarditis and myocarditis coexist because they share common etiologic agents, mainly ...cardiotropic viruses. The term “myopericarditis” indicates a primarily “pericarditic syndrome” and it is responsible for the majority of cases. The clinical presentation is varied, reflecting the variability of myocardial involvement, that may be focal or diffuse, affecting any or all cardiac chambers. Probably many cases may be subclinical and subtle cardiac symptoms and signs may be overshadowed by the systemic manifestations of the viral infection. Echocardiography is essential for the diagnosis of left ventricular dysfunction in even subclinical cases and for follow-up of patients with apparently normal left ventricular function. Magnetic resonance imaging holds promise for an effective non-invasive diagnostic tool. Either for acute pericarditis or myopericarditis there is a lack for adequate controlled clinical trials. In myopericarditis the use of NSAID should be cautious, because in animal models of myocarditis, NSAID are not effective and may actually enhance the myocarditic process and increase mortality. In clinical practice lower anti-inflammatory doses are mainly considered to control symptoms. The natural history of myopericarditis in large populations is not known with accuracy. On follow-up, the majority of these cases had objective normalization of echocardiography, electrocardiography, laboratory testing, and functional status, although up to 14% may report atypical, non-limiting chest discomfort. Unfortunately, few data have been published on myopericarditis, the paper reviews current available evidence on the presentation, management, and prognosis of myopericarditis.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
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