Quiz: Hypertrophic Cardiomyopathy in Cats

B is the correct answer.

A systolic heart murmur may be present in dogs with heartworm disease (Dirofilaria immitis) when there is pulmonary hypertension or worms entangled around the tricuspid valve. The murmur is typically caused by tricuspid regurgitation. However, in cats, the lungs are the primary organ affected, as the relatively low worm burden makes development of pulmonary hypertension and a resultant murmur less likely in cats than in dogs.^1-4 Thus, a systolic heart murmur is a rare clinical examination finding.^5,6

Hyperthyroidism, a significant cause of functional murmurs in cats, produces changes in cardiac contractility, myocardial oxygen consumption, cardiac output, blood pressure, and systemic vascular resistance.^7,8 These changes can lead to turbulent flow in the outflow tracts secondary to increased cardiac output, which can manifest as a murmur during auscultation. Hyperthyroidism can also lead to significant cardiac hypertrophy, primarily through the increased work load on the heart by way of an increase in the hemodynamic load.⁹ Because these changes can mimic hypertrophic cardiomyopathy (HCM), it is important to check thyroid levels in cats showing echocardiographic evidence of HCM (eg, left ventricular hypertrophy, eccentric hypertrophy of the left ventricle).

Physiologic heart murmurs are relatively common in cats and are typically caused by dynamic right ventricular outflow tract obstruction (DRVOTO),¹⁰ a unique physiologic condition in cats in which the flow velocity through the proximal right ventricular outflow tract is increased, possibly due to the comparatively hyperdynamic ventricular systolic function in cats.

The most common causes for heart murmurs in cats are underlying cardiac disease resulting from HCM (specifically, dynamic left ventricular outflow tract obstruction [DLVOTO]) and DRVOTO.^10-15 HCM is the most common form of underlying heart disease affecting cats. Other types of heart disease (eg, congenital heart disease, restrictive cardiomyopathy, unclassified cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy) are also possible differentials.^10,12-19

Hypertension in cats can lead to left ventricular hypertrophy (LVH), subsequent diastolic dysfunction, and development of changes that could result in development of a heart murmur. However, it is important to note that hypertension is not a direct cause of a heart murmur; rather, the secondary effects of sustained systemic hypertension to the left ventricle and valvular structures can lead to LVH and hemodynamic alterations that may result in development of a heart murmur.

Correct!

A systolic heart murmur may be present in dogs with heartworm disease (Dirofilaria immitis) when there is pulmonary hypertension or worms entangled around the tricuspid valve. The murmur is typically caused by tricuspid regurgitation. However, in cats, the lungs are the primary organ affected, as the relatively low worm burden makes development of pulmonary hypertension and a resultant murmur less likely in cats than in dogs.^1-4 Thus, a systolic heart murmur is a rare clinical examination finding.^5,6

Hyperthyroidism, a significant cause of functional murmurs in cats, produces changes in cardiac contractility, myocardial oxygen consumption, cardiac output, blood pressure, and systemic vascular resistance.^7,8 These changes can lead to turbulent flow in the outflow tracts secondary to increased cardiac output, which can manifest as a murmur during auscultation. Hyperthyroidism can also lead to significant cardiac hypertrophy, primarily through the increased work load on the heart by way of an increase in the hemodynamic load.⁹ Because these changes can mimic hypertrophic cardiomyopathy (HCM), it is important to check thyroid levels in cats showing echocardiographic evidence of HCM (eg, left ventricular hypertrophy, eccentric hypertrophy of the left ventricle).

Physiologic heart murmurs are relatively common in cats and are typically caused by dynamic right ventricular outflow tract obstruction (DRVOTO),¹⁰ a unique physiologic condition in cats in which the flow velocity through the proximal right ventricular outflow tract is increased, possibly due to the comparatively hyperdynamic ventricular systolic function in cats.

The most common causes for heart murmurs in cats are underlying cardiac disease resulting from HCM (specifically, dynamic left ventricular outflow tract obstruction [DLVOTO]) and DRVOTO.^10-15 HCM is the most common form of underlying heart disease affecting cats. Other types of heart disease (eg, congenital heart disease, restrictive cardiomyopathy, unclassified cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy) are also possible differentials.^10,12-19

Hypertension in cats can lead to left ventricular hypertrophy (LVH), subsequent diastolic dysfunction, and development of changes that could result in development of a heart murmur. However, it is important to note that hypertension is not a direct cause of a heart murmur; rather, the secondary effects of sustained systemic hypertension to the left ventricle and valvular structures can lead to LVH and hemodynamic alterations that may result in development of a heart murmur.

B is the correct answer.

A systolic heart murmur may be present in dogs with heartworm disease (Dirofilaria immitis) when there is pulmonary hypertension or worms entangled around the tricuspid valve. The murmur is typically caused by tricuspid regurgitation. However, in cats, the lungs are the primary organ affected, as the relatively low worm burden makes development of pulmonary hypertension and a resultant murmur less likely in cats than in dogs.^1-4 Thus, a systolic heart murmur is a rare clinical examination finding.^5,6

Hyperthyroidism, a significant cause of functional murmurs in cats, produces changes in cardiac contractility, myocardial oxygen consumption, cardiac output, blood pressure, and systemic vascular resistance.^7,8 These changes can lead to turbulent flow in the outflow tracts secondary to increased cardiac output, which can manifest as a murmur during auscultation. Hyperthyroidism can also lead to significant cardiac hypertrophy, primarily through the increased work load on the heart by way of an increase in the hemodynamic load.⁹ Because these changes can mimic hypertrophic cardiomyopathy (HCM), it is important to check thyroid levels in cats showing echocardiographic evidence of HCM (eg, left ventricular hypertrophy, eccentric hypertrophy of the left ventricle).

Physiologic heart murmurs are relatively common in cats and are typically caused by dynamic right ventricular outflow tract obstruction (DRVOTO),¹⁰ a unique physiologic condition in cats in which the flow velocity through the proximal right ventricular outflow tract is increased, possibly due to the comparatively hyperdynamic ventricular systolic function in cats.

