9) myocardial diseases in cats and dogs Flashcards
types of myocardial diseases
- Dilated Cardiomyopathy (DCM)
- Hypertrophic Cardiomyopathy (HCM)
- Restrictive unclassified Cardiomyopathy (RCM)
- Arrhythmogenic right ventricular cardiomyopathy (ARVC)
dilated cardiomyopathy
❖ Progressive loss of myocyte number & function, decrease of contractility → leading to eccentric hypertrophy
- 2nd most common cardiac disease in dogs, cat: rare! Used to be common due to taurine-deficiency, but balanced commercial diets decreased occurrence drastically
predisposing factors DCM
- middle-aged to older large-breed dogs, males
- Doberman pinscher, boxer, great Dane, Irish wolfhound, standard poodle, cocker spaniels
- incidence in cats low since substitution of taurine in commercial cat food (rare!)
- juvenile onset: Portuguese water dog
pathogenesis of DCM
- variety of myocardial insults can lead to DCM → toxic, viral, nutritional (carnitine, taurine), genetic → but the etiology is often never determined → idiopathic
- Protracted subclinical phase: progressive loss of cardiac contractile function → cardiac output decreases → renal blood flow decreases
→ compensatory mechanisms:
o Sympathetic nervous system: heart rate increases
o RAAS: sodium and water retention → increases blood volume and renal return → eccentric hypertrophy of right ventricle → hypertrophy of both left and right ventricle and especially atria possible - After initial benefit of compensatory mechanism → deleterious effects
o Excessive stimulation by sympathetic nervous system → ventricular arrhythmias and myocyte death
o Excessive activation of the RAAS → vasoconstriction and edema/effusion
➔ Congestive Heart failure, left and/or right
Clinical findings and diagnosis in DCM
- Depending on side of heart failure (always left +/- right)
- Early signs: heart murmur, weak peripheral pulses, exercise intolerance
- Left sided CHF (usually predominating):
tachypnea, dyspnea, pulmonary edema (→ cough), weakness, exercise intolerance
inappetence, weight loss (cachexia)
weakness, syncope, collapse
cyanosis (hydrothorax!), weak pulse quality, jugular pulse, distension
pulse deficit - Right sided CHF: ascites, v. jugularis distention, subcutaneous edema
- Pleural effusion usually in dogs with both sided CHF
- Increased cardiac dullness
- Weak heart beats and pulse
- Cats: typically with severe respiratory signs, pulmonary edema, pleural effusion
- Systolic heart murmur heard at left cardiac apex, sometimes gallop sound
- Weak femoral pulse
- Arrhythmia (ventricular ectopy or atrial fibrillation) with associated pulse deficit
- Blood work can show prerenal azotemia (increased creatinine, BUN) but rather non-informative
- X-ray: (not adequate for exact diagnosis, but good to see secondary alterations)
Cardiomegaly (generalized), variable venous dilation (vena cava caudalis), pulmonary venal enlargement
pulmonary edema/perihilar infiltrate if decompensated (dogs), pleural effusion
hepatomegaly, ascites - Echocardiography → best for diagnosis (dilated cardiac chambers, decrease in left ventricular fractional shortening; mitral insufficiency due to left ventricular chamber dilation)
• Left atrial and ventricular dilation = enlargement + thin walls
• Mitral +/- tricuspid valve regurgitation → displaced papillary muscles
• +/- right atrial and ventricular dilation
• Eccentric hypertrophy
• Evidence of poor contractility: prolonged end-point septal separation (EPSS)
• Decreased fractional shortening (FS) normal > 30%, DCM < 15%, severe < 10%
• +/- right heart enlargement - ECG → to detect arrhythmias, can show ventricular premature complexes, ventricular tachycardia, atrial fibrillation and cardiac enlargement
• Sinus tachycardia, supraventricular tachycardia
• Wide and/or tall QRS complexes (enlarged LV), wide P wave (LA enlargement.)
