The enigma of fine mobile structures on the aortic surface in a patient undergoing transcatheter aortic valve replacement: a case report.

Background: The surface of the aorta generally does not show motion unless mobile atheroma, thrombi, vegetations, or intimal flaps are present. We previously described unusual mobile filamentous structures in the carotid artery. Here, we describe similar findings in the aorta and their possible cause. Case summary: An 88-year-old female with progressive exertional dyspnoea and severe aortic stenosis had a successful transcatheter aortic valve replacement (TAVR). A filamentous structure was noted on the focused pre-operative 2D transoesophageal echocardiography in the proximal descending aorta and post-TAVR as long strand-like structures attached to the thickened intimal wall with a planar component on 3D imaging. These findings were not associated with symptoms or clinical sequelae on short- and long-term follow-up. Discussion: The mobile structures that we describe are atypical for atheroma, thrombi, vegetations, and dissections in terms of their form and clinical presentation. 2D imaging showed that the filaments had focal thickening and emerged from the aortic surface. These findings suggest a relationship with the intima, perhaps from atherogenesis or injury with disruption or lifting of the intimal surface. No clinical sequelae were detected that may also relate to their position in the descending aorta and not the arch.

Role of long non-coding RNA TCONS_02443383 in regulating cell adhesion and peroxisome proliferator-activated receptor (PPAR) signaling genes in atherosclerosis: A New Zealand white rabbit model study.

OBJECTIVE: In this study, we performed RNA sequencing (RNA-seq) on the abdominal aorta tissue of New Zealand rabbits and investigated the potential association of lncRNA TCONS_02443383 with the development of AS through bioinformatics analysis of the sequencing data. The obtained results were further validated using quantitative real-time polymerase chain reaction (qRT-PCR). METHOD: We induced an AS model in New Zealand rabbits by causing balloon injury to the abdominal aorta vascular wall and administering a high-fat diet. We then upregulated the expression level of the lncRNA TCONS_02443383 by injecting lentiviral plasmids through the ear vein. RNA sequencing (RNA-seq) was performed on the abdominal aorta tissues. We conducted Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathway and Gene Ontology (GO) analyses. RESULT: The overexpression of the lncRNA TCONS_02443383 led to an upregulation of peroxisome proliferator-activated receptor (PPAR) signaling pathways as well as genes related to cell adhesion. CONCLUSION: The overexpression of the lncRNA TCONS_02443383 can inhibit the occurrence and development of AS by upregulating peroxisome proliferator-activated receptor (PPAR) signaling pathways and genes related to cell adhesion.

Multiple exposures to low-dose ionizing radiation induced the initiation and progression of pro-atherosclerotic phenotypes in mice and vascular endothelial cell damage.

OBJECTIVE: This study aimed to investigate the effects of low-dose radiation on the abdominal aorta of mice and vascular endothelial cells. METHODS: Wild-type and tumor-bearing mice were exposed to 15 sessions of low-dose irradiation, resulting in cumulative radiation doses of 187.5, 375, and 750 mGy. The effect on the cardiovascular system was assessed. Immunohistochemistry analyzed protein expressions of PAPP-A, CD62, P65, and COX-2 in the abdominal aorta. Microarray technology, Gene Ontology analysis, and pathway enrichment analysis evaluated gene expression changes in endothelial cells exposed to 375 mGy X-ray. Cell viability was assessed using the Cell Counting Kit 8 assay. Immunofluorescence staining measured γ-H2AX levels, and real-time polymerase chain reaction quantified mRNA levels of interleukin-6 (IL-6), ICAM-1, and Cx43. RESULTS: Hematoxylin and eosin staining revealed thickening of the inner membranes and irregular arrangement of smooth muscle cells in the media membrane at 375 and 750 mGy. Inflammation was observed in the inner membranes at 750 mGy, with a clear inflammatory response in the hearts of tumor-bearing mice. Immunohistochemistry indicated increased levels of PAPP-A, P65, and COX-2 post-irradiation. Microarray analysis showed 425 up-regulated and 235 down-regulated genes, associated with processes like endothelial cell-cell adhesion, IL-6, and NF-κB signaling. Cell Counting Kit 8 assay results indicated inhibited viability at 750 mGy in EA.hy926 cells. Immunofluorescence staining demonstrated a dose-dependent increase in γ-H2AX foci. Reverse transcription quantitative PCR results showed increased expression of IL6, ICAM-1, and Cx43 in EA.hy926 cells post 750 mGy X-ray exposure. CONCLUSION: Repeated low-dose ionizing radiation exposures triggered the development of pro-atherosclerotic phenotypes in mice and damage to vascular endothelial cells.