The most common causes for heart murmurs in cats are underlying cardiac disease resulting from HCM (specifically, dynamic left ventricular outflow tract obstruction [DLVOTO]) and DRVOTO.^10-15 HCM is the most common form of underlying heart disease affecting cats. Other types of heart disease (eg, congenital heart disease, restrictive cardiomyopathy, unclassified cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy) are also possible differentials.^10,12-19

Hypertension in cats can lead to left ventricular hypertrophy (LVH), subsequent diastolic dysfunction, and development of changes that could result in development of a heart murmur. However, it is important to note that hypertension is not a direct cause of a heart murmur; rather, the secondary effects of sustained systemic hypertension to the left ventricle and valvular structures can lead to LVH and hemodynamic alterations that may result in development of a heart murmur.

B is the correct answer.

A systolic heart murmur may be present in dogs with heartworm disease (Dirofilaria immitis) when there is pulmonary hypertension or worms entangled around the tricuspid valve. The murmur is typically caused by tricuspid regurgitation. However, in cats, the lungs are the primary organ affected, as the relatively low worm burden makes development of pulmonary hypertension and a resultant murmur less likely in cats than in dogs.^1-4 Thus, a systolic heart murmur is a rare clinical examination finding.^5,6

Hyperthyroidism, a significant cause of functional murmurs in cats, produces changes in cardiac contractility, myocardial oxygen consumption, cardiac output, blood pressure, and systemic vascular resistance.^7,8 These changes can lead to turbulent flow in the outflow tracts secondary to increased cardiac output, which can manifest as a murmur during auscultation. Hyperthyroidism can also lead to significant cardiac hypertrophy, primarily through the increased work load on the heart by way of an increase in the hemodynamic load.⁹ Because these changes can mimic hypertrophic cardiomyopathy (HCM), it is important to check thyroid levels in cats showing echocardiographic evidence of HCM (eg, left ventricular hypertrophy, eccentric hypertrophy of the left ventricle).

Physiologic heart murmurs are relatively common in cats and are typically caused by dynamic right ventricular outflow tract obstruction (DRVOTO),¹⁰ a unique physiologic condition in cats in which the flow velocity through the proximal right ventricular outflow tract is increased, possibly due to the comparatively hyperdynamic ventricular systolic function in cats.

The most common causes for heart murmurs in cats are underlying cardiac disease resulting from HCM (specifically, dynamic left ventricular outflow tract obstruction [DLVOTO]) and DRVOTO.^10-15 HCM is the most common form of underlying heart disease affecting cats. Other types of heart disease (eg, congenital heart disease, restrictive cardiomyopathy, unclassified cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy) are also possible differentials.^10,12-19

Hypertension in cats can lead to left ventricular hypertrophy (LVH), subsequent diastolic dysfunction, and development of changes that could result in development of a heart murmur. However, it is important to note that hypertension is not a direct cause of a heart murmur; rather, the secondary effects of sustained systemic hypertension to the left ventricle and valvular structures can lead to LVH and hemodynamic alterations that may result in development of a heart murmur.

B is the correct answer.

A systolic heart murmur may be present in dogs with heartworm disease (Dirofilaria immitis) when there is pulmonary hypertension or worms entangled around the tricuspid valve. The murmur is typically caused by tricuspid regurgitation. However, in cats, the lungs are the primary organ affected, as the relatively low worm burden makes development of pulmonary hypertension and a resultant murmur less likely in cats than in dogs.^1-4 Thus, a systolic heart murmur is a rare clinical examination finding.^5,6

Hyperthyroidism, a significant cause of functional murmurs in cats, produces changes in cardiac contractility, myocardial oxygen consumption, cardiac output, blood pressure, and systemic vascular resistance.^7,8 These changes can lead to turbulent flow in the outflow tracts secondary to increased cardiac output, which can manifest as a murmur during auscultation. Hyperthyroidism can also lead to significant cardiac hypertrophy, primarily through the increased work load on the heart by way of an increase in the hemodynamic load.⁹ Because these changes can mimic hypertrophic cardiomyopathy (HCM), it is important to check thyroid levels in cats showing echocardiographic evidence of HCM (eg, left ventricular hypertrophy, eccentric hypertrophy of the left ventricle).

Physiologic heart murmurs are relatively common in cats and are typically caused by dynamic right ventricular outflow tract obstruction (DRVOTO),¹⁰ a unique physiologic condition in cats in which the flow velocity through the proximal right ventricular outflow tract is increased, possibly due to the comparatively hyperdynamic ventricular systolic function in cats.

The most common causes for heart murmurs in cats are underlying cardiac disease resulting from HCM (specifically, dynamic left ventricular outflow tract obstruction [DLVOTO]) and DRVOTO.^10-15 HCM is the most common form of underlying heart disease affecting cats. Other types of heart disease (eg, congenital heart disease, restrictive cardiomyopathy, unclassified cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy) are also possible differentials.^10,12-19

Hypertension in cats can lead to left ventricular hypertrophy (LVH), subsequent diastolic dysfunction, and development of changes that could result in development of a heart murmur. However, it is important to note that hypertension is not a direct cause of a heart murmur; rather, the secondary effects of sustained systemic hypertension to the left ventricle and valvular structures can lead to LVH and hemodynamic alterations that may result in development of a heart murmur.

C is the correct answer.

