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Amara Estrada, DVM, DACVIM (Cardiology), University of Florida
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Clinical heart disease is the stage of disease when a patient has or had signs attributable to cardiovascular disease. However, similar to human heart disease, determining when veterinary heart disease becomes clinical or progresses to heart failure is variable; it is often unclear exactly when preclinical heart disease evolves to clinical heart disease (see Definitions). Congestive heart failure (CHF) is easily recognized when there is radiographic evidence of pulmonary edema or cardiogenic effusion. Subtle signs of CHF (eg, pulmonary venous enlargement, exercise intolerance, weakness, lethargy) may be noted on thoracic radiographs or patient history.
Therapeutic planning for heart failure patients includes diagnosing the underlying heart disease and identifying the stage or class of heart disease.
Heart failure is failure of the heart to pump and distribute blood appropriately and results in tissue hypoxia.
Congestive heart failure is cardiac dysfunction resulting in increased venous/capillary pressures that lead to edema or effusions.
Related Article: Finding a Consensus on Canine CVHD
In veterinary medicine, a modified version of the American College of Cardiology and American Heart Association classification system for humans is commonly used; the author follows a modified version for hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM; see Stages of Heart Disease). This classification can help veterinarians effectively identify and treat heart disease, but there is no perfect standard for treating all heart disease patients as they are expected to advance through the stages unless progression is altered by treatment. Other classification schemes include modified NYHA (New York Heart Association) classes, ISACHC (International Small Animal Cardiac Health Council) classes, and ACVIM (American College of Veterinary Internal Medicine) Consensus Statement Classes for canine valvular disease (CVD).
Stages of Heart Disease: CVD, DCM, & HCM Cases
Stage APatients at high risk for developing heart disease with no identifiable structural heart disorders (eg, Cavalier King Charles spaniel, Maine coon cat without heart murmurs) Stage BPatients with structural heart disease (eg, mitral insufficiency murmur) but without signs associated with CHF; because of important clinical implications for prognosis and treatment, patients are subdivided into B1 and B2 for many diseases
Stage CPatients with past or current clinical signs of heart failure associated with structural heart diseaseStage DPatients with end-stage disease and clinical signs of heart failure refractory to standard therapy and requiring advanced or specialized treatment to remain clinically comfortable
Related Article: Feline Enlarged Heart
One of the most important tools for assessing heart disease is a complete cardiovascular examination (see How I Diagnose), including assessment of peripheral perfusion, femoral pulse quality, body condition, respiratory rate and character, and auscultation of the heart sounds, rhythm, and rate. Assessment of systolic blood pressure via Doppler sphygmomanometry can be part of a thorough cardiovascular examination in patients with suspected underlying heart disease (ie, patients at stage B1 and greater). Assessment of blood pressure provides information about afterload, making it an important part of the cardiovascular examination and therapeutic planning. Ultrasound skills to assess left atrial size, ventricular contractility, and presence or absence of effusion are useful. Echocardiographic assessment by a veterinary cardiologist is ideal. In patients requiring diuretic therapy, baseline assessment of renal values and electrolytes is recommended.
Related Article: Canine Heart Murmur
Consider the specifics for CVD.
Consider the specifics for canine DCM.
Consider the specifics for feline HCM.
How I Treat Congestive Heart Failure
Reduce excessive preload.
Improve myocardial contractility.
Consider the specifics for DCM.
Enact follow-up measures
Although the stage of CHF often determines treatment, it is essential to assess and therapeutically support the 5 primary determinants of stroke volume and cardiac output: preload, afterload, inotropic state (myocardial contractility), heart rate, and synergy (see 5 Primary Determinants of Stroke Volume & Cardiac Output). These determinants help guide the measures necessary for patients with cardiac disease, regardless of the underlying disease process.
5 Primary Determinants of Stroke Volume & Cardiac Output
Preload Preload depends on venous return, total blood volume, and blood distribution within the vascular system. Increased diastolic stretching (ie, preload) results in more forceful cardiac contraction (ie, Frank-Starling mechanism). If diastolic myocardial function is normal, increased end-diastolic volume induces a more forceful contraction with only modest increases in end-diastolic pressure. Myocardial fibrosis and hypertrophy impede diastolic filling because they prevent optimal stretch by the myofibers even when filling pressures are increased. With many cardiac diseases, excessive preload can result in pleural effusion, ascites, pulmonary edema, or peripheral edema.
Afterload Afterload, the intraventricular systolic tension experienced during ejection, is determined by peripheral vascular resistance, physical properties (compliance) of the arterial tree, and volume of blood in the ventricle at onset of systole. Increased afterload leads to reduced rate or amount of ejection at preload. Reducing the afterload in patients with CHF may improve forward cardiac output, reduce regurgitant jet size, and speed resolution of CHF signs.
