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.


Philip R Fox, DVM, Dipl ACVIM, ECVIM-CA (Cardiology), ACVECC

The Animal Medical Center.; 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.

Diastolic Dysfunction

…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

may result.

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.

Systolic Dysfunction

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

be relevant…

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.

Recurrent CHF

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


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