Heart murmurs are common in cats, with a prevalence of up to 40.8%, and are more commonly found in older cats.²⁰ 

In one study, higher intensity murmurs, such as those producing a precordial thrill, seemed more likely to be associated with LVH as compared with lower grade murmurs.¹³ However, there was a large overlap in heart murmur grade in cats with and without LVH, limiting the usefulness of auscultation in identifying cats with LVH.¹³ Between 31% and 62% of cats with heart murmurs show evidence of LVH.¹³ Although no direct correlation between murmur intensity/grade and evidence of disease can be made, a more intense murmur may more strongly warrant further diagnostics (eg, echocardiography). Other auscultatory abnormalities (eg, gallop sounds, arrhythmias) may be more reliable for identifying cats with more advanced underlying cardiac disease and an increased risk for developing congestive heart failure (CHF).²¹ Thus, in apparently healthy cats, detection of a heart murmur is not a reliable indicator of cardiomyopathy. Conversely, auscultatory abnormalities (eg, heart murmur, arrhythmia, gallop sound) are not always present in cats with cardiac disease.²⁰ However, it may be considered prudent to pursue advanced diagnostics because of the negative sequelae associated with undetected heart disease.

C is the correct answer.

Heart murmurs are common in cats, with a prevalence of up to 40.8%, and are more commonly found in older cats.²⁰ 

In one study, higher intensity murmurs, such as those producing a precordial thrill, seemed more likely to be associated with LVH as compared with lower grade murmurs.¹³ However, there was a large overlap in heart murmur grade in cats with and without LVH, limiting the usefulness of auscultation in identifying cats with LVH.¹³ Between 31% and 62% of cats with heart murmurs show evidence of LVH.¹³ Although no direct correlation between murmur intensity/grade and evidence of disease can be made, a more intense murmur may more strongly warrant further diagnostics (eg, echocardiography). Other auscultatory abnormalities (eg, gallop sounds, arrhythmias) may be more reliable for identifying cats with more advanced underlying cardiac disease and an increased risk for developing congestive heart failure (CHF).²¹ Thus, in apparently healthy cats, detection of a heart murmur is not a reliable indicator of cardiomyopathy. Conversely, auscultatory abnormalities (eg, heart murmur, arrhythmia, gallop sound) are not always present in cats with cardiac disease.²⁰ However, it may be considered prudent to pursue advanced diagnostics because of the negative sequelae associated with undetected heart disease.

Correct!

Heart murmurs are common in cats, with a prevalence of up to 40.8%, and are more commonly found in older cats.²⁰ 

In one study, higher intensity murmurs, such as those producing a precordial thrill, seemed more likely to be associated with LVH as compared with lower grade murmurs.¹³ However, there was a large overlap in heart murmur grade in cats with and without LVH, limiting the usefulness of auscultation in identifying cats with LVH.¹³ Between 31% and 62% of cats with heart murmurs show evidence of LVH.¹³ Although no direct correlation between murmur intensity/grade and evidence of disease can be made, a more intense murmur may more strongly warrant further diagnostics (eg, echocardiography). Other auscultatory abnormalities (eg, gallop sounds, arrhythmias) may be more reliable for identifying cats with more advanced underlying cardiac disease and an increased risk for developing congestive heart failure (CHF).²¹ Thus, in apparently healthy cats, detection of a heart murmur is not a reliable indicator of cardiomyopathy. Conversely, auscultatory abnormalities (eg, heart murmur, arrhythmia, gallop sound) are not always present in cats with cardiac disease.²⁰ However, it may be considered prudent to pursue advanced diagnostics because of the negative sequelae associated with undetected heart disease.

C is the correct answer.

Heart murmurs are common in cats, with a prevalence of up to 40.8%, and are more commonly found in older cats.²⁰ 

In one study, higher intensity murmurs, such as those producing a precordial thrill, seemed more likely to be associated with LVH as compared with lower grade murmurs.¹³ However, there was a large overlap in heart murmur grade in cats with and without LVH, limiting the usefulness of auscultation in identifying cats with LVH.¹³ Between 31% and 62% of cats with heart murmurs show evidence of LVH.¹³ Although no direct correlation between murmur intensity/grade and evidence of disease can be made, a more intense murmur may more strongly warrant further diagnostics (eg, echocardiography). Other auscultatory abnormalities (eg, gallop sounds, arrhythmias) may be more reliable for identifying cats with more advanced underlying cardiac disease and an increased risk for developing congestive heart failure (CHF).²¹ Thus, in apparently healthy cats, detection of a heart murmur is not a reliable indicator of cardiomyopathy. Conversely, auscultatory abnormalities (eg, heart murmur, arrhythmia, gallop sound) are not always present in cats with cardiac disease.²⁰ However, it may be considered prudent to pursue advanced diagnostics because of the negative sequelae associated with undetected heart disease.

C is the correct answer.

Heart murmurs are common in cats, with a prevalence of up to 40.8%, and are more commonly found in older cats.²⁰ 

In one study, higher intensity murmurs, such as those producing a precordial thrill, seemed more likely to be associated with LVH as compared with lower grade murmurs.¹³ However, there was a large overlap in heart murmur grade in cats with and without LVH, limiting the usefulness of auscultation in identifying cats with LVH.¹³ Between 31% and 62% of cats with heart murmurs show evidence of LVH.¹³ Although no direct correlation between murmur intensity/grade and evidence of disease can be made, a more intense murmur may more strongly warrant further diagnostics (eg, echocardiography). Other auscultatory abnormalities (eg, gallop sounds, arrhythmias) may be more reliable for identifying cats with more advanced underlying cardiac disease and an increased risk for developing congestive heart failure (CHF).²¹ Thus, in apparently healthy cats, detection of a heart murmur is not a reliable indicator of cardiomyopathy. Conversely, auscultatory abnormalities (eg, heart murmur, arrhythmia, gallop sound) are not always present in cats with cardiac disease.²⁰ However, it may be considered prudent to pursue advanced diagnostics because of the negative sequelae associated with undetected heart disease.

D is the correct answer.

Twenty-four–hour ambulatory electrocardiographic monitoring (using Holter monitors) are valuable diagnostic tools for canine patients, for which more information is required about electrical activity, or for patients in which an arrhythmia is an important part of the pre-clinical stages of the disease. However, for most feline cardiomyopathic patients, primary arrhythmias or arrhythmias that precede the development of structural echocardiographic abnormalities do not occur.

