Cardiovascular Disorders in Companion Animals
- Dr Andrew Matole, BVetMed, MSc
- Jul 13
- 13 min read
Updated: Jul 13
Introduction
At The Andys Veterinary Clinic, we care about your pet’s heart health. Like humans, cardiovascular disorders in companion animals, such as dogs and cats, encompass a range of medical conditions affecting the heart and blood vessels. These disorders can be congenital (present at birth) or acquired (developing later in life), and their causes may include genetic predisposition, infections, age-related degeneration, endocrine (hormonal) abnormalities, or lifestyle influences such as diet and physical activity (Ettinger & Feldman, 2017).
Common Cardiovascular Disorders
a. Congenital Heart Diseases
Patent Ductus Arteriosus (PDA)
Patent Ductus Arteriosus (PDA) is a congenital heart defect in dogs and cats where a normal fetal blood vessel, the ductus arteriosus, fails to close after birth. Before birth, this vessel allows blood to bypass the lungs since oxygen is supplied through the placenta. However, after birth, as the lungs take over oxygenation, the blood vessel is expected to close within the first few days of life. When it remains open (or “patent”), it causes abnormal blood flow from the aorta to the pulmonary artery, leading to increased blood volume in the lungs and overworking of the heart (Bonagura & Twedt, 2013; Ettinger & Feldman, 2017).
Clinically, PDA may result in signs such as rapid breathing, coughing, exercise intolerance, or poor growth. Left untreated, it often leads to congestive heart failure within the first year of life (Kittleson & Kienle, 1998).
PDA is typically diagnosed using echocardiography and auscultation of a characteristic continuous heart murmur. Treatment involves surgical ligation or transcatheter device occlusion, both of which offer an excellent prognosis when performed early (Buchanan, 2001; Ettinger & Feldman, 2017).
Ventricular Septal Defect (VSD)
Ventricular Septal Defect (VSD) is a congenital heart condition in which an abnormal opening (a "hole") in the wall (septum) that separates the two lower chambers of the heart—the left and right ventricles—occurs. This defect allows blood to flow directly from the left ventricle (which pumps oxygen-rich blood) to the right ventricle (which carries oxygen-poor blood), resulting in inefficient circulation (Bonagura & Twedt, 2013; Ettinger & Feldman, 2017).
In healthy hearts, the septum prevents the mixing of oxygenated and deoxygenated blood. But with a VSD, the extra blood volume entering the lungs can overload the heart and lead to pulmonary overcirculation and eventually congestive heart failure, especially in moderate to large defects (Kittleson & Kienle, 1998).
Clinical signs depend on the size of the defect and may include:
Rapid breathing or shortness of breath
Poor growth or weight gain
Exercise intolerance
Heart murmur detected on physical exam
VSDs are commonly diagnosed via echocardiography, which allows visualisation of the defect and measurement of blood flow. Small VSDs may close spontaneously or remain clinically insignificant, while larger ones may require surgical or interventional closure (Buchanan, 2001; Fuentes et al., 2003).
Pulmonic and Aortic Stenosis
Pulmonic and Aortic Stenosis are two types of congenital heart defects in dogs and, less commonly, in cats, where one of the heart’s outflow valves is narrowed, making it difficult for blood to flow out of the heart properly. These conditions increase the workload on the heart, potentially leading to heart enlargement, reduced blood flow, and eventually heart failure if not managed appropriately.
Pulmonic Stenosis (PS)
Pulmonic stenosis is a narrowing of the pulmonary valve, which regulates blood flow from the right ventricle into the pulmonary artery and lungs.
Causes & Pathophysiology
Often valvular (leaflets fused or thickened)
It can also be subvalvular or supravalvular
Leads to right ventricular hypertrophy due to increased pressure (Bonagura & Twedt, 2013)
Clinical Signs
Heart murmur (typically systolic, loudest at the left base)
Exercise intolerance
Syncope (fainting)
Right-sided heart failure (in severe cases)
Diagnosis & Treatment
Diagnosed with echocardiography and Doppler studies
Balloon valvuloplasty is the treatment of choice for many dogs with valvular PS (Buchanan, 2001)
Beta-blockers like atenolol may be used to reduce heart workload in moderate to severe cases
Aortic Stenosis (AS)
Aortic stenosis is a narrowing at or just below the aortic valve, restricting blood flow from the left ventricle to the aorta and the rest of the body.