Myocardial Contractility and/or Inotropy Myocardial contractility, the innate property of the myocardium that defines force of contraction, is affected by sympathetic nerve activity, concentration of circulating catecholamines, and, to some extent, heart rate. Anoxia, ischemia, acidosis, and disease processes (eg, DCM, chronic mitral insufficiency with severe volume overload) can reduce contractility and inotropic state. Reduced myocardial contractility can be assessed by echocardiography and more indirectly via systemic blood pressure measurement. Drugs that can increase myocardial contractility (ie, positive inotropes) can help alleviate acute and chronic clinical signs of CHF.
Heart Rate Heart rate is determined by automaticity of the sinoatrial (SA) node, which is subject to autonomic regulation and other environmental (eg, temperature) and metabolic (eg, thyroid levels) factors. Cardiac output increases linearly with heart rate when stroke volume is constant; however, at extremely rapid heart rates, ventricular filling, stroke volume, and cardiac output are reduced. Patients can present with clinical signs attributed to bradyarrhythmias (eg, third-degree atrioventricular [AV] block, high-grade second degree AV block) and tachyarrhythmias (eg, ventricular or supraventricular tachycardia). Arrhythmias can contribute to clinical signs in patients with structural heart disease (eg, atrial fibrillation in patient with severe mitral insufficiency and CHF, ventricular tachycardia in patient with dilated cardiomyopathy). Addressing arrhythmias in a patient with CHF may help speed resolution of signs.
SynergyVentricular synergy is orderly synchronized contraction of the ventricles. Dyssynergy can lead to a reduction of stroke volume and cardiac output. Resynchronization therapy, fairly common in human cardiology, is starting to be investigated in veterinary cardiology (ie, in patients with a pacemaker-induced myocardial dysfunction).
CHF = congestive heart failure, CVD = canine valvular disease, DCM = dilated cardiomyopathy, HCM = hypertrophic cardiomyopathy, LAE = left atrial enlargement, NT proBNP = N terminal prohormone of brain natriuretic peptide, TT4 = total thyroxine
AMARA ESTRADA, DVM, DACVIM (Cardiology), is associate professor and associate chair in the department of small animal clinical sciences at University of Florida. Dr. Estrada’s interests include electrophysiology, pacing therapy, complex arrhythmias, cardiac interventional therapy, and cardiac stem-cell therapy. She has contributed to numerous research and clinical publications on emergency and critical care medicine and is associate editor of Journal of Veterinary Cardiology. Dr. Estrada earned her DVM from University of Florida before completing her internship at University of Tennessee and her residency in cardiology at Cornell University.
A splice site mutation in a gene encoding for PDK4, a mitochondrial protein, is associated with the development of dilated cardiomyopathy in the Doberman pinscher. Meurs KM, Lahmers S, Keene BW, et al. Hum Genet 131:1319-1325, 2012.
Association of dilated cardiomyopathy with the striatin mutation genotype in boxer dogs. Meurs KM, Stern JA, Sisson DD, et al. JVIM 27:1437-1440, 2013.
Submit DNA for testing. The Veterinary Health Complex at the College of Veterinary Medicine, NC State University; http://www.ncstatevets.org/genetics/submitdna/; accessed Mar 2014.
Prevalence of the myosin-binding protein C mutation in Maine Coon cats. Fries R, Heaney AM, Meurs KM. JVIM 22:893-896, 2008.
Re: Association of A31P and A74T polymorphisms in the myosin binding protein C3 gene and hypertrophic cardiomyopathy in Maine Coon and other breed cats. Kittleson MD, Meurs K, Munro M. JVIM 24:1242-1243, 2010.
A substitution mutation in the myosin binding protein C gene in ragdoll hypertrophic cardiomyopathy. Meurs KM, Norgard MM, Ederer MM, et al. Genomics 90:261-264, 2007.
Analysis of 8 sarcomeric candidate genes for feline hypertrophic cardiomyopathy mutations in cats with hypertrophic cardiomyopathy. Meurs KM, Norgard MM, Kuan M, et al. JVIM 23:840-843, 2009.
Hypertrophic cardiomyopathy in the sphinx cat: A retrospective evaluation of clinical presentation and heritable etiology. Silverman SJ, Stern JA, Meurs KM. J Feline Med Surg 14:246-249, 2012.
Clinical usefulness of an assay for measurement of circulating N-terminal pro-B-type natriuretic peptide concentration in dogs and cats with heart disease. Oyama MA, Boswood A, Connolly DJ, et al. JAVMA 243:71-82, 2013.
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