‘Eosinophilic myocarditis in the era of multi-modality cardiac imaging: A case report’

IntroductionEosinophilic myocarditis is a rare form of myocarditis. It is characterized pathologically by diffuse or focal myocardial inflammation with eosinophilic infiltration, often in association with peripheral blood eosinophilia. We report a case of eosinophilic myocarditis secondary to hypereosinophilic syndrome.Case presentationA 74-year-old Caucasian woman with a history of asthma, paroxysmal atrial fibrillation, stroke and coronary artery disease presented to the emergency department of our hospital with chest pain. Evaluations revealed that she had peripheral blood eosinophilia and elevated cardiac enzymes. Electrocardiographic findings were nonspecific. Her electrocardiographic finding and elevated cardiac enzymes pointed to a non-ST-elevated myocardial infarction. Echocardiogram showed a severe decrease in the left ventricular systolic function. Coronary angiogram showed nonobstructive coronary artery disease. She then underwent cardiac magnetic resonance imaging, which showed neither infiltrative myocardial diseases nor any evidence of infarction. This was followed by an endomyocardial biopsy which was consistent with eosinophilic myocarditis. Hematologic workup regarding her eosinophilia was consistent with hypereosinophilic syndrome. After being started on steroid therapy, her peripheral eosinophilia resolved and her symptoms improved. Her left ventricular ejection fraction, however, did not improve.ConclusionEosinophilic myocarditis can present like an acute myocardial infarction and should be considered in the differential diagnosis of acute coronary syndrome in patients with a history of allergy, asthma or acute reduction of the left ventricular function with or without peripheral eosinophilia.

Determining the etiology of cardiac dysfunction in patients with heart failure influences management and prognosis.1 Myocarditis, diagnosed by the current histopathological Dallas criteria, accounts for &10% of patients with new-onset cardiac dysfunction submitted to endomyocardial biopsy.1,2 Despite complete evaluation including history, physical examination, blood work, echocardiography, coronary angiography, and endomyocardial biopsy, &50% of patients with dilated cardiomyopathy have no etiology identified.1 Recent data suggest that patients in the “idiopathic” category may be suffering from myocardial inflammation due to persistent viral replication or autoimmune activation after a viral infection. These studies raise the question of whether the current histopathological criteria for myocardial inflammation (the Dallas criteria) are sensitive enough to identify the population with viral or autoimmune-related heart compromise. The Dallas criteria were proposed in 1986 and provided a histopathological categorization by which the diagnosis of myocarditis could be established. Dallas criteria myocarditis requires an inflammatory infiltrate and associated myocyte necrosis or damage not characteristic of an ischemic event. Borderline myocarditis requires a less intense inflammatory infiltrate and no light microscopic evidence of myocyte destruction.3 These criteria have been used exclusively by American investigators over the last 2 decades. Sampling error, variation in expert interpretation, variance with other markers of viral infection and immune activation in the heart, and variance with treatment outcomes all suggest that the Dallas criteria are no longer adequate. Chow et al and Hauck et al4,5 demonstrated by biopsying postmortem hearts of patients who had died with myocarditis that, from a single endomyocardial biopsy, histological myocarditis could be demonstrated in only 25% of samples. With >5 biopsies, Dallas criteria myocarditis could be diagnosed in approximately two thirds of subjects. A recent MRI study used focal imaging abnormalities to guide heart biopsy investigation of possible myocarditis. The authors showed that the earliest myocardial …

Dobutamine-Induced Fever and Isolated Eosinophilic Myocarditis in a 66-Year-Old Male Awaiting Heart Transplantation: A Case Report

Loeffler Endocarditis as a Manifestation of Paraneoplastic Hypereosinophilia

Options for ventricular tachycardia ablation after double valve replacement

BackgroundEosinophilic myocarditis is characterized by myocardial eosinophilic infiltration and is largely associated with hypereosinophilia. However, eosinophilic myocarditis with a normal peripheral eosinophilic count has been previously reported. Since the absence of eosinophilia poses a challenge for therapeutic management, we evaluated whether troponin I (TnI) levels can be used in the management of eosinophilic myocarditis where peripheral eosinophilia is absent.Case summaryWe report the case of a 77-year-old woman who developed cardiogenic shock due to acute necrotizing eosinophilic myocarditis, which required mechanical circulatory support. She did not have hypereosinophilia, but endomyocardial biopsy confirmed massive infiltration of eosinophils into the myocardium. We administered high-dose corticosteroids for 3 days and she dramatically improved. Along with this, the TnI level, which was elevated at the time of patient presentation, also decreased after steroid therapy. Troponin I level did not increase again without taking any oral prednisolone, and the follow-up biopsy after 6 months showed complete recovery of eosinophilic myocarditis.DiscussionTroponin I-guided treatment is a useful tool in the management of eosinophilic myocarditis because it helps with therapeutic decisions, especially in the absence of eosinophilia.

