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Murmurs in puppies and kittens (Proceedings)

Article

Congenital heart disease (CHD) is a morphologic defect of the heart or great vessels which is present at birth. "Congenital" does not imply the defect was inherited, although many CHD are heritable. CHD may also be caused by de novo spontaneous mutations, which have the potential to be transmitted to progeny. Diagnosis of CHD is important for the health of the patient and also to eliminate affected individuals from the breeding pool.

Congenital heart disease (CHD) is a morphologic defect of the heart or great vessels which is present at birth. "Congenital" does not imply the defect was inherited, although many CHD are heritable. CHD may also be caused by de novo spontaneous mutations, which have the potential to be transmitted to progeny. Diagnosis of CHD is important for the health of the patient and also to eliminate affected individuals from the breeding pool.

Cardiac auscultation often helps narrow the differential list and can be pathognomic for particular congenital defects such as patent ductus arteriosus (PDA). Evaluation of femoral arterial pulse strength, jugular veins, and mucous membrane color are also important aspects of the physical examination. Diagnostic approach for the CHD patient includes thoracic radiographs, echocardiography, electrocardiography, and complete blood count and arterial blood gas in cyanotic heart diseases.

Innocent murmurs

Innocent physiologic murmurs are not uncommon in healthy puppies, but are impossible to distinguish from pathologic murmurs due to structural cardiac disease. Therefore, an echocardiogram is needed to evaluate whether the murmur is innocent versus secondary to congenital heart disease. In a large 6-year study of over 1200 Boxer dogs, 52% of healthy Boxer dogs had left basilar systolic murmurs and normal echocardiograms with no evidence of congenital heart disease. A majority (97%) of these physiologic murmurs were soft (I-II/VI). Likewise, of the Boxers diagnosed with congenital heart disease, 85% had soft I-II/VI systolic murmurs, making it impossible to differentiate physiologic innocent murmurs from pathologic murmurs due to congenital heart disease. The cause of innocent physiologic murmurs in healthy animals is unknown. A possible explanation is that the stroke volume is greater in proportion to the size of the great vessels in puppies compared to adult dogs. Soft innocent murmurs in Boxer puppies have been shown to be highly variable in presence and intensity both within days and between days. Although often innocent murmurs are stated to commonly resolve by 6 months of age, a prospective study of growing Boxer puppies showed that these innocent murmurs commonly persisted into adulthood. In contrast, another study found that murmurs disappeared in half of adult Boxers who had soft murmurs as puppies.

Congenital heart diseases are divided into 4 main categories: ventricular outflow obstructions, left to right shunts, right to left shunts, and atrioventricular valve dysplasia or stenosis, along with other less common defects.

Ventricular outflow obstructions

Subaortic stenosis is the most common CHD of large breed dogs. It is caused by a fibrotic ridge, tunnel, or ring arising in the left ventricular outflow tract just below the level of the aortic cusps. SAS develops over the first few months of life, and may progress up to 12 months of life. SAS is heritable in Newfoundlands, likely as an autosominal dominant single trait, and is also common in Golden Retrievers, Rottweilers, Boxers, German Shepherd dogs, and Great Danes. Increased resistance to left ventricular ejection results in a high left ventricular systolic pressure, which causes concentric left ventricular hypertrophy and subendocardial fibrosis. Myocardial ischemia may result from reduced capillary density and reduced coronary blood flow. Exertional syncope or sudden death is common in severe SAS. Ventricular arrhythmias are the probable cause of sudden death. Physical examination abnormalities include a left basilar holosystolic murmur which often radiates to the right and to the carotid arteries. In moderate to severe SAS, femoral pulses are dampened. Thoracic radiographs are often unremarkable or may depict a post-stenotic dilation of the ascending aorta. Echocardiography is necessary to determine the diagnosis and severity of obstruction. Measurement of peak aortic blood flow velocity (and calculated pressure gradient by the modified Bernouilli equation of PG = 4V2) using the left apical 5-chamber view is necessary to determine the severity of obstruction: 20-50 mmHg (mild), 50-80 mmHg (moderate), > 80 mmHg (severe). Recent studies have identified that neither balloon valvuloplasty nor open heart surgical correction of the fibrotic ring improve survival over beta blockade alone. Patients with moderate or severe SAS should be placed on a beta blocker in efforts to reduce risk of sudden death. Patients with mild SAS have greatly diminished risk of sudden death, and it is debatable whether they should be placed on a beta blocker. Prophylactic antibiotics should be given prior to any surgical or dental procedure to prevent development of aortic valve infective endocarditis.

