Two-dimensional echocardiography is increasingly used to measure aortic root dimensions, which provide prognostic information in aortic regurgitation and the Marfan syndrome. Aortic root dilatation is currently detected by nomograms based on M-mode echocardiographic data. Aortic root diameters measured by 2-dimensional echocardiography at the anulus, sinuses of Valsalva, supra-aortic ridge and proximal ascending aorta in 135 normal adults and 52 normal children were compared with age, gender, body habitus, blood pressure and stroke volume, and with M-mode findings and normal limits. Two-dimensional measurements at the sinuses of Valsalva were larger than M-mode aortic root values (p less than 0.001), and use of 2-dimensional values with M-mode nomograms falsely diagnosed aortic dilatation in 40% of normal children and 19% of normal adults. Two-dimensional measurements at the sinuses closely correlated with body surface area in children (r = 0.93, p less than 0.0005), moderately in adults younger than 40 years of age (r = 0.71, p less than 0.0005) and weakly in older adults (r = 0.40, p less than 0.0005). In adults, gender influenced aortic root size at all levels (p less than 0.001), but dimensions were similar when indexed for body surface area. Age strongly influenced supraaortic ridge and ascending aortic diameters; blood pressure and stroke volume had no independent effect on aortic size. In conclusion, (1) 2-dimensional echocardiographic aortic root dimensions are influenced by age and body size but not by blood pressure; (2) aortic root dilatation is overdiagnosed when aortic diameter at the sinuses of Valsalva is compared with M-mode nomograms; (3) nomograms comparing aortic diameter with body surface area should be used in children; and (4) although use of nomograms based on body size in adults should maximize sensitivity for aortic dilatation, 98% specificity is attained by use of an upper normal limit of 2.1 cm/m2 for aortic diameter at the sinuses of Valsalva in both men and women.

Two-dimensional echocardiographic aortic root dimensions in normal children and adults.

Among 161 necropsy cases of aortic dissection, 87 (54%) were type I, 34 (21%) type II, and 40 (25%) type III, and an intimal tear was identified in each. Systemic hypertension had been present in 63 of 121 cases (52%) with type I or II dissection and in 30 of 40 (75%) with type III dissection. Aortic dissection involved 7 of 16 cases (44%) with the Marfan syndrome. In the 154 cases without the Marfan syndrome, grade 3 or 4 medial degeneration (cystic medial necrosis) was observed in the ascending aorta in only 27 (18%). The risk of aortic dissection in persons with congenitally bicuspid and unicommissural aortic valves, respectively, was 9 and 18 times that in subjects with tricuspid aortic valves. The mean age of those with aortic dissection and tricuspid, bicuspid and unicommissural aortic valves was 63, 55 and 40 years, respectively, and aortic dissection was more common in men than in women. Grade 3 or 4 atherosclerosis involved the intimal tear in only 11 of 121 type I or II dissections (9%) but 32 of 40 type III dissections (80%). Accordingly, the major risk factors for aortic dissection were systemic hypertension, the Marfan syndrome, and, for type I and II dissections, congenitally bicuspid or unicommissural aortic valves. Aortic medial degeneration was a less important risk factor. Rupture of ulcerocalcific aortic atheromas may have initiated the intimal tear in some type III dissections.

Risk factors for aortic dissection: A necropsy study of 161 cases

https://www.annalsthoracicsurgery.org/article/S0003-4975(07)02254-0/pdf

Expert consensus document on the treatment of descending thoracic aortic disease using endovascular stent-grafts.

Vascular smooth muscle cells (VSMCs) are the stromal cells of the vascular wall, continually exposed to mechanical signals and biochemical components generated in the blood compartment. They are involved in all the physiological functions and the pathological changes taking place in the vascular wall. Owing to their contractile tonus, VSMCs of resistance vessels participate in the regulation of blood pressure and also in hypertension. VSMCs of conduit arteries respond to hypertension-induced increases in wall stress by an increase in cell protein synthesis (hypertrophy) and extracellular matrix secretion. These responses are mediated by complex signalling pathways, mainly involving RhoA and extracellular signal-regulated kinase1/2. Serum response factor and miRNA expression represent main mechanisms controlling the pattern of gene expression. Ageing also induces VSMC phenotypic modulation that could have influence on cell senescence and loss of plasticity and reprogramming. In the early stages of human atheroma, VSMCs support the lipid overload. Endocytosis/phagocytosis of modified low-density lipoproteins, free cholesterol, microvesicles, and apoptotic cells by VSMCs plays a major role in the progression of atheroma. Migration and proliferation of VSMCs in the intima also participate in plaque progression. The medial VSMC is the organizer of the inwardly directed angiogenic response arising from the adventitia by overexpressing vascular endothelial growth factor in response to lipid-stimulated peroxisome proliferator-activated receptor-γ, and probably also the organizer of the adventitial immune response by secreting chemokines. VSMCs are also involved in the response to proteolytic injury via their ability to activate blood-borne proteases, to secrete antiproteases, and to clear protease/antiprotease complexes.

