Porcelain Aorta

Article Author:
Anan Abu Rmilah

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F Brian Boudi

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Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi

2/1/2019 12:09:43 AM


Porcelain aorta is a structural aortic wall disease characterized by an extensive heavy calcification of the ascending thoracic aorta extending to the aortic arch and descending aorta. The calcification occurs in a diffuse complete or near complete circumferential pattern involving, predominantly, the anterior wall of the ascending aorta and the superior wall of the aortic arch.[1][2]


Calcium deposition in PA can be located in the tunica intima, starting at the base of atherosclerotic plaques, which is known as the atherosclerotic type. While in non-atherosclerotic type, calcification usually happens in the tunica media of the aortic wall.[2]

Furthermore, PA can also be classified into two main types based on the site of calcification in the thoracic aorta as follows:

  1. Type I - implies the localization of circumferential calcification of the ascending aorta independent of further extensions. This type is subdivided into two subtypes according to the assessment of clamping possibility of the aorta during cardiac surgery by a calcification score proposed by Nishi et al.[3] and defined as the ratio of the circumferential length of calcification to the entire ascending aortic circumference.[2]
    1. Type IA in which the calcification score is above 75%, impeding the possibility of aorta clamping during cardiac surgeries[2]
    2. Type IB shows a calcification score below 75%, allowing the possibility to clamp the aorta but with increased risk[2]
  2. Type II - refers to the calcification localized only in the aortic arch and/or descending aorta.[2]


Porcelain aorta is a relatively rare entity in the general population, but its incidence has been recently increasing in older patients above 60 years old and in patients with coronary artery disease (CAD) or aortic stenosis (AS). The reported incidence rate ranges from 1% to 20% based on different studies. Leyh et al. found that 23 out of 1861 (1.2%) patients who underwent coronary artery bypass grafting (CABG) had PA.[4] PA was also detected in 15.1% (54 of 358) of patients enrolled in an inoperable cohort of PARTNER (Placement of AoRTic TraNscathetER Valves) trial.[5] Rodes-Cabau et al.reported TAVR procedures in 339 patients, and PA was present in 61 of 339 patients (18%).[6] FRANCE-2 TAVI Registry and German TAVI Registry published PA incidence rates of 5% and 11% respectively.[7][8] Faggiano et al. also evaluated 240 patients for aortic stenosis (AS) and noted that 7.5% (18/240) had porcelain aorta.[9]

Several studies have reported discordant results for gender differences in the prevalence of PA. The evaluation of PA among the heterogenic population has revealed some discrepancies in sex distribution, showing a male predominance in some[10][11] and a female predominance in others.[12][13][14] Moreover, a series of patients with PA who underwent transaortic valve replacement (TAVR) for severe aortic stenosis (AS) demonstrated a female predominance (52.8% to 75.4%).[6][8][15] On the other hand, there is a substantial male predominance in PA prevalence among patients who underwent coronary revascularization surgery.[16]


The exact cause of PA is still elusive, but two pathophysiological processes have been described in the pathogenesis of this condition. These mechanisms allowed us to divide PA into the following two entities:

Atherosclerotic PA

It is characterized by calcification of tunica intima of the aortic wall as a result of atherosclerotic plaques development. These atheromatous lesions are induced by an endothelial inflammatory injury that activates the endothelial cells to express adhesion molecules that attract inflammatory cells mainly monocytes and T lymphocytes into the subendothelial intima. These monocytes undergo a specific differentiation into macrophages which phagocytose the modified lipoproteins producing foam macrophages. The activated macrophages secrete cytokines to recruit more inflammatory cells and growth factors that induce the proliferation of inflammatory cells as well as vascular smooth muscle cells (VSMCs) and endothelial cells. This, in turn, stimulates the migration of VSMCs from the tunica media into the tunica intima. The intimal VSMCs proliferate and ingest lipoproteins forming lipid-laden VSMCs. The layers of foam macrophages and lipid-laden VSMCs are collectively known as fatty streaks which are designated as an early sign of stable atherosclerosis. The advanced, stable atherosclerosis is characterized by further enlargement of fatty streaks and secretion of extracellular matrix proteins by VSMCs, forming a fibrous cap that covers the lesion. This is followed by apoptosis of foam macrophages, leading to necrosis of VSMCs and degradation of extracellular matrix proteins, thus producing a necrotic core which is associated with the advanced unstable lesion. The destabilization of atheromatic plaques increases the liability of getting ruptured, resulting in platelets accumulation at the site of rupture and formation of atherothrombosis that occludes the artery.[1]

