Calcification of the Arteries

Arterial Calcification

Peripheral Arterial Disease

Thickening of the Arteries is an indicator of Vascular Disease and Heart Attack and Stroke. Peripheral arterial disease (PAD) (note peripheral vascular disease is called PVD), is a very common condition affecting 12-20 percent of Australians age 65 and older.

​PAD   develops most commonly as a result of atherosclerosis, or “hardening of the arteries,”  which occurs when cholesterol and scar tissue build up, forming a substance called plaque inside the arteries that narrows and clogs the arteries. In the elderly we are now more commonly seeing calcified material that is similar to bone or a coral reef. Circumscribing large areas of the main aorta and its branches  and in many areas developing as large masses and clumps that occlude the lumen of the vessel.

 


The following article by Sage is worth perusing for the various mechanisms being explored that are likely to effect the deposition and distribution of calcium in the arteries

 

. A generation ago longevity was limited and this problem presented infrequently, most had died from more significant other complications. It is now becoming increasingly common and images of recent patients demonstrate the massive problem we as interventional surgeons are facing not only with coronary disease but whole body effects threatening the kidneys, gut, legs and pelvis.


Regulatory mechanisms in vascular calcification

Andrew P. Sage, Yin Tintut and Linda L. Demer

Abstract |

 

In the past decade, the prevalence, significance, and regulatory mechanisms of vascular calcification
have gained increasing recognition.

 

Over a century ago, pathologists recognized atherosclerotic calcification as a form of extraskeletal ossification. Studies are now identifying the mechanism of this remarkable process as a recapitulation of embryonic endochondral and membranous ossification through phenotypic plasticity of vascular cells that function as adult mesenchymal stem cells.

 

These embryonic developmental programs, involving bone morphogenetic proteins and potent osteochondrogenic transcription factors are triggered and modulated by a variety of inflammatory, metabolic, and genetic disorders, particularly hyperlipidemia, chronic kidney disease, diabetes, hyperparathyroidism, and osteoporosis. They are also triggered by loss of powerful inhibitors, such as fetuin A, matrix Gla protein, and pyrophosphate, which ordinarily restrict biomineralization to skeletal bone. Teleologically, soft-tissue calcification might serve to create a wall of bone to sequester noxious foci such as chronic infections, parasites, and foreign bodies. This Review focuses on atherosclerotic and medial calcification. The capacity of the vasculature to produce mineral in culture and to produce de novo, vascularized, trabecular bone and cartilage tissue, even in patients with osteoporosis, should intrigue investigators in tissue engineering and regenerative biology.


Sage, A. P. et al. Nat. Rev. Cardiol. 7, 528–536 (2010); published online 27 July 2010; doi:10.1038/nrcardio.2010.115


A paper from Cleveland clinic has demonstrated that with IVUS studies STATIN drugs have been shown to be associated with increased calcification in the coronary arteries with a little unassociated regression of soft plaque. Quick comments by physicians to protect statins suggested that this might stabilise plaque but as Sage has suggested in his article the interfaces between hard and soft areas (& see images) are likely to be a source of vulnerability.

Introduction by Sage


In 2009, a  meta-analysis of 30 prospective cohort studies demonstrated the consistent finding that presence of vascular calcification poses an increased risk of cardiovascular and all-cause mortality.

 

 In coronary arteries, plaque independently predicts a 1.7-fold increase in mortality. When coronary calcification is extensive, mortality is increased 60-fold.

 

Calcification of peripheral arteries also independently predicts mortality,as well as risk of amputation.

By far, the most-extensive vascular calcification occurs in patients with chronic kidney disease  followed by those with type II diabetes mellitus. Nevertheless, nearly all patients with cardiovascular disease have some degree of calcification and, in asymptomatic adults, prevalence of coronary calcification corresponds roughly with age; among 60-year-olds, approximately 60% have calcific vasculopathy.

Controversy remains with respect to whether vascular calcification is a cause or consequence of cardio vascular disease. Most likely, it is both; a consequence, in that atherosclerosis induces cellular osteogenic differentiation; and a cause, in that vascular calcification stiffens the aorta and affects plaque stability.

