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Close window to return to IVIS Proceeding of the NAVC North American Veterinary Conference Jan. 8-12, 2005, Orlando, Florida Reprinted in the IVIS website with the permission of the NAVC http://www.ivis.org/ Published in IVIS with the permission of the NAVC Small Animal - Cardiology HOW WORRIED SHOULD I BE ABOUT THIS HEART MURMUR? Rebecca L. Stepien DVM, MS, DACVIM School of Veterinary Medicine University of Wisconsin, Madison, WI Heart murmurs are common findings in routine veterinary physical examinations, but it may be difficult to discern the underlying cause and severity of the heart disease responsible for the murmur by auscultation alone. Common questions owners may ask include: 1. Why does my pet have a heart murmur? 2. How will the murmur affect his/her life? 3. What diagnostic tests are necessary and why? 4. Does he/she need medication/lifestyle changes? WHY DOES MY PET HAVE A HEART MURMUR? The importance of age and breed cannot be overstated when formulating a differential diagnosis list for causes of cardiac murmurs. With rare exception, cats or dogs with audible heart murmurs prior to 3 years of age are affected by congenital heart disease (CHD); the specific abnormality can often be suspected based on the characteristics (timing, point of maximal intensity [PMI]) of the murmur. The most common congenital heart murmur timings/PMI and their differential diagnoses are listed in Table 1. The auscultatory characteristics of the murmur are used to develop a differential diagnosis list. In dogs, many congenital diseases have specific breed predilections; knowledge of these breed-associated abnormalities can narrow the differential list. Although most CHD show some breed predilection1, it is important to remember that some abnormalities occur frequently in many breeds (e.g. PDA), and that any animal can have any abnormality, regardless of the breed. Cats show less breed predilection for specific CHD, but mitral valve dysplasia and ventricular septal defects are the most common abnormalities in all cats. Discovery of a “new” murmur in an older animal usually occurs as the animal develops degenerative valvular disease (primarily dogs) or myocardial disease (cats, dogs). Other causes of acquired murmurs include vegetative endocarditis, anemia, and systemic hypertension (Table 2). In cases of endocarditis or anemia, systemic derangements are often evident on physical examination. A high index of suspicion must be maintained to diagnose systemic hypertension in many patients as this disease is often clinically ambiguous (see diagnostic work-up, below). A special case of an acquired murmur is the systolic murmur frequently heard in Close window to return to IVIS www.ivis.org thin, athletic dogs (PMI: left base). Many athletic dogs belong to breeds that have been associated with aortic or subaortic stenosis and differentiation of an “athletic” murmur and a murmur of CHD can be problematic. This differentiation frequently requires use of Dopplerechocardiographic studies. In cases involving breeding animals, consider referral to a cardiologist experienced in diagnosis of congenital heart disease. Note: “New” murmurs may represent previously undiagnosed congenital disease; this situation may occur in patients new to your practice or very active or uncooperative animals that are difficult to auscult with confidence. In addition, some congenital murmurs increase in intensity as the animal grows, and the murmurs may not attain their full intensity until the animal is an adult. HOW WILL THE MURMUR AFFECT HIS/HER LIFE? Congenital Murmurs Reliable indicators of moderate to severe congenital malformations include lethargy (may be interpreted as a “quiet” animal), poor growth (as compared to littermates) or cyanosis or signs of congestive heart failure accompanying a consistent murmur. More problematic are the outwardly “normal” pediatric patients with easily audible murmurs. In these animals, differentiation of an innocent murmur from a significant murmur may be based on several criteria (Table 3). Acquired Murmurs Acquired murmurs in dogs that are thought to be due to endocardiosis and are not associated with noticeable clinical or physical examination abnormalities may not affect the animal’s lifestyle a great deal at the time of diagnosis. Endocardiosis is a slowly progressive disease, however, and congestive heart failure is a likely outcome over the months to years following first auscultation of the murmur. Myocardial diseases tend to progress faster than valvular disease, and most animals with DCM are not diagnosed before the onset of clinical signs. Acquired heart murmurs in cats may be identified early in the course of cardiomyopathic disease (esp. HCM) and may not be