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LAIM: Cardiology > ACVIM Required Literature - Cardiology > Flashcards

ACVIM Required Literature - Cardiology Flashcards

1
Q

What are the classical clinical signs and alternate presenting clinical signs associated with pericarditis in the horse?

A

Classic signs: muffled heart sounds and/or friction rubs, tachycardia and jugular distention.
Alternate signs: fever, mild abdominal pain, ventral oedema, weight loss and/or lethargy.

Ref: Equine Vet. Educ. (2013) 25 (7) 334-338.

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2
Q

What is the treatment of choice for pericarditis, when effusions are moderate to severe?

A

Pericardial drainage. Minimal evidence to support benefit of pericardial lavage over drainage alone.

Ref: Equine Vet. Educ. (2013) 25 (7) 334-338.

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3
Q

What are the reported rates of remission or recovery following aggressive treatment of pericarditis in the horse?

A

60-100%.

Ref: Equine Vet. Educ. (2013) 25 (7) 334-338.

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4
Q

What insect has been associated with development of pericarditis in horses and what is the prognosis in these cases?

A
  • Eastern Tent Caterpillar.
  • Prognosis is guarded as pericardial constriction is an important fatal sequelae which may occur up to 2 years after initial diagnosis and treatment.

Ref: Equine Vet. Educ. (2013) 25 (7) 334-338.

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5
Q

What treatment can be attempted for horses with constrictive pericarditis and what is the success rate of this procedure?

A
  • Thorascopic pericardectomy.
  • In 4 cases of Eastern Tent Caterpillar pericarditis: 2 attempts at transecting the visceral pericardium –> 1 fatal haemorrhage, 1 fatal arrhythmia; 2 attempts at transecting parietal pericardium –> recovery up to 3y follow-up.

Ref: Equine Vet. Educ. (2013) 25 (7) 334-338.

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6
Q

Septic pericarditis can be treated via pericardial lavage with/installation of antibiotics. What is the potential risk involved with this procedure?

A

Caution should be exercised when contemplating intra-pericardial medication since pericardial irritation alone can induce pericarditis and constriction.

Ref: Equine Vet. Educ. (2013) 25 (7) 334-338.

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7
Q

List the two components of medical therapy indicated in treating most cases of equine percarditis.

A
  • NSAIDs
  • Broad-spectrum ABs as opportunistic or haematogenous infections of sterile pericardial fluid may develop and some cases of equine pericarditis accompany lower airway infections.

Ref: Equine Vet. Educ. (2013) 25 (7) 334-338.

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8
Q

Aseptic effusive fibrinous pericarditis is the most common form of equine pericarditis. What medication is indicated to treat this condition?

A

Corticosteroids. Reported to be highly effective at reducing pericardial fluid volume however does not appear to reduce the risk of pericardial restriction.

Ref: Equine Vet. Educ. (2013) 25 (7) 334-338.

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9
Q

Horses with Atypical Myopathy often have elevated cardiac troponin I concentrations. Is the magnitude of cTnI elevation correlated with survival?

A

No.
cTnI typically takes 2-10 wks to return to normal range.

Ref: J Vet Intern Med 2012;26:1019–1026.

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10
Q

What ECG changes have been described in horses with Atypical Myopathy?

A

Ventricular premature depolarisations, ventricular tachycardia, prolonged QT interval (prolonged ventricular repolarisation).
In survivors these abnormalities resolved in 2d-10wk.

Ref: J Vet Intern Med 2012;26:1019–1026.

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11
Q

What echocardiographic changes have been described in horses with Atypical Myopathy?

A

Systolic wall motion abnormalities: biphasic contractions.

Ref: J Vet Intern Med 2012;26:1019–1026.

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12
Q

List objective negative prognostic indicators of heart disease in horses.

A
  • Progressive chamber remodelling (dilation, change in chamber shape).
  • Great vessel enlargement.
  • Development of pulmonary hypertension.
  • Development of congestive heart failure.
  • Development of potentially dangerous arrhythmias.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

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13
Q

What three diagnoses in horses with heart disease indicate that a horse is dangerous to ride?

A
  • Pulmonary hypertension.
  • Congestive heart failure.
  • Ventricular arrhythmias.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

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14
Q

List eight specific incidences in which echocardiography is indicated in horses.

A
  • Prev dz ‘functional murmur’ is louder on repeat exam.
  • Grade 3-6/6 L heart murmur compatible with MR or AR.
  • Grade 3-6/6 R heart murmur compatible with TR.
  • Suspected VSD or other congenital heart defect.
  • Continuous or combined systolic-diastolic murmurs.
  • Clinically important arrhythmias (+/- murmurs).
  • Suspected myocardial injury.
  • Suspected congestive heart failure.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

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15
Q

Describe exercise testing for evaluation of cardiac function in horses.