• Atrial or ventricular premature contractions
• Ventricular ectopic beats are common
• May see significant ventricular arrhythmias early in Dobermans
• Atrial fibrillation in advanced disease
• Holter monitoring to determine: severity of arrhythmia, if therapy indicated - Taurine deficiency DCM: diagnosis with measurement of plasma or whole blood taurine cc
- Effusion analysis: modified transudate (cat, dog), chylous effusion (cat)
Treatment of DCM
- Can’t treat the cause (unknown!), except for in nutritional DCM → symptomatic and palliative
1. Lessen edema/effusion = reduce congestive signs : e.g. Diuretics e.g. furosemide
2. improve contractility = improve cardiac pump function: e.g. pimobendane
3. Reduce adverse effects of angiotensin II and other neurohormonal changes: e.g. ACE inhibitor (like enalapril, benazepril) - DCM due to taurine deficiency: taurine supplementation
- Severity of cardiac cachexia might be reduced by supplementing fish oil
- Severe CHF → CHF therapy (see other topic)
- Antiarrhythmic therapy (especially in Doberman pinschers with ventricular arrhythmia) → sodium-channel blockers e.g. Mexiletine (5-10mg/kg, tid), Digoxin, beta-blockers (e.g. carvedilol),
Prognosis of DCM
- Cats with DCM due to taurine deficiency → initially high risk of sudden death but as soon as taurine supplementation becomes effective the disease is completely reversible
- Dogs with DCM: poor prognosis, survival time about ½ to 1 year
- Depends on breed, Doberman pinscher and boxer worse prognosis
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
❖ Boxer cardiomyopathy
- Fatty or fibrofatty infiltrate of the right ventricular myocardium
Pathogenesis and Clinical Signs
- Non-sustained ventricular tachycardia (>400bpm) → no blood flow to the brain → lasting longer than 6-8 seconds → syncope → has to spontaneously stop for death not to occur
- some develop DCM and go into heart failure
Diagnosis
- Holter monitor → >100-300 PVCs (Premature ventricular complexes) are considered diagnostic (picture with monomorphic ventricular tachycardia in a dog with ARVC)
- Heart looks normal on x-ray and echocardiographs, except for cases that developed DCM
Treatment
- Without DCM: sotalol (1-3 mg/kg po bid), or combo of mexiletine (5-10mg/kg PO tid) and atenolol (12.5-25 mg/dog, PO, bid)
Prognosis
- Without DCM → good prognosis, can survive for several years on antiarrhythmic drugs
- With DCM → poor prognosis, most live for several months only
Hypertrophic Cardiomyopathy (HCM) - predisposed
❖ concentric left ventricular hypertrophy
Predisposed:
- especially cats (most common primary heart disease in cats), rarely small dogs
- Maine coon and ragdoll cats showed mutations in a number of sarcomere genes → production of dysfunctional sarcomeres → body tries to compensate dysfunctional ones with the production of even more sarcomeres → enlargement
Pathogenesis of HCM
- Causes primary inherent myocardial disorders, less common: pressure overload, hormonal stimulation, infiltration of the myocardium or other noncardiac disease
- Leading to muscle enlargement (concentric) → severe hypertrophy → accompanied by cellular necrosis → replacement fibrosis = myocardial scarring → stiffer than normal ventricle during diastole → increased diastolic pressure → backward-flow into the left atrium → left atrial enlargement → if severe enough → left HF
- if left atrial enlargement severe enough → stagnation of blood flow → thrombus formation → systemic thromboembolism
- enlarged papillary muscles → cranial displacement of the anterior mitral valve leaflet during ventricular systole (“systolic anterior motion of the mitral valve”)
Clinical findings of HCM
- Signs of left sided HF: pulmonary edema, pleural effusion → leading to tachypnea and dyspnea
- Tiredness/exercise intolerance, asphyxia, cyanosis, collapse if severe, (coughing is not typical)
- Tachycardia, murmur, gallop rhythm, arrhythmia with pulse deficit, sometimes ascites but not typical
- Acute life-threatening situation → cannot do full physical exam BUT must decide if dyspnea is from pulmonary edema or hydrothorax → furosemide or thoracentesis as life-saving treatment?!
