By Mark D. Kittleson, DVM, PhD, DACVIM (Cardiology), School of Veterinary Medicine, University of California, Davis
Heart Disease and Heart Failure
Overview of Heart Disease and Heart Failure
Diagnosis of Heart Disease
Specific Cardiac Diseases
Heart failure is a clinical syndrome that occurs secondary to severe, overwhelming cardiac disease. It occurs because the heart is no longer able to maintain normal venous/capillary pressures, cardiac output, and/or systemic blood pressure. It is most commonly caused by a chronic disease that results in a severe decrease in myocardial contractility, severe regurgitation or shunting, or severe diastolic dysfunction. It is common to have all three abnormalities present simultaneously (but with one predominating). By far, the most common clinical manifestations seen with heart failure are directly due to edema and effusion (congestive or backward heart failure). Much less commonly, animals present because of signs referable to a decrease in cardiac output (forward heart failure). Very rarely, they present in cardiogenic shock (low blood pressure due to decreased cardiac output). This occurs because the cardiovascular system operates under a system of priorities. Its three primary functions are to maintain a normal blood pressure and normal cardiac output, both at a normal venous/capillary pressure. When the system is overwhelmed, it allows venous/capillary pressure to increase first (and so allows edema or effusion to form) and then allows cardiac output to fall. Only after cardiac output has fallen remarkably does cardiogenic shock occur. In acute heart failure, before any compensation has occurred, cardiogenic shock may predominate, but even in this situation, acute chordal rupture is the most common cause of acute heart failure in animals and results in an increased left atrial pressure and thus pulmonary edema.
Initial changes in cardiac chamber dimension (volume) or wall thickness that occur are best understood in relation to preload (the tension imposed by venous return on the ventricular walls at end-diastole) and afterload (the tension imposed on the ventricular walls at end-systole). Alterations in preload or afterload may be caused by structural cardiac abnormalities, systemic compensatory mechanisms, or both. Volume overload states, such as those that occur with chronic valvular disease/valvular insufficiencies, patent ductus arteriosus, atrial or ventricular septal defects, peripheral left-to-right shunts, anemia, or hyperthyroidism, cause an increase in preload that leads to ventricular growth and chamber enlargement (euphemistically called dilation) via eccentric myocyte hypertrophy. Pressure overload states, such as those that occur with systemic or pulmonary hypertension, and pulmonic or aortic stenosis, cause an increase in afterload (systolic intraventricular pressure) that leads to ventricular wall thickening via concentric hypertrophy. Neither volume nor pressure overload is synonymous with heart failure; either state may result in heart failure, depending on the severity of the overload and the degree of compensation.
Systolic function is a broad classification of cardiac function that encompasses all of the entities in systole that are capable of altering blood flow into the aorta. It includes (but is not limited to) heart rate, myocardial contractility, preload, afterload, hypertrophy (volume and pressure overload), leaks, and shunts. Again, the left ventricle grows larger to compensate for this disease, but when the myocardial failure is severe, compensation can no longer maintain a normal diastolic pressure in the left ventricle (kidneys continue to retain sodium and water) and this increased pressure backs up into the left atrium, pulmonary veins, and pulmonary capillaries, creating pulmonary edema.
Most ventricular diastolic dysfunction severe enough to cause heart failure is due to myocardial fibrosis, thus due to a decrease in ventricular compliance (an increase in stiffness). Diastolic dysfunction also occurs in pericardial diseases that cause cardiac compression (pericardial effusion, constrictive pericarditis). With pericardial disease, right heart failure (eg, ascites) predominates because systemic (eg, hepatic) capillaries leak more easily (leak profusely at a pressure of 10 mmHg) than pulmonary capillaries (which can generally withstand a pressure up to 20 mmHg without leaking).
CHF may also occur if a tumor or other anatomic obstruction impedes venous return to one or both atria. Pericardial disease or effusion leading to decreased ventricular filling may also be thought of as an extracardiac cause of CHF. Iatrogenic volume overload (ie, aggressive IV fluid therapy) can lead to edema formation in the absence of primary heart disease.
Acute compensatory mechanisms, such as increased sympathetic tone, are useful and generally short-lived only for situations that demand an acute change in cardiac function (eg, hypovolemia). Chronic mechanisms of cardiac compensation generally take over within days of the onset of a cardiac disease and are viable for years. Only at the very end of a chronic disease do they contribute to the formation of heart failure and require medical intervention.
When a decline in stroke volume occurs secondary to cardiac dysfunction, cardiac output decreases. The acute response is an increase in sympathetic tone leading to peripheral vasoconstriction, increased heart rate, and increased cardiac contractility that serve to restore cardiac output and maintain systemic blood pressure. This effect fades within days as events such as β-receptor down-regulation occur. Chronically, the renin-angiotensin-aldosterone system (RAAS) is activated. Activation is initiated by events such as decreased renal perfusion, leading to decreased sodium delivery to the macula densa (which interacts with the juxtaglomerular apparatus). The juxtaglomerular cells release renin, which converts angiotensinogen (synthesized in the liver) to angiotensin I. Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II, chiefly in the lungs. A separate tissue RAAS exists in the brain, vascular, and myocardial tissues, which can generate angiotensin II independently of the renal, or systemic, RAAS.
