DON’T COMPARE YOURSELF TO OTHERS “ Everyone is a genius, but if you judge a fish by its ability to climb a tree, it will live its whole life believing its stupid.” -Albert Einstein

DISEASES OF THE CARDIOVASCULAR SYSTEM: CARDIOMYOPATHIES

PATIENT PRESENTATION v=X-wLIoYTpOU CiC7SXjk

FELINE HYPERTROPHIC CARDIOMYOPATHY NEUTERED MALE CATS BETWEEN 1-16 YRS. OF AGE THE MOST COMMON CARDIOMYOPATHY IN CATS!

FELINE HYPERTROPHIC CARDIOMYOPATHY: CLINICAL SIGNS and DIAGNOSIS  Soft, sytolic murmur  Gallop rhythms or other arrhythmias  ECG: ↑ p wave duration, ↑ QRS width, sinus tachycardia  Echo: shows ↑ ventricular wall thickness, dilated left atrium  Acute onset of heart failure  Acute onset of systemic thromboembolism  Hindlimb paresis  Cold rear legs  Painful rear legs

FELINE HYPERTROPHIC CARDIOMYOPATHY  THE PREDOMINANT PATHOLOGY OF THIS DISEASE IS LEFT VENTRICULAR HYPERTROPHY  CAUSE:  Genetics  Related to abnormal myocardial myosin or calcium transport within the muscles of the heart

FELINE HYPERTROPHIC CARDIOMYOPATHY

FELINE HYPERTROPHIC CARDIOMYOPATHY: DIAGNOSIS

FELINE HYPERTROPHIC CARDIOMYOPATHY: Pathophysiology PROBLEM #1: The walls lose compliance and resist filling during diastole! (diastolic failure)

FELINE HYPERTROPHIC CARDIOMYOPATHY: Pathophysiology  PROBLEM #2: If the left ventricle cannot fill adequately with blood, the blood backs up into the left atrium (enlargement) → pulmonary veins → pulmonary edema!  PROBLEM #3: The left atrium becomes dilated with blood → the blood becomes static → blood stasis leads to clot formation → clot becomes dislodged and trapped elsewhere in the arterial system → thromboembolism! ***90% of thrombi become lodged in the aortic trifurcation causing “saddle thrombus”***

FELINE HYPERTROPHIC CARDIOMYOPATHY: SADDLE THROMBUS ACUTE, PAINFUL CONDITION CAUSING PARESIS, COLD REAR LEGS/FEET!

FELINE HYPERTROPHIC CARDIOMYOPATHY: SADDLE THROMBUS

FELINE HYPERTROPHIC CARDIOMYOPATHY: TREATMENT OR PROPRANOLOL (B-BLOCKER) DILTIAZEM (CALCIUM CHANNEL BLOCKER) FUROSEMIDE (DIURETIC) ANTICOAGULANT ASPIRIN

FELINE HYPERTROPHIC CARDIOMYOPATHY: TREATEMENT  LASIX (furosemide): a diuretic used to treat pulmonary edema  DILTIAZEM: a calcium channel blocker used to inhibit cardiac and vascular smooth muscle contractility; reduces blood pressure and cardiac afterload; overall improvement in diastolic function  Or Propranolol: a beta-blocker to decrease heart rate and myocardial oxygen demand  ASPIRIN: an anticoagulant used to thin blood and help prevent clot formation in HCM  TPA (Activase): serves as a fibrolysin resulting in the breakdown of clots that have already formed  Or Heparin, Warfarin: acts on the coagulation factors to inhibit the formation of a stable clot

FELINE HYPERTROPHIC CARDIOMYOPATHY: CLIENT INFO  There is no cure!  Cats with HCM may experience heart failure, arterial embolism, or SUDDEN DEATH!  Cats whose heart rates stay below 200 beats/min have a better prognosis than those whose heart rate is >200 beats/min

CANINE HYPERTROPHIC CARDIOMYOPATHY:  An UNCOMMON canine disease, but the cause appears to be heritable  CLINICAL SIGNS:  Fatigue  Sudden death  Tachypnea  Syncope  Cough  BREEDS: German Shepherds, Rottweilers, Cocker Spaniels, and others

DISEASES OF THE CARDIOVASCULAR SYSTEM: CONGENITAL DEFECTS

CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS CHIHUAHUAS, MALTESE, POODLE, POMERANIAN, SHELTIE PUPPIES COMMONLY AFFECTED

CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS Normally, the ductus arteriosus carries blood from the pulmonary artery to the aorta during fetal development. It bypasses the lungs of the fetus.

CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS The duct should close in the first hours after birth. If it does not, the blood begins to shunt from the aorta into the pulmonary artery and hyperperfuse the lungs. The left side of the heart will have an increase in blood return and become volume overloaded. THIS IS CALLED A LEFT-TO-RIGHT SHUNT

LOL! “ People who think they know everything are a great annoyance to those of us who do.” -Isaac Asimov

CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS (PDA)

CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS  CLINICAL SIGNS:  A loud murmur best heard over the left base  Sometimes called a “machinery” murmur or a continuous murmur  If the shunt is small some animals may be asymptomatic  In large shunts the animal will develop left-sided heart failure  Pulmonary edema  Cough  Exercise intolerance  Tachypnea  Weight loss  ECG: wide range of arrhythmias including APCs and VPCs  Echocardiography (ultrasound)  Radiographs: left atrial and ventricular enlargement

PATENT DUCTUS ARTERIOSUS: TREATMENT EXCELLENT PROGNOSIS WITH SURGICAL CORRECTION: LIGATION OF THE DUCTUS ARTERIOSUS

PATENT DUCTUS ARTERIOSUS: TREATMENT  CLIENT INFO:  64% OF ANIMALS WILL DIE WITHIN 1 YEAR IF NOT TREATED SURGICALLY  Dogs with this condition should not be used for breeding

CONGENITAL DEFECTS: ATRIAL AND VENTRICULAR SEPTAL DEFECTS During fetal life, the foramen ovale is an openingi n the interatrial septum, allowing shunting of blood from the right atrium to the left atrium in order to bypass the nonfunctioning fetal lungs. It should close at birth. If it doesn’t, after birth, the blood will shunt from left to right resulting in overload of the right side of the heart. Atrial Septal Defect

CONGENITAL DEFECTS: ATRIAL AND VENTRICULAR SEPTAL DEFECTS  CLINICAL SIGNS: ATRIAL SEPTAL DEFECTS  Result in overload of the right side of the heart → dilation and hypertrophy of the right- sided chambers  Systolic murmur  Right-sided heart failure  Radiographs: right ventricular enlargement  Echo: right ventricular dilatation

CONGENITAL DEFECTS: ATRIAL AND VENTRICULAR SEPTAL DEFECTS Blood is shunted from the oxygen-rich left ventricle into the right ventricle. The blood goes through pulmonary circulation and right back into the left atrium and ventricle resulting in volume overload of the left side of the heart. The right ventricle may dilate as well.

CONGENITAL DEFECTS: ATRIAL AND VENTRICULAR SEPTAL DEFECTS  CLINICAL SIGNS: VENTRICULAR SEPTAL DEFECTS:  Animals with small defects may have minimal or no signs  Larger defects may result in acute left-sided heart failure, usually by 8 weeks of age  A harsh holosystolic murmur  CLIENT INFO:  Repair of these defects requires open-heart surgery or cardiopulmonary bypass. These procedures are uncommon in the dog and cat  Most of these animals will eventually experience development of congestive heart failure

CONGENITAL DEFECTS: PULMONIC STENOSIS Chihuahuas, English Bulldogs, are commonly affected. CAUSE: polygenic inheritance

PULMONIC STENOSIS In pulmonic stenosis, the right ventricular outflow tract is narrowed, either at the valve itself, just below it, or just after it.

PULMONIC STENOSIS The most common form of pulmonic stenosis involves a deformed pulmonary valve such that the valve leaflets are too thick, the opening is too narrow, or the valve cusps are fused. The heart must pump extra hard to get blood through This unusually narrow, stiff valve. The right ventricle becomes thickened from all this extra work. The right atrium May become dilated and hypertrophied.

