Philip R. Fox, DVM, DACVIM, DECVIM-CA (Cardiology), DACVECC
Incidence of Heart Disease in the Cat
Many healthy, normal cats have systolic heart murmurs. Echocardiography is the best method to assess cardiac structure and function and determine whether the murmur is related to important underlying disease. Gallop rhythms are not normal and can be detected in 15% of cats with cardiomyopathy.
Heart Disease vs. Heart Failure
Occult cardiomyopathy refers to myocardial disease without a history of failure. Because heart failure is a syndrome and not a disease, there is no single test that reliably identifies the failing heart.
Cardiac Morbidity and Mortality
More than 95% of cardiac morbidity and mortality is caused by cardiomyopathy (myocardial disease). While the majority of affected cats appear to remain asymptomatic for life, the proportion that develops morbidity has not been identified. Diastolic heart failure is the most common cause of heart failure.
This principal pathophysiologic consequence results from a wide range of phenotypically heterogeneous myocardial disorders - most commonly hypertrophy (HCM) and restrictive (RCM) cardiomyopathy.
Diastolic Heart Failure
When alterations in diastolic function lead to increased left ventricular filling pressure and mean left atrial pressure, CHF may result. Diastolic heart failure is present when pulmonary edema occurs in the setting of abnormal diastolic function and relatively normal systolic function. It is the most common condition associated with acute CHF in the cat.
This may represent an end-stage consequence of HCM in some cases, while in others it results from infarction, inflammation, or unknown causes. Segmental or global myocardial thinning and/or dysfunction is best detected by echocardiography. Taurine deficiency is now rare.
Test for Discriminating Cardiac vs. Respiratory Cause of Dyspnea
Biomarkers: Echocardiography, the gold standard to assess cardiac structure and function, has limited availability and requires trained personnel. Recent studies have reported high sensitivity and specificity using the cardiac biomarker, NT-proBNP, as an adjunct test to help differentiate cardiac vs. non-cardiac causes of respiratory distress. Moreover, assessment of NT-proBNP concentration in combination with conventional evaluation significantly improves accuracy of this test.
The Role of Genetics and Feline Heart Disease
Feline HCM is inherited in Maine Coon, Sphynx, Ragdoll, Siberian and Norwegian Forest cat breeds, and is suspected in the Persian, American shorthair, and others. Genetic mutation testing for HCM is relatively simple and can utilize DNA obtained from an oral swab to test for mutations found predominantly in the Main Coon cat and Ragdoll cat. The absence of a detectible mutation does not mean that the cat will never develop HCM.
Goals for Managing Heart Disease
The Asymptomatic Cat
There is currently no evidence that treatment of asymptomatic cats prevents disease progression, reduces risk factors, or affects morbidity and mortality. Nevertheless, certain factors appear to increase risk of cardiovascular morbidity.
Potential Cardiovascular Risk Factors
In certain circumstances, abnormalities of myocardial structure or function might promote adverse outcome, thereby providing raison d'être for pharmacologic intervention. The following may warrant therapy, although efficacy remains to be proven.
Myocardial infarction might justify use of ACE inhibitors and/or beta-blockers. 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 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).
Massive left ventricular hypertrophy (severe HCM). Cats with greatly increased left ventricular mass (maximal diastolic septal or left ventricular wall thickness > 8 mm) may be at increased risk for cardiovascular events.
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, Plavix) 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).
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.
Dynamic LV outflow tract obstruction. When HCM is associated with systolic anterior motion (SAM) of the mitral valve, the obstructive form of HCM is present. While this carries increased risk in humans, limited veterinary literature is mixed as to whether it promotes cardiac morbidity.
Arrhythmic right ventricular cardiomyopathy (arrhythmic 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.
Restrictive LV filling (diastolic dysfunction). Cats who develop restrictive diastolic filling (detected via Doppler echocardiography) are at increased risk of morbidity and death.