Angiotensin II has widespread effects, including stimulation of aldosterone synthesis and release from the adrenal glands, increased thirst via stimulation of antidiuretic hormone (ADH) release, increased norepinephrine and endothelin release, and stimulation of cardiac hypertrophy. This, plus the effect of ADH, causes an increase in circulating blood volume. The increased blood volume leads to an increase in venous return to the affected ventricle.
In response to these compensatory mechanisms, counter-regulatory systems are in place such as the release of atrial natriuretic peptide (ANP) from the atria, and B-type natriuretic peptide (BNP) from the atria and ventricles. ANP and BNP are released in response to stretch of the atrial and ventricular chambers. Both hormones serve to increase natriuresis (with subsequent diuresis) and decrease systemic vascular resistance, thus countering the effects of the RAAS. The effects of ANP and BNP are greatly outweighed by those of the RAAS and other systems in animals with chronic disease. Again, this is beneficial up until the end, when the RAAS continues to force sodium and water retention despite the presence of edema and effusion.
In situations when the heart must deal with higher than normal systolic intraventricular pressures (eg, subaortic stenosis, pulmonic stenosis, systemic arterial hypertension), the affected ventricle must contract against a greater force. Much like skeletal muscle when it is forced to lift a heavier weight, cardiac muscle undergoes concentric or pressure overload hypertrophy. In this situation, sarcomeres again replicate within cardiac myocytes but in parallel (side by side), to grow a wider myocyte and a thicker ventricular wall.
A biomarker is a measurable characteristic that reflects the severity or presence of some disease state. Blood pressure, cholesterol, gamma-glutamyl transferase, and BUN are all biomarkers. Studies in cats and dogs have shown that increased blood concentrations of BNP (most commonly N-terminal pro-B-type natriuretic peptide [NT-proBNP], ANP, and endothelin-1 are indicators of cardiac disease that increase proportionately with progressive cardiac disease and CHF. Cardiac troponin I (cTnI), which is released after cardiomyocyte death, has also been evaluated as a biomarker for cardiac disease but found to be less sensitive than those mentioned above. ANP, BNP, and cTnI have also been evaluated as screening tools for occult DCM (before onset of CHF) in dogs. Increased levels of BNP were found to be highly sensitive for the detection of occult DCM, whereas ANP and cTnI were relatively less sensitive. NT-proBNP is cleaved from BNP in equal amounts in response to increased cardiac filling pressures (myocardial stretch) and ischemia, and its greater stability and longer half-life make it more suitable for use as a diagnostic biomarker. Several studies have demonstrated the usefulness of NT-proBNP in differentiating between primary and cardiac respiratory causes of dyspnea in cats and dogs. A rapid assay is available for this use in cats. Biomarkers such as NT-proBNP and troponin I should never be evaluated in isolation, because they are not 100% accurate. Instead, they should be used in concert with other diagnostic modalities.
Chronic mechanisms of cardiac compensation generally take over within days of the onset of a cardiac disease and are viable for years. When a decline in stroke volume occurs secondary to cardiac dysfunction, cardiac output decreases. The acute response is an increase in sympathetic tone leading to peripheral vasoconstriction, increased heart rate, and increased cardiac contractility that serve to restore cardiac output and maintain systemic blood pressure., ANP, and endothelin-1 are indicators of cardiac disease that increase proportionately with progressive cardiac disease and CHF. Cardiac troponin I (cTnI), which is released after cardiomyocyte death, has also been evaluated as a biomarker for cardiac disease but found to be less sensitive than those mentioned above.
Mistakes In Heart Development :
Dogs and cats are sometimes born with abnormal hearts. We call this congenital heart disease.
Subaortic Stenosis (SAS) :
This problem is most common in big dogs (Rotties, Boxers, Newfoundlands, Goldens, Great Danes etc.) It is the most common inherited heart disease in large dogs.
In subaoritic stenosis the puppy is born with an abnormally narrow passage way leading from the heart to the aorta. It comes in all degrees, from a very mild case, requiring no treatment to a life-endangering problem.
When you take a puppy to the vet for his first vaccinations, the veterinarian should listen to the puppy’s heart. In a puppy with SAS, there will usually be a heart murmur over chest near the left base of the heart. If the puppy is not severely anemic with hookworms, then SAS is the most common cause of the murmur. This is how most cases of SAS are first diagnosed. Not every puppy with a heart murmur has SAS. Puppies often outgrow heart murmurs without our really knowing what caused them in the first place. Only some complicated tests can tell which murmur is important. But if your puppy still has a murmur when it is 6 months old, SAS becomes likely.
When a puppy has a significant degree of SAS, its heart has to work harder to force the blood through the narrow area just below the aortic valve. With time, the heart muscles get thicker due to the extra effort. As the walls thicken, the full heart holds less and less blood and needs more and more oxygen. Eventually, the heart begins to fail. Unlike older dogs with CHF, SAS puppies often die suddenly when clots form in the heart muscle or its electrical system fails.
Neither parent of an SAS puppy should ever be bred again.