Valvular pulmonic stenosis is the third most common congenital heart disease in dogs, and occurs most frequently in small breeds. Bulldogs and Boxer dogs are predisposed to develop either valvular PS or subvalvular extramural PS due to an anomalous left coronary artery that originates from the right coronary artery and encircles the pulmonary artery. PS causes a left basilar holosystolic murmur and normal femoral pulses. Thoracic radiographs typically show right heart enlargement and post-stenotic dilation of the pulmonary artery. Echocardiography is useful to determine the diagnosis, the severity, and whether the obstruction is subvalvular or valvular. Other concurrent defects such as tricuspid valve dysplasia (TVD) or right to left shunting patent foramen ovale should also be evaluated with echocardiography. The combination of TVD and PS commonly result in severe right sided congestive heart failure (i.e. ascites, hepatomegaly, jugular distension, +/- pleural effusion). Transesophageal echocardiography or aortic root angiography may be necessary to diagnose the anomalous left coronary artery. Dogs with severe PS are at risk for sudden death, syncope, or development of right sided CHF due to either diastolic dysfunction or worsening tricuspid regurgitation. Balloon valvuloplasty is the treatment of choice of severe valvular PS, and is associated with a 53% reduction in risk of sudden death as well as improved quality of life.

Left to right shunts (patent ductus arteriosus, atrial septal defect, and ventricular septal defect)

Patent ductus arteriosus (PDA) is the second most common CHD, and is heritable as a polygenic trait with sex as a modifier in poodles. Auscultation reveals the pathognomonic continuous left basilar murmur. Femoral pulses are bounding. Thoracic radiographs show left heart enlargement, pulmonary overcirculation, the pathognomonic aortic-ductal aneurysm, and possibly left sided CHF. Echocardiography is necessary to confirm the diagnosis and to evaluate for concurrent CHDs. M-mode and 2- dimensional echocardiography show left ventricular eccentric hypertrophy and often there is mild to moderate systolic failure. There is usually mild or moderate left atrial enlargement. Assessment of ductal morphology and measurement of minimal ductal opening help assess whether the patient is a suitable candidate for percutaneous coil embolization. Color flow Doppler at the right parasternal short-axis basilar view and left parasternal long axis view shows continuous turbulent blood flow from the ductus arteriosus into the pulmonary artery. Peak systolic velocity of the ductal flow is measured to assess whether there is pulmonary hypertension (i.e. reduced velocity may indicate pulmonary hypertension). Surgery or percutaneous closure with cather based devices are the two treatment options. Ductal closure should not be postponed since there is always a risk of the PDA reversing and becoming uncorrectable. Mortality rate with an experienced surgeon is ≤ 5.6 % and mortality rate for percutaneous catheter based closure ranges from 0- 2.4 %.

Ventricular septal defect is uncommon in dogs and is one of the most common CHDs in cats. A right basilar holosystolic murmur is typically ausculted. Murmur intensity is inversely proportional to the size of the defect. Perimembranous defects are the most common and occur just below the aortic cusps. This often results in variable degrees of aortic insufficiency. Thoracic radiographs are normal if there is a small shunt, and may show left heart enlargement, pulmonary overcirculation, and possibly left sided CHF in large left to right shunts.

Echocardiography is used to determine the diagnosis and to assess the hemodynamic significance of the shunt. Left ventricular eccentric hypertrophy and left atrial dilation occur secondary to significant left to right shunting. The right heart remains normal in size, unless there is pulmonary hypertension secondary to Eisenmenger's syndrome, which is discussed in the right to left shunting category. Peak systolic velocity of the shunt is necessary to assess presence of pulmonary hypertension (reduced left ventricular to right ventricular pressure gradient of <80 mmHg indicate pulmonary hypertension). Treatment is not necessary unless there is significant left heart enlargement and congestive heart failure. Pulmonary artery banding may be performed to reduce the pulmonary artery diameter by 50% and decrease the left to right shunting.11 Patch closure of the VSD during cardiopulmonary bypass is another treatment option. Medical treatment with lasix, enalapril, and arteriolar vasodilators is indicated if surgery is not an option.

