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Background Cardiac sarcoidosis (CS) is known to be associated with congestive heart failure, conduction disorders, and tachyarrhythmias. Ventricular arrhythmias are the most feared cardiac manifestation because they often are unpredictable, may be the first manifestation of the disease, and may be fatal. The propensity for the development of supraventricular arrhythmias (SVAs) in patients with CS has not been described. The aim of this study was to assess the prevalence as well as the predictors of SVA. Methods We retrospectively investigated 100 patients with biopsy specimen-proven systemic sarcoidosis and evidence of cardiac involvement (defined by cardiac biopsy specimen, PET scan, or cardiac MRI). The mean follow-up was 5.8 ± 3.6 years. ECG, Holter monitoring, implantable cardioverter defibrillator interrogations, or electrophysiology studies were used to document SVA. Echocardiographic data, demographics, and extracardiac involvement were recorded, and univariate and Poisson regressions were performed to compare characteristics of patients with and without documented SVA. Results The prevalence of SVA was 32%, and atrial fibrillation was the most common arrhythmia, comprising 18% of the total burden, followed by atrial tachycardias (7%), atrial flutter (5%), and other supraventricular tachycardias (2%). Of the patients with SVA, 96% were symptomatic. Left atrial enlargement (LAE) was more frequent in the group with SVA, with an incidence of 267.8 per 1,000 person-years, and it significantly increased the likelihood of SVA on multivariate analysis (risk ratio, 6.12; 95% CI, 2.19-17.11). Diastolic dysfunction, systemic hypertension, and right atrial enlargement were predictors of SVA on univariate analysis. Left ventricular hypertrophy, right ventricular dysfunction, tricuspid valve disease, pulmonary hypertension, and pulmonary sarcoidosis were not associated with SVA on univariate analysis. Conclusions The study systematically evaluated the frequency of SVA in a large number of patients with CS. SVA in patients with CS is frequent and associated with symptoms. LAE was clearly associated with the development of SVA in this patient population. The extent to which LAE predicts the occurrence of SVA in larger, more diverse CS populations should be evaluated prospectively.

Background Cardiac sarcoidosis (CS) causes substantial morbidity and sudden death. Early diagnosis and risk stratification are warranted. Methods Ambulatory patients with sarcoidosis were interviewed to determine whether they experienced palpitations, syncope, or presyncope, and were evaluated with ECG, Holter monitoring, and echocardiography (transthoracic echocardiogram [TTE]). Those with symptoms or abnormal results were studied with cardiac MRI (CMRI) or positron emission tomography (PET) scanning. The diagnosis of CS was based on abnormalities detected by these imaging studies. Patients with CS were referred for risk stratification by electrophysiology study (EPS). Results Among the 62 patients evaluated, the prevalence of CS was 39%. Patients with CS had more cardiac symptoms than those without CS (46% vs 5%, respectively; p Conclusion CS is common among patients with sarcoidosis. A structured clinical assessment incorporating advanced cardiac imaging with PET scanning or CMRI is more sensitive than the established criteria for the identification of CS. Sarcoidal lesions seen on CMRI or PET scanning do not predict arrhythmias in ambulatory patients with preserved cardiac function, who appear to be at low risk for short-term mortality.

