Mayo Criteria Research Articles

Myocarditis mimicking Takotsubo cardiomyopathy or Takotsubo cardiomyopathy with secondary inflammation?: reply

We read with great interest the letter from Eitel et al. We would like to reemphasize that in the reported case of Takotsubo cardiomyopathy (TTC), endomyocardial biopsy (EMB), the diagnostic gold standard for myocarditis, had not been systematically performed, in spite of the fact that Mayo Criteria specify that myocarditis should be excluded in all cases of suspected TTC.1,2 As mentioned by Eitel, there are case reports of TTC that appear to be caused by myocarditis, in keeping with our findings.1 Our patient was virus-negative, thus the issue of virus pathogenicity is not relevant.3–5 In relation to Eitel's provocative proposal that our case may be a TTC with secondary inflammation, we think this is highly unlikely. Active myocarditis is not simply characterized by sparse mononuclear cell infiltrates, as suggested by Eitel et al., but is defined (Dallas criteria), as an inflammatory infiltrate of the myocardium with necrosis and/or degenerative changes of adjacent myocytes not typical of infarction.6 Our case fulfils state-of-the-art WHO histological (active myocarditis by the Dallas criteria), immunological (serum anti-heart autoantibodies), immunohistochemical (infiltrating activated lymphocytes and macrophages), and molecular (absence of viral genomes) diagnostic criteria of a virus-negative, immune-mediated form of acute myocarditis masquerading as TTC.3–6 Further, in our case the ‘stressful event’ dated back 3 months, thus the onset was not strictly time-related with clinical presentation; autoimmune myocarditis is more likely to occur in females, as other autoimmune diseases; the rapid resolution of cardiac dysfunction is a clinical hallmark of myocarditis.3,5 Last but not least, lymphocytic myocarditis can occur in relation to hypercatecholaminergic states, but it is not a feature known to be associated with microvascular ischaemia.5 Thus, a proportion of TTC patients with sympathetic overdrive may have an underlying virus-negative toxic myocarditis, explaining the reversible systolic dysfunction, chest pain and non-ischaemic troponin release. We propose1 in agreement with Eitel et al. that the role of inflammation in the pathogenesis of TTC merits further study, to differentiate myocarditis mimicking TTC from ‘idiopathic’ TTC, and/or to have a better understanding of the frequency of (viral, immune-mediated, or toxic) myocarditis in TTC. Takotsubo cardiomyopathy may be a syndrome, rather than a distinct pathological entity. Regarding Eitel's proposal that EMB is not an adequate method for the diagnosis of myocarditis, we disagree. First, EMB sensitivity is higher using immunohistochemistry.3–5,7 Secondly, EMB is safe with a complication rate that is similar to that of standard coronary angiography,3,7,8 which is always performed in TTC. Thirdly, myocarditis is challenging to identify clinically,3–5,7,8 and current validation studies of cardiac magnetic resonance imaging (CMR) are mainly based upon clinical presentation.9 Finally, CMR is unable to differentiate viral from non-viral myocarditis.9 Viral genome10 and chronic inflammation may have independent prognostic value in distinct subsets of patients.7 EMB, with adjunct immunohistology and molecular detection of the viral genome is the mainstay to achieve confirmation or exclusion of myocarditis3,5,9,10 as well as identify its aetiopathogenetic forms and aetiology-based therapies.3,5

Clinical correlates and prognostic significance of electrocardiographic abnormalities in apical ballooning syndrome (Takotsubo/stress-induced cardiomyopathy)

Apical ballooning syndrome (ABS) is a unique transient cardiomyopathy that mimics an acute myocardial infarction. The relative frequency of ST-segment elevation on the 12-lead electrocardiogram (ECG) and its prognostic significance is unknown. The aims of this study were to evaluate the frequency and the clinical correlates of ST- and T-wave abnormalities on the admission ECG in patients with ABS. Patients were retrospectively identified from the cardiac catheterization database--those who underwent coronary and left ventricular angiography and fulfilled the Mayo criteria for ABS during the period January 1988 to November 2006. They were divided into 3 groups according to the presence of (1) ST-segment elevation (>1 mm in 2 contiguous lead) or new left bundle branch block, (2) T-wave inversion (>3 mm in 3 contiguous leads) but no ST shift, and (3) nonspecific ST-T abnormalities or normal ECG at the time of admission. Clinical and echocardiographic findings were compared between groups. Among the 105 patients, 36 (34.2%), 32 (30.4%), and 37 (35.2%) patients were in the three respective groups. There were no differences in the clinical characteristics, ejection fraction, and outcomes between the 3 groups. Over a median follow-up of 2.5 years, there was no difference in the 5-year recurrence rate of ABS between the 3 groups (13%, 5%, 17% patients, respectively, P = .25). The 5-year mortality was similar in the 3 groups (24%, 7.3%, 10.8%, P = .58). ST-segment elevation is absent in two thirds of patients with ABS. Thus, the cardiomyopathy may mimic either ST-elevation or non-ST-elevation myocardial infarction. The ECG abnormalities at presentation do not correlate with the magnitude of ventricular dysfunction or outcomes.

Acute biopsy‐proven lymphocytic myocarditis mimicking Takotsubo cardiomyopathy

Endomyocardial biopsy (EMB), the diagnostic gold standard for myocarditis, has not been systematically performed in the reported case series of Takotsubo cardiomyopathy, although proposed Mayo Criteria specify exclusion of myocarditis. Moreover, there is no specific recommendation for infarct-like acute myocarditis in the recently published guidelines on the role of EMB. Here we present a thoroughly documented case fulfilling both the proposed Mayo criteria for Takotsubo cardiomyopathy and the World Health Organization criteria for active, virus-negative, immune-mediated myocarditis. Since myocarditis can mimic acute myocardial infarction with normal coronary arteries, EMB should be performed to rule out myocarditis in patients presenting with LV apical ballooning syndrome (or Takotsubo cardiomyopathy).