Echocardiography is currently considered the gold standard for antemortem diagnosis of underlying cardiac disease in cats, regardless of type of underlying cardiac disease. There is a broad range of phenotypic patterns of HCM and LVH; no one single pattern can be considered characteristic of the disease.^22-24 As compared with other diagnostic tests, echocardiography may provide superior information (eg, disease severity, presence of other comorbidities that may need to be addressed). 

Biomarkers such as N-terminal pro-B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) may aid the general practitioner but are not meant to definitively replace echocardiography. NT-proBNP appears most helpful in distinguishing cardiac from noncardiac causes of respiratory distress in cats. Cats with mild, and even moderate, subclinical heart disease are likely to be falsely identified as normal by both of these diagnostic tests. Additionally, concurrent disease states (eg, hypertension, hyperthyroidism, severe azotemia) may also cause elevations in biomarkers.^25-29 

Radiographs can provide information for a patient with heart disease or respiratory signs, but they are insensitive for detecting mild and moderate subclinical cardiomyopathy in cats.³⁰

HCM has been reported to be familial in specific cat breeds (eg, American shorthair, Maine Coon, Norwegian forest, Sphynx, ragdoll, Persian),^31-35 and genetic testing for HCM in some breeds is available (see Resources). As such, genetic testing in the colony would be an appropriate recommendation for this owner.

D is the correct answer.

Twenty-four–hour ambulatory electrocardiographic monitoring (using Holter monitors) are valuable diagnostic tools for canine patients, for which more information is required about electrical activity, or for patients in which an arrhythmia is an important part of the pre-clinical stages of the disease. However, for most feline cardiomyopathic patients, primary arrhythmias or arrhythmias that precede the development of structural echocardiographic abnormalities do not occur.

Echocardiography is currently considered the gold standard for antemortem diagnosis of underlying cardiac disease in cats, regardless of type of underlying cardiac disease. There is a broad range of phenotypic patterns of HCM and LVH; no one single pattern can be considered characteristic of the disease.^22-24 As compared with other diagnostic tests, echocardiography may provide superior information (eg, disease severity, presence of other comorbidities that may need to be addressed). 

Biomarkers such as N-terminal pro-B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) may aid the general practitioner but are not meant to definitively replace echocardiography. NT-proBNP appears most helpful in distinguishing cardiac from noncardiac causes of respiratory distress in cats. Cats with mild, and even moderate, subclinical heart disease are likely to be falsely identified as normal by both of these diagnostic tests. Additionally, concurrent disease states (eg, hypertension, hyperthyroidism, severe azotemia) may also cause elevations in biomarkers.^25-29 

Radiographs can provide information for a patient with heart disease or respiratory signs, but they are insensitive for detecting mild and moderate subclinical cardiomyopathy in cats.³⁰

HCM has been reported to be familial in specific cat breeds (eg, American shorthair, Maine Coon, Norwegian forest, Sphynx, ragdoll, Persian),^31-35 and genetic testing for HCM in some breeds is available (see Resources). As such, genetic testing in the colony would be an appropriate recommendation for this owner.

D is the correct answer.

Twenty-four–hour ambulatory electrocardiographic monitoring (using Holter monitors) are valuable diagnostic tools for canine patients, for which more information is required about electrical activity, or for patients in which an arrhythmia is an important part of the pre-clinical stages of the disease. However, for most feline cardiomyopathic patients, primary arrhythmias or arrhythmias that precede the development of structural echocardiographic abnormalities do not occur.

Echocardiography is currently considered the gold standard for antemortem diagnosis of underlying cardiac disease in cats, regardless of type of underlying cardiac disease. There is a broad range of phenotypic patterns of HCM and LVH; no one single pattern can be considered characteristic of the disease.^22-24 As compared with other diagnostic tests, echocardiography may provide superior information (eg, disease severity, presence of other comorbidities that may need to be addressed). 

Biomarkers such as N-terminal pro-B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) may aid the general practitioner but are not meant to definitively replace echocardiography. NT-proBNP appears most helpful in distinguishing cardiac from noncardiac causes of respiratory distress in cats. Cats with mild, and even moderate, subclinical heart disease are likely to be falsely identified as normal by both of these diagnostic tests. Additionally, concurrent disease states (eg, hypertension, hyperthyroidism, severe azotemia) may also cause elevations in biomarkers.^25-29 

Radiographs can provide information for a patient with heart disease or respiratory signs, but they are insensitive for detecting mild and moderate subclinical cardiomyopathy in cats.³⁰

HCM has been reported to be familial in specific cat breeds (eg, American shorthair, Maine Coon, Norwegian forest, Sphynx, ragdoll, Persian),^31-35 and genetic testing for HCM in some breeds is available (see Resources). As such, genetic testing in the colony would be an appropriate recommendation for this owner.

Correct!

Twenty-four–hour ambulatory electrocardiographic monitoring (using Holter monitors) are valuable diagnostic tools for canine patients, for which more information is required about electrical activity, or for patients in which an arrhythmia is an important part of the pre-clinical stages of the disease. However, for most feline cardiomyopathic patients, primary arrhythmias or arrhythmias that precede the development of structural echocardiographic abnormalities do not occur.

Echocardiography is currently considered the gold standard for antemortem diagnosis of underlying cardiac disease in cats, regardless of type of underlying cardiac disease. There is a broad range of phenotypic patterns of HCM and LVH; no one single pattern can be considered characteristic of the disease.^22-24 As compared with other diagnostic tests, echocardiography may provide superior information (eg, disease severity, presence of other comorbidities that may need to be addressed). 

Biomarkers such as N-terminal pro-B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) may aid the general practitioner but are not meant to definitively replace echocardiography. NT-proBNP appears most helpful in distinguishing cardiac from noncardiac causes of respiratory distress in cats. Cats with mild, and even moderate, subclinical heart disease are likely to be falsely identified as normal by both of these diagnostic tests. Additionally, concurrent disease states (eg, hypertension, hyperthyroidism, severe azotemia) may also cause elevations in biomarkers.^25-29 

Radiographs can provide information for a patient with heart disease or respiratory signs, but they are insensitive for detecting mild and moderate subclinical cardiomyopathy in cats.³⁰

HCM has been reported to be familial in specific cat breeds (eg, American shorthair, Maine Coon, Norwegian forest, Sphynx, ragdoll, Persian),^31-35 and genetic testing for HCM in some breeds is available (see Resources). As such, genetic testing in the colony would be an appropriate recommendation for this owner.