Managing Diastolic Heart Failure
Acute CHF (pulmonary edema) treatment goals include cardiac stabilization and rapid resolution of edema. Diuretics with supplemental O2 represent the cornerstone for emergency management. Intravenous furosemide causes peak diuresis within 15–30 minutes by inhibiting renal sodium tubular reabsorption or its accompanying anions. This reduces vascular volume, decreasing LV filling pressures (i.e., cardiac preload), and pulmonary congestion. Resolution of pulmonary edema may be enhanced by application of transdermal 2% nitroglycerin ointment, ¼ to ½ inch q6h. To reduce nitrate tolerance, alternate 12 h with and 12 h without nitroglycerine therapy. Supplemental oxygen (40–60% O2-enriched inspired gas) may improve pulmonary gas exchange. Dehydration, azotemia, and hypokalemia result from over-diuresis, so it is important to reduce the dosage or frequency of administration as soon as signs improve.
Chronic CHF. Long-term 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.
Furosemide is gradually decreased to the lowest effective dosage. Some cats remain stable on 1–2 mg/kg PO given daily or every other day. The author prefers to combine furosemide with long-term ACE inhibitor therapy (enalapril, 0.5 mg/kg daily) so long as renal function is normal. There is no evidence that beta blockers are effective. Some clinicians may add pimobendan, 0.625–1.25 mg per os q12h, although indications and efficacy for this therapy remain to be demonstrated.
Managing Systolic Heart Failure
Historically, myocardial failure was synonymous with taurine-deficient, reversible, dilated cardiomyopathy. This condition was nearly eliminated in the late 1980s after pet food companies reformulated diets to increase taurine content. Presently, idiopathic dilated is still detected. Many cases present with pulmonary edema or with edema and effusions; hypothermia is common; cardiogenic shock develops in some instances.
Acute management includes 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, 0.5 mg/kg q24h), pimobendan (1.25 mg q12h), physical removal of effusion, and generalized supportive measures including supplemental O2, preserving electrolyte balance and renal function. Supplemental feeding via nasoesophageal tube can help treat protracted anorexia. Chronic management includes reduction of furosemide to the lowest effective dose; adding spironolactone (6.25 mg q24h); ACEI; and pimobendan. Long-term prognosis is guarded.
Diuretic resistance may occur as heart failure progresses, and recurrent CHF is likely to benefit from IV furosemide which has higher bioavailability. A second diuretic (e.g., thiazide - 5 to 10 mg daily or every other day, or spironolactone - 6.25–12.5 mg daily) is reserved for diuretic resistance. It is prudent to assess creatinine, electrolytes and blood pressure routinely.
Antiplatelet 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 had previous thromboembolic episodes. Aspirin can be administered, 20 mg every three days. Clopidogrel (Plavix) is a new potent antiplatelet agent that has been shown to be superior to aspirin to prevent recurrent thrombosis (1/4 of a 75-mg tab q24h).
Low molecular-weight heparin drugs can be added when cats have thromboembolic complications. Two particular agents, enoxaparin (Lovenox) and dalteparin (Fragmin), have received the most attention. Fragmin (100 U/kg q12–24h SQ) or enoxaparin (1 mg/kg q12h SQ) have been used relatively safely. Administration rates of every 6 to 8 hours are ideal but are generally impractical for long-term administration.
Overall medical management must include evaluation of renal function and electrolytes. Hyperkalemia can occur acutely as a result of reperfusion injury. Continuous ECG monitoring is valuable during the first days of hospitalization to detect arrhythmias and alterations in the P-QRS-T wave related to hyperkalemia. Periodic evaluation of BUN and electrolytes is useful. Abdominal ultrasound examination can sometimes be helpful by identifying the location and extent of thrombosis and detecting renal involvement.
Indicators of a Relatively Favorable Prognosis - Arterial TE
1. Resolution of CHF and/or control of serious arrhythmias
2. Lack of LA/LV thrombi or spontaneous echo contrast
3. Reestablished appetite
4. Relatively normal BUN/creatinine/electrolytes
5. Return of limb viability
6. Return of femoral arterial pulses and pink nail beds
7. Lack of self-mutilation
Indicators of a Grave Prognosis - Arterial TE
1. Refractory CHF or malignant arrhythmias
2. Acute hyperkalemia
3. Declining limb viability; failure of these muscles to soften 48–72 hours after presentation, distal limb necrosis
4. Multiorgan/multisystemic embolization
5. History of previous embolic episodes
6. LA/LV thrombus or spontaneous echo contrast
7. Rising creatinine
8. Disseminated intravascular coagulation
9. Unresponsive hypothermia
10. Severe LA enlargement