H. Edward Durham Jr., CVT, LATG
Dental disease is perhaps the most common pathology presented in dogs today, especially small-breed dogs. In addition, chronic valvular heart disease is the most common source of murmurs and heart failure in small-breed dogs. It would seem reasonable that dental disease and heart murmurs would have a close association, especially in light of their connection in human medicine. It has been well documented that some people with periodontal disease are at risk for infections of the mitral valve after dental work, causing heart failure and, in severe cases, the need for valve replacement surgery.
Dental disease in dogs is ubiquitous across breeds. At some point in its life, virtually every domestic dog (and cat) develops some type of dental or periodontal disorder. Chronic periodontal disease can release bacteria into the bloodstream, damaging many organ systems. Unfortunately, even routine dental prophylaxis can release large amounts of bacteria into the bloodstream. Extractions are another source of bacterial release. Organ systems known to be damaged in the face of bacterial release are the kidneys, liver, lungs, and heart. Of these, the kidneys have the strongest link to periodontal disease.1
Veterinary technicians should become skilled in performing dental prophylaxis and understand how bacterial release can be minimized. The interactive CD-ROM Understanding Dental Hygiene is an excellent resource for learning or honing dental skills.
The Human Connection
Rheumatic fever is known to be the most common cause of acquired heart disease in children and young adults worldwide. Although uncommon in developed countries today, the condition was at one time common worldwide. An inflammatory process that attacks the connective tissues or vascular collagen, rheumatic fever is linked to untreated streptococcal tonsillopharyngitis. It can lead to significant valvular fibrosis, valvular regurgitation, and ultimately heart failure. The mitral valve is commonly affected and patients with a history rheumatic fever are advised by the American Heart Association to use prophylactic antibiotics before undergoing procedures such as dental work, which could result in bacteremia that may lead to infective endocarditis (IE). Given the incidence of dental disease and the prevalence of mitral endocardiosis in dogs, it is easy to see a connection between dogs and humans.
Valvular Deformities in Dogs
In veterinary medicine, valvular deformities can be viewed in three broad categories:
Dysplasia--Congenital malformation of the valve that can be stenotic, incompetent and leaky, or both.
Endocardiosis--Chronic degeneration of the valve tissue that is an acquired malformation related to age. It most commonly affects the atrioventricular valves, but all valves can be affected. It is non-inflammatory in nature and can lead to heart failure.
Endocarditis--Typically an inflammatory response initiated by an infective process. Damage to the valve as a result of bacterial growth can cause insufficiency leading to heart failure, even after the infection has been resolved. It can also lead to sepsis, septic shock, and death. Polyarthritis is a common condition in patients with IE as an inflammatory response in the connective joint tissue.
Chronic Myxomatous Valvular Degeneration
Chronic myxomatous valvular degeneration, or valvular endocardiosis, is by far the most common source of murmurs in small-breed dogs. It is estimated that up to 75% of dogs with signs of congestive heart failure have mitral endocardiosis.2 The cavalier King Charles spaniel is known to develop the condition much earlier in life, typically by 5 or 6 years of age. There is marked degeneration of the connective tissue of the mitral apparatus (leaflets and chordae tendineae), leading to regurgitation of the valve during systole. The valves become thick and "club like" at the leaflet tips. The leaflet may balloon or prolapse into the left atrium as well. In some cases, a chordae tendineae may rupture, leading to severe mitral regurgitation.
Currently, no evidence shows that this condition is infective and related to bacteremia from any source. There is one reported case of mitral valve IE following a dental prophylaxis. Although this case recognizes the temporal relationship between dental prophylaxis and the onset of IE, it acknowledges that the findings should not be applied broadly to all dogs because this is the only reported case.
Bacteremia is a condition in which bacteria enter the bloodstream through the mucous membranes or skin. The condition occurs in people every day during simple activities such as brushing one's teeth. Normally the immune system handles this influx of bacteria and no infection develops. Bacteremia has been shown to occur in two-thirds of dogs after dental prophylaxis, even with the use of prophylactic penicillin.3 In patients with chronic periodontal disease, this shower of bacteria can be constant. Under such a barrage the immune system loses ground and inflammation or systemic infections can follow.
Research has demonstrated that the severity of dental disease is related to histopathologic changes of the kidneys, liver, and lungs.1 Although histopathologic evaluation of heart tissue showed myocardial degeneration and inflammation related to the degree of dental disease, evidence of causation of mitral valve endocardiosis was lacking. However, research does show that dogs with sub-aortic stenosis have a higher risk of developing IE, and bacteremia could lead to disease.2,4 The connection between dental bacteremia and heart disease does not appear to be linked to mitral endocardiosis but rather to endocarditis.
Sub-aortic stenosis is a congenital defect of the heart that causes narrowing of the left ventricular outflow tract which is the area just inferior to the aortic valve. This narrowing causes the blood being ejected from the heart to move at an abnormally high velocity. The same effect can be seen when looking at a river where it narrows. As water approaches the narrowed area it increases in speed. The more narrow the area, the higher the velocity. As blood is ejected from the heart through the stenosis it impacts the aortic valve at increased velocity, thereby damaging the surface of the valve. This damaged area provides a place for bacteria to collect.
Golden retrievers, Boxers, and Newfoundlands are predisposed to sub-aortic stenosis. It is categorized as mild, moderate or severe based on the pressure gradient across the aortic valve calculated from the transvalvular velocity by Doppler echocardiography. Dogs with any degree of sub-aortic stenosis are at risk of developing IE.
IE is an infection of the valves or interior surfaces of the heart. The actual prevalence of IE is unknown, but published studies estimate it to be less than 1%. Most often, the aortic and mitral valves are targeted, although the tricuspid valve is occasionally affected. Pulmonic IE in dogs is rare.
