Sunday, July 24, 2011
Notes from July 2011 St. Louis AVMA Conference-Managing Feline Heart Failure
These are papers from the July 2011 St. Louis AVMA conference. I’ve edited them to delete some of the vet only jargon and for space considerations. If you see (…) that means that information has been deleted due to these considerations. The ones listed here include HCM, and other heart related papers, treatments, papers on x-rays and echos, thrombosis, kidney disease, idiopathic cystitis, pain management, anesthesia and cardiac disease, supplements and other hazards for pets, and some other basic information I hope is helpful.
MANAGING FELINE HEART FAILURE
Philip R Fox, DVM, Dipl ACVIM, ECVIM-CA (Cardiology), ACVECC
The Animal Medical Center.
Philip.firstname.lastname@example.org; Tel: 1 212 329 8606
More than 95% of feline cardiac morbidity and mortality is caused by cardiomyopathy
(myocardial disease). Many affected cats remain asymptomatic for life, although this
proportion has not been defined. Diastolic heart failure is the most common cause of
symptomatic heart disease Heart failure is a syndrome and not a disease. Therefore, there is no single test itself,
reliably identifies the failing heart. We therefore rely upon an integrated approach that
evaluates clinical symptoms and diagnostic findings.
…Hearts from cats with ventricular hypertrophy (HCM), and restrictive cardiomyopathy (RCM) are affected by complex intrinsic and extrinsic factors that affect left ventricular diastolic performance. Some of the better
recognized factors include altered loading conditions; increased myocardial mass
(hypertrophy); myocardial injury (inflammation, myocytolysis, necrosis) and repair (fibrosis,
matrix changes); myocyte disorganization; and ischemia. These alterations promote
ventricular stiffness and loss of compliance (diastolic dysfunction). Diastolic heart failure
Diastolic Heart Failure When alterations in diastolic function lead to increased left
ventricular filling pressure and mean left atrial pressure, congestive heart failure may result.
This clinical in which pulmonary edema occurs in the setting of abnormal diastolic function
and relatively normal systolic function has been termed diastolic heart failure.
Although relatively uncommon, some cats present with heart failure associated with
reduced LV contractility. Taurine deficiency, though rare, is still encountered. In most cats
with systolic failure, the cause is unknown. Segmental or global myocardial thinning and/or
dysfunction is best detected by echocardiography.
Screening for Heart Disease
Echocardiography is the gold standard for assessing cardiac structure and function.
Thoracic radiography is important to help document the presence of heart failure as well as
other non-cardiac conditions, but does not substitute for echocardiography.
Electrocardiography is valuable in the face of arrhythmia, but is insensitive for detecting the
presence of heart disease. Noninvasive measure out blood pressure can be useful to detect
the presence of systemic hypertension which could affect left ventricular wall thickness.
Blood pressure assessment is particularly relevant in face of diseases known to raise blood
pressure or effect heart structures such as chronic renal failure and hyperthyroidism.
Certain clinical pathology tests such as serum T4 (in cats older than six years of age) may
Goals for Managing Heart Disease
The goal for managing heart disease is to reduce morbidity and mortality…
Historically, in absence of prospective, randomized clinical trials in cats, treatment strategies have been extrapolated from human data, retrospective feline case studies, pharmacologic or physiologic studies of drug mechanisms in cats, and personal experience. Limitations of these approaches include lack of knowledge regarding
drug efficacy and long-term treatment benefit.
The Asymptomatic Cat
There is currently no evidence that treatment of asymptomatic cats prevents disease
progression, reduces risk factors, or affects morbidity and mortality. Moreover, there is no
data to guide whether therapies have to be implemented throughout the lifetime of an
individual, or indicate when a particular drug should be given. Nevertheless, certain
circumstances would appear to increase risk of cardiovascular morbidity.
Potential Cardiovascular Risk Factors
In several conditions, substantial abnormalities involving myocardial structure or function
appear to promote adverse outcome, thereby providing raison d'être for pharmacologic
intervention. The following may warrant therapy, although efficacy remains to be proven.
Myocardial Infarction In cats with myocardial infarction inferred by echocardiography, ACE
inhibitors and beta-blockers may be justified. Rationale for ACEI therapy is based upon the
potential of these agents to favorably influence ventricular remodeling and reduce mortality
in people and in experimental animals. Rationale for beta-adrenergic blockers similarly
include reduction of infarct size, myocardial oxygen utilization, and reduced mortality.
Tachyarrhythmia Rapid tachyarrhythmias can reduce cardiac filling, promote ischemia,
and result in hemodynamic instability. Sustained tachyarrhythmias are usually associated
with myocardial disease with attendant cardiac remodeling (myocyte necrosis, fibrosis,
inflammation, and interstitial matrix changes). Therefore, it is prudent to consider
antiarrhythmic therapy in selected cases, particularly when the ventricular rate is rapid.
Massive Left Ventricular Hypertrophy (Severe HCM) Although not confirmed, cats with
greatly increased left ventricular mass (maximal diastolic septal or left ventricular wall
thickness > 8mm) may be at increased risk for cardiovascular events.
Syncope Recurrent syncope is a risk factor for sudden death in humans with HCM, and
retrospective feline studies related syncope and poor outcome. In cats syncope can be
associated with tachyarrhythmias, dynamic LV outflow obstruction, and ischemia
(infarction). Symptoms can often be managed successfully with beta-blockers to reduce or
abolish LV outflow tract obstruction.