Atrial septal defects are rare in dogs and occasionally seen in cats. A soft left basilar holosystolic murmur is due to increased right ventricular stroke volume and functional pulmonic stenosis. Thoracic radiographs reveal right and left heart enlargement, pulmonary overcirculation, and possibly left-sided CHF. Color flow Doppler echocardiography shows laminar, low velocity left to right shunting flow across the defect. The right atrium and right ventricle are dilated to a greater degree than the left atrium and left ventricle. Treatment options for significant left to right shunting ASDs include: pulmonary artery banding, percutaneous cardiac catheterization closure with a clam-shell device, or open heart surgical correction during cardiopulmonary bypass. Medical treatment consists of furosemide and enalapril.

Right to left shunts (tetralogy of fallot, eisenmenger's syndrome, and right to left pda)

Tetralogy of fallot (TOF) is the most common cyanotic CHD. Components of TOF include: pulmonic stenosis, ventricular septal defect, over-riding aorta, and concentric right ventricular hypertrophy. TOF is inherited as a simple autosomal recessive trait in Keeshonds. The severity of PS and the systemic vascular resistance determine the severity of right to left shunting. Right to left shunting results in arterial hypoxemia (PaO2 usually 35-40 mmHg) and triggers erythropoietin production by the kidneys. Moderate polycythemia (55-65%) is beneficial, but PCV > 70% is often associated with hyperviscosity syndrome. Murmur severity is inversely related with the severity of the VSD. If there is severe PS and a large VSD, there will be no murmur. Thoracic radiographs typically show right heart enlargement and pulmonary undercirculation. Echocardiography shows right ventricular concentric hypertrophy, PS (usually infundibular and valvular), a VSD in the perimembranous sub-aortic region, and an over-riding (rightward shifted) aorta traversing the interventricular septum. Color flow Doppler and positive contrast echocardiography (using agitated saline injected into a peripheral vein) show right to left shunting blood flow across the VSD and out the aorta. The PS pressure gradient often equals the systemic systolic pressure when there is a large VSD and equilibration of right ventricular and left ventricular systolic pressures.

Eisenmenger's syndrome occurs when there is a large, unresistive defect (PDA, VSD, atrial septal defect, or atrioventricular canal defect) with an initial large left to right shunt that causes pulmonary arterial hypertension and ultimately results in right to left shunting. Initially, the pulmonic blood flow is greatly increased due to the large left to right shunt. Over time, the pulmonary arterioles develop irreversible pathologic changes that results in a severely elevated and fixed pulmonary vascular resistance. Blood flow then reverses to shunt from right to left, since systemic vascular resistance is lower than the pulmonic vascular resistance. This results in arterial hypoxemia, cyanosis, and secondary polycythemia.

Right to left PDA occurs when there is a large, unresistive PDA with virtually no smooth muscle in the ductus. The large communication between systemic and pulmonic vascular beds results in development of severe, irreversible pulmonary hypertension. Differential cyanosis occurs due to right to left shunting of unoxygenated blood from the pulmonary artery to the caudal half of the body. No murmur is present since there is laminar right to left shunting blood. Thoracic radiographs show right heart enlargement, pulmonary undercirculation, and a ductal aneurysm of the aorta. Echocardiography shows severe concentric right ventricular hypertrophy, pulmonary artery dilation, and a large non-tapered PDA with right to left or bidirectional flow on color flow Doppler or positive contrast bubblegram. Following peripheral venous injection of agitated saline, visualization of bubbles within the abdominal aorta in the absence of intracardiac right to left shunting confirms the right to left PDA.