CONGENITAL DEFECTS: PULMONIC STENOSIS NORMAL CANINE CHEST RADS THIS DOG HAS PULMONIC STENOSIS – THE HEART LOOKS “PREGNANT” IN THE FRONT DUE TO RIGHT VENTRICULAR ENLARGEMENT

CONGENITAL DEFECTS: PULMONIC STENOSIS  CLINICAL SIGNS:  Syncope  Tiring on exercise  Right-sided congested heart failure  Left basilar (base) murmur  Right ventricular enlargement  Radiographs: right ventricular enlargement, dilation of the pulmonary artery, pulmonary underperfusion  Echo: right ventricular hypertrophy and enlargement, dilation of the main pulmonary artery

PULMONIC STENOSIS: TREATMENT A special balloon is inserted into the valve where it is inflated and the obstruction is broken down. Unfortunately, medical management is not very beneficial in these cases. Beta-blockers may be used to relax the heart muscle and possibly dilate the stenosis.

CONGENITAL DEFECTS: SUBAORTIC STENOSIS LESION DEVELOPS IN THE FIRST 4-8 WEEKS OF LIFE Newfoundland, Boxer, Golden Retriever, and Bull Terrier are most commonly affected

CONGENITAL DEFECTS: SUBAORTIC STENOSIS  There is a scar-like narrowing just below the aortic valve. The heart must pump extra hard to get blood through the narrowed area. The blood is pushed through in a turbulent fashion creating a heart murmur.

CONGENITAL DEFECTS: SUBAORTIC STENOSIS THE HARD WORK RESULTS IN LEFT VENTRICULAR HYPERTROPHY, LEFT ATRIAL ENLARGEMENT, AORTIC DILATION

CONGENITAL DEFECTS: SUBAORTIC STENOSIS:  CLINICAL SIGNS:  Fatigue  Exercise intolerance (low cardiac output)  Syncope  Systolic murmur at the left heart base  ECG: evidence of left ventricular enlargement - ↑ QRS height  Echo: left ventricular hypertrophy, subvalvular fibrous ring, aortic dilation

ALWAYS FORGIVE “The person with no forgiveness in his heart, lives in even worse punishment than death.” - Mr. Miyagi, The Karate Kid 2

CONGENITIAL DEFECTS: SUBAORTIC STENOSIS  TREATMENT  Balloon catheter dilation – has been done with variable and temporary results  Medical management: THE GOAL IS TO SLOW THE HEART RATE AND DECREASE CONTRACTILITY; PROPRANOLOL (BETA- BLOCKER WILL DO THIS)

CONGENITAL DEFECTS: SUBAORTIC STENOSIS  CLIENT INFO:  Should not be used for breeding  Acute, left-sided congestive heart failure is possible  Sudden death is not uncommon

DCMHCMPDAAortic stenosis Pulmonic stenosis 1 – dogs Enlarged Heart bronchoconstric tion Dilated Flappy muscle Nutritional: no taurin in cats 1 – Cats Saddle thrombus Rarely in dogs (hereditary) Noncompliant heart muscle Aorta – pulmonary a – lungs back L side Stenotic aortic valve causes LV hypertrophy High pressure in aortic valve can lead to aortic dilatation Stenotic pulmonic valve Pregnant heart L sided heart failure (HF) LV hypertrophyRV hypertrophy R sided HF Increased HR Cough Increased HR Weakness in hindlimbs, acute pain, rear cold feet Pulmonary edema Sudden death if aorta ruptures Digoxin: increased contractibility Beta blocker: Slow HR Diuretic Blood thinner No cure Treat surgically or die No breedingBalloon valvuloplasty

CONGENITAL DEFECTS: TETRALOGY OF FALLOT Keeshonds are the most commonly affected breed, but bulldogs and cats have increased incidence as well. Cause: polygenic inheritance

CONGENITAL DEFECTS: TETRALOGY OF FALLOT  THERE ARE 4 MAIN ANATOMICAL ABNORMALITIES IN THIS DISEASE!  Pulmonic stenosis  Right ventricular hypertrophy  Ventricular septal defect  Overriding aorta

