History Of Aortic Aneurysm Research Articles

Aorto-pulmonary artery fistula with Laubry-Pezzi syndrome: A diagnostic enigma

Usually diagnosed post-mortem, aortopulmonary artery fistula is an exceptionally rare and often highly lethal condition. Here, we present a unique case of a 29-year-old woman with no history of aortic aneurysm or previous aortic surgery, referred for surgical management of Laubry-Pezzi syndrome in whom an aorto-pulmonary artery fistula bridging the ascending aorta and the main pulmonary artery was discovered intra operatively. The patient was successfully managed with an uneventful postoperative recovery. Our case outlines the inaugural reported occurrence of an aortopulmonary artery fistula coinciding with Laubry-Pezzi syndrome. Unique features include subtle onset of heart failure over months due to occult left ventricular volume overload, challenging diagnosis alongside known intracardiac shunts, emphasizing the need for vigilance, and demonstration of successful surgical outcomes despite high morbidity and mortality.

PS-C04-11: EFFECT OF ANKLE BRACHIAL INDEX EXAMINATION ON CENTRAL AORTIC BLOOD PRESSURE IN PATIENTS WITH PERIPHERAL ARTERY DISEASE

Background: Ankle brachial index (ABI) measurements are useful for detecting peripheral artery disease (PAD) as a screening test. In general, ABI examinations are contraindicated in patients with aortic aneurysm and history of aortic aneurysm. However, little is known whether ABI examinations elevate central aortic blood pressure (CBP). Method: From June 2018 to August 2020, we prospectively analyzed 66 patients who were performed cardiac catheterization through femoral approach and divided into peripheral artery disease complicated (PAD, N = 27) and uncomplicated (non-PAD, N = 39) groups. After insertion of pigtail catheter into both ascending (Asc), abdominal (Abd) positions, resting CBPs at Asc and Abd were measured. Subsequently, we measured each CBP during ABI, respectively. We compared resting CBP (R-CBP) and CBP during ABI (ABI-CBP) between PAD and non-PAD groups. Results: In non-PAD group, ABI-CBP at Abd was significantly higher than BL-CBP (P < 0.05). On the other hand, there were no significant ABI-CBP elevation at Asc and Abd in PAD. There was no case with CBP elevation more than 20mmHg during ABI measurements in both groups. Furthermore, no clinical events were observed after ABI measurements in both groups. Conclusion: ABI was considered a safe testing in patients with suspected PAD.

S2646 Role of Point-of-Care Ultrasound in Diagnosis of Upper GI Bleed Secondary to Aorto-Esophageal Fistula

Introduction: Aorto-esophageal fistula (AEF) is a rare etiology of upper gastrointestinal bleed (UGIB) with a high mortality rate. In patients with vascular pathology or aortic aneurysms presenting with hematemesis and Chiari’s triad (midthoracic pain, sentinel arterial hemorrhage and exsanguination after symptom-free interval), there should be high suspicion for AEF as mortality is high even with timely diagnosis and surgical intervention. Diagnostic endoscopy, aortography, or thoracic computed tomography angiography (CTA) are current standards of care but may be unobtainable in emergent cases. Here, we report a case of UGIB in which bedside Point-of-Care Ultrasound (POCUS) facilitated prompt diagnosis of AEF. Case Description/Methods: A 75-year-old male with history of diabetes, uncontrolled hypertension and abdominal aortic aneurysm presented with large volume hematemesis resulting in two episodes of PEA arrests. ROSC was achieved with aggressive hemodynamic support. Gastroenterology was consulted, but the patient was deemed too unstable for endoscopy. Octreotide and pantoprazole drips were initiated. Placement of a Blakemore tube was attempted. POCUS demonstrated descending aortic intraluminal flap consistent with aortic dissection. After stabilization, CTA was pursued which showed descending thoracic aortic aneurysm with penetrating ulcer and active extravasation into the subcarinal mediastinum. Vascular surgery was urgently consulted but the patient became increasingly unstable and ultimately expired. Discussion: AEF is a rare cause of UGIB that should be suspected in patients with large volume hematemesis, chest pain, hemodynamic compromise. Index of suspicion should be high in patients with a history of aortic aneurysm, esophageal malignancy, ingestion of foreign body or recent esophageal surgery. Temporization, rapid diagnosis, and surgical intervention are critical, but guideline directed diagnostic modalities are limited in hemodynamically unstable patients. Here, POCUS allowed prompt diagnosis several hours before the patient was stable enough for CTA. This case demonstrates that POCUS has a diagnostic role in massive UGIB in patients with a high pretest probability of vascular pathology and may limit unnecessary invasive testing in select patients who are unlikely to benefit from endoscopy. Further research is needed to determine the diagnostic role of POCUS in UGIB, but it should be considered in patients with high suspicion for AEF (Figure).Figure 1.: (A) POCUS showing descending aortic intraluminal flap consistent with aortic dissection. (B) CTA showing descending aortic aneurysm with penetrating ulcer resulting in hematoma of the subcarinal mediastinum.

