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Objective To evaluate the relationship between peripheral arterial disease (PAD) and incident atrial fibrillation (AF) and its clinical and pathophysiologic implications on ischemic stroke and all-cause mortality. Patients and Methods We identified all adult patients in the Mayo Clinic Health System without a previous diagnosis of AF undergoing ankle-brachial index (ABI) testing for any indication from January 1, 1996, to June 30, 2018. Retrospective extraction of ABI data and baseline echocardiographic data was performed. The primary outcome of interest was incident AF. The secondary outcomes of interest were incident ischemic stroke and all-cause mortality. Results A total of 33,734 patients were included in the study. After adjusting for demographic and comorbidity variables, compared with patients who had normal ABI (1.0 to 1.39), there was an increased risk of incident AF in patients with low ABI ( Conclusion In this large cohort of ambulatory patients undergoing ABI measurement, patients with PAD were at increased risk for incident AF, ischemic stroke, and mortality. In these high-risk patients with abnormal ABI, particularly severe PAD and cardiac structural abnormalities, routine monitoring for AF and management of cardiovascular risk factors may be warranted.

To describe the clinical features, treatment, and outcomes in a longitudinal cohort of patients with Takayasu arteritis (TAK).We retrospectively studied patients with newly diagnosed TAK evaluated from January 1, 1984, through December 31, 2009.The cohort included 126 patients who were predominantly white (85/103; 82.5%) and female (115/126; 91%). The median age at diagnosis was 31.6 years (interquartile range, 22.9-39.8 years). Median delay in diagnosis was 17.5 months (interquartile range, 7-41.8 months). Thirty-one patients (25%) were 40 years or older at diagnosis. Median delay in diagnosis for patients 40 years or older was 44.8 months compared with 28.3 months for those younger than 40 years (P.001). Limb claudication was the presenting symptom in 64 of 123 patients (52%). Hata type V arteriographic abnormalities were the most common (57/100; 57%). Renal artery abnormalities were observed in 24 of 41 patients (58%) with new-onset hypertension. Inflammatory markers were elevated at diagnosis in 85 of 119 patients (71%). Vascular interventions were performed in 69 patients (55%). Seventy-nine patients (63%) were followed up for more than 1 year (median follow-up, 5.5 years; interquartile range, 2.9-10.0 years). In this subset, treatment consisted of corticosteroids in 73 patients (92%) and additional immunosuppressants in 52 patients (66%). At 5 years, 96% experienced at least one remission of any duration. The overall survival was 97% at 10 years and 86% at 15 years. Mortality was increased compared with the general population (standardized mortality ratio, 3.0; 95% CI, 1.0-8.9).There continues to be an unacceptably long delay in the diagnosis of TAK. Awareness of TAK in patients older than 40 years is needed. Morbidity was high despite immunosuppressive treatment. Survival was decreased in this cohort.

Myocarditis, an inflammatory disease of heart muscle, is an important cause of dilated cardiomyopathy worldwide. Viral infection is also an important cause of myocarditis, and the spectrum of viruses known to cause myocarditis has changed in the past 2 decades. Several new diagnostic methods, such as cardiac magnetic resonance imaging, are useful for diagnosing myocarditis. Endomyocardial biopsy may be used for patients with acute dilated cardiomyopathy associated with hemodynamic compromise, those with life-threatening arrhythmia, and those whose condition does not respond to conventional supportive therapy. Important prognostic variables include the degree of left and right ventricular dysfunction, heart block, and specific histopathological forms of myocarditis. We review diagnostic and therapeutic strategies for the treatment of viral myocarditis. English-language publications in PubMed and references from relevant articles published between January 1, 1985, and August 5, 2008, were analyzed. Main keywords searched were myocarditis, dilated cardiomyopathy, endomyocardial biopsy, cardiac magnetic resonance imaging, and immunotherapy.

Peripheral arterial disease is a common but underdiagnosed and undertreated disorder with substantial morbidity and mortality. The pathophysiology of peripheral arterial disease and the risk factors for developing it are similar to those for atherosclerotic disease occurring at other sites. Peripheral arterial disease can be diagnosed accurately with simple, noninvasive, office-based tests that measure the severity of the disease and provide valuable prognostic information. Optimal medical therapy includes a supervised exercise program, tobacco cessation, and modification of treatable risk factors. Cilostazol can improve pain-free and peak walking distances in patients with intermittent claudication. As a general rule, patients with lifestyle-limiting claudication who do not respond to medical management or those with critical limb ischemia should be referred to a vascular specialist for consideration of revascularization.

Nonischemic dilated cardiomyopathy (DCM) is an uncommon cause of heart failure but has widespread importance because it is the cause of 45% of heart transplantations. Multiple experimental and clinical lines of evidence have implicated altered immunity in the pathogenesis of DCM. However, advances in the understanding of the mechanisms of altered immunity have not affected the diagnosis or treatment of DCM. In recognition of this problem, the National Institutes of Health sponsored an expert workshop with 2 aims: to review the current understanding of inflammation and immunity as they relate to DCM and to identify the most promising areas for future clinical research efforts in the field. This report summarizes the scientific opportunities, perceived needs and barriers, and workshop recommendations on research directions in DCM. The major recommendations from the members of the workshop are organized according to the following themes: cardiotropic viruses, innate and acquired immune responses, environmental factors, novel diagnostics, and novel therapeutics.

Dilated cardiomyopathy is a common cause of congestive heart failure. Despite a thorough cardiovascular evaluation, a specific cause is frequently not found, and the disorder then is considered idiopathic. Endomyocardial biopsy (EMB) may yield diagnostic and prognostic information in patients with idiopathic dilated cardiomyopathy; however, the yield of useful information with this procedure among patients with heart failure is low, and the risks of occasional cardiac perforation and death further limit its use. Recent publications in the field of myocarditis and cardiomyopathy have renewed interest in the use of EMB in select patients to diagnose specific and potentially treatable myocarditides; however, the role of EMB in the work-up of patients with dilated cardiomyopathy is not well defined. In this article, we discuss the risks and utility of EMB in the management of patients with dilated cardiomyopathy and specific myocarditides.

Giant cell myocarditis (GCM) is a rare and frequently fatal disorder with no proven treatment. Case reports and data from a rat model of GCM suggest that immunosuppressive therapy directed against T lymphocytes may have clinical benefit. We describe a 47-year-old man with severe acute heart failure due to GCM in whom the left ventricular ejection fraction normalized and the myocardial inflammatory infiltrate resolved rapidly after treatment with muromonab-CD3, cyclosporine, azathioprine, and corticosteroids. Three previously published cases with less impressive responses to treatment including muromonab-CD3 and a critical review of the published data on immunosuppressive therapy are included in this report. The response to immunosuppressive therapy is highly variable, and direct comparisons between immunosuppressive regimens do not exist. Therefore, despite individual reports of dramatic improvement after immunosuppressive treatment, firm conclusions cannot be made about the benefit of immunosuppression for GCM. The benefits of immunosuppressive therapy must be confirmed in a prospective, randomized trial.