CONGENITAL DEFECTS: TETRALOGY OF FALLOT  CLINICAL SIGNS and DIAGNOSIS:  Affected puppies are smaller than littermates  Exercise intolerance  Dyspnea, tachypnea  Syncope  Cyanosis  Polycythemia: occurs as a response to the large amount of deoxygenated blood going to the systemic circulation  Systolic murmur over the pulmonic area  ECHO: right ventricular hypertrophy, subaortic ventricular septal defect, right outflow tract obstruction

CONGENITAL DEFECTS: TETRALOGY OF FALLOT  TREATMENT:  Phlebotomy: to keep PCV below 65%  Surgery:  Create a left–to–right shunt by doing systemic artery to pulmonary artery anastamosis  Complete correction requires cardiopulmonary bypass which is uncommon in animals

CONGENITAL DEFECTS: TETRALOGY OF FALLOT  CLIENT INFO:  These dogs should not be bred  Congestive heart failure rarely develops  Affected animals need regular phlebotomy  Limit stress and exercise

CONGENITAL DEFECTS: PERSISTENT RIGHT 4 TH AORTIC ARCH Great Danes, German Shepherds, Irish Setters are most commonly affected

CONGENITAL DEFECTS: PERSISTENT RIGHT 4 TH AORTIC ARCH

Clinical signs include regurgitation due to megaesophagus, aspiration pneumonia, dyspnea, weight loss

CONGENITAL DEFECTS: PERSISTENT RIGHT 4 TH AORTIC ARCH  TREATMENT: Early surgical correction  Prognosis is poor without surgery  Even with surgery, some esophageal dilation may persist  CLIENT INFO:  These dogs should not be used for breeding

DISEASES OF THE CARDIOVASCULAR SYSTEM ACQUIRED VALVULAR DISEASES

CHRONIC MITRAL VALVE INSUFFECIENCY SMALL BREED/TOY BREED DOGS, USUASLLY OLDER THAN 10 YEARS THE PREVALENCE OF THIS DISEASE INCREASES WITH AGE, AND IS PROGRESSIVE. IT ACCOUNTS FOR ~95% OF ALL HEART FAILURE CASES

CHRONIC MITRAL VALVE INSUFFICIENCY ONE OF THE MOST COMMON CAUSES IS CHRONIC PERIODONTAL DISEASE! BACTERIA THAT LIVE IN TARTAR, GET SHOWERED INTO THE BLOOD STREAM AND COLONIZE IN THE VALVE LEAFLETS.

CHRONIC MITRAL VALVE INSUFFICIENCY 1.Lungs: Pulmonary fibrosis, bronchitis, and chronic obstructive pulmonary disease. 2.Heart: Endocarditis, mitral valve regurgitation, and myocardial degeneration. 3.Liver: Hepatic parenchymal inflammation and hepatopathy. 4.Kidneys: Interstitial nephritis and glomerulonephritis. CHRONIC PERIODONTAL DISEASE CAN AFFECT SEVERAL ORGAN SYSTEMS

MITRAL VALVE INSUFFICIENCY THIS IS THE OPEN LEFT VENTRICLE SHOWING THE MITRAL VALVE LEAFLETS. WHAT ARE THE STRING-LIKE STRUCTURES THAT ATTACH THE VALVES TO THE PAPILLARY MUSCLES?

MITRAL VALVE INSUFFICIENCY CHORDAE TENDINEAE

MITRAL VALVE INSUFFICIENCY BOTTOM LEAFLET IS THICKENED AND NODULAR. THIS IS DUE TO INCREASED FIBROBLASTIC TISSUE WITHIN THE VALVE LEAFLETS TOP LEAFLET IS NORMAL

CHRONIC MITRAL VALVE INSUFFICIENCY DURING LEFT VENTRICULAR CONTRACTION, BLOOD FLOWS BACK INTO THE LEFT ATRIUM THE STIFF MALFORMED VALVE FAILS TO CLOSE SUFFICIENTLY DURING SYSTOLE.