IntroductionThe aim of this study was to investigate the results of radiofrequency catheter ablation of ventricular tachycardia (VT) in patients with organic heart diseases utilising CARTO system and a saline-irrigated...

Refractory ventricular tachycardia secondary to cardiac sarcoid: Electrophysiologic characteristics, mapping, and ablation

We performed catheter ablation in 10 consecutive patients with idiopathic monomorphic right ventricular tachycardia and studied the long-term outcome. All ventricular tachycardias had a left bundle branch block configuration with an inferior axis, and originated from right ventricular outflow. Antiarrhythmic drugs (3-6 drugs) had been ineffective in controlling ventricular tachycardia. The 2 patients who underwent direct-current ablation (2 shocks of 150 J) had no recurrence of ventricular tachycardia and did not require antiarrhythmic drugs during a follow-up of 56 and 51 months, respectively. Of the 8 patients who underwent radiofrequency ablation (30-40 watt, 20-40 sec, 2-15 application, using Inter Nova RA 50, 13.56 MHz), 1 patient had no recurrence of ventricular tachycardias and did not require antiarrhythmic drugs, 4 patients had no recurrence of ventricular tachycardias but did require anti-arrhythmic drugs, and 3 patients experienced recurrence of non-sustained ventricular tachycardia despite the use of antiarrhythmic drugs during a follow-up of 15-40 months. There were no complications except for cardiac perforation which occurred immediately after direct-current ablation in 1 patient. In conclusion, long-term success in preventing ventricular tachycardia was achievable with direct-current ablation, but this success was associated with serious risks, such as cardiac perforation. Radiofrequency ablation was safer than direct-current ablation, but had a lower long-term success rate.

A Case Series of Biopsy-Proven Eosinophilic Myocarditis at a Tertiary Care Center

When to sear, when to burn, and when to chop: The art of substrate modification

BackgroundJ‐waves and fragmented QRS (fQRS) on surface ECGs have been associated with the occurrence of ventricular tachyarrhythmias. Whether these non‐invasive parameters can also predict ventricular tachycardia (VT) recurrence after radiofrequency catheter ablation (RFCA) is unknown. Of interest, patients with a wide QRS‐complex have been excluded from clinical studies on J‐waves, although a J‐wave like pattern has been described for wide QRS.MethodsWe retrospectively included 168 patients (67 ± 10 years; 146 men) who underwent RFCA of post‐infarct VT. J‐wave pattern were defined as J‐point elevation ≥ 0.1 mV in at least two leads irrespective of QRS width. fQRS was defined as various RSR` pattern in patients with narrow QRS and more than two R wave in those with wide QRS. The primary endpoint was VT recurrence after RFCA up to 24 months.ResultsJ‐wave pattern and fQRS were present in 27 and 28 patients, respectively. Overlap of J‐wave pattern and fQRS was observed in nine. During a median follow‐up of 20 (interquartile range 9–24) months, 46 (27%) patients had VT recurrence. Kaplan–Meier curves revealed that both J‐wave pattern and fQRS were associated with VT recurrence. Multivariate Cox regression analysis demonstrated that the presence of J‐wave pattern (hazard ratio [HR] 2.84; 95% confidence interval [CI] 1.45–5.58; P = .002) and greater number of induced VT (HR 1.29; 95% CI 1.15–1.45; P < .001) were the independent predictors of VT recurrence.ConclusionsA J‐wave pattern—but not fQRS—is independently associated with an increased risk of post‐infarct VT recurrence after RFCA irrespective of QRS width. This simple non‐invasive parameter may identify patients who require additional treatment.