Open surgical repair of TOF under cardiopulmonary bypass is a feasible option but has rarely been done in veterinary medicine. Surgical correction of right to left shunting PDA or closure of defects in patients with Eisenmenger's syndrome is contraindicated. Avoidance of systemic hypotension is essential in animals with right to left shunting defects to avoid worsened hypoxemia. Medical management is aimed at controlling the severity of polycythemia and avoidance of hyperviscosity syndrome. The goal of medical management is aimed at maintenance of PCV at 60-68%. Phlebotomy is a useful and safe technique to reduce polycythemia. If phlebotomies are poorly tolerated or must be performed too frequently, reversible bone marrow suppression of red blood cell production using hydroxyurea is another treatment option. Survival is variable in animals with cyanotic heart disease, and often ranges from 1-5 years.

Dysplasia of the atrioventricular valves (mitral and tricuspid valve dysplasia, mitral and tricuspid valve stenosis)

Mitral valve dysplasia (MVD) and tricuspid valve dysplasia (TVD) are malformations of the mitral valve apparatus or tricuspid valve apparatus including the valve leaflets, chordae tendinae, or papillary muscles that results in valvular insufficiency. There are many types of malformations including: short, thickened leaflets with clubbed tips, rolling of leaflet edges, short and thick chordae tendinae, fusion of chordae tendinae into a single chord, direct insertion of the papillary muscle to the leaflet, and upward malposition of the papillary muscle causing malalignment of the chordae tendinae. MVD is most commonly seen in large breed dogs, and Bull terriers and Great Danes are predisposed. TVD is the most common CHD of Labrador retrievers, and has been shown to be an autosomal dominant inherited trait with incomplete penetrance. MVD and TVD are the most common CHDs in cats, and MVD may also be seen in conjunction with atrioventricular canal defects.

Severe MVD and mitral regurgitation causes elevated left ventricular diastolic pressure, elevated left atrial and pulmonary venous pressures, and development of pulmonary edema. Congestive heart failure is seen in 75% of dogs with MVD in an early study. Severe TVD and tricuspid regurgitation causes elevated right ventricular end diastolic pressure, elevated right atrial pressure, and right congestive heart failure when right atrial pressure exceeds 10-15 mmHg.

Dogs with MVD commonly have a left apical holosystolic to pansystolic murmur whose intensity usually parallels the severity of the regurgitation. Auscultation of dogs with TVD reveals a right apical systolic murmur in dogs with moderate to severe TVD. However, in a study of Labrador retrievers screened by echocardiography for TVD, none of the dogs with mild TVD had a murmur, making auscultation an inappropriate screening test. ECG may show various supraventricular arrhythmias such as atrial premature complexes, supraventricular tachycardia, atrial fibrillation. Splintered QRS complexes (Rr', RR', rR', rr') are seen in 60% of dogs and cats with TVD. Labrador retrievers with TVD may also have an accessory pathway bridging the right atrium and the right ventricle, resulting in re-entrant supraventricular tachycardia. Thoracic radiographs demonstrate variable left atrial enlargement, left sided cardiomegaly, and possibly pulmonary venous distension and interstitial to alveolar pulmonary infiltrates of the perihilar to caudodorsal lung fields in dogs with MVD. Left sided congestive heart failure in cats may be characterized by atypical pattern of edema distribution and/or pleural effusion. Dogs with moderate to severe TVD often have profound right atrial dilation, as well as dilated caudal vena cava, hepatomegaly, and ascites. Cats with TVD have right atrial enlargement and a dilated and often tortuous caudal vena cava. Cats with right heart failure may develop pleural effusion with or without ascites.

Echocardiography reveals morphologic abnormalities of the mitral valve apparatus or tricuspid valve apparatus as described above. There may be left atrial enlargement, eccentric left ventricular hypertrophy secondary to volume overload, and possibly mild myocardial failure secondary to chronic volume overload in medium to large breed dogs and cats with MVD. TVD may cause profound right atrial dilation which may distort the position of the other chambers making it difficult to obtain normal standard views.

Standard medical management of congestive heart failure includes furosemide (1-4 mg/kg PO q 24 hr – TID) and an angiotensin converting enzyme (ACE) inhibitor. Treatment of tachyarrhythmias with antiarrhythmics may also be necessary. Intra-cardiac and extra-cardiac annuloplasty have been performed to reduce the severity of valvular insufficiency. Surgical valve repair or replacement during cardiopulmonary bypass has been successfully performed by a few highly experienced cardiac surgeons, but there is a high risk of mortality and is limited to medium and large breed fully grown dogs. Dogs must remain on life- long coumarin anticoagulant therapy.