D is the correct answer.

Twenty-four–hour ambulatory electrocardiographic monitoring (using Holter monitors) are valuable diagnostic tools for canine patients, for which more information is required about electrical activity, or for patients in which an arrhythmia is an important part of the pre-clinical stages of the disease. However, for most feline cardiomyopathic patients, primary arrhythmias or arrhythmias that precede the development of structural echocardiographic abnormalities do not occur.

Echocardiography is currently considered the gold standard for antemortem diagnosis of underlying cardiac disease in cats, regardless of type of underlying cardiac disease. There is a broad range of phenotypic patterns of HCM and LVH; no one single pattern can be considered characteristic of the disease.^22-24 As compared with other diagnostic tests, echocardiography may provide superior information (eg, disease severity, presence of other comorbidities that may need to be addressed). 

Biomarkers such as N-terminal pro-B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) may aid the general practitioner but are not meant to definitively replace echocardiography. NT-proBNP appears most helpful in distinguishing cardiac from noncardiac causes of respiratory distress in cats. Cats with mild, and even moderate, subclinical heart disease are likely to be falsely identified as normal by both of these diagnostic tests. Additionally, concurrent disease states (eg, hypertension, hyperthyroidism, severe azotemia) may also cause elevations in biomarkers.^25-29 

Radiographs can provide information for a patient with heart disease or respiratory signs, but they are insensitive for detecting mild and moderate subclinical cardiomyopathy in cats.³⁰

HCM has been reported to be familial in specific cat breeds (eg, American shorthair, Maine Coon, Norwegian forest, Sphynx, ragdoll, Persian),^31-35 and genetic testing for HCM in some breeds is available (see Resources). As such, genetic testing in the colony would be an appropriate recommendation for this owner.

Correct!

Although there is consensus for the treatment of cats with evidence of HCM,³⁶ no current data demonstrate a strong treatment benefit for cats with mild to moderate subclinical cardiomyopathy.²⁶ As such, differing opinions exist regarding an appropriate treatment protocol for a cat with subclinical HCM, and treatment is largely based on human trials and experimental research models. The goals of treating a clinically normally patient are to improve diastolic function, decrease myocardial ischemia, and prolong the time to CHF development. Left ventricular outflow tract obstruction (LVOTO) secondary to SAM is a common finding in patients with hypertrophic obstructive cardiomyopathy (HOCM).^24,32 SAM is an important factor to determine in cases of HCM because it may warrant additional medical management. Echocardiographic findings can generate important information regarding additional treatment and prognosis.¹⁷

Atenolol is a β-blocker that slows the heart rate and prolongs diastole, which may allow more efficient flow through the LVOT; in addition, atenolol can reduce myocardial oxygen demand.³⁶ It has been used to treat LVOTO and has been shown to reduce the velocity through the LVOT after a single oral dose.³⁷ A recent study evaluating cats with subclinical HCM demonstrated a reduction in heart rate, ventricular arrhythmia frequency and complexity, and LVOT velocity without a significant reduction in blood pressure after atenolol administration.³⁷ Although cats with HOCM are commonly administered atenolol, no strong evidence exists showing that treating cats with subclinical or preclinical HCM with β-blockers or ACE-inhibitors is effective at prolonging life.^{36, 38-40}

Because Bagheera shows no evidence of CHF, systolic dysfunction, or left atrial enlargement, diuretic therapy with furosemide, inotropic support with pimobendan, and antithrombotic agents (eg, clopidogrel) are not considered necessary.

Amlodipine is not recommended because it may cause peripheral vasodilation, which can decrease LV filling and worsen left ventricular outflow tract obstruction.

A is the correct answer.

Although there is consensus for the treatment of cats with evidence of HCM,³⁶ no current data demonstrate a strong treatment benefit for cats with mild to moderate subclinical cardiomyopathy.²⁶ As such, differing opinions exist regarding an appropriate treatment protocol for a cat with subclinical HCM, and treatment is largely based on human trials and experimental research models. The goals of treating a clinically normally patient are to improve diastolic function, decrease myocardial ischemia, and prolong the time to CHF development. Left ventricular outflow tract obstruction (LVOTO) secondary to SAM is a common finding in patients with hypertrophic obstructive cardiomyopathy (HOCM).^24,32 SAM is an important factor to determine in cases of HCM because it may warrant additional medical management. Echocardiographic findings can generate important information regarding additional treatment and prognosis.¹⁷

Atenolol is a β-blocker that slows the heart rate and prolongs diastole, which may allow more efficient flow through the LVOT; in addition, atenolol can reduce myocardial oxygen demand.³⁶ It has been used to treat LVOTO and has been shown to reduce the velocity through the LVOT after a single oral dose.³⁷ A recent study evaluating cats with subclinical HCM demonstrated a reduction in heart rate, ventricular arrhythmia frequency and complexity, and LVOT velocity without a significant reduction in blood pressure after atenolol administration.³⁷ Although cats with HOCM are commonly administered atenolol, no strong evidence exists showing that treating cats with subclinical or preclinical HCM with β-blockers or ACE-inhibitors is effective at prolonging life.^{36, 38-40}

Because Bagheera shows no evidence of CHF, systolic dysfunction, or left atrial enlargement, diuretic therapy with furosemide, inotropic support with pimobendan, and antithrombotic agents (eg, clopidogrel) are not considered necessary.

Amlodipine is not recommended because it may cause peripheral vasodilation, which can decrease LV filling and worsen left ventricular outflow tract obstruction.

A is the correct answer.