Spontaneous Echo Contrast (“Smoke”) Spontaneous echo contrast is associated with
blood stasis. This finding is considered to presage thrombosis and is associated with
increased thromboembolic risk. It should therefore warrant antiplatelet drugs (aspirin) and
perhaps more aggressive therapies.
“Malignant” Familial History of Sudden Death (High Risk Genotype) Pedigrees may be
identified with a documented heritable pattern of HCM with severe morbidity and mortality
(e.g., Maine coon cats, others). Early intervention with calcium channel blockers or betaadrenergic
blockers may be contemplated based on experimental considerations which
hold that a pathway to the phenotypic expression of LV hypertrophy is influenced by
triggers such as higher LV pressure and work load.
Myocardial Failure In some HCM cats LV contractility is reduced (e.g., fractional
shortening, 23-29%; LV end-systolic dimension, 12-15 mm) from acute or chronic
myocardial infarction, myocarditis, and other causes of LV remodeling. Therapies include
oral taurine supplementation, ACE inhibitors to counteract neurohormonal activation and
reduce remodeling, and judicious beta-blocker therapy if myocardial infarction is suspected
or with tachyarrhythmia.
Arrhythmic Right Ventricular Cardiomyopathy Cats with advanced structural lesions
(e.g., severe RV dilation, ventricular tachycardia) may be at risk for CHF. ACE inhibitors
and potentially, antiarrhythmics (sotalol) should be considered.
Managing Diastolic Heart Failure
Acute CHF (Pulmonary Edema) Pulmonary edema is rapidly progressive and
life threatening. Rapid resolution is the goal, and diuretics represent the cornerstone for acute,
emergency management. Furosemide administered intravenously causes peak diuresis
within 20- 30 minutes…Currently, two diuretic strategies are used, and there is no data to indicate which is the superior method. Use of intermittent IV bolus furosemide therapy (1- 2 mg/kg IV every 30-60 minutes) until dyspnea
associated with congestion is reduced…Resolution of pulmonary
edema may be enhanced by application of trans-dermal 2% nitroglycerin ointment, ¼ to ½
inch q 6hr…Supplemental oxygen (40-60% O2-enriched inspired gas) may
improve pulmonary gas exchange. Clinical improvement and resolution of congestion is
indicated by reduced respiratory rate and work of breathing, resolved lung crackles, and
radiographic clearing of alveolar infiltrates (usually by 24 to 36 hrs). Dehydration, azotemia,
and hypokalemia can result from over-diuresis.
Chronic CHF Chronic therapy is individualized to maintain a congestion-free state; prevent
arterial thromboembolism; halt, slow, or reverse myocardial dysfunction (theoretically);
promote enhanced quality of life; and prolong survival. Treatable and contributory diseases
should be identified and managed (e.g., systemic hypertension, hyperthyroidism, and
anemia). Therapy for each case must ultimately be individualized…
Managing Systolic Heart Failure
Historically, myocardial failure was most typified by reversible dilated cardiomyopathy
associated with taurine deficiency. This condition was nearly eliminated in the late 1980s
after a pet food companies reformulated diets to increase touring content. However, cases
are routinely encountered of idiopathic dilated cardiomyopathy that involve a number of
different etiologies such as myocardial infarction, inflammation, or idiopathic causes. Case
is usually present with effusions, hypothermia, and sometimes cardiogenic shock.
Acute management involves intensive care, administration of dobutamine (2-5 mcg per
kilogram per minute constant rate infusion), judicious furosemide administration (often
constant rate infusion), ACE inhibitor administration (enalapril, benazepril, ramipril, etc),
physical removal of effusion when severe, and generalized supportive measures, including
supplemental oxygen supplementation, care for preserving electrolyte balance, and
assessment of renal function). While the role of pimobendan in acute management is
unsubstantiated, many use it (0.625-1.25 mg q 12-24hr PO). Supplemental feeding via
naso esophageal tube can be useful. Chronic management includes the lowest effective
dose of furosemide, spironoactone, ACEI, and either digoxin or pimobendan. Generally,
long-term outlook is guarded.
Upward diuretic titration may be necessary with recurrent CHF. Diuretic resistance may
occur as heart failure progresses, and cats with recurrent CHF are likely to benefit acutely
from intravenous furosemide which has higher bioavailability. Addition of a second diuretic
(e.g., thiazide-5 to 10 mg daily, or spironolactone- 12.5 to 25 mg daily) is reserved for cases
of diuretic resistance. It is prudent to assess BUN, creatinine, electrolytes and blood
pressure in anorectic cats. Enalapril is added to current therapy if not already in place.
Addition of other drugs is contingent on individual needs and underlying disease.
Antiplatlet aggregating therapy may be considered when severe left atrial enlargement is
present, when spontaneous echo contrast is evident in the LA or LAV, or when cats have
have had preveious thromboembolic episodes. Aspirin may be used, dosed at
approximately 80mg every three days. Other agents are presently under investigation.
Clopidogrel (Plavix) is a new potent antiplatelet agent currently under evaluation to prevent
or treat arterial thromboembolism…Dosage is one quarter of a 75 mg
tabletop q 24 hrs…Low molecular weight heparin drugs are added when cats have
thromboembolic complications. Two particular agents, enoxaparin (Lovenox) and dalteparin
(Fragmin), have received the most attention. Both drugs are expensive but appear to have
a far greater safety margin than unfractionated heparin…Hyperkalemia
can occur acutely as a result of re-perfusion injury. Continuous ECG monitoring is valuable
during the first 3 days of hospitalization. Periodic evaluation of BUN and electrolytes are