Abstract 13865: Impact of Prior Aortic Aneurysm Diagnosis on Presentation and Outcomes in Stanford Type B Acute Aortic Syndromes

Introduction: Acute aortic syndromes (AAS) involving the descending, but not the ascending, aorta (Stanford type B) are medical emergencies that require multidisciplinary management. Aortic aneurysms are a known risk factor for AAS. We investigated the impact of a history of aortic aneurysm on presentation and outcomes in patients with type B AAS. Hypothesis: We hypothesize that patients with a history of aortic aneurysm have higher in-hospital mortality rate and adverse outcomes compared to those without. Methods: We performed a retrospective analysis of all patients admitted with AAS to our tertiary medical center between July 2012 and October 2020. Type B AAS presentations included aortic dissection, aortic rupture, intramural hematoma (IMH), penetrating atherosclerotic ulcer, and symptomatic aneurysm. Prior history included presence of a thoracic and/or abdominal aortic aneurysm. Results: A total of 169 patients with type B AAS were included in our analyses. Of these, 54 (32%) had a history of prior aortic aneurysm and 115 (68%) patients did not (Table). Patients with prior aortic aneurysm were significantly older (74.3±14.6 vs. 68.7±14.1 years, p <0.0001), had a lower proportion of aortic dissection (33.3% vs. 50.4%, p <0.05) and a higher proportion of symptomatic aneurysm (27.8% vs. 8.7%, p <0.001) as their presentation. Similar rates of mortality (8.9% vs. 7.4%), AAS related complications, and 30-day hospital readmission were observed between patients with a prior aortic aneurysm and those without. Conclusions: Among patients with type B AAS, those with a history of aortic aneurysm have a lower proportion of dissection and a higher proportion of symptomatic aneurysm at presentation. However, their rates of in-hospital mortality and 30-day readmission do not differ compared to those observed in patients without a history of aortic aneurysm.

FDG PET/CT in infected abdominal aortic aneurysm due to Brucellosis

A 66-year-old man with a history of aortic aneurysm, treated 5 years before by endovascular aneurysm repair (EVAR), underwent a follow-up CT angiography showing an increased aneurysm size to 64 mm, a proximal endoleak, and an inflammatory thickening of the aneurysm wall. The patient did not have fever or abdominal pain. Laboratory tests showed a normal blood count, a slightly elevated C-reactive protein and a normal procalcitonin.

Early and Midterm Results of Thoracoabdominal Aortic Aneurysm Repair in Patients with Marfan Syndrome

Objective To evaluate the early and midterm results of surgical repair of thoracoabdominal aortic aneurysm(TAAA)in patients with Marfan syndrome(MFS). Methods The clinical data of patients with MFS undergoing TAAA repair in Fuwai Hospital between January 2009 and December 2017 were retrospectively analyzed.These patients were divided into two groups:MFS group(n=58)and non-MFS group(n=98).The baseline data,early postoperative results,and midterm follow-up outcomes were compared between these two groups. Results MFS patients were significantly younger(32 years old vs. 45 years old,t=9.603,P=0.000)and more frequently had a history of aortic aneurysm or dissection(19% vs. 0,χ 2=19.996,P=0.000)than non-MFS patients.However,the proportions of males and smokers were significantly lower when compared with non-MFS patients(55.2% vs. 80.6%,χ 2=11.489,P=0.001;13.8% vs. 46.9%,χ 2=17.686,P=0.001).There was no significant difference in proportion of emergency operation,prophylactic cerebrospinal fluid drainage,operation time,intra-operative circulation management,and intra-operative blood transfusion(all P>0.05).The 30-day mortality rate was significantly lower in MFS group than in non-MFS group(0 vs. 9.2%, [Formula: see text]=5.034,P=0.025). Conclusions For patients with MFS,TAAA repair provides lower 30-day mortality and comparative middle-term survival.However,the re-intervention rate is higher among MFS patients,highlighting the importance of close follow-up.

