Clinical Presentation: a 51-years-old woman with history of palpitations and sporadic premature ventricular beats, presented to ED with chest pain.ECG revealed sustained polymorphic ventricular tachycardia (VT) with RBBB morphology.Amiodarone and lidocaine were partially effective while flecainide was initially able to maintain the sinus rhythm.The ECG showed a wide fragmented QRS (RBBB aspect) and negative T waves in lateral leads.Echocardiography disclosed dilated left ventricle (LV) with mild systolic dysfunction due to regional akinesia, prominent trabeculation in lateral wall.Troponin I and inflammatory markers were elevated as well.The patient underwent coronary angiography that ruled out any coronary disease and therefore, to identify the possible type of cardiomyopathy, an endomyocardial biopsy was performed but was inconclusive.Arrhythmia burden remained high with long episodes of VT despite antiarrhythmic therapy.Only esmolol seemed to reduce the episodes of VT.To better define the underlying disease, a cardiac magnetic resonance (CMR) during continuous esmolol injection was planned but, after functional sequences, the exam had to be stopped due to the occurrence of sustained VT.Amiodarone plus flecainide were needed to restore sinus rhythm beside esmolol.The few CMR data confirmed mild systolic biventricular dysfunction with LV non-compaction and dilated RV outflow tract.A second scan in a full body PET-CMR was scheduled showing an inflammatory cardiomyopathy with an enhanced uptake of FDG only in LV wall, Late Gadolinium Enhancement (LGE) was present transmurally in the apical and mid-segment of the anterolateral wall and as epicardial stria in inferolateral wall (Figure 1).The patient was discharged after 33 days on Flecainide and Metoprolol.Four months later a new CMR scan confirmed biventricular dilatation, a thinned and dyskinetic LV lateral wall with persistent areas of transmural LGE.Learning points: the clinical data led us to think of an ischemic heart disease.Once we ruled it out, the diagnosis became challenging.Noncompaction could be due to a dilated cardiomyopathy and may be a consequence of LV remodelling rather than the cause, moreover troponin release is atypical in this setting.Cardiac sarcoidosis is commonly seen in basal segments, particularly of the septum and wall thinning is not the first manifestation.PET-CMR showed a LV inflammation with biventricular dysfunction.By Literature, the increasing use of CMR showed that in arrhythmogenic cardiomyopathy, the LV involvement is much more common than expected and a sizeable proportion of patients has a LV disease which parallels or exceeds the severity of right ventricular involvement, as in this case.With disease progression an epicardial scar can became transmural, causing thinning of myocardial wall over time.In our opinion, the most likely diagnosis was a hot phase of arrhythmogenic cardiomyopathy.

Clinical presentation: Two middle-aged women with a history of Multiple Myeloma (MM)(IgG k and IgG lambda chains, respectively), both on treatment with Lenalidomide, were admitted to hospital because of atypical chest pain and raised Troponin I.They both complained of worsening asthenia and progressively developed ventricular arrhythmias, leading to ventricular fibrillation in one patient (successfully treated with DC-shock).Despite having normal biventricular function at admission, repeated echocardiographic scans showed progressive left ventricular (LV)dysfunction and mild pericardial effusion.Diagnostic Technique and their most important findings: Coronary angiography was performed, showing no coronary stenosis.Both patients underwent a CMR scan that showed similar findings: LV function was mildly impaired due to diffuse hypokinesia, with akinesia of the basal to mid-cavity septum and of the adjacent anterior and inferior segments; trivial pericardial effusion and severe bilateral pleural effusion were noted.Tissue characterisation showed extensive mid-wall and epicardial oedema (Fig. 1A andD, yellow arrows), early and late gadolinium enhancement (Fig. 1B-C andE-F, red arrows) of the basal to mid-cavity septum and of the adjacent anterior and inferior segments; these findings were consistent with acute myocardial inflammation.Endomyocardial biopsy was performed in both patients, showing different findings: while one patient had histological evidence of acute myocardial inflammation, with small amounts of adipose infiltration, necrosis and myocytolysis, the other only had mild signs of replacement fibrosis,with no evidenceof inflammation or necrosis, and showed focal spots of amyloid fibrils at electronmicroscopy. Learning points:Despite showing different histologic patterns, perhaps subtending different underlying causes, both patients presented similar clinical and imaging patterns, suggesting a common arrhythmicoutcome.CMR played a pivotal role in the diagnostic process, identifying the acute inflammatory process, and guiding the best clinical management.Chemotherapy treatment was discontinued, and modified, in both patients, with evidence of slow progressive recovery of LV function; a repeat 1-month scan in one of the patients, however,still showed extensive tissue damage.

Background:Troponin elevations are common in critically ill patients. Whether they are predictors of mortality independent of the severity of the underlying disease is unclear. Objective:To determine whether troponin elevations predict in-hospital, short-term, and long-term mortality in medical intensive care unit patients independent of the severity of the underlying disease as measured by Acute Physiology and Chronic Health Evaluation III prognostic system. Design:Retrospective study. Setting:We examined the Acute Physiology and Chronic Health Evaluation III database and cardiac troponin T levels of medical intensive care unit patients at Mayo Clinic, Rochester, MN. Patients:In all, 1,657 patients consecutively admitted to medical intensive care units between August 2000 and December 2001. Measurements:In-hospital, short-term (30-day), and long-term all-cause mortality. Results:During hospitalization, 12.5% of patients with a cardiac troponin T < 0.01 &mgr;g/L suffered deaths compared with 29.5% among those with cardiac troponin T ≥0.01 &mgr;g/L (p < .001). At 30 days, mortality was 13.7% without and 34.6% with elevations (p < .001). The expected probability of survival at 1-, 2-, and 3-yr follow-up was 43.7%, 33.8%, and 25.7% among patients with cardiac troponin T ≥0.01 &mgr;g/L and 75.3%, 67.6%, and 62.9% in those with cardiac troponin T < 0.01 &mgr;g/L, respectively (p < .001). After adjustment for the severity of disease and baseline characteristics, cardiac troponin levels were still associated with in-hospital, short-term, and long-term mortality (p = .006, p = .007, and p = .001, respectively). Limitations:This is a single-site retrospective study that included only patients in whom a troponin level was obtained on admission. Conclusions:In medical intensive care unit patients, admission troponin levels are independently associated with short- and long-term mortality, even after adjustment for severity of disease.

To the Editor: Constrictive pericarditis (CP) often is a challenging diagnosis despite sophisticated modalities ([1–4][1]). If a simple test could alert physicians to the possibility of CP in patients with evidence of heart failure, it would be valuable. Recent data ([5][2]) suggest that brain

It has been known for 50 years that transaminase activity increases in patients with acute myocardial infarction. With the development of creatine kinase (CK), biomarkers of cardiac injury began to take a major role in the diagnosis and management of patients with acute cardiovascular disease. In 2000 the European Society of Cardiology and the American College of Cardiology recognized the pivotal role of biomarkers and made elevations in their levels the “cornerstone” of diagnosis of acute myocardial infarction. At that time, they also acknowledged that cardiac troponin I and T had supplanted CK-MB as the analytes of choice for diagnosis. In this review, we discuss the science underlying the use of troponin biomarkers, how to interpret troponin values properly and how to apply these measurements to patients who present with possible cardiovascular disease.