Accuracy of Shunt Volume Measured by Three-Dimensional Echocardiography and Cardiac Magnetic Resonance in Patients with an Atrial Septal Defect and a Dilated Right Ventricle.

BACKGROUND: The accuracy of right ventricular (RV) quantification by three-dimensional echocardiography (3DE) has been reported mainly in patients with a normal RV. However, there are no data regarding the accuracy of 3DE in patients with a dilated RV, as in shunt diseases. In this study, we evaluated the accuracy of 3DE and that of volumetric cardiac magnetic resonance (CMR) for assessment of RV and left ventricular (LV) stroke volume (SV) and the pulmonary (Qp)/systemic (Qs) blood flow ratio in patients with an atrial septal defect (ASD) using the two-dimensional phase contrast (2DPC) method as the gold standard. METHODS: We retrospectively investigated 83 patients with ASD who underwent transcatheter closure and clinically indicated CMR and 3DE examinations. Qp/Qs was calculated using RV and LV SV measured by full-volume volumetric 3DE (Vol-3DE) and CMR (Vol-CMR) and by two-dimensional pulse Doppler quantification (2D-Dop); the parameters were compared using 2DPC-CMR as the gold standard. RESULTS: There was no significant difference in the Qp/Qs value between 2DPC-CMR and Vol-3DE (2.29 ± 0.70 vs. 2.21 ± 0.63, P=0.79) and 2D-Dop (vs. 2.21 ± 0.65, P=1.00); however, a significant difference was found between 2DPC-CMR and Vol-CMR (P<0.001). The Qp/Qs value obtained using Vol-3DE showed the best correlation with 2DPC-CMR (r=0.93, P<0.001). The RV and LV SV values obtained by Vol-3DE showed the best correlation with 2DPC-CMR (RV SV, r=0.82, P<0.001; LV SV, r=0.73, P<0.001), although the absolute values were underestimated. CONCLUSION: Qp/Qs was more accurately evaluated by Vol-3DE than by Vol-CMR or 2D-Dop. 3DE assessment was feasible and reproducible even in a dilated RV.

Cardioembolism after thoracoscopic left atrial appendage clipping in a patient on oral anticoagulation therapy.

Cardioembolism associated with atrial fibrillation is a major cause of ischemic stroke. Left atrial appendage occlusion in atrial fibrillation patients undergoing cardiac surgery reduces the risk of postoperative stroke. A 78-year-old man with a history of atrial fibrillation and severe mitral regurgitation underwent thoracoscopic mitral valve repair with left atrial appendage clipping and the cryo-maze procedure 4 years previously. He was taking a direct oral anticoagulant for stroke prevention because his atrial fibrillation had recurred. He presented with acute onset disturbed consciousness, omnidirectional gaze palsy, left facial palsy, severe dysarthria, bilateral limb ataxia, and sensory disturbance. National Institutes of Health Stroke Scale score was 16. Although non-contrast computed tomography showed no early ischemic changes, computed tomography angiography revealed occlusion of the basilar artery. Intravenous thrombolysis was performed, which resulted in recanalization. Transesophageal echocardiography showed left atrial spontaneous echo contrast and thrombus in the left atrial appendage. Contrast-enhanced chest computed tomography confirmed incomplete left atrial appendage occlusion. Cardioembolic stroke was diagnosed, and warfarin was initiated. Cardioembolism may occur after thoracoscopic left atrial appendage clipping despite direct oral anticoagulant therapy, particularly if appendage occlusion is incomplete. Occlusion status should be evaluated after thoracoscopic clipping. Learning objective: To illustrate, incomplete left atrial appendage closure may increase the risk of ischemic stroke even after thoracoscopic left atrial appendage clipping is performed to prevent embolism.

Diagnosis of cardiac sarcoidosis: histological evidence vs. imaging.