Mitral and tricuspid stenosis are uncommon variants of dysplasia. The atrioventricular valve leaflets are unable to open completely, which causes increased resistance to ventricular filling and elevated atrial pressure. There is always some degree of valve dysplasia and valvular insufficiency. Bull terriers and Newfoundlands are predisposed to develop mitral stenosis. Pulmonary hypertension may develop secondary to chronic elevated left atrial pressure in animals with mitral stenosis. Auscultation of a diastolic murmur is uncommon (27%) but animals usually have a systolic apical murmur.13 Echocardiography shows restricted, immobile valve leaflets that fail to open completely in diastole. Color flow Doppler shows aliasing to turbulent mitral or tricuspid diastolic inflow, and often also identifies systolic valvular insufficiency. Pulsed wave or continuous wave Doppler across the affected valve shows increased peak inflow velocity and prolonged pressure half times. The maximum atrial to ventricular pressure gradient is increased and may be used to non-invasively quantify atrial pressure.

Medical treatment is the same as for atrioventricular valve dysplasia. Control of tachycardia with negative chronotropic drugs is important to optimize diastolic filling. Balloon valvuloplasty or surgical commisurotomy are other treatment options.

References

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Hoglund K, Haggstrom J, Bussadori C, Kvart C. A prospective study of systolic ejection murmurs and left ventricular outflow tract in boxers. J Small Anim Pract.2011.Jan.;52.(1):11-7.doi.: 10.1111./j.1748.-5827.2010.01009.x.Epub.2010.Dec.9. 2011;52:11-17.

enni S, Gardelle O, Zini E, Glaus TM. Use of auscultation and Doppler echocardiography in Boxer puppies to predict development of subaortic or pulmonary stenosis. J Vet Intern Med.2009.Jan.-Feb.;23(1):81.-6. 2009;23:81-86.

MacDonald KA. Congenital heart diseases of puppies and kittens. Vet Clin.North Am Small Anim Pract.2006.May.;36.(3):503.-31., vi. 2006;36:503-31, vi.

Orton EC, Herndon GD, Boon JA, Gaynor JS, Hackett TB, Monnet E. Influence of open surgical correction on intermediate-term outcome in dogs with subvalvular aortic stenosis: 44 cases (1991-1998). J Am Vet Med.Assoc. 2000;216:364-67.

Meurs KM, Lehmkuhl LB, Bonagura JD. Survival times in dogs with severe subvalvular aortic stenosis treated with balloon vlavuloplasty or atenolol. JAVMA 2005;227:420-24.

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Gordon SG, Saunders AB, Achen SE, Roland RM, Drourr LT, Hariu C et al. Transarterial ductal occlusion using the Amplatz Canine Duct Occluder in 40 dogs. J Vet Cardiol.2010.Aug.;12.(2):85.-92.Epub.2010.Jul.7. 2010;12:85-92.

Eyster GE, Eyster JT, Cords GB, Johnston J. Patent ductus arteriosus in the dog: characteristics of occurrence and results of surgery in one hundred consecutive cases. J.Am.Vet.Med.Assoc. 1976;168:435-38.

Campbell FE, Thomas WP, Miller SJ, Berger D, Kittleson MD. Immediate and late outcomes of transarterial coil occlusion of patent ductus arteriosus in dogs. J Vet Intern Med.2006.Jan.-Feb.;20.(1):83.-96. 2006;20:83-96.

Eyster GE, Whipple RD, Anderson LK, Evans AT, O'Handley P. Pulmonary artery banding for ventricular septal defect in dogs and cats. J.Am.Vet.Med.Assoc. 1977;110:434-38.

Liu SK, Tilley LP. Malformation of the canine mitral valve complex. J.Am.Vet.Med.Assoc. 1975;167:465-71.

Lehmkuhl LB, Ware WA, Bonagura JD. Mitral stenosis in 15 dogs. J.Vet.Intern.Med. 1994;8:2-17.

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