associated with clinical signs for several years. In other cases, a murmur is detected when the animal is examined for a clinical sign of heart disease (e.g. lethargy, congestive signs or signs of thromboembolic disease) or of the underlying condition responsible for 2o heart diseases (e.g. hypertension, thyrotoxicosis). In some cases, the owners may not be aware of the cat’s clinical abnormalities (e.g. lethargy) until improvement occurs in response to appropriate medications. Table 1: Murmur characteristics of common congenital heart diseases Systolic Murmur Left apex: MD Left base: [S]AS, PS, ASD, VSD* Right apex: TD, PS* Right base/right sternal border: VSD, [S]AS* Systolic/Diastolic Murmur Left apex: bi-directional VSD Left base: [S]AS/AI, PS/PI Continuous Murmur# Left base: PDA # other systolic/diastolic murmurs may sound continuous and be heard over left or right heart structures *murmur listed is the secondary murmur, differential diagnosis applies if other appropriate murmurs are present [S]AS: [sub]aortic stenosis, AI: aortic insufficiency, ASD: atrial septal defect, MD: mitral dysplasia, PDA: patent ductus arteriosus, PS: pulmonic stenosis, PI: pulmonic insufficiency, TD: tricuspid dysplasia, VSD: ventricular septal defect 137 www.ivis.org Published in IVIS with the permission of the NAVC The North American Veterinary Conference – 2005 Proceedings Close window to return to IVIS www.ivis.org Table 2: Differential diagnosis of acquired heart disease based on murmur characteristics SYSTOLIC MURMUR Left apex: mitral insufficiency • mitral endocardiosis, mitral endocarditis (look for systemic signs) • myocardial disease with 2o mitral involvement • Dogs: dilated cardiomyopathy • Cats: cardiomyopathies • idiopathic HCM, RCM or DCM • secondary to systemic conditions • hypertrophic: hyperthyroidism, hypertension, growth hormone excess • dilated myocardial disease (rare): taurine deficiency • myocardial infiltration (usually neoplastic) in either species SYSTOLIC/DIASTOLIC MURMUR Left base: • aortic valve endocarditis (with insufficiency) • pulmonic valve endocarditis (with insufficiency) Right apex: tricuspid insufficiency • tricuspid endocardiosis, tricuspid endocarditis (look for systemic signs) • myocardial disease/ 2o tricuspid involvement • as above for dogs • rare murmur in cats Left base: “flow murmurs” e.g. anemia, “athletic” murmurs Table 3: Characteristics of innocent murmurs and murmurs associated with congenital heart disease Innocent Murmur Grade usually < III/VI Characteristics change with position of animal and heart rate Systolic only PMI: usually left base Decreased intensity with age up to 16 wks of age Inaudible after ~16 wks of age WHAT DIAGNOSTIC TESTS ARE NECESSARY, AND WHAT INFORMATION WILL WE GAIN BY SPENDING THE MONEY? Congenital Murmurs A complete cardiac assessment including radiographs, electrocardiography and Doppler-echocardiographic examination is recommended for animals suspected of having CHD. In some cases, the work-up will confirm the mild nature of the abnormality, and the owner can be informed of the relatively minor risk of development of serious complications. Confident identification and diagnosis of apparently mild congenital abnormalities is especially important in animals under consideration for breeding programs. In animals with more severe CHD, a complete diagnostic work-up allows accurate prognostication of survival and complications, based on clinical experience with animals with similar disease severity. The high expectations of many owners of potential breeding animals makes clear understanding of the known prevalence, suspected inheritance pattern and typical clinical course of CHD important, and cardiologic referral should be considered when a clinician experienced in CHD is not available in the primary practice. Possible Congenital Heart Disease Grade >/= III/VI Similar characteristics in all positions and heart rates Any timing possible PMI: any possible Same or increasing intensity up to and beyond 16 wks of age Persists after ~ 16 wks of age Acquired Murmurs The purpose of the diagnostic work-up in animals with acquired heart disease is to diagnose the disease, judge the severity of cardiac dysfunction and evaluate the animal for signs of heart failure or complications of disease. A thorough physical examination delineates cardiovascular signs, may help to rule out systemic disease and is followed by more focused diagnostic testing of the heart and cardiovascular systems: 1. Baseline renal function and electrolyte balance should be established in all animals that will be receiving cardiacrelated medication 2. Thoracic radiographs: Aid diagnosis of disease (“changes compatible with...”) and establish diagnosis of congestive heart failure 3. Electrocardiography: Aid diagnosis