P097: High-risk clinical features for acute aortic syndrome

Introduction: Acute aortic syndrome (AAS) is a rare clinical syndrome with a high mortality encompassing acute aortic dissection, intramural hematoma and penetrating atherosclerotic ulcer. The objective of our study was to assess the diagnostic accuracy of high risk historical, examination and basic investigative features for AAS, in confirmed cases of AAS and a low risk control group in order to address the spectrum bias in previous diagnostic accuracy studies. Methods: We performed a historical matched case-control study: participants were adults >18 years old presenting to two tertiary care emergency departments (ED) or one regional cardiac referral center. Cases: new ED or in-hospital diagnosis of non-traumatic AAS confirmed by computed tomography or echocardiography. Controls: triage diagnosis of truncal pain (<14 days) and an absence of a clear diagnosis on basic investigation. Cases and controls were matched in a 4:1 ratio by sex and age. A sample size of 165 cases and 660 controls was calculated based on 80% power and confidence interval of 95% to detect an odds ratio of greater than 2. Results: Data were collected from 2002-2014 yielding 194 cases of AAS and 776 controls (mean age of 65(SD 14.1) and 66.7% male). Of the 194 cases of AAS, 32 (16.5%) were missed on initial assessment. Chest pain unspecified (20.7%), abdominal pain unspecified (9.9%) and acute coronary syndrome (8.7%) were the top diagnoses in the control population. Absence of acute onset pain (Sensitivity 95.9% negative likelihood ratio (LR-) 0.07(0.03-0.14)), and a negative D-dimer (Sensitivity 96.7%, LR- 0.05(0.01-0.18)) can help rule out AAS. Presence of tearing/ripping pain (Specificity 99.7%, LR+42.1 (9.9-177.5), a history of aortic aneurysm (Specificity 97.8%, LR+6.35(3.54-11.42)), hypotension (Specificity 98.7%, LR+ 17.2(8.8-33.6)), pulse deficit (Specificity 99.3, LR+31.1(11.2-86.6)), neurological deficits (Specificity 96.9%, LR+ 5.26(2.9-9.3)), and a new murmur (Specificity 97.8%, LR+ 9.4(5.5-16.2) ) can help rule in the diagnosis of AAS. Conclusion: Patients with one or more high-risk feature should be considered high risk, whereas patients with no high risk and multiple low risk features are at low risk for AAS. Further research should focus on a combination of these factors to guide who warrants further investigation thus reducing miss rate, morbidity and mortality.