- In cases of mild to moderate disease often no signs
- Severe disease → left heart failure → thromboembolism → death
- Thromboembolism often leads to acute onset of hindlimb paralysis/paresis (feline aortic thromboembolism)
- Abnormal heart sounds: soft prominent systolic cardiac murmur and/or gallop sounds, dynamic murmur that increases with excitement (1/3 without murmur)
- X-ray:
➢ left atrial enlargement, variable left ventricular enlargement, but often cardiac silhouette appears normal,
➢ do just in stable patients
➢ good to check for pulmonary edema or hydrothorax - blood-work and urine analysis:
➢ non-informative for HCM but good for differential diagnosis - blood pressure measurement:
➢ important for differential diagnosis - Echocardiography → for diagnosis:
➢ left ventricular wall thickening (>6mm, generalized or regional) and papillary muscle hypertrophy, sometimes systolic anterior motion of the mitral valve
➢ thickened left ventricular septum
➢ shows decreased left ventricular end-systolic diameter → decreased systolic function
➢ dilated left atrium and narrowed left ventricular diameter (especially in systole) - ECG
➢ Less useful in cats!
➢ can show: supraventricular premature complex, ventricular premature complex, ventricular tachycardia, atrial fibrillation, electrical axis deviation (but often cats show normal ECG) - Increased plasma cc of NT-proBNP
Important to exclude other causes for left ventricular wall thickening
➢ High blood pressure/ hypertension
➢ Hypothyrosis
➢ Aortic stenosis
Treatment of HCM
- No causative treatment available
- Controlling signs of CHF; acute: furosemide (2-4mg/kg IV or IM as needed), oxygen therapy, ACE inhibitor (e.g. enalapril 0.5mg/kg/day PO)
- Cats without HF → no drug treatment has shown to change pathogenesis → no clinical signs, no treatment
- Acute situation:
➢ Decrease stress + oxygen therapy
➢ Pleural fluid/hydrothorax → thoracentesis (better US guided, but depends on needle)
➢ Pulmonary edema → furosemide, nitroglycerine - Chronic stages:
➢ Furosemide
➢ ACE-inhibitors ?
➢ Ca-channel blockers but controversial
➢ Beta-blockers but controversial, rather not, reduces survival time
➢ Repeated thoracentesis
Treatment of HCM
- No causative treatment available
- Controlling signs of CHF; acute: furosemide (2-4mg/kg IV or IM as needed), oxygen therapy, ACE inhibitor (e.g. enalapril 0.5mg/kg/day PO)
- Cats without HF → no drug treatment has shown to change pathogenesis → no clinical signs, no treatment
- Acute situation:
➢ Decrease stress + oxygen therapy
➢ Pleural fluid/hydrothorax → thoracentesis (better US guided, but depends on needle)
➢ Pulmonary edema → furosemide, nitroglycerine - Chronic stages:
➢ Furosemide
➢ ACE-inhibitors ?
➢ Ca-channel blockers but controversial
➢ Beta-blockers but controversial, rather not, reduces survival time
➢ Repeated thoracentesis
Prognosis of HCM
very variable
- Clinical signs → about 3 months
- In case of subsequent thoracoembolus very bad
Arterial Thromboembolism, feline aortic thromboembolism
Pathogenesis:
Enlargement of the left atrium → blood flow stasis → RBC aggregate when blood flow decreases below a critical velocity → thrombus is formed → most commonly in left auricle → breaks loose → enters systemic circulation
➔ Small thrombus can enter coronary artery → myocardial infarction
➔ Mid-sized thrombus can enter branches of aorta
➔ Large thrombus (most of them) → too big to leave through branches → gets to terminal aorta → occlude aortic flow → release of vasoactive amines → shut-down of collateral circulation → acute cessation of blood flow to the hindlimbs (sometimes only one affected) → pulselessness, pale or purple foot pads, poikilothermic (decreased rectal temperature and cold hindlimbs), extreme pain
Thrombus formation
Clinical Signs:
- Sudden onset of weakness to paralysis in hindlimbs
- Bluish, pale nailbed on hindlimbs and cooler temperature
- Absent or diminishing femoral pulse
- Vocalizing and anxiety
- Vomiting
- Heart murmur or arrhythmias
Diagnosis:
- On base of clinical signs
- Doppler blood flow readings of hindlimbs
- US to identify thrombus
- Neurological disorders are often misdiagnosed as thromboembolism (the other way around?)
Treatment/Prognosis:
- Often most effective treatment is to wait for the lysis of the thrombus on its own (1-72hr)
- Pain control!
- some might have residual problems
- euthanasia is common (prognosis significantly poorer if both hindlimbs are involved)
- prevention of thrombus formation/recurrence : Clopidogrel (18.75mg/d/cat)