Forms:
Subvalvular aortic stenosis (SAS) is the most common form in dogs
Most common in Boxers, Golden Retrievers, and Newfoundlands
Pathophysiology
Causes left ventricular hypertrophy due to resistance to outflow
Increased risk of arrhythmias and sudden death in severe cases (Kittleson & Kienle, 1998)
Clinical Signs:
Left basilar systolic murmur
Exercise intolerance
Fainting episodes
Sudden death (especially during exertion)
Diagnosis & Treatment:
Confirmed by echocardiography with Doppler
Beta-blockers (e.g., atenolol) are used in moderate to severe cases to reduce heart oxygen demand and arrhythmia risk
Surgical options are limited and usually reserved for severe, refractory cases
Congenital heart diseases are often diagnosed in younger animals and may require surgical intervention or medical management (Bonagura & Twedt, 2013).
b. Acquired Heart Diseases
Chronic Valvular Heart Disease (CVHD)
Chronic Valvular Heart Disease (CVHD)—also known as myxomatous mitral valve disease (MMVD) or endocardiosis — is the most common acquired heart disease in dogs, particularly in small and medium breeds. It involves progressive degeneration of the heart valves, especially the mitral valve (between the left atrium and ventricle), leading to valvular insufficiency and blood regurgitation.
Pathophysiology
In CVHD, the mitral valve becomes thickened and misshapen, failing to close properly during contraction.
This allows blood to leak backwards (regurgitate) into the left atrium.
Over time, the left atrium and ventricle enlarge, and pulmonary pressure increases, leading to congestive heart failure (CHF) if untreated (Atkins et al., 2009; Ettinger & Feldman, 2017).
Commonly Affected Breeds
Cavalier King Charles Spaniel
Dachshund
Miniature and Toy Poodles
Chihuahua
Cocker Spaniel
Onset is usually middle-aged to older dogs, and males are slightly more predisposed (Bonagura & Twedt, 2013).
Clinical Signs
Heart murmur (typically left apical systolic)
Coughing (especially at night or after exercise)
Exercise intolerance
Laboured breathing or panting
Syncope (fainting episodes)
Weight loss and muscle wasting in advanced disease
Diagnosis
Auscultation to detect murmurs
Thoracic radiographs (for heart enlargement and pulmonary oedema)
Echocardiography (gold standard to assess valve structure and function)
Biomarkers like NT-proBNP may support diagnosis and monitor progression
Treatment and Management (per ACVIM 2009 guidelines – Atkins et al.)
Stage | Condition | Treatment |
B1 | Murmur but no structural changes | Monitor; no treatment necessary |
B2 | Murmur with left atrial and ventricular enlargement | Start pimobendan ± ACE inhibitor |
C | Clinical signs of CHF (cough, dyspnea, oedema) | Add furosemide, enalapril/benazepril, pimobendan, oxygen if needed |
D | Refractory CHF | Intensify treatment (e.g., spironolactone, dietary adjustments, rechecks) |
Prognosis
Highly variable, depending on stage at diagnosis and response to therapy.
Dogs in stage B1 may remain stable for years.
With proper treatment, even stage C dogs can live months to years with a good quality of life (Atkins et al., 2009; Boswood et al., 2016).
Dilated Cardiomyopathy (DCM)
Dilated Cardiomyopathy (DCM) is a serious acquired heart disease seen primarily in medium - to large-breed dogs, and rarely in cats. It is characterised by a weakening of the heart muscle, leading to enlargement (dilation) of the heart chambers and reduced ability to pump blood effectively.
Pathophysiology
In DCM, the heart muscle (especially the left ventricle) becomes thin and weak, resulting in poor contractility.
This causes blood to back up into the lungs or body, leading to signs of congestive heart failure (CHF).
Over time, it can also result in arrhythmias and sudden death (Ettinger & Feldman, 2017).