Nonatherosclerotic PA

In this type, calcification takes place in the tunica media of the aortic wall in the absence of atherosclerosis. It is induced by vascular inflammation, radiation, and uremia via triggering a metaplastic transformation of VSMCs into osteoblasts leading to the production of bone-associated proteins such as alkaline phosphatase, bone sialoprotein, bone GLa protein, and bone morphogenic protein 2. In cases of vascular inflammation and aging, apoptotic vesicles arising from dead VSMCs, and elastin degradation mediated by matrix metalloprotease will act as a nidus for medial calcification by sending a paracrine osteogenic signal that will provoke the aortic calcium deposition as well as the collagen deposition and loss of the elastic fibers causing an arterial wall stiffness.[1][17]

Multiple risk factors have been implicated in PA in literature reviews. The factors that are commonly involved in both types are a familial factor, aging, diabetes mellitus (DM), radiation, uremia, and Takayasu arteritis. Whereas, the atherosclerotic type is associated with additional factors such as hypertension, hyperlipidemia, smoking, alcoholism, sedentary lifestyle, obesity, systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA).[1]


Porcelain aorta (PA) is an asymptomatic condition that usually appears as an incidental finding in patients being evaluated for cardiovascular or pulmonary diseases.[1]

Different diagnostic tools have been suggested to diagnose porcelain aorta and evaluate its extent and exact location before any cardiac intervention. The most accurate modality is a multislice computed tomography (MSCT). It is used to accurately diagnose PA and give valuable information about the exact level and site of aortic calcification, thereby distinguishing PA (circumferential calcification) from a less extensive aortic calcification. Furthermore, a 3-dimensional (3D), volume-rendered reconstructions of MSCT images can be done to allow 3D mapping of the aortic wall, thus providing us with useful information about the three-dimensional distribution of the calcification.[1][2][18][19][20]

Other modalities include:

  • Chest X-ray which may occasionally reveal a calcification in the thoracic aorta, but it is not accurate in defining PA.
  • Fluoroscopy during coronary angiography is somehow sensitive in detecting an aortic calcification that suggests PA, however, it lacks the precision in assessing the distribution and localization of this calcification.

On the other hand, there is no doubt that PA is highly recognized during the cardiac surgery by performing an epiaortic echocardiographic scanning of the aorta in conjunction with a manual palpation after sternotomy and exposure of the aorta. Such testing confirms the presence of PA as well as its extent and exact location.[1][2][18][19][20]

Treatment / Management

During any cardiac procedure, the need for advanced surgical techniques in patients with concomitant PA is mandatory to avoid manipulation of the heavily calcified aorta thus preventing unfavorable consequences such as atheroembolism from the calcified aorta leading to stroke and systemic embolism.

Porcelain Aorta During Coronary Bypass Surgery (CABG)

Patients with PA demonstrate an increased rate of morbidity and mortality during CABG operation because of the elevated risk of embolic stroke from the atheromatous heavily calcified aorta. Such complication usually takes place during manipulation of the diseased aorta in three different maneuvers in CABG: (1) cannulation of the aorta, (2) cross-clamping, and (3) partial clamping for construction of the proximal anastomosis.[4] 

Several amendments have been described to avoid cannulation and clamping of the porcelain aorta including no touch technique or aortic off-pump CABG[1][16][18][21][22][21]; CABG performed during deep hypothermic circulatory arrest (DHCA)[1][4][16][23]; femoral or axillary artery cannulation for cardiopulmonary bypass[1][4][16][24]; placement of proximal saphenous vein (SV) grafts onto the internal mammary artery (IMA), onto the innominate artery, onto the axillary artery, or onto the carotid artery[1][4][16][25][26]; single clamp technique[1][4][16][27]; intraluminal balloon catheter as a substitute for external clamps[1][4][16][28]; ascending aorta endarterectomy[1][4][16][29][30]; patch aortoplasty[1][4][16][31]; and graft replacement of the ascending aorta[1][4][16]

The most common and effective recent modality is "no touch technique" or aortic off-pump CABG (OPCABG) in which cannulation and clamping of the ascending aorta are averted. This technique is performed on the beating heart without the use of the heart-lung machine and, so-called, off-pump or beating heart CABG. It is achieved by an arterial grafting using bilateral internal mammary grafts in addition to radial artery or reverse saphenous venous grafts, forming a T or Y shaped graft that will be connected to the innominate artery or common carotid artery that will act as the inflow source, thereby bypassing the blockage area without touching the diseased aorta.[1][18][21][16][22] Lev-Ran eet al.[16] performed a retrospective analysis and comparison of the results of CABG with femoral artery cannulation in 15 patients and off-pump CABG in 41 patients with PA. He found that off-pump CABG group has only 1 case of perioperative mortality (2.4%) and no cases of perioperative stroke or transient ischemic attack. While in CABG with femoral cannulation, there was 1 case of perioperative mortality (6.6%) and 3 cases of perioperative strokes or transient ischemic attacks (20%). These results reveal that the off-pump technique has a beneficial impact in reducing the risk of perioperative mortality and stroke compared to the conventional CABG procedure. However, the major drawback of this technique in their study was the failure to achieve a complete revascularization in 24.3% of patients in contrast to the lower rate in the conventional CABG group. 

