Bidirectional Ventricular Tachycardia in a Patient With Fulminant Myocarditis Secondary to Cardiac Sarcoidosis Mimicking Giant Cell Myocarditis.
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ABSTRACT:
SUBMITTER: Durocher D
PROVIDER: S-EPMC8712583 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Giant cell myocarditis, but not cardiac sarcoidosis, is known to cause fulminant myocarditis resulting in severe heart failure. However, giant cell myocarditis and cardiac sarcoidosis are pathologically similar, and attempts at pathological differentiation between the two remain difficult. We are presenting a case of fulminant myocarditis that has pathological features suggestive of cardiac sarcoidosis, but clinically mimicking giant cell myocarditis. This patient was treated with cyclosporine and prednisone and recovered well. This case we believe challenges our current understanding of these intertwined conditions. By obtaining a sense of severity of cardiac involvement via delayed hyperenhancement of cardiac magnetic resonance imaging, we were more inclined to treat this patient as giant cell myocarditis with cyclosporine. This resulted in excellent improvement of patient's cardiac function as shown by delayed hyperenhancement images, early perfusion images, and SSFP videos.
| S-EPMC4008442 | biostudies-other
Project description:Myocarditis is a disease with variable clinical presentation, ranging from an uncomplicated febrile illness to cardiogenic shock. Herein, we report a case of fulminant myocarditis secondary to murine typhus in a 52-year-old male that initially mimicked an acute coronary syndrome. Emergent coronary angiography showed angiographically normal coronary arteries. Left ventriculography showed global hypokinesis with an ejection fraction of 10%. The patient required mechanical support with an intra-aortic balloon pump and fully recovered. <Learning objective:Fulminant myocarditis secondary to murine typhus may occur in urban areas. Clinical complications such as cardiogenic shock and acute heart failure can be overcome with supportive therapy such as an intra-aortic balloon pump and guideline-directed medical therapy.>.
| S-EPMC8380947 | biostudies-literature
Project description:A 69-year-old woman with isolated cardiac sarcoidosis was hospitalized for frequent appropriate implantable converter defibrillator therapies for ventricular tachycardia (VT) despite of favorably controlled condition with oral prednisolone. The patient underwent urgent catheter ablation with CARTO 3D mapping system. Although the voltage map, activation map, and propagation map during VT could not visualize the tachycardia circuit, the coherent map clarified entrance and exit sites of the tachycardia circuit with slow or nonconducting (SNO) zones, which seemed like a figure-of-eight circuit. Considering the risk of VT termination or acceleration to rapid unstable VT, neither entrainment nor pacing studies were performed. The VT was terminated near the exit site of the isthmus where tiny pre-systolic potential was detected. Any diastolic potentials could not be detected. This meant that the critical isthmus might be located at the epicardium or deep incite of the left-ventricular myocardium where the coherent map showed as SNO zones. We should recognize coherent map as artificial that may represent VT circuit as if complete endocardial reentry even if not. The procedural time from mapping to termination of VT was only 22 minutes. The patient has been free from any cardiovascular events after the procedure. Coherent map might be feasible for revealing the critical isthmus of hemodynamically stable VTs without using electrophysiological techniques, including entrainment, pacing study, and voltage map during own beats, and would enable us to achieve successful VT ablation in a short time.