Commonly Affected Breeds
Doberman Pinschers
Boxers
Great Danes
Irish Wolfhounds
Cocker Spaniels
Golden Retrievers
Note: Some cases in Golden Retrievers and Cocker Spaniels have been linked to taurine deficiency, a potentially reversible condition (Freeman et al., 2018).
Clinical Signs
Coughing
Laboured breathing (dyspnea)
Weakness or fainting (syncope)
Abdominal distension (ascites)
Exercise intolerance
Sudden death (especially in Dobermans)
Diagnosis
Echocardiography (gold standard): shows ventricular dilation and poor contraction
ECG: detects arrhythmias (esp. ventricular premature complexes in Dobermans)
Thoracic radiographs show an enlarged heart and pulmonary oedema
NT-proBNP and troponin I: useful biomarkers for early detection
Holter monitor: used in breeds prone to silent arrhythmias (e.g., Dobermans)
Note:
NT-proBNP and troponin I are two important cardiac biomarkers in veterinary cardiology to assess heart health.
NT-proBNP is a protein fragment released from the heart muscle (mostly the ventricles) when stretched or under stress, such as during heart enlargement or failure. It is a circulating marker of cardiac strain (Oyama et al., 2007).
Troponin I is a protein involved in muscle contraction. It is found in heart muscle cells and is released into the bloodstream when they are damaged or die (Sleeper et al., 2001).
NT-proBNP and troponin I Comparison Chart
Feature | NT-proBNP | Troponin I |
Released from | Ventricular myocardium | Damaged heart muscle cells |
Triggered by | Stretch/pressure overload | Cell injury/death |
Indicates | Volume overload/heart strain | Myocardial damage |
Common in | CHF, CVHD, DCM | Myocarditis, DCM, trauma, toxins |
Use | Screening, diagnosis, and monitoring | Diagnosis of cardiac injury |
Treatment
Treatment is aimed at improving heart function, controlling symptoms, and slowing progression:
Drug | Purpose |
Pimobendan | Positive inotrope to improve contractility |
ACE inhibitors | Reduce afterload and slow disease progression |
Diuretics | Manage fluid buildup (e.g., furosemide) |
Antiarrhythmics | Control abnormal rhythms (e.g., sotalol, mexiletine) |
Taurine supplementation | In taurine-deficiency cases (Freeman et al., 2018) |
Prognosis
Guarded to poor in most cases once clinical signs develop
Dobermans: high risk of sudden death; may benefit from early screening with Holter and NT-proBNP
Dogs with nutritional DCM (taurine deficiency) may improve significantly with diet change and supplements
Hypertrophic Cardiomyopathy (HCM)
Hypertrophic Cardiomyopathy (HCM) is the most common heart disease in cats and also occurs rarely in dogs. It is a primary myocardial disorder where the heart muscle (usually the left ventricle) becomes abnormally thickened (hypertrophied). This thickening interferes with the heart’s ability to relax and fill correctly, leading to diastolic dysfunction, decreased cardiac output, and sometimes congestive heart failure or sudden death.
Pathophysiology
The thickened heart wall reduces the size of the left ventricular chamber, impairing its ability to fill with blood.
The abnormal muscle also becomes stiff and noncompliant, leading to elevated pressures in the heart and lungs.
In some cases, the mitral valve is pulled abnormally into the outflow tract, causing dynamic left ventricular outflow tract obstruction (DLVOTO) (Fox, 2003).
Common in Cats
Breeds at higher risk include:
Maine Coon (linked to genetic mutations)
Ragdoll
British Shorthair
American Shorthair
Onset typically occurs in middle-aged to older cats, but can happen at any age.