Left ventricular assist device implantation combined with hemiarch replacement for severe aortic atherosclerosis.

Implantation of the left ventricular assist device (LVAD) has emerged as a widely employed therapeutic approach for specifically chosen individuals suffering from severe heart failure. Stroke is a well-known complication of LVAD implantation. Concomitant aortic surgeries in patients requiring LVAD implantation to avoid outflow graft anastomosis to a severe atherosclerotic aorta are unknown. We illustrate a successful LVAD implantation with hemiarch replacement for severe aortic atherosclerosis to decrease the risk of postoperative stroke. A 72-year-old male patient with advanced heart failure has chosen to undergo LVAD treatment. Preoperative examinations detected severe atherosclerosis in the ascending aorta. It was determined that clamping the ascending aorta and directly connecting the outflow graft could increase the risk of stroke after surgery. Therefore, it was decided to replace the diseased ascending aorta entirely. The HeartMate 3 was implanted under cardiopulmonary bypass (CPB) using right axillary artery cannulation. And moderate hypothermia and bilateral antegrade cerebral perfusion were utilized to perform hemiarch replacement. Subsequently, the outflow graft was connected to an artificial ascending aortic graft. The patient did not exhibit any specific complications, such as neurological abnormalities, after the surgery. Based on our observations, it appears that LVAD implantation combined with aortic replacement could be a viable option for specific patients, particularly those who have a perioperative stroke risk due to aortic atherosclerosis.

Ascending aorta cannulation for isolated liver procurement in extended criteria donors: a safe option in case of massive infrarenal aortic atherosclerosis.

The chronic organ shortage and the increased number of patients on the waiting list for liver transplantation have led to a progressive increase in the use of extended criteria donors. Nowadays more and more overweight donors with several comorbidities are selected for donation providing acceptable patient and liver graft survival. These donors have often aortic atherosclerosis which can spare the hepatic artery making suitable the liver for procurement. Massive aortic atherosclerosis localized to infrarenal aorta can challenge aortic cannulation for organ cooling. We herein describe in a stepwise approach the aortic cannulation realized at the ascending aorta level in case of massive infrarenal aortic atherosclerosis in ECD donors. This technique represents a safe option when abdominal aorta is not suitable for cannulation and it should be included into the surgical armamentarium of liver transplant surgeon.

Serial Changes of Aortic Vulnerable Plaques Observed via Non-Obstructive General Angioscopy.

Stabilization of aortic vulnerable plaques has not been fully elucidated. Non-obstructive general angioscopy (NOGA) is a novel method for the detailed evaluation of atheromatous plaques in the aortic intimal wall. A 57-year-old man presenting with acute myocardial infarction underwent percutaneous coronary intervention (PCI). NOGA was performed for the evaluation of aortic atherosclerosis, and vulnerable puff-chandelier plaques in the aortic arch were identified. After a strictly controlled low-density lipoprotein cholesterol lowering therapy with a strong statin for 8 months after the primary PCI, NOGA revealed stabilized aortic plaques in the same lesions. Therefore, NOGA may be helpful in evaluating the effects of lipid-lowering therapy on aortic plaque stabilization.

Intimal aortic atherosclerosis in cardiac surgery: surgical strategies to prevent embolic stroke.