| S-EPMC9237297 | biostudies-literature
Project description:Background Cardiac sarcoidosis (CS) and giant cell myocarditis (GCM) share many histopathologic and clinical features. Whether they are parts of a one-disease continuum has been discussed. Methods and Results We compared medical record data of 351 CS and 28 GCM cases diagnosed in Finland since the late 1980s and followed until February 2018 for a composite end point of cardiac death, aborted sudden death, and heart transplantation. Heart failure was the presenting manifestation in 50% versus 15% (P<0.001), and high-grade atrioventricular block in 21% versus 43% (P=0.044), of GCM and CS, respectively. At presentation, left ventricular ejection fraction was ≤50% in 81% of cases of GCM versus in 48% of CS (P=0.004). The median (interquartile range) of plasma NT-proBNP (N-terminal pro-B-type natriuretic peptide) was 5273 (2782-11309) ng/L on admission in GCM versus 859 (290-1950) ng/L in CS (P<0.001), and cardiac troponin T exceeded 50 ng/L in 17 of 19 cases of GCM versus in 48 of 239 cases of CS (P<0.001). The 5-year estimate of event-free survival was 77% (95% CI, 72%-82%) in CS versus 27% (95% CI, 10%-45%) in GCM (P<0.001). By Cox regression analysis, GCM predicted cardiac events with a hazard ratio of 5.16 (95% CI, 2.82-9.45), which, however, decreased to 1.58 (95% CI, 0.71-3.52) after inclusion of markers of myocardial injury and dysfunction in the model. Conclusions GCM differs from CS in presenting with more extensive myocardial injury and having worse long-term outcome. Yet the key determinant of prognosis appears to be the extent of myocardial injury rather than the histopathologic diagnosis.
| S-EPMC8174201 | biostudies-literature
Project description:Background Sarcoidosis is a granulomatous disease usually affecting the lungs, although cardiac morbidity may be common. The risk of these outcomes and the characteristics that predict them remain largely unknown. This study investigates the epidemiology of heart failure, atrioventricular block, and ventricular tachycardia among patients with and without sarcoidosis. Methods and Results We identified California residents aged ≥21 years using the Office of Statewide Health Planning and Development ambulatory surgery, emergency, or inpatient databases from 2005 to 2015. The risk of sarcoidosis on incident heart failure, atrioventricular block, and ventricular tachycardia were each determined. Linkage to the Social Security Death Index was used to ascertain overall mortality. Among 22 527 964 California residents, 19 762 patients with sarcoidosis (0.09%) were identified. Sarcoidosis was the strongest predictor of heart failure (hazard ratio [HR], 11.2; 95% CI, 10.7-11.7), atrioventricular block (HR, 117.7; 95% CI, 103.3-134.0), and ventricular tachycardia (HR, 26.1; 95% CI, 24.2-28.1) identified among all risk factors. The presence of any cardiac involvement best predicted each outcome. Approximately 22% (95% CI, 18%-26%) of the relationship between sarcoidosis and increased mortality was explained by the presence of at least 1 of these cardiovascular outcomes. Conclusions The magnitude of risk associated with sarcoidosis as a predictor of heart failure, atrioventricular block, and ventricular tachycardia, exceeds all established risk factors. Surveillance for and anticipation of these outcomes among patients with sarcoidosis is indicated, and consideration of a sarcoidosis diagnosis may be prudent among patients with heart failure, atrioventricular block, or ventricular tachycardia.
| S-EPMC8174291 | biostudies-literature
Project description:A 70-year-old woman was admitted to our hospital complaining of shortness of breath. She was diagnosed with acute decompensated heart failure due to left ventricular dysfunction. Her symptoms began to improve with standard therapy for heart failure with diuretics, noninvasive pressure ventilation, and inotropes, but paroxysmal atrial fibrillation and premature ventricular contractions (PVCs) occurred. After treatment with amiodarone, the number of PVCs decreased, and the left ventricular wall motion gradually improved. However, on day 28, ventricular fibrillation and cardiopulmonary arrest occurred suddenly, and she could not be resuscitated. She was diagnosed with giant cell myocarditis via an autopsy. The autopsy revealed diffuse inflammatory cells that comprised giant cells and eosinophils as well as cellular degeneration and necrosis. <Learning objective: We herein report a case of sudden cardiac death due to giant cell myocarditis diagnosed at an autopsy.>.