Abstract 37: A Multi-locus Genetic Risk Score for Abdominal Aortic Aneurysm

Background: Genome-wide association studies (GWAS) have identified several common variants associated with abdominal aortic aneurysm (AAA). We investigated whether a multi-locus genetic risk score (GRS) for AAA was associated with presence and progression of AAA in a case-control study. Methods: The study comprised of 1098 patients with AAA (74±8 years, 83% men) and 6538 controls (67±10 years, 58% men) enrolled in the Mayo Vascular Disease Biorepository. AAA was defined as a transverse diameter of abdominal aorta ≥ 3.0 cm or history of AAA repair. Controls were participants without known AAA. We found five single nucleotide polymorphisms (SNPs) previously shown to be associated with AAA at GWAS significance (P≤10^-8) in NHGRI GWAS catalog and PubMed. A GRS for AAA for each individual was calculated from four SNPs (rs2383107, rs7025486, rs599839, rs1466535) that were replicated in our cohort, by summing the number of risk alleles for each SNP weighted by their estimated effect sizes in GWAS catalog or published largest meta-analysis. Results: GRS was associated with presence of AAA: odds ratio (OR) (95% confidence interval): 1.06 (1.03-1.08). The association remained significant after adjustment for age, sex, cardiovascular risk factors, and atherosclerotic cardiovascular diseases: adjusted OR: 1.05 (1.03-1.08). Further adjustment for each SNP did not attenuate association of GRS with presence of AAA (All P<0.001). GRS was not associated with family history of aortic aneurysm (P=0.4). Adding GRS to conventional risk factors improved net reclassification index by 16% (P<0.001).In a subset of patients with AAA who had sequential imaging studies (n=628), GRS was associated with AAA growth rate ≥ 1.75 mm/year (median of the cohort) after adjustment for baseline AAA size: adjusted OR: 1.07 (1.00-1.14). No conventional risk factors were associated with AAA growth. Patients with GRS > 5.24 (median of the cohort) had 1.31 times higher odds of having AAA and 1.64 times higher odds of having AAA growth rate ≥1.75 mm/year compared to those with GRS ≤ 5.24 (both P≤0.005). Conclusions: A multi-locus GRS was associated with presence of AAA and aneurysm growth, suggesting genetic predisposition to disease initiation and progression.

Correlation between coronary artery calcium score and aortic diameter in a high-risk population of elderly male hypertensive patients.

Studies on the relationship between coronary artery calcium and aortic diameter are scarce. The aim of the current study was to evaluate the correlation between coronary artery calcium score (CACS) and maximal thoracic and abdominal aortic diameters in a population of elderly (>65 years) male hypertensive patients at high risk for coronary artery disease. From June 2012 to April 2013, we prospectively enrolled 393 male hypertensive patients older than 65 years of age who had no history of aortic aneurysm. Coronary artery calcium and maximal diameters of the ascending thoracic aorta (ATAmax), descending thoracic aorta (DTAmax), and abdominal aorta (AAmax) were measured using noncontrast computed tomography imaging. Aortic diameters are indexed to body surface area (BSA). Participants were divided into five groups according to CACS (0, 1-10, 10-100, 100-400, and >400). The mean ATAmax/BSA, DTAmax/BSA, and AAmax/BSA were 22.0±2.7, 16.3±1.9, and 13.0±2.9 mm, respectively. On multivariate analysis, ATAmax/BSA was associated independently with age, diabetes, and history of aortic valve replacement (all P<0.001). DTAmax/BSA was associated independently with age (P<0.001). However, there were no significant correlations between thoracic aorta diameter and CACS. In contrast, AAmax/BSA was associated independently with CACS as well as age and history of smoking (P=0.014, 0.003, and 0.019, respectively). Abdominal aortic aneurysm (>30 mm) was more prevalent in patients with a CACS of 400 or more compared with the others (14 vs. 3%, P<0.001). CACS was associated with increased abdominal aorta diameter, but not with thoracic aorta diameter. Therefore, screening for an abdominal aortic aneurysm is warranted in patients with a high risk of coronary artery disease and a high CACS. However, the necessity for thoracic aortic aneurysm screening is not clear in these patients.

Aortic Transgraft Hemorrhage after Intravenous Tissue Plasminogen Activator Therapy in Patients with Acute Ischemic Stroke

The safety of intravenous recombinant tissue plasminogen activator (IV tPA) therapy for patients with an aortic aneurysm or undergoing aortic graft replacement has not been established. We evaluated the incidence, bleeding site, coagulation factors, and clinical outcomes of patients treated with IV tPA for acute stroke. Between October 2005 and May 2013, 394 ischemic stroke patients were treated in our stroke center with IV tPA. Among these patients, we investigated those who had a history of aortic aneurysm with or without aortic graft replacement before IV tPA therapy and underwent computed tomography imaging. We compared the levels of D-dimer and hemoglobin (Hb) around IV tPA therapy between the patients with and without tPA-associated periaortic bleeding. Seven patients with a history of aortic aneurysm (3 men; mean age: 80.4 years) were examined; 3 had undergone aortic graft replacement, and 2 had experienced tPA-associated bleeding around vascular grafts. The serum D-dimer levels in those with bleeding were only slightly higher before tPA than in those without (median: 10.5 vs. 1.5 μg/mL) but were elevated 1 day after tPA (107.4 vs. 8.6 μg/mL). The Hb levels 2 days after tPA were comparable with those before tPA (11.9 vs. 11.8 g/dL) but were lower in the patients with bleeding than in those without (8.5 vs. 11.7 g/dL). Surgical intervention was not required, although 1 patient required blood transfusion. Our analysis provides reassurance regarding the risk of IV tPA therapy in patients undergoing aortic graft replacement.