The vascular smooth muscle cell in arterial pathology: a cell that can take on multiple roles.

ContextArterial stiffness increases with age. Thus, pulse
pressure, an index of arterial stiffening, may predict congestive heart
failure (CHF) in the elderly.ObjectiveTo study prospectively the association between pulse
pressure and risk of CHF.DesignProspective cohort study.SettingThe community-based East Boston Senior Health Project,
East Boston, Mass.PatientsA total of 1621 men and women (mean [SD] age, 77.9
[5.0] years) free of CHF who had blood pressure measurements taken in
1988-1989 and were followed up for 3.8 years.Main Outcome MeasureIncidence of CHF as ascertained by hospital
discharge diagnosis (n=208) and death certificates
(n=13).ResultsAfter controlling for age, sex, mean arterial pressure,
history of coronary heart disease, diabetes mellitus, atrial
fibrillation, valvular heart disease, and antihypertensive medication
use, pulse pressure was an independent predictor of CHF. For each 10-mm
Hg elevation in pulse pressure, there was a 14% increase in risk of
CHF (95% confidence interval, 1.05-1.24;
P=.003). Those in the highest tertile of pulse
pressure (>67 mm Hg) had a 55% increased risk of CHF
(P=.02) compared with those in the lowest
(<54 mm Hg). Pulse pressure was more predictive than systolic blood
pressure alone and was independent of diastolic blood pressure.ConclusionPulse pressure, an easily measurable correlate of
pulsatile hemodynamic load, is an independent predictor of risk of CHF
in this elderly cohort.

https://jamanetwork.com/journals/jama/articlepdf/188787/joc80370.pdf

Increased pulse pressure and risk of heart failure in the elderly.

The histologic changes that occur in the media of the normal aorta at various ages were studied in 100 normal aortas. These changes encompassed (1) cystic medial necrosis, defined as pooling of mucoid material; (2) elastin fragmentation, characterized by disruption of elastin lamellae; (3) fibrosis, defined as an increase in collagen at the expense of smooth muscle cells; and (4) medionecrosis, defined as areas with apparent loss of nuclei. The changes showed a striking correlation with age and may represent the normal aging process for the aorta as determined histologically. The alterations showed a close relation in onset and location within the media, suggesting a phenomenon of injury and repair caused by hemodynamic events. These findings in the normal aging aorta reveal that none of the histologic changes observed can be regarded as the specific structural alteration responsible for the development of dissecting aneurysm.

Histologic changes in the normal aging aorta: Implications for dissecting aortic aneurysm

In a previous investigation of the normal aging aorta, the claimed specificity of alterations in the media in the pathogenesis of dissecting aneurysm of the aorta was challenged The concept was promoted that these changes are nonspecific and caused by general hemodynamic events within the aorta In this investigation the aortic media was studied in patients with a dilated ascending aorta, whose hemodynamic profile is known to be altered The results were compared with data obtained from the study of aortas with complete or incomplete dissection and aortas from patients with Marfan's syndrome, a condition known to predispose to dissection Only quantitative differences were found between the normal “aging” aorta and the overtly abnormal aorta The pathogenesis of dissecting aneurysm, therefore, is considered to be initiated by processes of injury and repair within the aortic wall, consequent to hemodynamic forces The histologic features of the media previously implicated as the specific underlying defect appear to represent the morphologic substrate of this traumatizing and reparative process This process may gradually lead to dilatation of the aorta and, according to Laplace's law, a vicious cycle may ensue that may lead to further complications Local circumstances determine whether a dilated aorta will rupture or whether an incomplete or complete dissection will occur The fact that the aorta in patients with Marfan's syndrome shows basically the same structural alterations supports the concept proposed The underlying connective tissue disorder in these patients will lead to complications at an earlier age Dissecting aneurysm therefore is part of a spectrum of lesions that have as a common denominator the process of injury and repair

Thomas J.M. Schlatmann

Papers

Histologic changes in the normal aging aorta: Implications for dissecting aortic aneurysm

Pathogenesis of dissecting aneurysm of aorta: Comparative histopathologic study of significance of medial changes