A
  • Continuous ECG monitoring of horses exercising at or slightly above exercise level with intermittent, unexpected sympathetic stimulation.
  • Specific noninvasive cardiac assessments include (1) the effects of exercise on auscultation (rate, rhythm, and murmurs); (2) peak HR during exercise; (3) HR and rhythm during the different phases of the exercise test and during recovery; and, optionally, (4) echocardiography before and after exercise (stress echocardiogram).

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

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16
Q

When is exercise testing indicated for evaluation of heart disease in horses?

A
  • Pre-purchase exam when non-functional murmur or a sporadic arrhythmia is identified.
  • Clinically important structural lesions.
  • Intermittent premature complexes.
  • Lone atrial fibrillation that cannot be converted to sinus rhythm.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

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17
Q

When is exercise testing contradicted for evaluation of heart disease in horses?

A
  • Congestive heart failure.
  • Severe valulvar regurgitation with secondary atrial fibrillation.
  • Pulmonary hypertension.
  • Severely reduced systolic function.
  • Ventricular rhythm of dangerous intensity.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

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18
Q

What is the clinical significance of mitral regurgitation in affected horses?

A
  • Common finding in performance horses,
  • If mild normal performance and life expectancy,
  • Unlikely to affect performance unless severe but left atrial enlargement results in increase risk of atrial fibrillation.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

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19
Q

List negative prognostic indicators in horses with mitral regurgitation.

A
  • Moderate to severe regurgitation.
  • Endocarditis.
  • Ruptured chordae tendinae.
  • Flail leaflet.
  • Severe valvular thickening.
  • Concurrent pulmonary artery dilation.
  • Increased tricuspid regurgitation velocity.
  • Significant mitral regurgitation with atrial fibrillation or tachycardia.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

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20
Q

List the recommendations for assessment and management of mitral regurgitation.

A
  • Determine the most likely aetiology.
  • Assess severity: Hx, exercise test, PE, echo.
  • Examine every 2y (mild) or at least 1y (mod to severe).
  • Ensure HR and rhythm monitored reg (mod to severe).
  • Exercise test if mod to severe, AF, MR progresses rapidly.
  • Management of complications of advanced dz.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

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21
Q

What is the clinical significance of aortic regurgitation in affected horses?

A
  • Common finding in older horses.
  • Often incidental but sudden death is possible.
  • Risk for decreased performance or longevity if mod to severe or diagnosed at less than 10y of age.
  • Haemodynamically severe AR –> LV overload –> bounding pulses.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

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22
Q

List the recommendations for assessment and management of aortic regurgitation.

A
  • Determine the most likely aetiology.
  • Assess severity: Hx, exercise test, PE, echo.
  • Exercise ECG if moderate to severe AR.
  • Examine every 12mo if stable.
  • Examine at least every 6mo if mod to severe.
  • Monitor HR and rhythm regularly; inc HR or irregularly irregular rhythm indicates AF/PVC and progression.
  • Exercise induced ventric arrhythmias = neg prognostic indicator.
  • Horses w AR and PVC are less safe to work than age-matched peers.
  • Manage complications of advanced disease.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

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23
Q

What is the clinical significance of tricuspid regurgitation in affected horses?

A
  • Common benign finding in equine athletes.
  • Prevalence and severity are associated with age and level of training.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

24
Q

List negative prognostic indicators in horses with tricuspid regurgitation.

A
  • Structural valve lesions: endocarditis, ruptured chordae tendinae, flail leaflet.
  • Clinical signs of right congestive heart failure.
  • Concurrent severe mitral regurgitation or pulmonary hypertension.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

25
Q

List the recommendations for assessment and management of tricuspid regurgitation.

A
  • Appreciate the high prevalence of tricuspid regurgitation in high performance horses.
  • Perform clinical examination and echo with murmur is 4-6/6, poor performance, thrombophlebitis, FUO, PPE.
  • Re-examine yearly for moderate to severe tricuspid regurgitation.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

26
Q

Describe the breed dispositions, typical location of and typical murmur associated with ventricular septal defects (VSD) in horses.

A
  • Suspected breed predispositions: Section A Welsh Mountain ponies, Standardbreds and Arabian horses.)
  • Perimembranous located ventral to the tricuspid leaflet,
    and below the junction of the right and noncoronary cusps of the aortic valve.
  • R systolic murmur: PMI ventral to tricuspid valve; holo- or pansystolic; plateau (band-) shaped; grade 4–6/6.
  • Commonly part of more complex congenital defects, therefore murmur may be different.
27
Q

Describe diagnosis and evaluation of VSDs in horses.