Low yield of genetic testing for known vascular connective tissue disorders in patients with fibromuscular dysplasia

Patients with fibromuscular dysplasia (FMD) may have clinical features consistent with Mendelian vascular connective tissue disorders. The yield of genetic testing for these disorders among patients with FMD has not been determined. A total of 216 consecutive patients with FMD were identified. Clinical characteristics were collected and genetic test results reviewed for abnormalities in the following genes: transforming growth factor-β receptor 1 and 2 (TGFβR1 and TGFβR2), collagen 3A1, fibrillin-1, smooth muscle α-actin 2, and SMAD3. A total of 63 patients (63/216; 29.2%) were referred for genetic counseling with testing performed in 35 (35/63; 55.6%). The percentage of patients with a history of arterial or aortic dissection, history of aortic aneurysm, systemic features of a connective tissue disorder, and a family history of sudden death was significantly larger in the group that underwent genetic testing (62.9% vs 18.2%, p < 0.001; 8.6% vs 1.7%, p = 0.02; 51.4% vs 17.1%, p < 0.001; and 42.9% vs 22.7%, p = 0.04, respectively). Two patients were found to have distinct variants in the TGFβR1 gene (c.611 C>T, p.Thr204lle and c.1285 T>C, p.Tyr429His). The yield of genetic testing for vascular connective tissue disorders was low in a high-risk subset of FMD patients. However, two patients with a similar phenotype had novel and distinct variants in the TGFβR1 gene, a finding which merits further investigation.

Partial thrombosis of the false lumen in patients with acute type B aortic dissection. N Engl J Med. 2007;357:349-359

Background: Patency or thrombosis of the false lumen in type B acute aortic dissection has been found to predict outcomes. The prognostic implications of partial thrombosis of the false lumen have not yet been elucidated. Methods: We examined 201 patients with type B acute aortic dissection who were enrolled in the International Registry of Acute Aortic Dissection between 1996 and 2003 and who survived to hospital discharge. Kaplan-Meier mortality curves were stratified according to the status of the false lumen (patent, partial thrombosis, or complete thrombosis) as determined during the index hospitalization. Cox proportional-hazards analysis was performed to identify independent predictors of death. Results: During the index hospitalization, 114 patients (56.7%) had a patent false lumen, 68 patients (33.8%) had partial thrombosis of the false lumen, and 19 (9.5%) had complete thrombosis of the false lumen. The mean (±SD) 3-year mortality rate for patients with a patent false lumen was 13.7 ± 7.1%, for those with partial thrombosis was 31.6 ± 12.4%, and for those with complete thrombosis was 22.6 ± 22.6% (median follow-up, 2.8 years; P = 0.003 by the log-rank test). Independent predictors of postdischarge mortality were partial thrombosis of the false lumen (relative risk, 2.69; 95% confidence interval [CI], 1.45 to 4.98; P = 0.002), a history of aortic aneurysm (relative risk, 2.05; 95% CI, 1.07 to 3.93; P = 0.03), and a history of atherosclerosis (relative risk, 1.87; 95% CI, 1.01 to 3.47; P = 0.05). Conclusions: Mortality is high after discharge from the hospital among patients with type B acute aortic dissection. Partial thrombosis of the false lumen, as compared with complete patency, is a significant independent predictor of postdischarge mortality in these patients.

Perioperative spinal cord infarction in nonaortic surgery: report of three cases and review of the literature

Paraplegia caused by a spinal cord infarction (SCI) is a devastating perioperative complication, most often associated with aortic and spine surgery. We present two other clinical scenarios in which perioperative SCI may occur. They happened during surgical procedures performed with epidural anesthesia, in the presence of several specific risk factors such as spinal stenosis, vascular disease, intraoperative hypotension, or the use of epinephrine in the local anesthetic solution. Second, SCI may occur during episodes of postoperative hypotension in patients with a history of aortic aneurysms.