Clinical Signs
Many cats are asymptomatic until late in the disease. Others may show:
Tachypnea (fast breathing)
Open-mouth breathing
Lethargy or collapse
Acute paralysis of hind limbs (due to aortic thromboembolism)
Heart murmur or gallop rhythm on auscultation
Diagnosis
Echocardiography: Gold standard – shows wall thickening and impaired filling
Thoracic radiographs: May show enlarged heart or pulmonary oedema
ECG: May detect arrhythmias
NT-proBNP and troponin I: Elevated in many cases
Genetic testing: Available for some breeds like Maine Coons (MYBPC3 gene)
Treatment
There is no cure for HCM, but treatment focuses on:
Improving relaxation of the heart muscle (diastolic function)
Reducing congestion
Preventing thromboembolism
Medication | Purpose |
Atenolol | Beta-blocker to reduce heart rate and obstruction |
Diltiazem | Calcium channel blocker for diastolic relaxation |
Furosemide | Diuretic for pulmonary oedema |
Clopidogrel | Prevents blood clots (especially in cats with a large left atrium) |
Complications
Aortic thromboembolism (ATE): A blood clot that blocks blood flow to the hind limbs, causing painful, often sudden paralysis
Congestive heart failure
Sudden cardiac death
Prognosis
Varies: Some cats live many years with mild disease; others deteriorate quickly
Early detection (especially via echocardiogram in high-risk breeds) improves outcomes
c. Vascular Disorders
Systemic Hypertension
Systemic Hypertension in veterinary medicine refers to high blood pressure in the body’s systemic arteries, most commonly affecting older cats and dogs with chronic disease. It’s a significant cardiovascular disorder because it can damage vital organs like the kidneys, eyes, heart, and brain, earning it the nickname "target organ disease."
Definition
Systemic hypertension is defined as a persistent elevation of systolic blood pressure, typically:
≥160 mmHg = borderline
≥180 mmHg = hypertensive (per ACVIM consensus, Brown et al., 2007)
Types
Type | Description |
Primary (essential) | Rare in animals; no identifiable cause |
Secondary | Most common, linked to underlying disease, like: |
– Chronic kidney disease (CKD) | |
– Hyperthyroidism (cats) | |
– Diabetes mellitus | |
– Cushing's disease (dogs) |
Commonly Affected Animals
Cats: Especially seniors with CKD or hyperthyroidism
Dogs: With endocrine disorders (e.g., hyperadrenocorticism) or kidney disease
Clinical Signs
Often silent, but can present as:
Sudden blindness (retinal detachment or haemorrhage)
Dilated pupils (mydriasis)
Behaviour changes, disorientation
Nosebleeds
Proteinuria
Heart murmur or gallop sound
Diagnosis
Measured using Doppler or oscillometric devices
Best done in a quiet room, with multiple readings to rule out stress-related “white-coat” hypertension
Concurrent testing for renal function, thyroid levels, and urinalysis is advised.
Treatment
Goal: Lower blood pressure to protect organs while avoiding hypotension.
Drug | Species | Purpose |
Amlodipine | Cats | First-line treatment |
ACE inhibitors | Dogs (and some cats) | For proteinuria and renal-associated hypertension |
Telmisartan | Cats | An angiotensin receptor blocker (ARB); also reduces proteinuria |
Beta-blockers | Dogs | Occasionally used if tachycardia is present |
Target Organ Damage
Uncontrolled hypertension can damage:
Eyes → Retinal haemorrhage, detachment → Blindness
Kidneys → Worsens proteinuria and CKD
Heart → Left ventricular hypertrophy (LVH)
Brain → Seizures, stroke-like signs
Prognosis
Good if diagnosed early and managed appropriately
Monitoring is lifelong, with frequent rechecks and dose adjustments
Thromboembolism
Thromboembolism is a life-threatening condition in companion animals, where a blood clot (thrombus) forms in the circulatory system and then travels (embolizes) to block a blood vessel elsewhere in the body. This prevents oxygen and nutrients from reaching the tissues, leading to pain, tissue damage, or even death, especially when critical organs are affected.
Definition
A thromboembolism is the obstruction of a blood vessel by a clot that has broken loose from its site of origin and travelled through the bloodstream.
In veterinary practice, the most common form is:
Feline Aortic Thromboembolism (FATE): A clot blocks the end of the aorta, often at the point where it splits to the hind legs.
Common in Cats with HCM
HCM leads to enlarged, poorly contracting atria, especially the left atrium.
Blood pools and stagnates, increasing the risk of clot formation.
The clot travels and lodges at the aortic bifurcation, leading to paralysis of the hind limbs.