Although there is consensus for the treatment of cats with evidence of HCM,³⁶ no current data demonstrate a strong treatment benefit for cats with mild to moderate subclinical cardiomyopathy.²⁶ As such, differing opinions exist regarding an appropriate treatment protocol for a cat with subclinical HCM, and treatment is largely based on human trials and experimental research models. The goals of treating a clinically normally patient are to improve diastolic function, decrease myocardial ischemia, and prolong the time to CHF development. Left ventricular outflow tract obstruction (LVOTO) secondary to SAM is a common finding in patients with hypertrophic obstructive cardiomyopathy (HOCM).^24,32 SAM is an important factor to determine in cases of HCM because it may warrant additional medical management. Echocardiographic findings can generate important information regarding additional treatment and prognosis.¹⁷

Atenolol is a β-blocker that slows the heart rate and prolongs diastole, which may allow more efficient flow through the LVOT; in addition, atenolol can reduce myocardial oxygen demand.³⁶ It has been used to treat LVOTO and has been shown to reduce the velocity through the LVOT after a single oral dose.³⁷ A recent study evaluating cats with subclinical HCM demonstrated a reduction in heart rate, ventricular arrhythmia frequency and complexity, and LVOT velocity without a significant reduction in blood pressure after atenolol administration.³⁷ Although cats with HOCM are commonly administered atenolol, no strong evidence exists showing that treating cats with subclinical or preclinical HCM with β-blockers or ACE-inhibitors is effective at prolonging life.^{36, 38-40}

Because Bagheera shows no evidence of CHF, systolic dysfunction, or left atrial enlargement, diuretic therapy with furosemide, inotropic support with pimobendan, and antithrombotic agents (eg, clopidogrel) are not considered necessary.

Amlodipine is not recommended because it may cause peripheral vasodilation, which can decrease LV filling and worsen left ventricular outflow tract obstruction.

A is the correct answer.

Although there is consensus for the treatment of cats with evidence of HCM,³⁶ no current data demonstrate a strong treatment benefit for cats with mild to moderate subclinical cardiomyopathy.²⁶ As such, differing opinions exist regarding an appropriate treatment protocol for a cat with subclinical HCM, and treatment is largely based on human trials and experimental research models. The goals of treating a clinically normally patient are to improve diastolic function, decrease myocardial ischemia, and prolong the time to CHF development. Left ventricular outflow tract obstruction (LVOTO) secondary to SAM is a common finding in patients with hypertrophic obstructive cardiomyopathy (HOCM).^24,32 SAM is an important factor to determine in cases of HCM because it may warrant additional medical management. Echocardiographic findings can generate important information regarding additional treatment and prognosis.¹⁷

Atenolol is a β-blocker that slows the heart rate and prolongs diastole, which may allow more efficient flow through the LVOT; in addition, atenolol can reduce myocardial oxygen demand.³⁶ It has been used to treat LVOTO and has been shown to reduce the velocity through the LVOT after a single oral dose.³⁷ A recent study evaluating cats with subclinical HCM demonstrated a reduction in heart rate, ventricular arrhythmia frequency and complexity, and LVOT velocity without a significant reduction in blood pressure after atenolol administration.³⁷ Although cats with HOCM are commonly administered atenolol, no strong evidence exists showing that treating cats with subclinical or preclinical HCM with β-blockers or ACE-inhibitors is effective at prolonging life.^{36, 38-40}

Because Bagheera shows no evidence of CHF, systolic dysfunction, or left atrial enlargement, diuretic therapy with furosemide, inotropic support with pimobendan, and antithrombotic agents (eg, clopidogrel) are not considered necessary.

Amlodipine is not recommended because it may cause peripheral vasodilation, which can decrease LV filling and worsen left ventricular outflow tract obstruction.

A is the correct answer.

Although there is consensus for the treatment of cats with evidence of HCM,³⁶ no current data demonstrate a strong treatment benefit for cats with mild to moderate subclinical cardiomyopathy.²⁶ As such, differing opinions exist regarding an appropriate treatment protocol for a cat with subclinical HCM, and treatment is largely based on human trials and experimental research models. The goals of treating a clinically normally patient are to improve diastolic function, decrease myocardial ischemia, and prolong the time to CHF development. Left ventricular outflow tract obstruction (LVOTO) secondary to SAM is a common finding in patients with hypertrophic obstructive cardiomyopathy (HOCM).^24,32 SAM is an important factor to determine in cases of HCM because it may warrant additional medical management. Echocardiographic findings can generate important information regarding additional treatment and prognosis.¹⁷

Atenolol is a β-blocker that slows the heart rate and prolongs diastole, which may allow more efficient flow through the LVOT; in addition, atenolol can reduce myocardial oxygen demand.³⁶ It has been used to treat LVOTO and has been shown to reduce the velocity through the LVOT after a single oral dose.³⁷ A recent study evaluating cats with subclinical HCM demonstrated a reduction in heart rate, ventricular arrhythmia frequency and complexity, and LVOT velocity without a significant reduction in blood pressure after atenolol administration.³⁷ Although cats with HOCM are commonly administered atenolol, no strong evidence exists showing that treating cats with subclinical or preclinical HCM with β-blockers or ACE-inhibitors is effective at prolonging life.^{36, 38-40}

Because Bagheera shows no evidence of CHF, systolic dysfunction, or left atrial enlargement, diuretic therapy with furosemide, inotropic support with pimobendan, and antithrombotic agents (eg, clopidogrel) are not considered necessary.

Amlodipine is not recommended because it may cause peripheral vasodilation, which can decrease LV filling and worsen left ventricular outflow tract obstruction.

The correct answer is B.

One negative sequela associated with HCM is the generation of a thromboembolism, known as feline aortic thromboembolism (ATE, or saddle thrombus); ATE occurrence in cases of HCM ranges from 5% to 17%.^10,16,41 Treatment would ideally be implemented before the development of ATE (primary prevention).

