Acute coronary syndrome in Behcet's syndrome: A systematic review.

Behcet syndrome is a rare vasculitis that affects both arteries and veins. Vasculo-Bechet Syndrome (VBS) is seen predominantly in men. Genetic predisposition and immune dysregulation leading to inflammation, endothelial damage, and impaired fibrinolysis contribute to its pathogenesis. Isolated case reports of Behcet syndrome (BS) with associated acute coronary syndrome (ACS) have been reported in the past. In this study, we present the first systematic review of such cases. A systematic search was conducted using Pubmed, Google Scholar, CINAHL, Cochrane CENTRAL, and Web of Science databases from 1980-2018 to identify case reports of myocardial infarction associated with BS. Cases that fulfilled the criteria for BS were selected for analysis. Demographic data, electrocardiography, echocardiography, angiography findings, and management were analyzed when available. We identified 62 case reports. Most subjects were men with a mean age of 37 years. Twenty-one percent were smokers, but other traditional cardiovascular risk factors were less common. Myocardial infarction was confirmed in half of the cases with findings on electrocardiogram (ECG). Echocardiogram revealed wall motion abnormality in 76% of patients, and angiography showed double-vessel disease in more than half of the cases. Mortality was reported in 1.6% of the cases. This systematic review shows that ACS in BS affects young males with low prevalence of coronary artery disease risk factors. Chest pain is the most common presenting feature and ST-segment elevation myocardial infarction (STEMI) was the most common ECG finding. Immunotherapy may be helpful to prevent future ACS in these patients.

The Legacy Effect in Treating Hypercholesterolemia.

BACKGROUND: The duration of randomized controlled clinical trials usually is approximately 3 to 5 years although hypercholesterolemia and other risk factors for atherosclerotic cardiovascular disease (ASCVD) are lifelong conditions. OBJECTIVES: The legacy effect, defined as the persistence of benefit of pharmacologic interventions in clinical trials after the end of the randomized phase when all participants receive active therapy, is used to examine the long-term benefit. We summarize the evidence for the existence of the legacy effect as it pertains to hypercholesterolemia, describe underlying mechanisms, and discuss its relevance to clinical practice. METHODS: We examined all published (n = 13) randomized clinical trials of lipid-lowering agents compared to placebo or usual care with follow-up after the randomized phase for the presence or absence of a legacy effect. RESULTS: A legacy effect was demonstrated in all studies. The current US and European guidelines recommend treatment with high-intensity statins for patients with manifest ASCVD and that individualized approach be used for primary prevention. CONCLUSION: The legacy effect results in significant long-term clinical benefits by preventing fatal and nonfatal events. This implies that early therapy would result in lower event rates. Long-term follow-up should be a part of clinical trial design in order to evaluate the presence or absence of a legacy effect.

ACE Inhibitor-Induced Angioedema: a Review.

PURPOSE OF REVIEW: This study aims to examine current knowledge on the occurrence, pathophysiology, and treatment of angioedema among patients who receive angiotensin-converting enzyme inhibitors. RECENT FINDINGS: Angiotensin-converting enzyme inhibitors (ACE-I), a medication class used by an estimated 40 million people worldwide, are associated with angioedema that occurs with incidence ranging from 0.1 to 0.7%. The widespread use of ACE-I resulted in one third of all emergency department visits for angioedema. Angioedema occurs more frequently in African Americans, smokers, women, older individuals, and those with a history of drug rash, seasonal allergies, and use of immunosuppressive therapy. The pathophysiology of ACE-I-induced angioedema involves inhibition of bradykinin and substance P degradation by ACE (kininase II) leading to vasodilator and plasma extravasation. Treatment modalities include antihistamines, steroids, and epinephrine, as well as endotracheal intubation in cases of airway compromise. Patients with a history of ACE-I-induced angioedema should not be re-challenged with this class of agents, as there is a relatively high risk of recurrence. CONCLUSION: ACE-I are frequently used therapeutic agents that are associated with angioedema. Their use should be avoided in high-risk individuals and early diagnosis, tracheal intubation in cases of airway compromise, and absolute avoidance of re-challenge are important.