Partial thrombosis of the false lumen in patients with acute type B aortic dissection

Conclusion: After hospital discharge, patients with acute type B aortic dissection and partial thrombosis of the false lumen are at increased risk of death compared with patients with complete patency of the false lumen. Summary: The International Registry of Acute Aortic Dissection (IRAAD) tracks patients with acute aortic dissection at 22 aortic centers in 11 countries. This is a registry, and treatment during hospitalization is not standardized but is conducted at the discretion of each patient’s physician and institution. Patients with acute aortic type B dissection have low in-hospital mortality but survival rates after discharge range from 92% at 1 year to 48 to 82% at 5 years. It has been suggested that patients with complete thrombosis of the false lumen have improved outcomes compared with patients who have a patent false lumen, with the patent false lumen thought to place the patient at increased risk of aortic expansion and death (Am J Card 2001;87:1378-82). The authors sought to determine the influence on mortality of partial thrombosis of the false lumen. They defined partial thrombosis of the false lumen as both flow and thrombus present in the false lumen. Between 1996 and 2003, 201 patients with type B aortic dissection were enrolled in IRAAD and survived to discharge from the hospital. The authors developed mortality curves according to the status of the false lumen (complete thrombosis vs partial thrombosis vs patent). False lumen status was determined during the initial hospitalization. They used Cox proportional hazard analysis to identify independent predictors of death on follow-up. There were 114 patients (56.7%) who, during the index hospitalization, had a patent false lumen. Sixty-eight patients (33.8%) had partial thrombosis of the false lumen, and 19 (9.5%) had complete thrombosis of the false lumen. At 3 years, the mortality rate for patients with a patent false lumen was 13.7%. The mortality rate for patients with partial thrombosis of the false lumen was 31.6%, and mortality for those with complete thrombosis was 22.6% ± 22.6% (median follow-up, 2.8 years; P = .003, log-rank test). Postdischarge mortality was independently predicted by partial thrombosis of the false lumen (relative risk, 2.69; 95% confidence interval [CI], 1.45 to 4.98; P = .002), a history of atherosclerosis (relative risk, 1.87; 95% CI, 1.01 to 3.47; P < .05), and a history of aortic aneurysm (relative risk, 2.05; 95% CI, 1.07 to 3.93; P = .03). Comment: The authors postulate their findings may reflect that a patent false lumen is perfused by a proximal entry tear and then decompressed through re-entry tears distally. When thrombus partially occludes the lumen, these distal re-entry tears may be occluded, impeding outflow and leading to an increase in mean arterial and diastolic pressure that results in increased wall tension in the false lumen and increases the risk of aneurysm expansion, with increased risk of rupture and redissection.

Partial Thrombosis of the False Lumen in Patients with Acute Type B Aortic Dissection

Patency or thrombosis of the false lumen in type B acute aortic dissection has been found to predict outcomes. The prognostic implications of partial thrombosis of the false lumen have not yet been elucidated. We examined 201 patients with type B acute aortic dissection who were enrolled in the International Registry of Acute Aortic Dissection between 1996 and 2003 and who survived to hospital discharge. Kaplan-Meier mortality curves were stratified according to the status of the false lumen (patent, partial thrombosis, or complete thrombosis) as determined during the index hospitalization. Cox proportional-hazards analysis was performed to identify independent predictors of death. During the index hospitalization, 114 patients (56.7%) had a patent false lumen, 68 patients (33.8%) had partial thrombosis of the false lumen, and 19 (9.5%) had complete thrombosis of the false lumen. The mean (+/-SD) 3-year mortality rate for patients with a patent false lumen was 13.7+/-7.1%, for those with partial thrombosis was 31.6+/-12.4%, and for those with complete thrombosis was 22.6+/-22.6% (median follow-up, 2.8 years; P=0.003 by the log-rank test). Independent predictors of postdischarge mortality were partial thrombosis of the false lumen (relative risk, 2.69; 95% confidence interval [CI], 1.45 to 4.98; P=0.002), a history of aortic aneurysm (relative risk, 2.05; 95% CI, 1.07 to 3.93; P=0.03), and a history of atherosclerosis (relative risk, 1.87; 95% CI, 1.01 to 3.47; P=0.05). Mortality is high after discharge from the hospital among patients with type B acute aortic dissection. Partial thrombosis of the false lumen, as compared with complete patency, is a significant independent predictor of postdischarge mortality in these patients.

