HM Medical Clinic

Vjd_2009-dierenartsen.pdf

Cardiovascular Formulary for the Hypertensive Cat Lusitrope, Vasodilator, Negative chronotrope 180, 240 mg caps.
180, 240 mg caps.
Enacard (Vasotec) 1, 2.5, & 5 mg tablets ACE-I (CHF, Hypertension) Lotensin (Foretkor) 5 & 10 mg tablets .25-.5 mg/kg PO qd-bid Negative chronotrope, 6.25-12.5 mg PO qd Antiarrhythmic, Lusi-trope, Antihypertensive 1/8–¼ inch topically tid Nitrol, Nitro-Bid Venodilator (CHF) only 30% of cats with HC. Histological cardiac myofiber disarray is reported in 27% of affected cats and only in C A R D I O M YO PAT H Y
those with asymmetric septal hypertrophy. Other his- Clarke E. Atkins, DVM, Diplomate ACVIM (Internal Medi- tological features of feline HC include myocardial and cine & Cardiology) endocardial fibrosis and narrowed coronary arteries. Department of Clinical Sciences, College of Veterinary Dynamic aortic outflow obstruction, secondary mitral insufficiency, myocardial ischemia, and systemic arte- North Carolina State University, Raleigh NC, USA rial embolism (SAE) may complicate this syndrome.
The left heart is predominately affected and clinical signs manifested as sudden death or, more commonly, Etiology and Pathophysiology
acute left heart failure due to diastolic dysfunction. Pleu- Hypertrophic cardiomyopathy (HC/HCM) is the most ral effusion is occasionally associated with HC. Systolic prevalent feline cardiac disorder. It affects most com- function is usually adequate or enhanced but may de- monly middle-aged cats (average 6.5 years), but cline with myocardial infarction. Tilley and Lord demon- all ages are affected. There is a male predisposition strated an elevated resting left ventricular end diastolic (>75%). In humans, there is an important hereditary pressure (LVEDP) in feline HC. With the administration predisposition for HCM in 55% of cases. In people, this of isoproterenol, mimicking endogenous, stress-related disorder may be congenital or acquired, and probably sympathoadrenal activity, the LVEDP pressure doubled. represents a group of diseases. Although the etiology Left ventricular end diastolic pressure is indicative of of feline HCM is unknown, the Persian and Maine coon pressures in the left atrium and pulmonary veins, which cat have appeared to be predisposed in some case se- reflect the tendency for the development of pulmonary ries, suggesting a genetic influence. A case-controlled edema. In addition, during stressful situations, accelera- study in our laboratory, which showed a trend toward tion of the heart rate reduces cardiac filling time and a predisposition for Maine coon cats, was validated myocardial perfusion. The former further diminishes by work of Meurs, et al. which has shown that HCM in cardiac volume and the latter results in relative myocar- Maine coon cats and Ragdolls is heritable as an auto- dial ischemia in a rapidly beating heart with high oxy- somal dominant trait.
gen needs, thereby, aggravating diastolic dysfunction. Cardiac lesions are typified by severe left ventricular Stressful incidents, such as a car ride, restraint for an concentric hypertrophy and secondary left atrial dilata- ECG, confrontation with a dog, or an embolic event may tion. Asymmetric septal hypertrophy (ASH), present in precipitate in left heart failure and pulmonary edema. the majority of dogs and humans with HC, is present in Abstracts European Veterinary Conference Voorjaarsdagen 2009
Scientific proceedings: companion animals programme
ventricular wall, and papillary muscle enlargement. The With the aid of ECG, thoracic radiographs, and echocar- diagnosis of SAE (usually located at the aortic trifurac- diography, a high percentage of cases of HC are diag- ton: saddle thrombus) can be confirmed by the finding nosed prior to the onset of symptomatology. Suspicion of an abrupt termination of the dye column in the aorta is raised in such instances when the attending clinician at its trifurcation.
discovers a murmur, gallop, or arrhythmia. At the other Echocardiography is extremely useful for distinguish- end of the spectrum, cats may die unexpectedly with ing HC from DC, but, because of overlap of echocardio- no prior signs. The most common clinical sign is the graphic reference values, differentiation of normal from sudden onset of dyspnea, with or without evidence asymptomatic HC and HC from RC may be difficult. of SAE (the prevalence of which has ranged from 16 Concentric left ventricular hypertrophy and left atrial to 48%, in clinical and autopsy studies, respectively). enlargement are features useful in confirming the diag- Physical examination typically reveals a well-fleshed, nosis of HC. Cardiac function is normal to exaggerated, dyspneic cat with audible pulmonary crackles, murmur due to diminished afterload and possibly hypercontrac- (50% of cases) typically loudest at the left apex, gal- tility. Systolic anterior mitral valve motion may be evi- lop (40%, usually S4), and/or arrhythmia (25 to 40% of dent, suggesting dynamic aortic outflow obstruction. If cases). Heart sounds may be muffled. The oral mucosa present, ASH, left atrial thrombi, pleural effusion, and/ is ashen, the pulses normal, weak, or absent (SAE), the or pericardial effusion may be evident.
apex beat may be hyperdynamic, and the liver may rarely be palpably enlarged. Cats with HC are generally not hypothermic, providing information useful in differ- The treatment of HCM is different than that of DCM entiation from DC.
