A 72-year-old woman with no history of coronary artery disease presented with an acute left middle cerebral artery stroke and was found to have a large left ventricular pseudoaneurysm measuring 8.7 × 7.6 cm and 2 large left ventricular thrombi, the source of her systemic embolization. Despite initial medical management, she developed refractory New York Heart Association functional class III heart failure, uncontrolled atrial fibrillation, and further enlargement of her pseudoaneurysm to 5.5 × 10.6 × 9.2 cm. She underwent urgent aneurysmectomy. Left ventricular pseudoaneurysms are rare and most commonly occur following an acute myocardial infarction when a ventricular free-wall rupture is contained by pericardium or thrombi. Historically, left ventricular angiography displaying a lack of an overlying coronary artery was the gold standard for diagnosis. Now, noninvasive imaging such as computed tomography, magnetic resonance imaging, and echocardiogram with ultrasound-enhancing agent, are reliable diagnostic tools. They can distinguish a pseudoaneurysm from a true left ventricular aneurysm using characteristic findings such as a narrow aneurysm neck, bidirectional doppler flow between the pseudoaneurysm and the left ventricle, and abrupt changes in the cardiac wall structures. Progressive dilation, wall thinning, and dyskinesis can result in refractory heart failure, arrhythmias, and thrombi formation from venous stasis. Pseudoaneurysms have a 30% to 45% risk of rupture and can be treated with left ventricular aneurysmectomy.
C oronary artery disease (CAD) is the leading cause of death in both men and women in the United States. 1 Its diagnosis and risk stratifi cation are an important aspect of medical care for all practitioners, regardless of specialty.Coronary catheterization has been the technical standard for the diagnosis of CAD and is the recommended pathway for patients who are at high risk or who present with acute coronary syndrome. 2,3 However, given that chest pain and anginal-equivalent symptoms are frequent in patients presenting to community clinics and emergency rooms and on inpatient wards, many practitioners need the skills and knowledge to conduct cardiac risk evaluation.Noninvasive testing is often used to categorize patients as being at lower risk or having noncardiac chest pain vs those who are likely to have ischemia or obstructive CAD, which may require invasive coronary catheterization for further evaluation or intervention.Testing for CAD may be functional or anatomic (Table 1). In this article, we review what each test measures, its specifi c features, diagnostic and prognostic value, clinical utility, and limitations. These considerations help practitioners select the best test for a patient in a given setting or provide answers to a specifi c clinical question. ■ CORONARY ARTERY DISEASECAD is an infl ammatory pathologic process that starts as fatty streaks in the intimal layers of coronary arteries, then progresses to nonobstructive and then obstructive atherosclerotic REVIEW
Introduction: Preclinical studies demonstrated a potential role for aspirin (ASA) to slow the progression of abdominal aortic aneurysms (AAA) to rupture. We aim to investigate the association of long-term ASA use with progression and mortality in AAA. Methods: We queried the vascular ultrasound database at Cleveland Clinic for patients who underwent consecutive abdominal vascular ultrasound 2010-2020 if at least two available ultrasounds were conducted, without prior history of aneurysm repair, dissection, or rupture. ASA use was defined as at least one prescription of ASA during the during the follow-up period. The primary outcome was all-cause mortality, assessed by survival analysis with multivariable-adjust Cox regression. The secondary outcome was the mean annualized change of aneurysm diameter, assessed by multivariable-adjusted linear regression. Results: A total of 3,803 patients were included, with an average age of 73, and of which 826 (22%) were female and 2,380 (62.5%) were prescribed ASA (median duration of use ~ 9 years). ASA use was not significantly associated with all-cause mortality irrespective of age, sex and smoking status, except among those with a baseline diameter > 3.5 cm (Figure 1). ASA use was negatively associated with the mean annualized AAA diameter change only in males (0.25 vs 0.38 cm/year, p = 0.002) and in nonsmokers (0.26 vs 0.37 cm/year, p = 0.003). Conclusions: ASA use reduces the expansion of abdominal aortic aneurysms with altering all-cause mortality except in certain high-risk individuals in men and non-smokers. Mechanistic and randomized studies are needed to ascertain the role of ASA in patients with abdominal aortic aneurysms.
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