SUMMARYCoronary artery ectasia (CAE) or aneurysm is usually defined as dilation ≥1.5-fold the normal vessel diameter. It has an incidence of 1.4-5.3% and is associated with a wide variety of etiologies-mainly congenital, atherosclerotic, and inflammatory ones. CAE is very common in sickle cell disease, and possibly sickle cell trait, with an incidence of 17.7%. It is likely related to the inflammatory process associated with hemoglobin S. Prognosis depends mainly on the underlying etiology. Atherosclerotic CAE does not carry additional risks compared to atherosclerotic coronary artery disease (ACAD) without ectasia. However, isolated CAE in the absence of ACAD carries an increased risk of myocardial infarction (MI) due to vasospasm, slower coronary blood flow, and thrombosis, typically within the dilated segments. Due to lack of studies and guidelines, management recommendations are based on personal experiences. Therapy should be tailored to each individual case after assessment of severity, history of complications, underlying etiology, and comorbidities. Treatment of underlying condition and avoidance of exacerbating factors are essential. Medical therapy in general may include antiplatelets, b-blockers, angiotensin-converting enzyme inhibitors statins, and dihydropyridine calcium channel blockers. In severe CAE or history of MI, the addition of anticoagulation therapy after assessing bleeding risk may be warranted. In acute MI, the large thrombus burden in the dilated segment makes the percutaneous approach very challenging. Aspiration attempts can result in distal thromboembolization. Survival is better in bypass grafting than with medical therapy. Nonetheless, bypass grafting does not improve survival in atherosclerotic CAE. Depending on the physical characteristics of aneurysm, different surgical approaches can be sought; however, the ideal one is unclear.

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The renal actions of endothelin were examined by infusing it intrarenally in anesthetized dogs at 4 ng.min-1.kg-1 without affecting arterial blood pressure or cardiac output. Endothelin infusion caused a transient and significant increase in renal blood flow (RBF) by 13 +/- 2%, followed by large decreases in RBF and glomerular filtration rate (GFR; by 26 +/- 2 and 23 +/- 7%, respectively) but did not alter urine flow rate or absolute sodium excretion. After endothelin infusion, renal venous and arterial plasma 6-ketoprostaglandin F1 alpha increased from 250 +/- 58 and 117 +/- 31 to 1,044 +/- 249 and 617 +/- 211 pg/ml, respectively, and its renal output increased from 339 +/- 99 to 963 +/- 202 pg.min-1.g-1 (P less than 0.01 for all). The renal prostacyclin synthesis was augmented by endothelin without stimulating the renal renin release or norepinephrine output. Inhibition of prostaglandin synthesis with indomethacin partially prevented the early renal vasodilation induced by endothelin, which then caused a more pronounced decline in RBF and GFR (by 65 +/- 7 and 54 +/- 8%, respectively). With suppression of prostacyclin synthesis, inhibition of renin release by endothelin was observed. Thus the vasoconstrictive effects of endothelin on renal hemodynamics are significantly modified by its ability to enhance production of vasodilators, including prostacyclin.

Esophageal perforation is a rare condition that is commonly missed. Male gender and alcohol use are predisposing risk factors. Most of the cases are iatrogenic or traumatic; nonetheless, spontaneous cases are not uncommon. It typically occurs after vomiting or straining as the increased intra-abdominal pressure transmits into the esophagus and results in the tear. One of the main complications is acute bacterial mediastinitis from contamination with esophageal flora. This condition can be life-threatening because it is very frequently misdiagnosed and appropriate management is often delayed.A 49-year-old man presented with worsening sudden-onset interscapular back pain that then changed to chest pain with odynophagia and was found to have fever and leukocytosis.Chest computed tomography revealed signs of mediastinitis with possible esophageal perforation. He reported symptoms started 2 days ago after lifting of heavy objects. Empiric antimicrobial was begun with conservative management and avoidance of oral intake. Barium esophagram and esophagogastroduodenoscopy revealed no signs of perforation or inflammation. His symptoms resolved and he gradually resumed oral intake. Blood cultures grew Methicillin-sensitive Staphylococcus aureus and he was discharged on appropriate antibiotics for 4 weeks. He did well on follow-up 3 months after hospitalization.The case highlights the importance of considering esophageal etiologies of chest pain.

Background: Use of high-sensitivity troponin (hs-Tn) assays can detect small levels of myocardial damage previously undetectable with conventional troponin (c-Tn) assays. However, prognostic utility of these hs-Tn assays in prediction of mortality remains unclear in the presence of nonelevated c-Tn levels on admission. A systematic review and meta-analysis was performed to assess mortality risk of patients with hs-Tn elevations in the setting of normal c-Tn levels. Hypothesis: Patients with hs-Tn elevations with normal c-Tn levels on admission blood samples, drawn to rule out acute coronary syndrome (ACS), have a higher mortality risk than those without hs-Tn or c-Tn elevations. Methods: A search was made of the PubMed, CENTRAL, EMBASE, CINAHL, EBSCO, and Web of Science databases. Studies evaluating patients with suspected ACS that reported mortality rates for those with elevated hs-Tn levels but normal c-Tn levels on admission were included. A random-effects model was used to pool event rates, and data were reported in odds ratios (95% confidence interval). Results: Four studies (N = 2033, mean age 64-75 years, 49%-70% male) revealed that nearly 32% of suspected ACS patients with normal c-Tn levels on admission had elevated hs-Tn levels. Elevated hs-Tn levels conferred a significantly higher risk of all-cause mortality vs normal hs-Tn levels (odds ratio: 4.35, 95% confidence interval: 2.81-6.73, P < 0.01), with negligible heterogeneity (I 2 = 0%). Conclusions: Elevation of hs-Tn levels predicted a higher risk of mortality in patients with suspected ACS and may aid in the early identification of higher-risk patients in this setting. Future studies are needed to investigate further optimal management strategies.