MITRAL VALVE INSUFFICIENCY IF BLOOD CONTIUES THIS BACKWARD FLOW, THE ANIMAL MAY EXPERIENCE LEFT-SIDED HEART FAILURE CHARACTERIZED BY PULMONARY EDEMA

CHRONIC MITRAL VALVE INSUFFICIENCY   DIAGNOSIS:   Radiographs   Echo   Systolic murmur at left apex; “whooping” quality   There is no treatment to delay the onset of clinical signs. Treatment is aimed at improving symptoms of heart failure   Diuretics (lasix)   ACE inhibitor, vasodilator (Enalapril)   Diet change: low sodium

TRICUSPID VALVE INSUFFICIENCY

TRICUSPID INSUFFICIENCY RESULTS IN RIGHT-SIDED HEART FAILURE CHARACTERIZED BY PLEURAL EFFUSION

TRICUSPID VALVE INSUFFICIENCY RIGHT-SIDED HEART FAILURE ALSO LEADS TO ASCITES NOTE: THE LOSS OF ABDOMINAL DETAIL

TRICUSPID VALVE INSUFFICIENCY   Treatment and client info are the same as for mtiral insufficiency; repeated abdominocentesis may be needed in these cases.

LIVE LIFE TO THE FULLEST! “You only live once, but if you work it right, once is enough.” -Joe E. Lewis, comedian

DISEASES OF THE CARDIOVASCULAR SYSTEM HEARTWORM DISEASE

CANINE HEARTWORM DISEASE   PARASITE CAUSING HEARTWORM DISEASE: DIROFILARIA IMMITIS MICROFILARIA OF D. IMMITIS ADULT HEARTWORMS

CANINE HEARTWORM DISEASE ONLY FEMALE MOSQUITOES BITE

DISTRIBUTION OF CANINE HEARTWORM DISEASE

CANINE HEARTWORM DISEASE ADULT HEARTWORMS LIVE IN THE PULMONARY ARTERIES. THE HEART MUST WORK EXTRA HARD TO PUMP AGAINST THIS OBSTRUCTION.

CANINE HEARTWORM DISEASE ADULT HEARTWORMS IN RIGHT VENTRICLE AND PULMONARY ARTERY

CANINE HEARTWORM DISEASE   PREDOMINANT PATHOLOGY: DAMAGE TO THE PULMONARY ARTERY FROM ADULT HEARTWORMS   Endothelial damage and sloughing   Inflammation (leukocytes, platelets)   Risk of thromboemboli   Pulmonary hypertension   Disruption of vascular integrity   Thickened, fibrosed   RIGHT VENTRICULAR HYPERTROPHY AND RIGHT-SIDED HEART FAILURE   The right ventricle compensates by dilating and increasing muscle thickness   Ultimately, there is decompensation and heart failure

CANINE HEARTWORM DISEASE   Severe infection can lead to CAVAL SYNDROME   Worms back up into the right atrium and venae cavae   Found in heavy worm burdens (>60)   Associated with a poor prognosis   Surgical treatment: pull worms from the right heart and venae cavae via jugular venotomy

CANINE HEARTWORM DISEASE

IDEXX SNAP TEST ADULT FEMALE ANTIGEN

CANINE HEARTWORM DISEASE

CANINE HEARTWORM DISEASE: PREVENTION   HEARTGARD/IVERHEART   Ivermectin/pyrantel pamoate   INTERCEPTOR/SENTINEL   Milbemycin oxime/ milbemycin oxime+lufeneron   REVOLUTION   Selamectin   ADVANTAGE MULTI/PROHEART 6   Moxidectin   Q 6 month injectable   TRIFEXIS   Milbemycin oxime + spinosad

CANINE HEARTWORM DISEASE: TREATMENT STANDARD PROTOCOL: 1 epaxial injection, followed By a second injection on the opposite side 24 hours later ALTERNATIVE PROTOCOL: 1 Injection given followed in 4-6 weeks by 2 injections given 24 hours apart ONLY KILLS ADULT (L5) STAGE WORMS; DOXYCYCLINE IS REC. AS COMPLIMENTARY TX