OBJECTIVES: Although the incidence of perioperative stroke after cardiac surgery gradually decreased over the last decades, there is much variation between centres. This review aimed to create a concise overview of the evidence on possible surgical strategies to prevent embolic stroke in patients with intimal aortic atherosclerosis. METHODS: The PubMed and EMBASE databases were searched for studies on surgical management of aortic atherosclerosis and the association with perioperative stroke in cardiac surgery, including specific searches on the most common types of surgery. Articles were screened with emphasis on studies comparing multiple strategies and studies reporting on the patients' severity of aortic atherosclerosis. The main findings were summarized in a figure, with a grade of the corresponding level of evidence. RESULTS: Regarding embolic stroke risk, aortic atherosclerosis of the tunica intima is most relevant. Although several strategies in general cardiac surgery seem to be beneficial in severe disease, none have conclusively been proven most effective. Off-pump surgery in coronary artery bypass grafting should be preferred with severe atherosclerosis, if the required expertise is present. Although transcatheter aortic valve replacement is used as an alternative to surgery in patients with a porcelain aorta, the risk profile concerning intimal atherosclerosis remains poorly defined. CONCLUSIONS: A tailored approach that uses the discussed alternative strategies in carefully selected patients is best suited to reduce the risk of perioperative stroke without compromising other outcomes. More research is needed, especially on the perioperative stroke risk in patients with moderate aortic atherosclerosis.

ACR Appropriateness Criteria® Nontraumatic Aortic Disease.

Nontraumatic aortic disease can be caused by a wide variety of disorders including congenital, inflammatory, infectious, metabolic, neoplastic, and degenerative processes. Imaging examinations such as radiography, ultrasound, echocardiography, catheter-based angiography, CT, MRI, and nuclear medicine examinations are essential for diagnosis, treatment planning, and assessment of therapeutic response. Depending upon the clinical scenario, each of these modalities has strengths and weaknesses. Whenever possible, the selection of a diagnostic imaging examination should be based upon the best available evidence. The American College of Radiology Appropriateness Criteria are evidence-based guidelines for specific clinical conditions that are reviewed annually by a multidisciplinary expert panel. The guideline development and revision include an extensive analysis of current medical literature from peer reviewed journals and the application of well-established methodologies (RAND/UCLA Appropriateness Method and Grading of Recommendations Assessment, Development, and Evaluation or GRADE) to rate the appropriateness of imaging and treatment procedures for specific clinical scenarios. In those instances where evidence is lacking or equivocal, expert opinion may supplement the available evidence to recommend imaging or treatment. The purpose of this document is to assist physicians select the most appropriate diagnostic imaging examination for nontraumatic aortic diseases.

Ischemic Stroke Patients with Non-Valvular Atrial Fibrillation have a Risk for Aortogenic Embolizations.

We have a great interest in the article in Journal of Atherosclerosis and Thrombosis by Suzuki et al. titled Complex Aortic Arch Atherosclerosis in Acute Ischemic Stroke Patients with Non-Valvular Atrial Fibrillation. The authors demonstrated that 38.7% transesophageal echocardiography-derived complex aortic arch plaques (CAPs) among 106 patients with acute ischemic strokes with atrial fibrillation (AF), suggesting that patients with acute ischemic stroke and AF often had CAPs. The atheromatous lesions at the aortic arch are one of the causes of ischemic strokes. The cause of acute ischemic strokes in patients with AF could not only be cardiogenic embolisms due to AF but also aortogenic embolisms due to CAPs. The possibility of concomitant CAPs should be considered for stroke patients with AF. Non-obstructive general angioscopy has the possibility to detect aortic plaques in the aortic arch more accurately than TEE and might help to diagnose atheromatous plaques and embolic materials in the aortic arch. Further studies are needed to elucidate the causes of ischemic strokes and are expected to improve the outcomes for acute ischemic strokes in patients with AF.