of disease and establish complications (e.g. conduction abnormalities, dysrhythmias) 4. Echocardiography: recommended in all cases to delineate disease, but required in canine cases if DCM is suspected in atypical breed or signs are confusing in a “typical” breed, and in all cats when definitive diagnosis is required, since forms of myocardial disease cannot be reliably differentiated based on ancillary testing. In both species, echocardiography is required if presenting signs 138 www.ivis.org Published in IVIS with the permission of the NAVC Small Animal - Cardiology are confusing or complications (e.g. dysrhythmias) develop, if the animal does not respond as expected to therapy, or previous response is not sustained or when more than one cardiac abnormality is suspected (e.g. mitral endocardiosis with myocardial failure). 5. Resting serum T4 measurement is recommended in cats with heart murmurs who are >6 years old or have a palpable cervical nodule or compatible clinical signs, but T4 levels may be abnormal even if cat not showing “typical” thyrotoxic signs. 6. Resting blood pressure and retinal examination is recommended for all cats with acquired heart murmurs, but is especially important if renal dysfunction (but not necessarily failure) is present, or if retinal detachment is suspected. DOES HE/SHE NEED MEDICATION/LIFESTYLE CHANGES? Congenital Murmurs Animals with CHD that have signs of congestive failure require palliative or curative procedures or aggressive medical therapy to maintain reasonable quality of life. Therapy of asymptomatic animals is more controversial. Animals with known hypertrophic diseases (e.g. [S]AS, PS) may be treated with therapies to slow heart rate or increase diastolic function (e.g. beta-blockers or calcium channel blockers). To date, little published information is available regarding the risk/benefits of long-term therapy with these drugs in asymptomatic animals with normal sinus rhythm. In many cases of CHD, no therapy is used unless the animal has clinical signs of inadequate cardiac function or dysrhythmias are present. Acquired Murmurs There is little argument that animals with signs of low output or congestive heart failure require specific cardiac therapy. More controversial is the therapy of asymptomatic (or perhaps “pre-symptomatic”) animals. It is generally accepted (although proof of long-term benefit in asymptomatic animals is lacking) that use of calcium channel blockers to promote diastolic function in cats with asymptomatic HCM is reasonable2. Whether similar or other theoretic benefits could be obtained with beta-blocker therapy is unknown3, and ultimately, client dedication and compliance may be the deciding factor in treating any cat without easily discernible clinical signs. Many people would agree that dogs with known DCM but no clinical signs may benefit from early therapy with ACE inhibitors with or without digoxin, but no proof of such benefit in dogs has been published. 139 Close window to return to IVIS www.ivis.org In the case of asymptomatic mitral or tricuspid insufficiency, some evidence suggests that early activation of the renin-angiotensin-aldosterone system (RAAS) may be a desirable intervention point for pre-symptomatic disease, but some research has shown that intervention itself (with diuretics or non-ACE inhibitor vasodilators) may lead to activation of the RAAS4. It is still unclear which arm of the neuroendocrine response to cardiac disease or what imbalance in the response is the most likely cause of development of signs,5 thus therapy of nonsymptomatic endocardiosis cases remains controversial. REFERENCES 1. Buchanan JW. Causes and prevalence of cardiovascular disease. In: Kirk’s Current Veterinary Therapy XI: Small Animal Practice. Kirk RW, Bonagura JD (eds). Philadelphia: W.B. Saunders Company. 1992, pp.647-655. 2. Bright J, Golden AL, Gompf RE, Walker MA, Toal RL. Evaluation of the calcium channel-blocking agents diltiazem and verapamil for treatment of feline hypertrophic cardiomyopathy. J Vet Int Med 1991;5:272282. 3. Fox PR. Evidence for or against efficacy of betablockers and aspirin for management of feline cardiomyopathies. Vet Clin N America: Small An Prac 1991;21(5):1011-1022. 4. Haggstom J, Hansson K, Karlberg BE, Kvart C, Madej A, Olsson K. Effects of long-term treatment with enalapril of hydralazine on the renin-angiotensin-aldosterone system and fluid balance in dogs with naturally acquired mitral valve regurgitation. Am J Vet Res 1996;57(11):16451652. 5. Haggstom J, Hansson K, Kvart C, Karlberg BE, Vuolteenaho O, Olsson K. Effects of naturally acquired decompensated mitral valve regurgitation on the reninangiotensin-aldosterone system and atrial natriuretic peptide concentration in dogs. Am J Vet Res 1997;58(1)77-82. www.ivis.org