Patients with IE often present with fever, polyarthropathy, new murmurs, general malaise, and possibly signs of heart failure. Diagnosis is complicated and relies on multiple tests as no single diagnostic tool is definitive. A system of major and minor criteria and definitions of likelihood has been developed to aid in diagnosis. Echocardiography and blood cultures are the mainstay of diagnostics in conjunction with patient history and physical examination findings (e.g., fever, joint swelling, lethargy, anorexia).
Achieving a diagnosis of many valvular disorders including IE requires gathering as much patient data as possible before conducting diagnostic tests. Blood cultures and echocardiography are key diagnostic criteria.
Adhering to proper technique in collecting blood samples for culture is paramount to avoid contamination. A venous blood sample of 10 ml should be collected using sterile technique as follows: The hair over the vein should be clipped and a standard aseptic scrub performed. The technician collecting the sample should wear sterile gloves and maintain a sterile field. The samples need to be transferred directly into a culture bottle, some of which contain antibiotic-suppressing agents. In order to maintain the proper dilution, it is important not to overfill the bottle. Typically, several samples should be collected about every 30 minutes for a 90- to 120-minute period. The bottles should then be processed for anaerobic and aerobic bacterial identification and sensitivity. Several organisms have been linked to IE in dogs, including Streptococcus spp, Corynebacterium spp, Erysipelothrix rhusiopathae, and Bartonella spp.
Echocardiography is an excellent tool to help achieve a definitive diagnosis of valvular disease. Vegetative lesions can sometimes be seen attached to a cardiac valve but if the vegetation is small discrete visual clues may be lacking. Highly reflective thickening of a valve and valvular regurgitation in conjunction with other clinical signs can be suspicious, especially in young animals, but are inconclusive. Vegetative lesions often appear as a pedunculated mass attached to the valve, sometimes flopping in and out of one chamber.
Echocardiography can also be exceedingly useful in assessing cardiac dysfunction and the consequences of murmurs, if present. Specific changes in cardiac chambers and valve function can likewise be determined.
Because IE has several sequelae that must be addressed, therapy involves aggressive use of antibiotics, treatment of congestive heart failure, and management of any other systemic abnormalities. Antibiotic therapy is typically broad-spectrum and potent. Contrary to popular belief, circulating antibiotics have a difficult time penetrating a vegetative lesion. Even though the lesion is bathed in the bloodstream, antibiotics have no direct perfusion into tissues. Antibiotic therapy must be continued for several weeks.
Aggressive treatment of heart failure may be necessary including diuretics, oxygen therapy, and nitroglycerin paste. If the valve damage is extensive, normal cardiac function may never return, and drugs such as angiotensin-converting enzyme (ACE) inhibitors or digoxin may be needed to manage chronic congestive heart failure. Cardiac arrhythmias are also occasionally seen in dogs with IE, some of which can be life-threatening. Standard antiarrhythmic therapy is recommended as needed.
Even though the prevalence of periodontitis and heart murmurs is high in veterinary medicine, there appears to be no substantial link between poor dental hygiene in dogs and chronic valvular degeneration. IE is a rare but potentially deadly condition that can be caused by bacteremia associated with dental prophylaxis. Dogs with sub-aortic stenosis have been shown to be at higher risk of developing IE when exposed to bacteremia. Therefore, it is recommended that dogs with sub-aortic stenosis receive antibiotics before dental, surgical, or with traumatic events. Prophylactic antibiotic therapy for all patients with murmurs undergoing dental treatment is controversial.
Table 1. Diagnostic criteria for the diagnosis of infective endocarditis in dogs and cats.4
1. Major criteria:
a. Positive echocardiographic findings:
i. Vegetative lesions
ii. Destructive lesions
iii. Thickened aortic valve leaflets
b. Positive blood cultures in the absence of diskospondylitis or obvious sepsis:
i. At least three positive cultures when common skin contaminants are cultured
ii. Preferably at least two positive blood cultures with other organisms
c. The recent onset of a diastolic heart murmur or evidence of more than trivial aortic regurgitation on a Doppler echocardiographic examination in the absence of sub-aortic stenosis or annuloaortic ectasia
2. Minor criteria:
b. Large (greater than 15 kg) dog
c. New or worsening systolic heart murmur
3. Supporting evidence:
a. Embolic disease:
ii. Renal failure; hematuria
b. Immunologic disease:
iii. Positive immunologic test (Antinuclear Antibody (ANA), Coombs')
c. Sub-aortic stenosis in a dog greater than 5 years of age
Table 2. Criteria for the diagnosis of infective endocarditis in dogs and cats.4
1. Definite or very probable infective endocarditis:
a. Pathologic criteria:
i. Microorganisms demonstrated by culture or histology in a vegetation
ii. Pathologic lesions confirmed by histology to show active endocarditis
b. Clinical criteria:
i. Two major criteria, or
ii. Positive echocardiographic finding plus one minor criterion, or
iii. Three minor criteria
2. Possible infective endocarditis:
a. One major criterion
b. Two minor criteria
c. Supporting evidence with at least two minor criteria
3. Not infective endocarditis:
a. Identification of alternative diagnosis to explain signs compatible with infective endocarditis
b. Resolution of clinical signs with short-term antibiotic therapy
c. No pathologic evidence of infective endocarditis
1. DeBowes LJ, Mosier D. J Vet Dent 1996, 13(2):57-60
2. Fox P, Sisson D, Moïse S. 1999Textbook of Canine and Feline Cardiology WB Saunders
3. Black AP, Crichlow AM, Saunders JB; 1980 JAAHA 16:611-616
4. Kittleson M, Kienle R. 1998 Small Animal Cardiovascular Medicine, Mosby