1. DCM

2. Clinical examination Auscultation Radiology Ultrasound examination ECG Laboratory tests Genetic testing Blood pressure measurement

3.  Grade 1 weak murmur requiring careful auscultation  Grade 2 weak murmur that can be heard immediately  Grade 3 moderate murmur  Grade 4 strong murmur without thrill  Grade 5 strong murmur with thrill  Grade 6 murmur can be heard without stethoscope

4.  Lateral projection  VD projection

5.  Dilatation and kongestion lat  Dilatation and kongestion VD

9. DCM

10.  The most common cardiac disease in the large and giant breed dogs  The disease has a long preclinical period lasting from 1-4 years  Congestive heart failure develops at the later stages of the disease  Disease is more common in male dogs

11.  DCM is a primary form of myocardial disease leading to impaired cardiac contractility and cardiac dilatation  To compensate the reduced contractility the heart enlarges and the heart rate often increases  Arrhytmias are common, most often dogs develop atrial fibrillation or ventricular premature complexes

12.  The cause of the disease is not verified but genetic predisposition is obvious  Symptoms often start suddenly without earlier signs of the disease  Sudden cardiac death may be caused by arrhytmias

13.  Prevalent opinion is that DCM is a group of diseases with genetic predisposition  For this reason there are significant differences in clinical outcome between different breeds  First genetic tests are available  Ultrasound examination can be used to seek for preclinical cases

14.  At least the following breeds are at increased risk  Doberman pincher, boxer, Finnish hound, Great dane, Irish wolfhound, Newfoundland, St. Bernard, cockerspaniel, English springerspaniel, Islandic sheepdog, Portuguese Water Dog, Dalmatian

15.  Autosomal dominant – boxer and Doberman pincher  Great Dane – not known  Irish Wolfhound –combined monogenic/polygenic inheritance  Genetic mutation has so far been found in Doberman ja boxer breeds

16.  Two different forms has been found  In doberman pincher and boxer fatty infiltrates develop in the heart muscle cells (fatty infiltrate)  This form of the disease seems to be clinically more severe

17.  Giant breed dogs seem to have so called wavy fiber form of the disease  Is the mode of inheritance same?  Irish wolfhounds seem to have a mutation that affects lipid metabolism of the heart muscle cells

18.  Impaired cardiac contractility may be caused by noncardiac disease  Most common causes of secondary cardiomyopathy are hypothyroid disease, myocarditis and tumors  Fs value often decreases between 20-25 %, rarely below 20 %

19.  Chocolate poisoning  Adriamycin (chemotherapy)  Prolonged tachycardia  Increased blood pressure?

20.  Cough  Respiratory distress  Exercise intolerance  Nightly restlessness  Ascites  Loss of weight  Reduced apetite  Syncophy  Very common  Common  Rare

21.  Auscultation may be normal  Murmur or arrhytmia may be heard  Rtg finding may be normal at the early stages  Rtg findings are not spesific  Ultrasound examination is needed to confirm the diagnosis  Preclinical stage may be challenging

22.  Cardiac neurohormones  Holter monitoring  How many VPC:s is abnormal?  Boxer over 100/24 hours is suspicious  Doberman – yli 50/24 hours suspicious, over 100/24 hours abnormal

26.  Normal Fs  Reduced Fs

36. Pimobendane 0,1-0,3 mg/kg bid Furosemide 0,5-3 mg/kg sid-tid ACE inhibitor Digitalis 0,005-0,01 mg/kg bid Spironolaktone 1-2 mg/kg sid-bid Hydrochlorotiatside 2-4 mg/kg bid L-karnitine 1-2 g/dog bid-tid, taurin 500 mg/dog bid

37.  Normal rhytmm  Sinustachycardia

39.  AF with slow ventricular rate  AF with rapid ventricular rate

40.  Digoxin 0,005-0,01 mg/kg bid  Sotalol 1-2 mg/kg bid  Atenolol 6,25-25 mg bid  Propranolol 0,2-2 mg/kg tid  Diltiazem 0,5-2 mg/kg tid  Digoxin may be combined with either betablocker or calsium channel blocker