Inflammatory rheumatic disease and smoking are predictors of aortic inflammation: A controlled study of biopsy specimens obtained at coronary artery surgery

Several inflammatory rheumatic diseases are associated with accelerated atherosclerosis. Atherosclerosis may result from systemic and/or local vascular inflammation. The aim of this study was to evaluate the occurrence of chronic inflammatory infiltrates in the aortas of patients with and those without inflammatory rheumatic disease who had undergone coronary artery bypass graft (CABG) surgery, and to assess the relationship between the infiltrates and other factors thought to play a role in atherosclerosis, such as smoking. Aortic specimens routinely removed during CABG surgery in 66 consecutive patients with inflammatory rheumatic disease and 51 control patients without inflammatory rheumatic disease were examined by light microscopy for the occurrence, location, and severity of chronic inflammatory infiltrates and atherosclerotic lesions. Mononuclear cell infiltrates in the inner adventitia (apart from those localized along the epicardium) were more frequent in the group of patients with inflammatory rheumatic disease (47% versus 20%; P = 0.002, odds ratio [OR] OR 3.6, 95% confidence interval [95% CI] 1.6-8.5), and the extent of these infiltrates was greater. Multivariate analyses revealed that the occurrence of mononuclear cell infiltrates was associated with inflammatory rheumatic disease (OR 2.99, P = 0.020) and current smoking (OR 3.93, P = 0.012), and they were observed in 6 of 7 patients with a history of aortic aneurysm. Inflammatory infiltrates in the media were seen only in patients with inflammatory rheumatic disease. The frequency of atherosclerotic lesions, inflammation within the plaques, and epicardial inflammatory infiltrates in the 2 groups was equal. Among aortic samples collected during CABG surgery, those obtained from patients with inflammatory rheumatic disease had more pronounced chronic inflammatory infiltration in the media and inner adventitia than those obtained from control patients. Current smoking was an independent predictor of chronic inner adventitial infiltrates. The infiltrates may represent an inflammatory process that promotes atherosclerosis and formation of aneurysms.

Polymorphisms in the promoter regions of MMP-2, MMP-3, MMP-9 and MMP-12 genes as determinants of aneurysmal coronary artery disease.

Our hypothesis was that functional polymorphisms in matrix metalloproteinase (MMP) genes may act as susceptibility factors for the development of coronary aneurysms (CAs). Different forms of remodeling have been described at the level of coronary arteries; CA, reported in 1% to 5% of patients with angiographic evidence of coronary artery disease (CAD), are one of them. Matrix metalloproteinases have been implicated in the pathogenesis of aneurysm development through increased proteolysis of extracellular matrix proteins. We screened 3,862 patients who underwent coronary angiography and identified 113 patients with CAD with at least one CA (CA group); these patients were matched with 226 patients with CAD without CA (control group). The -1,306 C/T MMP-2, 5A/6A MMP-3, CA-repeat MMP-9 and -82 A/G MMP-12 polymorphisms were determined. The MMP-2, MMP-9 and MMP-12 polymorphisms were not associated with CA. By contrast, the 5A/5A genotype of MMP-3 was significantly more frequent in the CA group than in the control group (31% vs. 18%, p = 0.015); similarly, the MMP-3 5A allele was more frequent in the CA group (p = 0.009). Three variables were independently associated with CA: the MMP-3 5A/5A genotype (odds ratio [OR] = 2.23, 95% confidence interval [CI] [1.27 to 3.93]), a previous myocardial infarction (OR = 1.91, 95% CI [1.14 to 3.20]) and a history of aortic aneurysm (OR = 21.06, 95% CI [2.35 to 188]). The MMP-3 5A allele is associated with the occurrence of CA. Our results suggest that an increased proteolysis in the arterial wall may act as a susceptibility factor for the development of CA in patients with coronary atherosclerosis.