Atherosclerotic Vascular Disease

Atherosclerotic vascular disease (AVD) is a chronic process that occurs when the blood vessels carrying oxygen and nutrients from the heart to the rest of the body develop a buildup of plaques formed by fat, cholesterol and other substances in the blood.39 These plaque deposits cause narrowing of the blood vessels, a decrease in the elasticity of the vessel musculature, and changes in the smooth flow of blood through the lumen of the vessels.39 The formation of these plaques occur in response to inflammatory stimuli, which increase the expression of endothelial adhesion molecules. This allows for the recruitment and firm attachment of leukocytes to the vessel wall.39-41 Monocytes in the circulating blood attach to the vessel walls and then enter the intima of the vessels. They are then activated and mature in macrophages and scavenge the lipoproteins modified by inflammation.41,42 As low-density lipoproteins (LDLs) accumulate in the macrophages, they become “foam cells,” which characterize the initial plaque formations or fatty streaks.42 The macrophages and foam cells produce pro-inflammatory mediators, such as interleukin-1ß (IL-1ß) and tumor necrosis factor alpha which amplify the local inflammatory response. A feedback loop develops that leads to atherosclerosis. Apoptosis of the foam cells then results in a release and accumulation of lipids in the intima of the blood vessels.42

Approximately 11% of adults in the United States have some form of heart disease (Figure 1).33 AVD leads to high rates of morbidity and mortality. There is significant overlap of the risk factors for periodontal disease and for AVD. Dental care providers aware of the interactions will be able to adequately counsel their patients and customize treatment protocols. Additionally, dental health care providers should be aware of current pharmacotherapeutic management strategies for cardiovascular diseases and their implications on periodontal therapies (Table 2).

Figure 1. Heart disease death rates in the U.S. amongst adults ages 35+, 2011-2013.33
Map of US showing common CVD drugs used 2011-2013.
Table 2. Common drugs used for management of cardiovascular diseases and their oral sequelae.109
Drug Mechanism of Action Potential Oral Manifestations Other Considerations
α Adrenergic blockers Produce dialation due to antagonizing alpha receptors on blood vessels Xerostomia Orthostatic Hypotension
Prolonged NSAID use can decrease anti-hypersensitivity effects
α, β-Adrenergic blockers Alpha and nonselective beta-adrenergic receptor blockade Xerostomia
Altered taste
Lichenoid reaction
Orthostatic hypotension
Prolonged NSAID use can decrease anti-hypertensive effects
β- Adrenergic blockers Compete with catecholemines for beta-adrenergic receptor sites; may be cardioselective (CS) or nonselective (NS) Xerostomia NS may have a possible interaction with sympathomimetics
Orthostatic hypotension
Central sympatholytics Inhibition of sympathetic outflow from the central nervous system Xerostomia
Lichenoid reaction
Parotid pain/swelling
Orthostatic hypotension
Nausea/vomiting
Enhance CNS depressants
Prolonged NSAID use can decrease anti-hypersensitive effects
Peripheral adrenergic antagonists (seldom used) Deplete tissue stores of catecholamines and serotonin Xerostomia Orthostatic hypotension
Enhance CNS depressants
Prolonged NSAID use can decrease anti-hypersensitive effects
Anglotensin-converting enzyme (ACE) inhibitors Block conversion of angiotensin II to angiotensin II Cough
Angioedema of lips, face, tongue
Altered/decreased taste
Prolonged NSAID use can decrease anti-hypertensive effects
Neutropenia, thrombocytopenia
Angiotensin receptor blockers Competitively block angiotensin II at blood vessels and renal receptors Angioedema of lips, face, tongue Nausea/vomiting
Dizziness
Calcium channel blockers Inhibit calcium-ion influx into the cardiac and vascular smooth muscle Xerostomia
Gingivial overgrowth
Orthostatic hypotension
Drowsiness
Nausea/vomiting
Nitrates Venours and arterial dilation; reduction of oxygen demand by mycardium Facial flushing May decrease effects of epinephrine and levonordefin
Orthostatic hypotension
Headache
Dizzines
Nausea/vomiting