Factors associated with ATE include LA enlargement and SEC visible on an echocardiogram42; thus, current recommendations include considering primary prevention in cats with echocardiographic evidence of LA enlargement or evidence of SEC.⁴³

Clopidogrel is commonly used for primary prevention of ATE. A recent study evaluating antithrombotic therapy in cats with underlying cardiac disease and previous ATE formation found that cats treated with clopidogrel were significantly less likely to have a recurrent ATE event and that clopidogrel-treated cats had a longer median time to a recurrent event as compared with cats treated with aspirin.⁴⁴ Of the clopidogrel-treated cats, 26% did not have a recurrent ATE event or die from a cardiac cause, as compared with 11% of cats in the aspirin-treated group; in addition, the clopidogrel-treated cats had a longer median survival time.⁴⁴ However, the cats assessed in this study had already had a thromboembolic event, unlike cats considered “at risk” like Bagheera. Note: Because clopidogrel is extremely bitter, it can be combined into a gelatin capsule with other medications to make administration easier for the owner.

Other therapies exist for the treatment of ATE, including warfarin and streptokinase, though typically these medications are not used in primary prevention; additionally, there are limited data on how these other thromboembolic therapies (particularly those used in human medicine) compare with clopidogrel. 

Cyclosporine is an immunosuppressive agent that is not associated with treatment of ATE.

Correct!

One negative sequela associated with HCM is the generation of a thromboembolism, known as feline aortic thromboembolism (ATE, or saddle thrombus); ATE occurrence in cases of HCM ranges from 5% to 17%.^10,16,41 Treatment would ideally be implemented before the development of ATE (primary prevention).

Factors associated with ATE include LA enlargement and SEC visible on an echocardiogram42; thus, current recommendations include considering primary prevention in cats with echocardiographic evidence of LA enlargement or evidence of SEC.⁴³

Clopidogrel is commonly used for primary prevention of ATE. A recent study evaluating antithrombotic therapy in cats with underlying cardiac disease and previous ATE formation found that cats treated with clopidogrel were significantly less likely to have a recurrent ATE event and that clopidogrel-treated cats had a longer median time to a recurrent event as compared with cats treated with aspirin.⁴⁴ Of the clopidogrel-treated cats, 26% did not have a recurrent ATE event or die from a cardiac cause, as compared with 11% of cats in the aspirin-treated group; in addition, the clopidogrel-treated cats had a longer median survival time.⁴⁴ However, the cats assessed in this study had already had a thromboembolic event, unlike cats considered “at risk” like Bagheera. Note: Because clopidogrel is extremely bitter, it can be combined into a gelatin capsule with other medications to make administration easier for the owner.

Other therapies exist for the treatment of ATE, including warfarin and streptokinase, though typically these medications are not used in primary prevention; additionally, there are limited data on how these other thromboembolic therapies (particularly those used in human medicine) compare with clopidogrel. 

Cyclosporine is an immunosuppressive agent that is not associated with treatment of ATE.

The correct answer is B.

One negative sequela associated with HCM is the generation of a thromboembolism, known as feline aortic thromboembolism (ATE, or saddle thrombus); ATE occurrence in cases of HCM ranges from 5% to 17%.^10,16,41 Treatment would ideally be implemented before the development of ATE (primary prevention).

Factors associated with ATE include LA enlargement and SEC visible on an echocardiogram42; thus, current recommendations include considering primary prevention in cats with echocardiographic evidence of LA enlargement or evidence of SEC.⁴³

Clopidogrel is commonly used for primary prevention of ATE. A recent study evaluating antithrombotic therapy in cats with underlying cardiac disease and previous ATE formation found that cats treated with clopidogrel were significantly less likely to have a recurrent ATE event and that clopidogrel-treated cats had a longer median time to a recurrent event as compared with cats treated with aspirin.⁴⁴ Of the clopidogrel-treated cats, 26% did not have a recurrent ATE event or die from a cardiac cause, as compared with 11% of cats in the aspirin-treated group; in addition, the clopidogrel-treated cats had a longer median survival time.⁴⁴ However, the cats assessed in this study had already had a thromboembolic event, unlike cats considered “at risk” like Bagheera. Note: Because clopidogrel is extremely bitter, it can be combined into a gelatin capsule with other medications to make administration easier for the owner.

Other therapies exist for the treatment of ATE, including warfarin and streptokinase, though typically these medications are not used in primary prevention; additionally, there are limited data on how these other thromboembolic therapies (particularly those used in human medicine) compare with clopidogrel. 

Cyclosporine is an immunosuppressive agent that is not associated with treatment of ATE.

The correct answer is B.

One negative sequela associated with HCM is the generation of a thromboembolism, known as feline aortic thromboembolism (ATE, or saddle thrombus); ATE occurrence in cases of HCM ranges from 5% to 17%.^10,16,41 Treatment would ideally be implemented before the development of ATE (primary prevention).

Factors associated with ATE include LA enlargement and SEC visible on an echocardiogram42; thus, current recommendations include considering primary prevention in cats with echocardiographic evidence of LA enlargement or evidence of SEC.⁴³

Clopidogrel is commonly used for primary prevention of ATE. A recent study evaluating antithrombotic therapy in cats with underlying cardiac disease and previous ATE formation found that cats treated with clopidogrel were significantly less likely to have a recurrent ATE event and that clopidogrel-treated cats had a longer median time to a recurrent event as compared with cats treated with aspirin.⁴⁴ Of the clopidogrel-treated cats, 26% did not have a recurrent ATE event or die from a cardiac cause, as compared with 11% of cats in the aspirin-treated group; in addition, the clopidogrel-treated cats had a longer median survival time.⁴⁴ However, the cats assessed in this study had already had a thromboembolic event, unlike cats considered “at risk” like Bagheera. Note: Because clopidogrel is extremely bitter, it can be combined into a gelatin capsule with other medications to make administration easier for the owner.

Other therapies exist for the treatment of ATE, including warfarin and streptokinase, though typically these medications are not used in primary prevention; additionally, there are limited data on how these other thromboembolic therapies (particularly those used in human medicine) compare with clopidogrel. 