Cardiac sarcoidosis (CS) is known to be associated with congestive heart failure, conduction disorders, and tachyarrhythmias. Ventricular arrhythmias are the most feared cardiac manifestation because they often are unpredictable, may be the fi rst manifestation of the disease, and may be fatal. The propensity for the development of supraventricular arrhythmias (SVAs) in patients with CS has not been described. The aim of this study was to assess the prevalence as well as the predictors of SVA.We retrospectively investigated 100 patients with biopsy specimen-proven systemic sarcoidosis and evidence of cardiac involvement (defi ned by cardiac biopsy specimen, PET scan, or cardiac MRI). The mean follow-up was 5.8 3.6 years. ECG, Holter monitoring, implantable cardioverter defibrillator interrogations, or electrophysiology studies were used to document SVA. Echocardiographic data, demographics, and extracardiac involvement were recorded, and univariate and Poisson regressions were performed to compare characteristics of patients with and without documented SVA.The prevalence of SVA was 32%, and atrial fibrillation was the most common arrhythmia, comprising 18% of the total burden, followed by atrial tachycardias (7%), atrial fl utter (5%), and other supraventricular tachycardias (2%). Of the patients with SVA, 96% were symptomatic. Left atrial enlargement (LAE) was more frequent in the group with SVA, with an incidence of 267.8 per 1,000 person-years, and it significantly increased the likelihood of SVA on multivariate analysis (risk ratio, 6.12; 95% CI, 2.19-17.11). Diastolic dysfunction, systemic hypertension, and right atrial enlargement were predictors of SVA on univariate analysis. Left ventricular hypertrophy, right ventricular dysfunction, tricuspid valve disease, pulmonary hypertension, and pulmonary sarcoidosis were not associated with SVA on univariate analysis.The study systematically evaluated the frequency of SVA in a large number of patients with CS. SVA in patients with CS is frequent and associated with symptoms. LAE was clearly associated with the development of SVA in this patient population. The extent to which LAE predicts the occurrence of SVA in larger, more diverse CS populations should be evaluated prospectively.

Cardiac sarcoidosis (CS) causes substantial morbidity and sudden death. Early diagnosis and risk stratification are warranted.Ambulatory patients with sarcoidosis were interviewed to determine whether they experienced palpitations, syncope, or presyncope, and were evaluated with ECG, Holter monitoring, and echocardiography (transthoracic echocardiogram [TTE]). Those with symptoms or abnormal results were studied with cardiac MRI (CMRI) or positron emission tomography (PET) scanning. The diagnosis of CS was based on abnormalities detected by these imaging studies. Patients with CS were referred for risk stratification by electrophysiology study (EPS).Among the 62 patients evaluated, the prevalence of CS was 39%. Patients with CS had more cardiac symptoms than those without CS (46% vs 5%, respectively; p0.001), and were more likely to have abnormal Holter monitoring findings (50% vs 3%, respectively; p0.001) and TTE findings (25% vs 5%, respectively; p = 0.02). The degree of pulmonary impairment did not predict CS. Two of the 17 patients who underwent EPS had abnormal test findings and received implantable cardioverter-defibrillators. No patients died, had ventricular arrhythmias that triggered defibrillator therapy, or had heart failure develop during almost 2 years of follow-up. This diagnostic approach was more sensitive than the established criteria for identifying CS.CS is common among patients with sarcoidosis. A structured clinical assessment incorporating advanced cardiac imaging with PET scanning or CMRI is more sensitive than the established criteria for the identification of CS. Sarcoidal lesions seen on CMRI or PET scanning do not predict arrhythmias in ambulatory patients with preserved cardiac function, who appear to be at low risk for short-term mortality.

Based on multiple recent studies, anticoagulant therapy is recommended prior to elective cardioversion for patients with atrial fibrillation of more than 24 h duration. The value of anticoagulation in patients with atrial flutter, however, is less well established. Published recommendations for pericardioversion anticoagulation of atrial fibrillation often do not extend to patients with atrial flutter. We evaluated the risk of thromboembolism in our patient population undergoing cardioversion for atrial flutter. Over a period of 30 months, clinically indicated electrical cardioversions were performed in 41 patients with "common" atrial flutter. Sixteen of these patients underwent transesophageal echocardiograms immediately prior to cardioversion to exclude a left atrial thrombus. Three of the 41 patients with atrial flutter developed neurologic ischemic syndromes within 48 h of elective cardioversion. All three patients who developed ischemic neurologic complications had undergone transesophageal echocardiography immediately prior to cardioversion and did not have any evidence of left atrial clot. One patient had cardiomyopathy and the other two had left ventricular hypertrophy. Thus, electrical cardioversion without anticoagulation in patients with atrial flutter and associated heart disease is associated with a risk of thromboembolic events. A normal transesophageal echocardiogram is of doubtful value in prevention of thromboembolic complications.

A woman had a 40-year history of vomiting associated with syncope. Spontaneous and induced vomiting was predictably associated with sinus bradycardia, paroxysmal atrioventricular block, and ventricular asystole. The clinical and laboratory studies carried out to illustrate the mechanism of this unusual complication of vomiting demonstrated it to be due to a vagovagal reflex initiated by distension of upper esophagus.