 Calcium deposits might affect plaque stability by introducing compliance mismatch at the interface of the rigid mineral with the more distensible artery wall tissue. Under mechanical stress, this interface has an increased risk of mechanical failure (plaque rupture). Such plaque rupture is believed to cause most myocardial infarction and stroke events. Finite element analysis has demonstrated that calcium deposits dramatically redistribute stress in plaque, reducing it in some regions at the cost of increasing it in others.

 

 The net effect of calcium deposition
on risk of rupture depends on the anatomic orientation of the calcium deposits relative to the plaque and any necrotic core. Aortic rigidity—the most insidious effect of vascular calcification—results in hypertension,left ventricular hypertrophy, ischemia, heart failure, amputation, and death.

Much can be done to improve the blood flow in these cases with endovascular procedures using Duplex ultrasound, Angiography, Angioplasty, Stents, Stent Grafts and Drug Eluting Balloons but as the disease progresses there comes a time that instruments may not penetrate the calcium and if the material is extreme standard surgery is excluded as the vessels are unable to be clamped, and there are no places to attach a graft either superiorly or inferiorly.

 

RECENT REPORT

The Following report coordinated from John Hopkins University supports the data from Prof Reid in New Zealand demonstrating a significant risk of ionic calcium supplements, whereas a higher intake of food based calcium was found to be associated with lower risk

 

Calcium Intake From Diet and Supplements and the Risk of Coronary Artery Calcification and its Progression Among Older Adults:

10-Year Follow-up of the Multi-Ethnic Study of Atherosclerosis (MESA)


John J.B. Anderson, PhD; Bridget Kruszka, MPH; Joseph A.C. Delaney, PhD; Ka He, MD, ScD; Gregory L. Burke, MD, MSc; Alvaro Alonso, MD, PhD; Diane E. Bild, MD, MPH; Matthew Budoff, MD; Erin D. Michos, MD, MHS, FACC, FAHA


Background-

 

Recent randomized data suggest that calcium supplements may be associated with increased risk of cardiovascular disease (CVD) events.

 

Using a longitudinal cohort study, we assessed the association between calcium intake, from both foods and supplements, and atherosclerosis, as measured by coronary artery calcification (CAC).


Methods and Results

 

We studied 5448 adults free of clinically diagnosed CVD (52% female; aged 45–84 years) from the Multi-Ethnic Study of Atherosclerosis. Baseline total calcium intake was assessed from diet (using a food frequency questionnaire) and calcium supplements (by a medication inventory) and categorized into quintiles. Baseline CAC was measured by computed tomography, and CAC measurements were repeated in 2742 participants 10 years later. At baseline, mean calcium intakes across quintiles were 313.3, 540.3, 783.0, 1168.9, and 2157.4 mg/day. Women had higher calcium intakes than men.

 

After adjustment for potential confounders, among 1567 participants without baseline CAC, the relative risk (RR) of developing incident CAC over 10 years, by quintile 1 to 5 of calcium intake, were 1 (reference), 0.95 (0.79–1.14), 1.02 (0.85–1.23), 0.86 (0.69–1.05),
and 0.73 (0.57–0.93).

 

After accounting for total calcium intake, calcium supplement use was associated with increased risk for incident CAC (RR=1.22 [1.07–1.39]). No relation was found between baseline calcium intake and 10-year changes in log transformed
CAC among those participants with baseline CAC >0.


Conclusions

 

High total calcium intake was associated with a decreased risk of incident atherosclerosis over long-term followup, particularly if achieved without supplement use.

 

However, calcium supplement use may increase the risk for incident CAC.


( J Am Heart Assoc. 2016;5:e003815 doi: 10.1161/JAHA.116.003815)
Key Words: calcium • cardiovascular imaging • coronary artery calcium • diet • epidemiology

 Surgery  gives better results in the groin region where we often find large masses of occlusive calcium and stents are prone to fracture and failure at this site. Often we can combine Surgical and EndoVascular procedures using  Xray in the operating theatre, Special “Hybrid” theatres are being developed  to facilitate this and some will have CT scans incorporated to allow assessment during spinal surgery particularly where this involves combined vascular reconstruction.

Particularly in Combined arrangements with Spinal and Vascular Surgeons  we have developed procedures that can resolve both the spinal and the vascular components and give a solution that can reduce Multiple Major Surgeries (e.g. aortic aneursym and multiple anterior disk reconstructions)  to a Single Operation