If there is a small non-calcified area confirmed by epiaortic ultrasound, a safe proximal anastomosis construction can be done using a proximal seal system.[1][25][21][16] to allow the surgeon to perform an anastomosis between the graft and the aorta without the need to do an aortic clamping. Hilker and his colleagues[32] published a study that reveals a stroke rate of 0.48% of 412 patients in which 542 had proximal anastomoses using Heartstring device during OPCABG were performed. Dohmen G et al [21] reported 25 successful PAS-Port® anastomoses in 17 patients undergoing CABG. It was shown that 8 patients had porcelain aorta. Two of them developed neurological deficits (prolonged reversible ischemic neurological deficits, (PRIND)) after the procedure. 

The other beneficial method is performing CABG during deep Hypothermic circulatory arrest (DHCA). In this practice, myocardial revascularization is performed using moderate hypothermia with a core temperature of 28-32°C for up to 40 minutes without harming the patient. In this case, a sufficient time is given for the surgeon to perform safe proximal anastomoses without placing clamps on the aorta, and so minimizing the rate of cerebral complications.  Salenger et al.[23] studied the outcome of this approach in 71 patients and found that one patient (1.4%) developed a mild stroke which resolved afterward. (D. Damodar Reddy, H. Storm Floten, and Hugh L. Gately) [26] analyzed six patients that are not suitable for clamping due to the severely calcified aorta. A deep hypothermic circulatory arrest for proximal anastomosis was conducted in all patients with complete recovery free of neurological problems.

Ascending aorta is the usual cannulation site in cardiac surgery[18]. The existence of a porcelain aorta precludes the conventional arterial cannulation[18]. Therefore, a convenient cannulation site should be chosen for safe surgery. Several sites have been proposed and the classic approach is performing an arterial perfusion via the common femoral artery (CFA) because it can be done easily but carries the risk of embolization from the atherosclerotic thoracic and abdominal aorta due to retrograde perfusion. If the CFA is atherosclerotic and cannot be used for cannulation, the alternative location will be through the axillary artery[25]. Perfusion through the axillary artery has the following advantages: 1) It carries a lower risk of cerebral embolization, the rate of atherosclerosis is less than that of the ascending aorta or the femoral artery, and 3) the risk of severe distal ischemic-reperfusion injury or embolization after cannulation is decreased due to the presence of abundant collaterals. However, axillary artery cannulation can be accompanied with several local complications, including axillary artery dissection, thrombosis, and brachial plexus injury [25].

Svensson et al.[24] conducted an arterial perfusion via the axillary side graft in 299 patients and femoral artery in 375 patients. They observed that the stroke occurred in 4% (12/299) of the axillary side graft group and 6.7% (25/375 patients) of the femoral artery group. The risk of hospital mortality was higher with femoral perfusion (11%, 42/375 patients) than axillary side graft perfusion (7.0%, 21/299). 

Cannulation via the brachiocephalic artery could also be a feasible option in patients with porcelain aorta. Banbury et al. endorsed that brachiocephalic arterial cannulation is a good alternative in cases whose aorta cannot be manipulated. This option can avoid making a second incision in axillary artery cannulation or retrograde perfusion issues in femoral artery cannulation [25].

Porcelain Aorta During Mitral Valve Surgery 

Hypothermia and a fibrillating heart have been considered a good technique to avoid an aortic cross-clamping in mitral valve surgeries performed in patients with porcelain aorta [1][25][27]. Loulmet et al. reported outstanding results of using hypothermia and a fibrillating heart method during mitral valve surgeries in patients with PA [28]

Porcelain Aorta and Aortic Stenosis 

Strategies like deep hypothermic circulatory arrest, the apico-aortic conduit technique have been proposed in the scholarly literature to avoid a cross-clamping of the aorta during surgical aortic valve surgery in patients with aortic stenosis and porcelain aorta[1][25][21]. Unfortunately, these methods are technically challenging, require significant surgeon experience, and don't completely avoid manipulation of the PA [1]

 Another new promising invention is transcatheter aortic valve replacement (TAVR) or transcatheter aortic valve implantation (TAVI). It is a minimally invasive procedure to replace the aortic valve in high surgical risk patients with severe aortic stenosis. Patients having PA will benefit from this approach via replacing the aortic valve without an aortic cross-clamping. Multiple articles have published excellent results of utilizing this technique in these patients [1][25][21]. Rodés-Cebau et al.[6] described the results of the TAVR procedure in 339 patients, including 61 patients (18%) with a porcelain ascending aorta. The procedure was successful in 98.4% of the patients with porcelain aorta. The stroke rate and 30-day mortality rate were 1.6% (1/61 patients) and 11.5% (7/61 patients), respectively, showing no differences from patients without porcelain aorta. Pascual et al. stated that 449 patients underwent TAVR, of which 36 patients  (8%) had a porcelain ascending aorta. The procedure was successful in 94.4%. The stroke rate and 30-day mortality rate were 2.8% (1/36 patients) and 5.6% (2/36 patients), respectively, which are similar to patients without porcelain aorta.