Cyclosporine is an immunosuppressive agent that is not associated with treatment of ATE.

The correct answer is B.

One negative sequela associated with HCM is the generation of a thromboembolism, known as feline aortic thromboembolism (ATE, or saddle thrombus); ATE occurrence in cases of HCM ranges from 5% to 17%.^10,16,41 Treatment would ideally be implemented before the development of ATE (primary prevention).

Factors associated with ATE include LA enlargement and SEC visible on an echocardiogram42; thus, current recommendations include considering primary prevention in cats with echocardiographic evidence of LA enlargement or evidence of SEC.⁴³

Clopidogrel is commonly used for primary prevention of ATE. A recent study evaluating antithrombotic therapy in cats with underlying cardiac disease and previous ATE formation found that cats treated with clopidogrel were significantly less likely to have a recurrent ATE event and that clopidogrel-treated cats had a longer median time to a recurrent event as compared with cats treated with aspirin.⁴⁴ Of the clopidogrel-treated cats, 26% did not have a recurrent ATE event or die from a cardiac cause, as compared with 11% of cats in the aspirin-treated group; in addition, the clopidogrel-treated cats had a longer median survival time.⁴⁴ However, the cats assessed in this study had already had a thromboembolic event, unlike cats considered “at risk” like Bagheera. Note: Because clopidogrel is extremely bitter, it can be combined into a gelatin capsule with other medications to make administration easier for the owner.

Other therapies exist for the treatment of ATE, including warfarin and streptokinase, though typically these medications are not used in primary prevention; additionally, there are limited data on how these other thromboembolic therapies (particularly those used in human medicine) compare with clopidogrel. 

Cyclosporine is an immunosuppressive agent that is not associated with treatment of ATE.

B is the correct answer.

Overall prognosis in cases of HCM depends on the rate of disease progression but is generally good (>5 years) if subclinical; this decreases significantly if CHF is present (18 months) or if there is evidence of ATE (7 months).^16,17,41 Cats with ATE have much shorter median survival times as compared with cats with subclinical disease or cats with CHF, mostly due to low acute survival rates.⁴⁷ CHF and ATE are the most common causes of cardiac death, followed by sudden cardiac death.^17,41 Decreased LA systolic function, decreased LV systolic function, and extreme hypertrophy (>9mm) have been shown to be independent predictors of an increased hazard of cardiac death.²¹ Left atrial size is reported to have prognostic value in cats with HCM.¹⁷ Age is also a negative prognostic indicator.²¹ Young male purebreed cats may also have a more aggressive disease progression and thus a shorter survival time.^45,46

Correct!

Overall prognosis in cases of HCM depends on the rate of disease progression but is generally good (>5 years) if subclinical; this decreases significantly if CHF is present (18 months) or if there is evidence of ATE (7 months).^16,17,41 Cats with ATE have much shorter median survival times as compared with cats with subclinical disease or cats with CHF, mostly due to low acute survival rates.⁴⁷ CHF and ATE are the most common causes of cardiac death, followed by sudden cardiac death.^17,41 Decreased LA systolic function, decreased LV systolic function, and extreme hypertrophy (>9mm) have been shown to be independent predictors of an increased hazard of cardiac death.²¹ Left atrial size is reported to have prognostic value in cats with HCM.¹⁷ Age is also a negative prognostic indicator.²¹ Young male purebreed cats may also have a more aggressive disease progression and thus a shorter survival time.^45,46

B is the correct answer.

Overall prognosis in cases of HCM depends on the rate of disease progression but is generally good (>5 years) if subclinical; this decreases significantly if CHF is present (18 months) or if there is evidence of ATE (7 months).^16,17,41 Cats with ATE have much shorter median survival times as compared with cats with subclinical disease or cats with CHF, mostly due to low acute survival rates.⁴⁷ CHF and ATE are the most common causes of cardiac death, followed by sudden cardiac death.^17,41 Decreased LA systolic function, decreased LV systolic function, and extreme hypertrophy (>9mm) have been shown to be independent predictors of an increased hazard of cardiac death.²¹ Left atrial size is reported to have prognostic value in cats with HCM.¹⁷ Age is also a negative prognostic indicator.²¹ Young male purebreed cats may also have a more aggressive disease progression and thus a shorter survival time.^45,46

B is the correct answer.

Overall prognosis in cases of HCM depends on the rate of disease progression but is generally good (>5 years) if subclinical; this decreases significantly if CHF is present (18 months) or if there is evidence of ATE (7 months).^16,17,41 Cats with ATE have much shorter median survival times as compared with cats with subclinical disease or cats with CHF, mostly due to low acute survival rates.⁴⁷ CHF and ATE are the most common causes of cardiac death, followed by sudden cardiac death.^17,41 Decreased LA systolic function, decreased LV systolic function, and extreme hypertrophy (>9mm) have been shown to be independent predictors of an increased hazard of cardiac death.²¹ Left atrial size is reported to have prognostic value in cats with HCM.¹⁷ Age is also a negative prognostic indicator.²¹ Young male purebreed cats may also have a more aggressive disease progression and thus a shorter survival time.^45,46

B is the correct answer.

Overall prognosis in cases of HCM depends on the rate of disease progression but is generally good (>5 years) if subclinical; this decreases significantly if CHF is present (18 months) or if there is evidence of ATE (7 months).^16,17,41 Cats with ATE have much shorter median survival times as compared with cats with subclinical disease or cats with CHF, mostly due to low acute survival rates.⁴⁷ CHF and ATE are the most common causes of cardiac death, followed by sudden cardiac death.^17,41 Decreased LA systolic function, decreased LV systolic function, and extreme hypertrophy (>9mm) have been shown to be independent predictors of an increased hazard of cardiac death.²¹ Left atrial size is reported to have prognostic value in cats with HCM.¹⁷ Age is also a negative prognostic indicator.²¹ Young male purebreed cats may also have a more aggressive disease progression and thus a shorter survival time.^45,46