Diagnostic challenge in autoimmune pancreatitis: beware of shipwreck!

Assessing the differential diagnosis between autoimmune pancreatitis (AIP) and pancreatic adenocarcinoma is like sailing between two rocks. Rock number 1 is to perform a surgical pancreatic resection in patients with...

Review of diagnostic criteria for autoimmune pancreatitis; for establishment of international criteria.

Along with worldwide expansion of the disease concept of autoimmune pancreatitis (AIP), the necessity of international diagnostic criteria for the disease is increasing. Since the first diagnostic criteria for AIP by the Japan Pancreas Society was proposed in 2002, certain groups in several countries have reported criteria for AIP. We reviewed the criteria proposed to date. Among three systematic criteria from Japan, the Mayo Clinic and Korea, there is no fundamental difference in the three major diagnostic categories: findings on pancreatic imaging, laboratory and histological studies. Notable differences are that typical imaging findings are essential for the diagnosis in Japanese and Korean criteria, but not in the Mayo criteria, while, the Mayo criteria emphasize the histological findings as a gold standard for the diagnosis. The critical differences between the Japanese and the other two criteria are the use of the diagnostic factors "other organ involvement" and "steroid responsiveness." Employment of these factors in clinical diagnostic criteria for general physicians possibly confuses the disease concept and definitely increases the risk for treating patients with pancreatic or biliary malignancies with steroids. Even if the sensitivity of criteria goes down, their use might be limited to certain kinds of specific criteria, such as that for epidemiological study, patient selection for research purposes, or use in expert hospitals. The disease entity of AIP postulated in Europe includes two histological types of pancreatitis with different clinical phenotypes, suggesting two syndromic spectra of autoimmune-related chronic pancreatitis.

Primary sclerosing cholangitis - What is the difference between east and west?

Primary sclerosing cholangitis (PSC) is a chronic, progressive, cholestatic liver disease characterized by inflammation and fibrotic obliteration of the hepatic biliary tree. It is commonly associated with inflammatory bowel disease (IBD). A number of complications can occur which require special consideration, the most important of which is the development of cholangiocellular carcinoma (CCC). Unfortunately, no medical therapy is currently available for the underlying liver disease. Liver transplantation is an effective, life-extending option for patients with advanced PSC. Geographical variations between East and West include a second peak for age with a lower association with IBD in a Japanese population and female predominance in a lone study from Turkey. The clinical and biochemical Mayo criteria may not be universally applicable, as different patients show variations regarding the initial presentation and natural course of the disease. Directing research towards explaining these geographical differences and understanding the pathogenesis of PSC is required in order to develop better therapies for this devastating disease.

Significance of fecal lactoferrin in evaluation of disease activity in ulcerative colitis

To explore the possibility and clinical application value of fecal lactoferrin as a marker of the activity of ulcerative colitis (UC). Specimens of feces were collected from 66 UC patients and 20 healthy persons or irritable bowel syndrome patients. ELISA was used to measure the concentration of lactoferrin in feces, and CRP and ESR were also measured. The disease activity of UC was determined by Mayo criteria. The fecal lactoferrin concentration of the patients with active UC was (61.6 +/- 4.8) microg/g, significantly higher than that of the patients with inactive UC and the controls [(7.9 +/- 1.1) microg/g and (3.0 +/- 0.5) microg/g, both P < 0.01], and the fecal lactoferrin concentration of the patients with inactive UC group was also significantly higher than that of the controls (P < 0.05). The higher the grade of activity of disease the higher the concentration of lactoferrin (P < 0.05 or P < 0.01). The area under curve of receiver operating characteristic (AUCROC) of fecal lactoferrin was 0.982, significantly larger than those of the CRP and ESR (0.740 and 0.692 respectively, both P < 0.01). However, there was no significant difference in AUCROC between CPR and ESR. The fecal lactoferrin concentration was positively correlated with the endoscopic grades of UC (r = 0.871, P < 0.01). Lactoferrin in feces reflects the disease activity of UC and is a rational fecal marker of intestinal inflammation for clinical application. A precise, simple, and noninvasive method, lactoferrin examination is better than common clinically used markers, such as CRP and ESR.

Chronic active hepatitis in Sweden. The etiologic spectrum, clinical presentation, and laboratory profile.

An epidemiologic study covering about 1/3 of the adult Swedish population showed an annual incidence of chronic active hepatitis (CAH) of 1.6 per 100,000. At least 45% had a viral cause of their CAH, the proportion being distinctly higher in large cities than in rural ones. Drugs, alcohol, and metabolic disorders were rarely identified as etiologic factors. The prevalence of ulcerative colitis and gluten enteropathy was remarkably high in idiopathic CAH. Compared with antibody-negative patients with idiopathic CAH, antibody-positive patients showed higher rates of the female sex, IgG increase, anti-HBs negativity, compliance with the Mayo criteria for treatment, and absence of previous episode of jaundice. Furthermore, in autoantibody-negative idiopathic CAH the prevalence of anti-HBs antibodies was at least three times greater than in the Swedish population, suggesting a viral cause of some forms of idiopathic CAH, a suggestion supported by the clinical pattern of the disease.