Challenges in porcelain aorta (PA):

PA is highly associated with valvular and coronary calcification, thus increasing the risk of valvular stenotic disorders and ischemic heart diseases due to coronary atherosclerosis in these patients. Furthermore, a severe calcification of the aorta narrows down its lumen and increases the resistance to the blood flow coming out from the left ventricle, and so it exerts too much load on the heart that results in the development of hypertension, hypertrophy cardiomyopathy, congestive heart failure and arrhythmia over time. PA is also listed in the second consensus document of the Valve Academic Research Consortium as a risk factor in aortic valve replacement [19]. Eisen et al [29] reported that 253 out of 361 patients (70%) with stable angina pectoris have also porcelain aorta. Jacobs et al [30] also investigated the impact of PA on the development of cardiovascular events in 1723 patients and found that PA has increased these events by a factor of 2.7 compared to non-PA patients. 

PA significantly increases the morbidity and mortality in patients undergoing cardiac surgeries [18]. It is considered as a challenging issue for cardiac surgeons and interventional cardiologists because it precludes and complicates the aortic cannulation, aortic clamping, aortotomy, and central coronary bypass anastomosis, thereby raising substantially the complexity and the risks associated with cardiac procedures particularly cardiopulmonary bypass graft (CABG) and aortic valve replacement procedures. This, in turn, necessitates the employment of advanced surgical techniques to minimize the manipulation of the heavily calcified aorta because clamping of the diseased aorta may cause an excessive aortic injury and/or release of thromboembolic material, thus increasing the risk of embolic stroke and systemic embolism [17]. Van der Linden et al [31] noticed that 26.2% of 921 patients who underwent a cardiac surgery had PA. The incidence of postoperative stroke was 1.8% in patients without and 8.7% in patients with PA. The risk of stroke significantly increased to 33% with extensive involvement of more than half of the ascending aorta.

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Porcelain Aorta - Questions

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Which of the following is considered inappropriate for a 60-year-old with porcelain aorta and coronary artery disease?

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A calcified, rigid aorta, often seen in elderly people, requires an increased cardiac performance for an adequate cardiac output because it:

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A 45-year-old female presented to the Emergency Department suffering from chest pain, dyspnea, and hemoptysis. She endorsed smoking two packets per day and drinking alcohol two times a week. Her vital signs were unremarkable. Blood samples were withdrawn for biochemical testings. CBC shows a hemoglobin level of 10 mg/dl, hematocrit level of 34%, MCV equals 95 fl and MCH is 30 pg. Her EKG revealed normal sinus rhythm without any abnormalities. Blood chemistry tests showed low serum osmolarity and hyponatremia. Imaging studies including chest x-ray and chest CT scan were consistent with bilateral lower lobar lung nodules with deposits appeared in the mediastinal lymph nodes. A bronchoscopic biopsy was performed, and histological findings were consistent with small cell lung cancer with metastasis to mediastinal lymph nodes and the contralateral lung in association with the syndrome of inappropriate secretion of antidiuretic hormone. Therefore, the patient started with intense chemotherapy accompanied by radiotherapy. A few months later, the patient came to the hospital for a follow-up CT scan that showed a severe calcification in the thoracic aorta which was regarded as porcelain aorta. Which of the following factor plays a role in mediating this calcification?

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A 75-year-old male with a history of asymptomatic aortic stenosis, hypertension and diabetes mellitus was brought to the emergency department by the ambulance after experiencing an episode of syncope. He stated that he developed substernal chest discomfort and shortness of breath before fainting. On examination, his vital signs looked normal, whereas the cardiac auscultation revealed an increased intensity of the ejection systolic, crescendo-decrescendo murmur at the upper right sternal border, and the second right intercostal space associated with a systolic thrill and radiation to carotid arteries bilaterally. EKG was essentially normal. Echocardiography showed an aortic valve area of 0.8 cm2 and mean aortic valve pressure gradient of 50 mmHg. Based on these findings a diagnosis of symptomatic severe aortic stenosis was considered and valve replacement intervention was decided. CT angiography was performed as a part of the preoperative evaluation process and was notable for a severe calcification in the thoracic aorta. What is the best approach to replace the aortic valve in this patient?

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Porcelain aorta can be classified into several types based on multiple parameters. Which of the following statements describes the classification of PA correctly?

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Porcelain Aorta - References


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