Clinical Signs (FATE):
Sudden, severe pain and hind limb paralysis
Cold, pale, or blue paw pads
No femoral pulse in one or both hind legs
Vocalisation, tachypnea, distress
⚠️ This is an emergency — the sooner treatment starts, the better the outcome.
Thromboembolism in Dogs
Less common but can occur secondary to:
Immune-mediated haemolytic anaemia (IMHA)
Cushing's disease
Protein-losing nephropathy (PLN)
Cardiac disease or neoplasia
Diagnosis
Clinical presentation + absence of limb pulses
Doppler ultrasound to confirm the absence of blood flow
Echocardiography (especially in cats with heart disease)
Elevated D-dimers, cardiac troponin I, or NT-proBNP may support diagnosis
Treatment Options
Management focuses on:
Pain relief (e.g., opioids)
Antithrombotics (to prevent further clots):
Clopidogrel (platelet inhibitor) – first-line in cats
Heparin (unfractionated or LMWH)
Aspirin (less effective in cats; risk of GI side effects)
Supportive care (oxygen, fluids, nursing)
In dogs, managing the underlying disease (e.g., IMHA, neoplasia) is critical.
Prognosis
Species | Prognosis |
Cats | Guarded to poor for FATE, especially if both hind limbs are affected. Some cats recover and regain function with aggressive care (Smith et al., 2003). |
Dogs | Varies depending on the underlying disease and the organ involved. Prognosis improves with early detection. |
Prevention in At-Risk Cats
Clopidogrel for cats with an enlarged left atrium
Monitor with echocardiography
Manage underlying HCM or systemic disease
Influence of Lifestyle Factors
While genetic predisposition plays a major role, lifestyle and environmental factors can also influence cardiovascular health:
Obesity increases cardiac workload and is associated with hypertension and respiratory compromise.
Obesity Dietary deficiencies, especially taurine in cats and some breeds of dogs, can precipitate dilated cardiomyopathy (Freeman et al., 2018).
Dietary deficiencies A sedentary lifestyle may exacerbate heart disease by reducing cardiovascular fitness.
Key Differentiations
Heart Disease
Definition:
A general term for any disorder that affects the structure or function of the heart.
Examples:
Valvular disease, cardiomyopathy, and congenital defects.
Progression:
It may remain asymptomatic for long periods and may not necessarily exhibit clinical signs until the late stages.
Diagnosis:
Detected by auscultation, echocardiography, ECG, or radiography.
"Heart disease is not synonymous with heart failure. Many animals with heart disease never develop clinical signs" (Bonagura & Twedt, 2013).
Heart Failure
Definition:
A clinical syndrome that occurs when the heart is unable to pump sufficient blood to meet the body’s needs.
Types:
Left-sided heart failure leads to pulmonary oedema.
Right-sided heart failure causes ascites and pleural effusion.
Clinical Signs:
Coughing, exercise intolerance, dyspnea, and ascites.
Treatment:
Diuretics, ACE inhibitors, positive inotropes (e.g., pimobendan).
"Heart failure represents the end-stage consequence of heart disease and is marked by fluid accumulation and reduced perfusion" (Ettinger & Feldman, 2017).
Hypertension
Definition:
Persistently elevated systemic arterial blood pressure.
Causes:
Often secondary to diseases like chronic kidney disease, hyperthyroidism (in cats), and diabetes.
Target Organ Damage:
Eyes (retinal detachment), brain (seizures), heart (left ventricular hypertrophy), kidneys (proteinuria).
Diagnosis:
Measured using Doppler or oscillometric methods; confirmed with multiple readings.
Management:
Amlodipine (cats), ACE inhibitors (dogs), dietary sodium restriction.
"Systemic hypertension in pets is often secondary and requires treatment to prevent damage to vital organs"(Brown et al., 2007).
Conclusion
Cardiovascular disorders in companion animals are diverse, with both congenital and acquired forms. Understanding the distinction between heart disease (structural abnormalities), heart failure (functional insufficiency), and hypertension (vascular disorder) is essential for effective diagnosis and management. Lifestyle factors such as diet and exercise, while not primary causes in most veterinary cases, play a supportive role in disease prevention and long-term care.
References
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