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Calcification of the Arteries

By Jonas Wilson, Ing. Med.

Arterial calcification is a gradual and progressive process that is seen in most people after the 6th decade of life. This results in a reduction of arterial elasticity and an increased propensity for morbidity and mortality due to the impairment of the cardiovascular system’s hemodynamics.

Implicated in this impairment as a direct consequence of the calcification are aortic stenosis (narrowing), hypertension (high blood pressure), congestive heart failure, cardiac hypertrophy (enlarged heart), myocardial ischemia, and general compromised structural integrity of the heart.

Arterial calcification consists mainly of apatite calcium salt precipitates, similar to hydroxyapatite, which is found in bone. There are several risk factors associated with the pathogenesis of vascular calcification. Older age, African descent, no college education, high total cholesterol, smoking, and hypertension are the risk factors associated with arterial calcification.

Several proteins have also been identified in playing a role in the development of vascular calcification. Some of the proteins are inhibitory, while others are activating.

Failure in the compliance and elasticity of the aorta (the main artery in the body) leads to congestive heart failure due to the resultant increased workload placed on the heart. The increased load on the heart also results in increased left ventricular size and diastolic dysfunction. Calcification of the aortic valve results in aortic narrowing, a life-threatening condition.

Calcium deposits also cause weakening of the vasomotor responses. The ultimate result is a compliance mismatch within the cardiovascular system that leads to early mechanical failure.

Histological, anatomical, and etiological considerations are used in order to categorize the different types of arterial calcifications. Amorphic, chondromorphic, or osteomorphic are the classifications on a histological basis, whereas metastatic (diffuse calcification) or dystrophic (not metastatic) are used to determine etiology. Anatomically, the calcifications may be intimal or medial, which occur in a patchy or diffuse pattern, respectively.

Co-morbidities Associated with Arterial Calcification

Patients with chronic kidney disease who are on dialysis frequently have elevated calcium and phosphate. These minerals are directly implicated in increased vascular calcifications together with the risk factors for arterial calcification. Atherosclerotic factors such as lipid oxidation and inflammation play roles that have not yet been fully elucidated.

While some studies implicate PTH as another culprit in calcification pathogenesis, there are others that claim there is no association of PTH with arterial calcification. However, uremia, based on some studies has been suggested to behave as a natural stent by it’s stabilizing effect on atherosclerotic plaques.

Diabetes mellitus type 2 is another comorbidity that presents with increased rates of cardiovascular morbidity and mortality. In particular, there is high risk of medial artery calcification with increased age and hyperglycemia, where the arteries are not occluded, but stiffened.

These patients tend to have a significantly higher risk for stroke and cardiovascular mortality than patients without medial artery calcification.  In addition to this, these patients are also at a significantly higher risk for amputations of the lower extremities.

Prevention of Calcifications

The evidence demonstrating an effective therapy that reduces arterial calcifications is lacking. Regimens such as calcium channel inhibitors and/ or statins have not showed any promising results. Nonetheless, it is reasonable to assume that reducing the reducible risk factors associated with arterial calcification may be a step in the right direction.

Care should also be taken with the use of certain drugs, such as vitamin K antagonists, which seem to have an accelerating effect on arterial calcification.

Reviewed by Susha Cheriyedath, MSc

Further Reading

Last Updated: Jul 18, 2016

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