INTRODUCTION: The prognosis for cardiac sarcoidosis (CS) remains unfavorable. Although early and accurate diagnosis is crucial, the low detection rate of endomyocardial biopsy makes accurate diagnosis challenging. AREAS COVERED: The Heart Rhythm Society (HRS) consensus statement and the Japanese Circulation Society (JCS) guidelines are two major diagnostic criteria for the diagnosis of CS. While the requirement of positive histology for the diagnosis in the HRS criteria can result in overlooked cases, the JCS guidelines advocate for a group of 'clinical' diagnoses based on advanced imaging, including cardiovascular magnetic resonance and 18F-fluorodeoxyglucose positron emission tomography, which do not require histological evidence. Recent studies have supported the usefulness of clinical diagnosis of CS. However, other evidence suggests that clinical CS may sometimes be inaccurate. This article describes the advantages and disadvantages of the current diagnostic criteria for CS, and typical imaging and clinical courses. EXPERT OPINION: The diagnosis of clinical CS has been made possible by recent developments in multimodality imaging. However, it is still crucial to look for histological signs of sarcoidosis in other organs in addition to the endomyocardium. Additionally, phenotyping based on clinical manifestations such as heart failure, conduction abnormality or ventricular arrhythmia, and extracardiac abnormalities is clinically significant.

Trajectory of serum chloride levels during decongestive therapy in acute heart failure.

BACKGROUND: Hypochloremia is a risk factor for poor outcomes in patients with acute heart failure (AHF). However, the changes in serum chloride levels during decongestion therapy and their impact on prognosis remain unknown. METHODS: In total, 2798 patients with AHF were retrospectively studied and divided into four groups according to their admission and discharge serum chloride levels: (1) normochloremia (n=2,192, 78%); (2) treatment-associated hypochloremia, defined as admission normochloremia with a subsequent decrease (<98 mEq/L) during hospitalization (n=335, 12%); (3) resolved hypochloremia, defined as admission hypochloremia that disappeared at discharge (n=128, 5%); (4) persistent hypochloremia, defined as chloride <98 mEq/L at admission and discharge (n = 143, 5%). The primary outcome was all-cause death, and the secondary outcomes were cardiovascular death and a composite of cardiovascular death and rehospitalization for heart failure after discharge. RESULTS: The mean age was 76 ± 12 years and 1584 (57%) patients were men. The mean left ventricular ejection fraction was 46 ± 16%. During a median follow-up period of 365 days, persistent hypochloremia was associated with an increased risk of all-cause death (adjusted hazard ratio [95% confidence interval]: 2.27 [1.53-3.37], p < 0.001), cardiovascular death (2.38 [1.46-3.87], p < 0.001), and a composite of cardiovascular death and heart failure rehospitalization (1.47 [1.06-2.06], p = 0.022). However, the outcomes were comparable between patients with resolved hypochloremia and normochloremia. CONCLUSIONS: Persistent hypochloremia was associated with worse clinical outcomes, while resolved hypochloremia and normochloremia showed a comparable prognosis. Changes in serum chloride levels can help identify patients with poor prognoses and can be used to determine subsequent treatment strategies.

Comparisons between biopsy-proven versus clinically diagnosed cardiac sarcoidosis.

OBJECTIVES: Diagnosis of cardiac sarcoidosis (CS) without histological evidence remains controversial. This study aimed to compare characteristics and outcomes of histologically proven versus clinically diagnosed cases of CS, which were adjudicated using Heart Rhythm Society or Japanese Circulation Society criteria. METHODS: A total of 512 patients with CS (age: 62±11 years, female: 64.3%) enrolled in the multicentre registry were studied. Histologically confirmed patients were classified as 'biopsy-proven CS', while those with the presence of strongly suggestive clinical findings of CS without histological evidence were classified as 'clinical CS'. Primary outcome was a composite of all-cause death, heart failure hospitalisation and ventricular arrhythmia event. RESULTS: In total, 314 patients (61.3%) were classified as biopsy-proven CS, while 198 (38.7%) were classified as clinical CS. Patients classified under clinical CS were associated with higher prevalence of left ventricular dysfunction, septal thinning, and positive findings in fluorodeoxyglucose-positron emission tomography or Gallium scintigraphy than those under biopsy-proven CS. During median follow-up of 43.7 (23.3-77.3) months, risk of primary outcome was comparable between the groups (adjusted HR: 1.24, 95% CI: 0.88 to 1.75, p=0.22). Similarly, the risks of primary outcome were comparable between patients with clinical isolated CS who did not have other organ/tissue involvement, and biopsy-proven isolated CS (adjusted HR: 1.23, 95% CI: 0.56 to 2.70, p=0.61). CONCLUSIONS: A substantial number of patients were diagnosed with clinical CS without confirmatory biopsy. Considering the worse clinical outcomes irrespective of the histological evidence, the diagnosis of clinical CS is justifiable if imaging findings suggestive of CS are observed.