Neurologic complications of diseases of the aorta.

Neurologic complications of diseases of the aorta are common, as the brain and spinal cord function is highly dependent on the aorta and its branches for blood supply. Any disease impacting the aorta may have significant impact on the ability to deliver oxygenated blood to the central nervous system, resulting in ischemia-and if prolonged-cerebral and spinal infarct. The breadth of pathology affecting the aorta is diverse and neurologic complications can vary dramatically based on the location, severity, and underlying etiology. This chapter outlines the major pathology of the aorta while highlighting the associated neurologic complications. This chapter covers the entire spectrum of neurologic complications associated with aortic disease by beginning with a detailed overview of the spinal cord vascular anatomy followed by a discussion of the most common aortic pathologies affecting the nervous system, including aortic aneurysm, aortic dissection, aortic atherosclerosis, inflammatory and infectious aortopathies, congenital abnormalities, and aortic surgery.

An unexpected paradox: wall shear stress in the aorta is less in patients with severe atherosclerosis regardless of obesity.

BACKGROUND: Obesity is a widespread condition that is more prevalent in Western countries compared to others. Aortic atherosclerosis (AA) is a condition that frequently has been associated with obesity. An obesity paradox, where morbidly obese decedents had either no or minimal AA compared to nonobese decedents, recently has been described by some of us. The explanation for this almost counterintuitive paradox has yet to be determined, but a number of hypotheses were advanced, including hemodynamic factors producing aortic wall shear stress (WSS). The purpose of the present study was to determine if there was a relationship between AA and WSS, as determined by postmortem measurement of aortic wall diameters. METHODS: Circumferences of the aorta at the levels of the ascending, thoracic and abdominal aorta were measured in 274 consecutive autopsies over 2-year period of time. AA was assessed using a previously described grading scale as either mild or severe. Circumferences were mathematically converted to diameters and WSS was calculated using the Hagen-Poiseuille formula. Two different methods to estimate cardiac output were used, both based on literature methods, one of which was body mass index (BMI) dependent, and the other BMI independent. Univariate and multivariable analyses of the relationship between WSS, age, BMI, gender, race and severity of AA were performed. RESULTS: Of the 274 decedents, 140 had mild and 134 had moderate to severe AA. BMI <35 was associated with moderate to severe AA. WSS was inversely correlated with AA in all these segments of the aorta in each BMI subgroup with the exception of the ascending aorta for decedents with BMI ≤35 kg/m2. Contrary to what we had hypothesized, WSS was not a determinant of the obesity paradox. However, among all the variables analyzed, a history of hypertension, diabetes mellitus and age were significant factors for developing AA (relative risk [RR] 0.35, P = .039; RR 1.51, P = .0006, RR 1.19, P = .0001, respectively). CONCLUSIONS: Our data demonstrate that WSS was unexpectedly lower in decedents with moderate and severe AA as compared to those with mild AA. This observation, which requires further investigations, was seen in all BMI ranges and was confirmed by 2 methods to calculate WSS.

Anatomical References to Evaluate Thoracic Aorta Calcium by Computed Tomography.

PURPOSE OF REVIEW: Thoracic aortic calcium (TAC) has received some interest in recent studies as an important subclinical marker of atherosclerosis. Besides that, using computed tomography (CT) scans performed with cardiac or chest protocols, ECG-gated, or non-gated, TAC can be easily evaluated with no addition in radiation dose. This review discusses the particularities of the aortic wall calcium formation, as well as the differences between the aortic segments and summarizes the current status of TAC evaluation, mainly concerning the anatomical references used in the studies. RECENT FINDINGS: The studies have evaluated TAC considering different anatomical references. It was identified two different study groups. In the first one, researchers have analyzed the aorta as the sum of calcium in the ascending aorta (ATAC), aortic arch (AAC), and descending thoracic aorta (DTAC). The second group has used cardiac CT scans to assess TAC; therefore, they did not include AAC; however, the aortic root calcium (ARC) was added in the analysis. So, caution is advisable when interpreting and comparing studies that used different TAC anatomical references. The broad methodological variability, in addition to the variations in the population characteristics of the studies on TAC, may be in part contributing to the differences between results of different studies. Currently TAC does not have a role in clinical decisions, so it is necessary to create a standard protocol for the aortic calcium research as well as exists for the coronary artery calcium evaluation.