(systolic myocardial failure) and entails the goals of re-ducing LVEDP, abolishing sinus tachycardia and other arrhythmias, improving myocardial oxygenation, and Diagnosis of HC is not difficult, but does require special alleviating and preventing pulmonary edema. Positive testing to confirm clinical suspicions. Without the aid of inotropic agents are not needed and generally contrain- echocardiography, dilated and restrictive (RC) cardio- dicated because they may increase LVEDP and aggra- myopathies can be difficult to distinguish from HC vate outflow obstruction. The latter precaution should The ECG is abnormal in 35 to 70% of cases and can pro- be exercised in the use of arterial vasodilators and, to vide useful diagnostic information. Many ECG findings a lesser degree, preload reducing agents (diuretics and are not specific, but left axis deviation and left anterior mixed or venodilators). fascicular block are strongly suggestive of HC, but also Diuretic therapy is indicated to eliminate pulmonary may be recognized in RC, hyperkalemia, hyperthyroid- edema. Furosemide is the diuretic of choice in emer- ism, hypertension and, rarely, DC. Other ECG abnormal- gencies because it reduces LVEDP and, hence, left atrial, ities include P-mitrale and P-pulmonale (10% and 20%, and pulmonary venous pressures through diuresis and respectively), tall R waves (40%), wide QRS complexes venodilation. In the emergency situation, treatment (35%), conduction disturbances (50%, including left with parenteral furosemide (2-4 mg/kg IV or IM) is ac- axis deviation in 25% and left anterior fascicular block companied by the use of topical nitroglycerin (1/8-1/4 in 15%), and arrhythmias (55%, usually ventricular in inch tid-qid for first 24 hours, then "8 hours on, 8 off" only if necessary) and oxygen supplementation (40%). Thoracic radiographic findings suggestive of HC in- Although furosemide diuresis is usually successful, the clude cardiomegaly with a prominent left ventricle addition of enalapril (.25-.5 mg/kg sid) is indicated in and atrium, and pulmonary congestion and/or edema. refractory cases or when biventricular failure (pleural In the ventrodorsal projection, the heart may appear effusion) ensues. It should be kept in mind that drugs "valentine-shaped," reflecting the concentric ventricu- which reduce preload (and afterload) may worsen out- lar hypertrophy and enlarged left auricle. Additionally, flow obstruction in hypertrophic obstructive cardio- the apex is often shifted to the right. On the lateral view, myopathy (HOCM).
the heart is enlarged with increased sternal contact, Drugs that enhance ventricular relaxation and slow the left atrial prominence, left ventricular convexity, and a heart include the beta adrenergic (atenolol), and cal- prominent caudal cardiac waist. Pleural effusion may be cium channel (diltiazem) blockers. Such therapy is indi- noted in 25 to 33% of cases in heart failure, but is usu- cated in treatment of the diastolic failure of HCM. Beta ally of much less volume than that noted in DC. Nonse- blockers improve diastolic performance only indirectly, lective angiography is of less risk in HC than in DC. This enhancing ventricular filling by reducing heart rate and procedure typically reveals normal or enhanced circu- improving myocardial perfusion. Traditionally, beta- lation, pulmonary venous tortuosity, left atrial enlarge- blockers have been administered orally after stabiliza- ment, small left ventricular lumen, thickening of the left tion (24 to 36 hours after institution of diuretic therapy) Abstracts European Veterinary Conference Voorjaarsdagen 2009

to reduce and prevent elevations in LVEDP, to lower systolic pressure gradients and myocardial oxygen re- Cats with asymptomatic HCM should be evaluated at quirements, to prevent stress-induced tachycardia and 12 month intervals, while those with symptoms should reduce resting heart rate, and for its antiarrhythmic ef- ideally be seen more frequently until stabilized for a fects. When arrhythmias are present, this drug may be period of time. The prognosis for asymptomatic HCM is initiated earlier in the disease course. This is the author's guarded to good, with a median survival of over 5 years. treatment of choice for asymptomatic HCM, for cats Cats presented in heart failure survive a median of ap- with documented outflow obstruction (HOCM), and proximately 18 months, while cats with emboli carry a when tachycardia persists.
much poorer prognosis.