What Signs Would I See In A Puppy ?
Most often, you will see no signs at all in your puppy. But as time goes by and the puppy’s heart muscles thicken, problems in the electrical system of the heart can cause fainting or unexpected sudden death.
What Tests Might My Veterinarian Perform ?
To decide how serious a heart murmur really is, your pet needs to have an echocardiograpy (doppler ultrasound) performed by a veterinarian experienced in interpreting the results. An x-ray and an EKG will also be required to see how much damage has already occurred.
What Are The Treatment Choices I Have ?
The most popular drugs used to treat SAS are known as beta blockers (ß-blockers). The most commonly used ones are Propranolol (Inderal) and atenolol (Tenormin). Beta blockers reduce heart rate, help control abnormal heart rhythm and reduce blood pressure. They are proven in their ability to extend the lives of dogs with SAS.
Open heart surgery to correct this problem in dogs has not been as successful as one might hope. Dogs that have had the surgery, live about as long as dogs that just receive medicine.
Balloon Valvuloplasty :
This technique is similar to balloon angioplasties that are done to dilate blocked coronary arteries in people. A catheter is threaded into the heart and a balloon is expanded in the narrowed area of the heart. So far, this technique has not led to increased life span.
How Long Will A Puppy With Heart Problems Live ?
This is very difficult to predict. They younger the puppy is when the problem is first noticed, and the louder the heart murmur, the bleaker the outlook. Most dogs with the typical signs of SAS do not live over 3 years without medication.
A cardiac work-up at a regional veterinary center that includes all the diagnostic tests, might give you more insight. But all pets with this condition can die suddenly – and often do.
Feline Dilated Cardiomyopathy :
This problem was due to a deficiency in an amino acid, taurine. Now that we know that cats must have sufficient taurine in their diet, all major brands of cat food have adequate taurine levels.
Hypertrophic Cardiomyopathy Of Cats :
In this disease the walls of the heart thicken, leading to inefficient pumping of blood. Blood pressure rises and fluid accumulates in the lungs. Eventually the chambers of the heart enlarge and abnormal heart rhythms occur. Signs of this disease are labored breathing, rapid heart rate, heart murmurs, weakness, collapse and death. Rare heart valvular disease, hyperthyroidism and asthma can mimic hypertrophic cardiomyopathy. We diagnose this disease with x-rays electrocardiograms (EKG = ECG) and cardiac ultrasound.
We treat the disease with low salt diets, diuretics, aspirin to prevent blood clots, and medications such as diltiazem and atenelol to stabilize blood pressure and heart rate. Do not give aspirin to your cat without veterinary supervision – cats do not handle aspirin well and Never give them Tylenol.
Corticosteroid-related Congestive Heart Failure in Cats
In 2004, the University of Minnesota Veterinary Center noticed an occasional link between heart failure and a recent dose of a number of corticosteroid medications in their feline patients (particularly with injectable methyl prednisolone acetate = Depomedrol aka “Depo”). Of the 160 cats with heart failure that passed through their clinic between 1992 and 2001, at least 8% that developed congestive heart failure had received those medications within the 1-3 weeks preceding their developing heart problem symptoms. This unique form of heart disease often resolved itself with time. Corticosteroids are often given to cats with respiratory problems that are believed to be asthmatic. In other cases , they were given for allergic skin conditions or as appetite stimulants. (ref)
Dilated Cardiomyopathy Of Dogs :
In this condition, as in cats, the heart chambers enlarge to the point where they can no longer pump blood efficiently. It is most common in large breeds of dogs and rare in small breeds. Doberman Pinschers, Great Danes, German Shepherds and Labrador Retrievers are particularly at risk. The disease is most common in middle-aged dogs, especially males. Usually the cause is unknown. However, we think that taurine deficiencies, parvovirus and the use of adriamycin have all caused the disease.
The overly-stretched heart muscle that occurs in this disease is an inefficient pump. Signs of the disease are those of congestive heart failure: difficult breathing, weakness, coughing and fluid enlargement of the abdomen. These dogs may need oxygen until medicines have an opportunity to work. Low salt diets as well as supplements that contain taurine, L-carnitine (carnatine) and coenzyme Q may also be helpful. Dogs do not survive long with this condition.
Hypertrophic Cardiomyopathy Of Dogs :
This disease is quite rare. As in cats, the muscles of the heart thicken and become inefficient at pumping blood. The signs of the disease are the signs of congestive heart failure e.g. difficulty breathing, coughing, heart murmurs and exercise intolerance.
How Will I Know If The Medications My Veterinarian Gives Me Are Working ?
The most common reason pets with heart problems come to see veterinarians is because of breathing problems. These pets tend to breath faster than they should and they tend to be congested. One can have complicated tests performed to evaluate if the medications are doing their job, but monitoring your pet’s breathing rate and freedom from congestion at home is just as accurate – perhaps more so. If the medications are working, your pet will breath slower and easier when it is at rest. If you want to confirm your decision about its progress based on its respiration, do so by having your vet run occasional proBNP tests (or Cardio-BNP if your pet is a dog) to confirm their level is dropping or holding steady. You can read an article that confirms that here.