Colon cancer laterality is associated with atherosclerosis and coronary artery disease.

BACKGROUND: Primary right-sided colon cancer (RCC) is associated with a higher mortality than left-sided colon cancer (LCC), but the etiology of this phenomenon remains unclear. We sought to study whether cancer laterality is associated with the prevalence of clinical coronary artery disease, calcific atherosclerosis as measured by computed tomography (CT), and cardiovascular risk factors. METHODS: We conducted a single center retrospective study of 546 participants who had previously been diagnosed with colon cancer between January 2005 and December 2014. The presence of coronary and aortic calcifications was assessed by CT in 486 of these patients. We examined the prevalence of clinical cardiovascular disease (CAD) (prior myocardial infarction or revascularization), comorbidities, coronary and aortic calcification in patients with RCC (n=261) and LCC (n=285). Logistic regression analysis was performed to assess the likelihood of clinical CAD and calcific atherosclerosis by cancer laterality. RESULTS: Compared to patients with LCC, patients with RCC were more likely to have hypertension, hyperlipidemia, hypothyroidism and clinical CAD. In the patients with available CT scans, RCC was associated with higher prevalence of coronary, thoracic, and abdominal calcifications than LCC. On univariate and multivariate analyses, RCC was associated with higher likelihood of clinical CAD (adjusted risk ratio 2.15, 95% CI, 1.37-3.38, P=0.001) as well as radiological evidence of calcific atherosclerosis compared to LCC. CONCLUSIONS: we found that both clinical CAD and vascular calcifications are prevalent in patients with colon cancer, and are independently increased in patients with RCC compared to LCC.

Risk Factors of Contralateral Microembolic Infarctions Related to Carotid Artery Stenting.

This study sought to analyze the incidence of contralateral microembolic infarctions (MIs) on diffusion-weighted imaging (DWI) following protected carotid artery stenting (CAS) and compared the difference of risk factors between ipsilateral and contralateral lesions. From April 2010 to March 2017, 147 CASs in 140 patients were performed. All the patients underwent DWI within 1 week before and 24 hrs after the procedures. CAS was successfully completed in 145 (98.6%) of the 147 procedures. Forty-nine (33.8%) patients with new MIs revealed on postprocedural DWI were enrolled. They were divided into ipsilateral and contralateral groups based on the side of the CAS and MIs. The ipsilateral group indicates patients with MIs exclusively on the side of CAS. The contralateral group includes patients with MIs on the opposite side of the CAS or both sides. Patients with MIs at vertebrobasilar territory were excluded. Patient characteristics, morphology of the carotid artery and aortic arch, and procedural data were retrospectively assessed and compared between the two groups. Twenty-two (15.2%) and 14 (9.7%) patients were assigned to the ipsilateral and contralateral groups, respectively. Advanced age, left-sided stenosis, severe aortic arch calcification (AAC) on chest X-ray and contralateral carotid occlusion significantly increased the occurrence of contralateral MIs. On multivariable logistic regression analysis, severe AAC was statistically more frequent in the contralateral group. In the present study, the incidences of contralateral MIs after CAS is relatively not low. Advanced aortic atherosclerosis is statistically predictive for contralateral MIs. AAC on chest X-ray is a useful finding for estimating aortic atherosclerosis in candidates for CAS.

Aortic atherosclerosis is a key modulator of the prognostic value of postural blood pressure changes.