Studies show mixed results regarding the effect of coronary revascularization on mortality benefit and ventricular tachycardia (VT) recurrence in patients with monomorphic VT without acute coronary syndrome (ACS). This meta-analysis aimed to assess the effect of ischemia testing and/or coronary revascularization on mortality and VT recurrence in a pooled data set. Databases including PubMed, Google Scholar, and the Cochrane Library were searched from January 2000 to December 2023 for studies reporting event data on mortality and VT recurrence in patients without ACS who presented with monomorphic VT. Data were pooled and analyzed using random effects meta-analysis. The pooled sample consisted of a total of five studies, with 1062 patients, of whom 433 underwent ischemia testing and/or coronary revascularization and 629 did not. There was no statistically significant difference in the mortality and VT recurrence in the patients who underwent ischemia testing and/or revascularization versus those who did not (mortality odds ratio [OR]: 0.98; [95% confidence interval (CI): 0.62 to 1.53]; p = 0.92; VT recurrence OR: 1.07; [95% CI: 0.51 to 2.26]; p = 0.86). No publication bias was detected by examination of the funnel plot, Begg-Mazumdar's test (p = 0.80), and Egger's test (p = 0.91). In conclusion, in patients with sustained monomorphic VT in the absence of ACS, ischemia testing and/or revascularization does not lead to improved mortality or a decrease in the incidence of VT recurrence.

In many cases, the diagnosis of eosinophilic myocarditis is suggested by an elevated peripheral blood eosinophil count. However, no detailed studies have been performed on the sequential changes in the initial peripheral blood eosinophil count over the course of the disease. We measured the peripheral blood eosinophil count at the time of presentation in eight patients with eosinophilic myocarditis proven by endomyocardial biopsy and intermittently thereafter. The eosinophil count at the time of onset was <500/mm(3) in four patients, >500/mm(3) but <1,000/mm(3) in three patients, and > or =1,000/mm(3) in one patient. In three of the four patients with an initial eosinophil count of <500/mm(3), an increase to > or =500/mm(3) occurred 7-12 days after the onset. The remaining patient did not develop peripheral eosinophilia. In conclusion, in the early stage of eosinophilic myocarditis, peripheral hypereosinophilia is not present initially in some patients, and may not develop during the course of the illness in a subset of these patients.

Background: The identification of ventricular tachycardia (VT) substrate is crucial for optimizing the success of VT ablation. Recently, multi-modality imaging has gained interest in VT substrate identification before ablation. Objective: This study aims to compare VT recurrence and all-cause mortality in patients undergoing MRI-guided versus MRI-aided VT ablation. Methods: A systematic literature review was conducted from inception until November 30, 2024, following PRISMA guidelines. Two independent reviewers screened studies meeting the following inclusion criteria: VT due to ischemic (ICM) or non-ischemic cardiomyopathy (NICM), MRI-guided ablation (MRI data integrated with electroanatomic mapping), or MRI-aided ablation (MRI reviewed by radiologists and electrophysiologists), age &gt;18 years, and clinical trials or observational studies. Primary endpoints included VT recurrence and all-cause mortality. A stratified subgroup analysis for ICM and NICM was performed. Event rates were estimated using a generic variance random-effects model (CMA IV), with heterogeneity assessed via Cochrane’s Q-statistic (I2&gt;75% indicating high heterogeneity) and study quality evaluated using the Newcastle-Ottawa Scale. Results: Fifteen studies (N=565, MRI-guided: n=238; MRI-aided: n=327) were included, with a mean follow-up of 24 months. VT recurrence was 25% (CI: 15%-38%, I2=41%, p=0.012) and all-cause mortality was 5.7% (CI: 2.5%-13%, I2=0%, p=0.64) in the MRI-guided group. Subgroup analysis showed VT recurrence rates of 27% in ICM (CI: 17%-40%, I2=11%, p=0.342) and 35% in NICM (CI: 18%-56%, I2=0%, p=0.963). In the MRI-aided group, VT recurrence was 29% (CI: 18%-45%, I2=69%, p=0.04) and all-cause mortality was 4.2% (CI: 1.5%-11%, I2=0%, p=0.669). Subgroup analysis showed VT recurrence of 46.5% in ICM (CI: 29%-65%, I2=37%, p=0.205) and 41% in NICM (CI: 23%-63%, I2=74%, p=0.004). Study quality ranged from moderate to high. Conclusion: MRI-guided VT ablation is associated with lower VT recurrence rates compared to MRI-aided VT ablation, while all-cause mortality remains similar between both techniques. Stratified analysis suggests that MRI-guided VT ablation may be particularly beneficial in reducing VT recurrence in the ICM subgroup.