44.  When to treat?  Sotalol 1-2 mg/kg bid  Atenolol 6,25-25mg bid  Propranolol 0,2-2 mg/kg tid  Diltiazem 0,5-3 mg/kg tid

47.  No treatment unless heart rate is elevated  Tachycardia as atrial fibrillation

50.  Lidocaine iv 2 mg/kg slow bolus  No more than 8 mg/kg (4 boluses)  Continued 40-100 g/kg/min  Sotalol 1-22 mg/kg bid  Atenolol 6,25-25 mg bid  Mexiletine

51.  About 20 % of Irish Wolfhounds develop dilated cardiomyopathy at some point of their life  Mean age of onset is 4,5 years  Most dogs develop the disease between 3-7 years of age  Male dogs have significantly higher risk than females

52.  Most affected dogs have concurrent atrial fibrillation which may be a first sign of the disease  The left ventricular function does not often become severely compromised until the later stages of the disease, which improves the survival time

53.  Survival time may be longer than in many other breeds  Some dogs developing the disease at middle age may survive to old age  A dog may still die of sudden cardiac death  DCM is in any case a major cause of death in this breed

54.  Fs below 25 %  End diastolic diameter over 61 mm  End systolic diameter over 41 mm  EF measured by Simpsons method below 45 %  Atrial fibrillation diagnosed by ECG

55.  Two studies trying to establish a mode of inheritance for DCM in IWH has been published 2007 and 2012  Both groups published similar conclusions  In both studies a simple dominant monogenic mode of inheritance coud be rejected

56.  The model that best explained the results was a mixed monogenic-polygenic model with an autosomal dominant sex dependant major gene and further polygenic effects  5 minor loci associated with development of DCM coud be identified

57.  A most propable mode of inheritance in IWH is a model where one dominant major gene needs futher polygenic effects for the disease to develop  The major gene is located on CFA37  Its gene action is significantly different between male and female dogs  The major risk allele is a common variant widely spread in the population

58.  Detected genes affect lipid metabolism  Cells in the heart muscle use lipids as they energy source  Impaired cardiac function seems to be the result of increased lipid production in the heart muscle cells

59.  In the last three years I have performed a cardiac examination for 45 individual Irish Wolfhounds  9 of these dogs have so far been assessed to have DCM  Only three of these dogs show a typical mode of the disease with impaired cardiac function and cardiac dilatation

60.  On the other dogs diagnosis is based on development of arrhytmias  The dogs have acguired atrial fibrillation with of without VPC:s  Five of these dogs are on medication either because of congestive heart failure or atrial fibrillation with rapid ventricular rate

61.  Three dogs have been assessed as equivocal  They have arrhytmias that are not severe enough to establish a diagnosis of DCM  One dog has been diagnosed a mitral regurgitation  Findings are consistent with other similar studies

62.  Results send to the Irish wolfhound association show lesser incidense  This is because of three reasons  Some of the dogs have been so young when examined that the disease may not yet be detectable  Many dogs are female with a smaller risk  Dogs assessed equivocal having atrial fibrillation shoud be assessed DCM

63.  Examining dogs below the age of three is not effective  Ultrasound examination does not find all cases before dogs are used for breeding  ECG examination shoud always be performed together with ultrasound  Holter monitoring ?

64.  Genetic testing is not yet available for IWH  Cardiac biomarkers are not sensitive enough to recognize the disease in early stages  Available method is ultrasound examination combined with ECG and possibly Holter monitoring

65.  Hopes were these woud prove to be an easy method to recognise cardiac disease at early stages  Blood sampling does not require the expertese needed to perform cardiac ultrasound or ECG

66.  Troponine is released in conjuction with sudden cardiac injury  It can be measured in the blood sample  Unfortunately the halflife of troponine is short and its release is not spesific for particular cardiac disease

67.  High sensitive troponine is elevated for some months  Lack of specifity makes troponine unsuitable for breeding examinations  Elevated value indicates cardiac injury

68.  Brain natriuretic peptide  Is released almost entirely from heart muscle cells  Overlap between individuals is too wide to make BNP suitable for detecting the early disease

69.  BNP is suitable for assessing the progression of the heart disease, increasing value indicates the increase in severity  Simpler test methods have been developed