BACKGROUND AND AIMS: Orthostatic blood pressure decrease or increase has been related to cardiovascular events in hypertensive patients. Large blood pressure changes after orthostatic stress are associated with autonomic and neurohormonal abnormalities; aortic atherosclerosis (ATS) may also play a role. METHODS: We investigated the interaction of ATS on the prognostic value of postural blood pressure changes. In a cohort of 958 hypertensive patients with an aortography (mean ± standard deviation age 44 ± 11 years, 61% men, mean blood pressure 182/110 mmHg), blood pressure was measured after 10 min of rest in the supine position. Systolic blood pressure (SBP) was also measured in standing position, 1 min after the supine position. Blood pressure changes were calculated as supine SBP minus standing SBP and analyzed as absolute or arithmetic means. ATS was assessed using an aortography score. RESULTS: After 15 years of follow-up, 280 all-cause and 167 cardiovascular deaths occurred. In a multivariable Cox regression analysis adjusted for major cardiovascular risk factors and stratified according to ATS status, SBP changes were statistically associated with all-cause and cardiovascular mortality only in the presence of ATS: tertile 3 versus 1, 2.99 (1.37-6.49) and 4.08 (1.55-10.72) respectively, tertile 3 versus 2, 2.89 (1.29-6.46) and 4.82 (1.79-12.98), respectively (p for interaction: 0.003 for all-cause and 0.003 for cardiovascular mortality) for absolute changes. The hazard associated with the magnitude of SBP changes was more important than that associated with its direction. CONCLUSIONS: The prognostic significance of postural SBP changes is markedly influenced by ATS in hypertensive patients.

Ascending Aortic Rupture through a Penetrating Atherosclerotic Ulcer: A Rare Cause of Sudden Unexpected Death.

Spontaneous rupture of the aorta through an atherosclerotic lesion without preexisting aortic aneurysm, dissection, or history of trauma is very rare. Without prompt aortic repair, all cases result in sudden death with a definitive diagnosis made only intraoperatively or during autopsy. The phenomenon has been uniformly found in individuals with hypertension. The author reports a sudden unexpected death caused by spontaneous rupture of the ascending aorta in a 57-year-old man with a history of hypertension. The ascending aortic wall showed a longitudinal intimal tear measuring approximately 1 cm in length and rupture of the ascending aorta through an atherosclerotic ulcer, leading to massive hemopericardium and eventual death. Chronic hypertension and a penetrating atherosclerotic ulcer of the ascending aorta were the apparent underlying etiologies of the aortic rupture in the present case. This case illustrates not only the association between a rupture and a penetrating atherosclerotic ulcer with a silent death, but also raises awareness of possible such deaths.

The role of L-arginine/L-homoarginine/nitric oxide pathway for aortic distensibility and intima-media thickness in stroke patients.

Asymmetric dimethylarginine (ADMA) and L-homoarginine (hArg) are L-arginine (Arg) metabolites derived from different pathways. Protein arginine N-methyltransferase (PRMT) and subsequent proteolysis of proteins containing methylarginine residues release ADMA. Arginine:glycine amidinotransferase (AGAT) converts Arg to hArg and guanidinoacetate (GAA). While high concentrations of ADMA and low concentrations of hArg in the blood have been established as cardiovascular risk markers, the cardiovascular relevance of GAA is still unexplored. Arg and hArg are substrates and ADMA is an inhibitor of nitric oxide (NO) synthase (NOS). The cardiovascular effects of ADMA and hArg have been related to NO, a potent endogenous vasodilator. ADMA and hArg are considered to exert additional, not yet explored, presumably NO-unrelated effects and to act antagonistically in the renal and cardiovascular systems. Although the physiological role of Arg, ADMA, hArg and NO for endothelial function in small- and medium-sized arteries has been intensively studied in the past, the clinical relevance of aortic wall remodeling still remains unclear. Here, we evaluated potential relation between aortic distensibility (AD) or aortic intima-media thickness (aIMT) and circulating ADMA, hArg, GAA, and the NO metabolites nitrite and nitrate in the plasma of 78 patients (24 females, 54 males; aged 59 ± 14 years) with recent ischemic stroke or transient ischemic attack (TIA). All biochemical parameters were determined by stable-isotope dilution gas chromatography-mass spectrometry. AD and aIMT were measured by transesophageal echocardiography. Arg, hArg, ADMA and GAA median plasma concentrations (µM) were determined to be 61, 1.43, 0.50 and 2.16, respectively. hArg, ADMA and GAA correlated closely with Arg. Nitrite, nitrate and creatinine median plasma concentrations (µM) were 2.49, 48.7, and 84.1, respectively. Neither AD (2.61 vs. 1.85 10-6 × cm2 × dyn-1, P = 0.064) nor aIMT (1.25 vs. 1.13 mm, P = 0.596) differed between females and males. The hArg/ADMA molar ratio (r = -0.351, P = 0.009), nitrate (r = 0.364, P = 0.007) and nitrite (r = 0.329, P = 0.015) correlated with aIMT but not with AD. Arg, hArg, ADMA and GAA correlated with aIMT but not with AD. The results demonstrate a strong relation between the Arg/NO pathway and aortic atherosclerosis but not with AD suggesting different mechanisms underlying the two aspects of aortic wall remodeling.