Calcium channel blocking agents have been effective in human HCM by reducing heart rate, myocardial oxygen consumption, and diastolic dysfunction. In addition to directly enhancing myocardial relaxation, these drugs dilate peripheral and coronary arteries. Bright has dem-onstrated the utility of diltiazem (3-7.5 mg po tid) in the treatment feline HCM, including those cases refractory to the beta-blocker, propranolol. Unfortunately, current packaging for human use, makes accurate feline dosing of diltiazem difficult. Long-acting diltiazem may be sub-stituted and includes Cardizem CD (45 PO sid; requires disassembling capsules) or Dilacor (30 mg PO bid; re-quires disassembling capsules). Combining a calcium channel blocker and a beta blocker has theoretical ad-vantages and is often done, using a long-acting form of each drug, one in the morning and one in the evening. There is no role for amlodipine in the normotensive cat with HCM as it has no theoretical or proven benefit and it may precipitate hypotension.
A report by Rush, et al. demonstrated a reduction in wall thickness with the administration of enalapril to cats with HCM. This suggests a potential role for ACE-inhib-itors in the treatment of HCM. These drugs are gener-ally safe and do play a role in cases which are refractory or in which pleural effusion is present. In asymptom-atic patients, it is logical that the renin-angiotensin-aldosterone system is not pathologically activated, and hence ACE-inhibitors might not be useful. Recent data from McDonald and colleagues, using an ACE-Inhibitor in asymptomatic Maine Coon Cats and followed them for one year, failed to show benefits in regression of hy-pertophy, improvement in diastolic function or onset of CHF. While this does not prove "ineffectiveness" of this drug class in HCM, it does not produce confidence of their use. When used, at NCSU, we employ enalapril at .5 mg/kg daily.
Other therapies, including oxygen, aspirin or low mo-lecular weight heparin, home confinement, and moder-ate salt restriction should be instituted as needed. Tau-rine supplementation is not indicated in the treatment of HCM. In asymptomatic cats with HCM, the author advises home confinement, moderate salt restriction, Beta- and/or calcium channel blockade, and aspirin in-definitely.
Abstracts European Veterinary Conference Voorjaarsdagen 2009
Scientific proceedings: companion animals programme
Cardiovascular Formulary for Cats
Lusitrope, Vasodilator, Negative chronotrope 180, 240 mg caps.
180, 240 mg caps.
Enacard (Vasotec) 1, 2.5, & 5 mg tablets ACE-I (CHF, Hypertension) Lotensin (Foretkor) 5 & 10 mg tablets .25-.5 mg/kg PO qd-bid Negative chronotrope, 6.25-12.5 mg PO qd Antiarrhythmic, Lusi-trope, Antihypertensive 10 & 250 mg/ml inject- 50-500 (100 usually) ug/ Pronestyl, Procan SR 2-5 mg/kg PO bid-tid 100 mg/ml inject.
1-4 mg/kg PO bid-q48h; 50 mg/ml inject.
.5-2 mg/kg SQ, IM, IV PRN 1/8–¼ inch topically tid Nitrol, Nitro-Bid Venodilator (CHF) 1, 2, 2.5, 4 mg tabs.
250-300 U/kg SQ tid Positive inotrope, Nega- .007 mg/kg PO q48h tive chronotrope (CHF, (check serum [digoxin]) Taurine deficiency *Selected name brands; some available as generic. **Most appropriate formulations for cats – other sizes available for many drug cyanotic foot pads or nail beds, the latter not bleeding upon quicking. If SAE is partial, a pulse (weak or even Clarke E. Atkins, DVM, Diplomate ACVIM (Internal Medi- normal unilaterally) may be detected, carrying a better cine & Cardiology) prognosis. If the attending clinician cannot ascertain Department of Clinical Sciences, College of Veterinary with certainty whether SAE is present, Doppler technol- ogy (Doppler diagnostic ultrasound or blood pressure North Carolina State University, Raleigh NC, USA monitoring equipment) or non-selective angiography may be used to confirm the diagnosis.
Physical Examination & Diagnosis
When SAE affects alternative sites, the signs may range SAE is typically associated with an acute or peracute from sudden death (coronary or cerebral arteries or presentation, usually with rear limb paralysis/paresis. proximal aorta) to an acute abdomen (aorta at level of Classical findings include posterior limb pain, lack of kidneys or mesenteric arteries) or to front leg lameness. pulse, gradual (over days) hardening of the gastrocne- When affected, the kidneys can be isolated and are firm mius and quadriceps muscles, lack of pulse and pale/ and quite painful to palpation. Often (approximately Abstracts European Veterinary Conference Voorjaarsdagen 2009

Source: http://voorjaarsdagen.nl/index.php?option=com_phocadownload&view=category&id=36:companion-animal-scientific-proceedings-2009&download=809:atkins-feline-hypertrophic-cardiomyopathy&Itemid=20