| S-EPMC7283290 | biostudies-literature
Project description:Objectives: Fulminant myocarditis (FM) is a rapidly progressive and frequently fatal form of myocarditis that has been difficult to classify. This study aims to compare the clinical characteristics, treatments and outcomes in patients with fulminant giant cell myocarditis (FGCM) and fulminant lymphocytic myocarditis (FLM). Methods and Results: In our retrospective study, nine patients with FGCM (mean age 47.9 ± 7.5 years, six female) and 7 FLM (mean age 42.1 ± 12.3 years, four female) patients confirmed by histology in the last 11 years were included. Most patients with FGCM and FLM were NYHA functional class IV (56 vs. 100%, p = 0.132). Patients with FGCM had significantly lower levels of high-sensitivity C-reactive protein [hs-CRP, 4.4 (2.0-10.2) mg/L vs. 13.6 (12.6-14.6) mg/L, P = 0.004, data shown as the median with IQR], creatine kinase-myoglobin [CK-MB, 1.4 (1.0-3.2) ng/ml vs. 14.6 (3.0-64.9) ng/ml, P = 0.025, median with IQR], and alanine aminotransferase [ALT, 38.0 (25.0-61.5) IU/L vs. 997.0 (50.0-3,080.0) IU/L, P = 0.030, median with IQR] and greater right ventricular end-diastolic diameter (RVEDD) [2.9 ± 0.3 cm vs. 2.4 ± 0.6 cm, P = 0.034, mean ± SD] than those with FLM. No differences were observed in the use of intra-aortic balloon pump (44 vs. 43%, p = 1.000) and extracorporeal membrane oxygenation (11 vs. 43%, p = 0.262) between the two groups. The long-term survival rate was significantly lower in FGCM group compared with FLM group (0 vs. 71.4%, p = 0.022). A multivariate cox regression analysis showed the level of hs-CRP (hazard ratio = 0.871, 95% confidence interval: 0.761-0.996, P = 0.043) was an independent prognostic factor for FM patients. Furthermore, the level of hs-CRP had a good ability to discriminate between patients with FGCM and FLM (AUC = 0.94, 95% confidence interval: 0.4213-0.9964). Conclusions: The inflammatory response and myocardial damage in the patients with FGCM were milder than those with FLM. Patients with FGCM had distinctly poorer prognoses compared with those with FLM. Our results suggest that hs-CRP could be a promising prognostic biomarker and a hs-CRP level of 11.71 mg/L is an appropriate cutoff point for the differentiating diagnosis between patients with FGCM and FLM.
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Project description:Electrical storm during the acute inflammatory phase caused by myocarditis may be resistant to antiarrhythmic therapy. Cardiac imaging including magnetic resonance tomography, positron emission tomography, and endomyocardial biopsy are crucial to guide potential therapeutic options. Optimal management involves a multidisciplinary approach, including expertise beyond cardiology.
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Project description:Bidirectional ventricular tachycardia (BVT), which is characterized by an alternating beat-to-beat ECG QRS axis, is a rare but intriguing arrhythmia associated with digitalis toxicity, familial catecholaminergic polymorphic ventricular tachycardia (CPVT), and several other conditions that predispose cardiac myocytes to delayed afterdepolarizations (DADs) and triggered activity. Evidence from human and animal studies attributes BVT to alternating ectopic foci originating from the distal His-Purkinje system in the left and/or right ventricle, respectively.The purpose of this study was to evaluate a simple "ping pong" model of reciprocating bigeminy to explain BVT.We constructed a two-dimensional anatomic model of the rabbit ventricles with a simplified His-Purkinje system, in which different sites in the His-Purkinje system had different heart rate thresholds for DAD-induced bigeminy.When the heart rate exceeded the threshold for bigeminy at the first site in the His-Purkinje system, ventricular bigeminy developed, causing the heart rate to accelerate and exceed the threshold for bigeminy at the second site. Thus, the triggered beat from the first site induced a triggered beat from the second site. The triggered beat from the second site next reciprocated by inducing a triggered beat from the first site, and so forth. Bigeminy from two sites produced BVT, and that from three or more sites produced polymorphic VT.This "ping pong" mechanism of reciprocating bigeminy readily produces the characteristic ECG pattern of BVT and its degeneration to polymorphic VT if additional sites develop bigeminy.
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