An obesity paradox: an inverse correlation between body mass index and atherosclerosis of the aorta.

BACKGROUND AND AIMS: Morbid obesity generally has been associated with higher morbidity and mortality for a variety of diseases. However, a number of exceptions to this have been reported and referred to as the "obesity paradox." The purpose of the present study was to obtain objective data on aortic atherosclerosis and its relationship to body mass index (BMI, kg/m2), based on autopsy findings in a large cohort of overweight and obese decedents. METHODS: Decedents were ≥18 years who had autopsies between 2003 and 2014, a subset of whom were morbidly obese (BMI≥40). Autopsy findings were reviewed and compared to a control group (BMI<40) who had consecutive autopsies performed between January 2013 and June 2014. Atherosclerosis was assessed by gross pathologic examination using a semiquantitative grading scale (from 0 to 3), and for statistical analysis, the scores were stratified into two groups: nonsevere (<2) or severe (≥2). RESULTS: There were 304 decedents in the study: 66 were morbidly obese (BMI≥40), 94 were either Class I or II obese (BMI 30-40), 127 were either overweight (BMI 25.0-29.9) or normal weight (BMI 20-24.9), and 17 were underweight (BMI<20). Decedents with mild atherosclerosis were significantly younger than those with severe disease (55.2 vs. 67.3, P<.0001). Decedents were further stratified by age and BMI. Univariate analysis revealed that decedents >60 years were more likely to have severe atherosclerosis than those ≤60 years (61% vs. 30%, P<.0001). There was a highly significant (P=.008) inverse relationship between severe aortic atherosclerosis and BMI. Twenty of 66 decedents (30%) with a BMI≥40 had severe atherosclerosis vs. 122 of 238 decedents (51%) with BMIs<40 (P=.001). As BMI increased, the probability of developing severe disease decreased. Hypertension increased the probability of having severe atherosclerosis (54% vs. 33%, P=.007). After adjusting for other covariates, multivariable analysis revealed that age and hypertension were still positively correlated with the severity of atherosclerosis (P=.014 and 0.028, respectively), and the inverse relationship between BMI and atherosclerosis remained (adjusted relative risk of BMI≥40 vs. <40=0.64, 95% confidence interval: 0.4-1; P=.03). CONCLUSIONS: Our data extend the previously described obesity paradox to another disease entity, atherosclerosis of the aorta. Morbid obesity appeared to have a protective effect for developing severe aortic atherosclerosis, for the reasons for which are yet to be determined. However, the mean age at death of decedents with BMIs≥40 was younger than those with BMIs in the 20-30 range (55.9 vs. 63.2 years, P=.001), confirming that morbid obesity was not associated with increased longevity.