Irish wolfhound DCM Cardiac examination Clinical examination Auscultation
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Irish wolfhound DCM
Cardiac examination • • Clinical examination Auscultation Radiology Ultrasound examination ECG Laboratory tests Genetic testing Blood pressure measurement
Murmur � 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
Normal heart Lateral projection VD projection
Dilated heart Dilatation and kongestion lat Dilatation and kongestion VD
Left atrium/aortic root ratio
ECG examination
Normal rhythm
Dilated cardiomyopathy DCM
Dilated cardiomyopathy � 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
Dilated cardiomyopathy � 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
Dilated cardiomyopathy � 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
Dilated cardiomyopathy � 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
Dilated cardiomyopathy � 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
Etiology and inheritance � 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
Histological changes � 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
Histological changes � 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
Secondary cardiomyopathy � 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 %
Secondary cardiomyopathy � Chocolate poisoning � Adriamycin (chemotherapy) � Prolonged tachycardia � Increased blood pressure?
DCM - symptoms Cough Respiratory distress Exercise intolerance Nightly restlessness Ascites Loss of weight Reduced apetite Syncophy Very common Common Rare
Diagnosis � 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
Diagnosis � 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
Cardiac enlargement
Enlarged left atrium
Reduced Fs
Reduced Fs Normal Fs Reduced Fs
Reduced Fs
DCM
Preclinical DCM
Preclinical DCM
Myocarditis
Mitral regurgitation
Simpsons EDV
Simpsons ESV
Shperical index
DCM - treatment • • 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
Arrhytmias Normal rhytmm Sinustachycardia
Atrial fibrillation
Atrial fibrillation AF with slow ventricular rate AF with rapid ventricular rate
AF - treatment � 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
Multifocal premature ventricular beats
AV – junctional VPC
AF and VPC
VPC - treatment � When to treat? � Sotalol 1 -2 mg/kg bid � Atenolol 6, 25 -25 mg bid � Propranolol 0, 2 -2 mg/kg tid � Diltiazem 0, 5 -3 mg/kg tid
Atrial premature complexes
APC
APC - treatment � No treatment unless heart rate is elevated � Tachycardia as atrial fibrillation
Ventricular tachycardia
Ventricular tachycardia
Ventricular tachycardia - treatment � 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
Irish Wolfhound � 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
IWH � 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
IWH � 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
Diagnostic criteria � 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
Inheritance � 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
Inheritance � 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
Inheritance �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 CFA 37 � Its gene action is significantly different between male and female dogs � The major risk allele is a common variant widely spread in the population
Inheritance � 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
Study material � 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
Study material � 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
Study material � 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
Study material � 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
Recommendations � 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 ?
Recommendations � 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
Cardiac biomarkers � 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
Troponine � 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
Troponine � High sensitive troponine is elevated for some months � Lack of specifity makes troponine unsuitable for breeding examinations � Elevated value indicates cardiac injury
BNP � 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
BNP � BNP is suitable for assessing the progression of the heart disease, increasing value indicates the increase in severity � Simpler test methods have been developed
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