A
  • Definitive diagnosis = echocardiogram.
  • Measure largest systolic diameter of the defect in two mutually perpendicular planes; defects ≤2.5 cm in a 450–500 kg horse, less likely to be hemodynamically important.
  • Peak velocities >4.5 m/s suggest a restrictive defect with a better prognosis.
  • Lower shunt velocities (
28
Q

Describe prognostic indicators in horses with VSDs.

A
  • Most important prognostic criteria for an isolated VSD:
    1. Size of VSD.
    2. Size of the cardiac chambers.
    3. Maximal shunt velocity.
    4. Presence of significant AR or MR.
    5. PHT.
    6. CHF.
  • Small VSD –> excellent Px for normal performance/life.
  • Moderate defects: often well-tolerated at rest; perform in high-intensity sports might be affected.
  • Progressive MR or AR and cardiac remodeling can facilitate dev of AF, PHT, or LVD with progressively negative impact on exercise capacity and eventually on survival.
  • Large diameter, unrestrictive VSD portends a poor
    prognosis and shortened life expectancy.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

29
Q

List key recommendations for evaluation and management of horses with VSDs.

A
  • Perform comprehensive clinical and echo exams.
  • Re-examine annually.
  • Perform exercise (ECG) testing mod to large VSDs, in prepurchase exams, or when performance is suboptimal.
  • Consider horses with a small VSD and minimal cardiomegaly as safe to compete; evaluate larger defects on a case-by-case basis in consultation with a specialist experienced in equine cardiology.
  • Consider affected horses unsuitable for breeding.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

30
Q

Describe clinical findings in horses with aorto-cardiac fistulas.

A
  • A continuous machinery murmur loudest on the RHS of the thorax with bounding arterial pulses is characteristic.
  • Many horses present with an acute onset of exercise intol and pain, often perceived as colic, and ventricular tachy.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

31
Q

Describe clinical findings in horses with aorto-pulmonary fistulas.

A
  • Friesian horses with aorto-pulmonary fistulation present with bounding arterial pulses, tachycardia, and a grade 1–3/6 holosystolic and early-to-mid diastolic murmur loudest dorsal to the aortic valve.
  • Often results in acute heart failure or even SCD, but might also present with a chronic history of poor performance.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

32
Q

List key recommendations for evaluation and management of horses with aorto-cardiac or aorto-pulmonary fistulas.

A
  • Consider aorto-cardiac fistula in horses with acute colic and VT, or when a continuous RHS murmur is detected.
  • Affected horses are not safe to use.
  • These horses can experience SCD at any time.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

33
Q

Discuss second degree atrioventricular block in horses.

A
  • This rhythm is normal in equine athletes.
  • HR is low normal.
  • Several conducted P waves before the AVB.
  • Auscultation: an irregular rhythm with a repetitive pattern. - Physical activity or increased sympathetic tone should cause the arrhythmia to disappear.
  • In some cases, an exercising ECG is needed to confirm the physiologic basis of the arrhythmia.
  • “High-grade”: when second degree AV block results
    in more than 2 consecutively blocked P waves; considered abnormal; if the horse cannot be exercised an atropine resp test can be used to determine if a 1 : 1 conduction dev.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

34
Q

List key recommendations for evaluation and management of horses with second degree atrioventricular block.

A
  • Horses with high-grade 2nd degree AVB that disappears with exercise should only be ridden or driven by an informed adult, and the HR and rhythm should be frequently monitored.
  • Horses with high-grade 2nd degree AVB during exercise or after atropine administration should be rested and re-evaluated; they are considered less safe to ride or drive than their age matched peers.
  • Horses with symptomatic bradyarrhythmias generally have a poor prognosis and are not safe to ride or drive.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

35
Q

Describe atrial fibrillation in horses.

A
  • Most common arrhythmia affecting performance.
  • Heritable lesions in some Standardbred racehorses.
  • Paroxysmal AF: acute onset of AF, spont conversion to normal sinus rhythm (NSR) can occur, usually w/in 24–48h.
  • Lone AF: in absence of detectable underlying heart dz.
  • Structural heart dz can predispose horses to recurrent or persistent AF.
  • Charac by an irregularly irregular rhythm that can sound like a combination of premature beats and long pauses.
  • Atrial (4th) sound is absent, resting HR is usually normal.
  • Resting tachycardia suggests underlying heart dz, SNS stim because of stress or pain, or presence of an accessory atrioventricular conduction pathway.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

36
Q

Describe the diagnosis of atrial fibrillation in horses.

A
  • ECG: irregularly irregular R-R interval with normal QRS
    morphology, absent P, f waves, +/- concurrent PVCs.
  • AV conduction in atrial flutter is usually variable, resulting in a ventricular rate response that can be irregular or regular during periods of increased sympathetic tone.
  • Echo to ID any underlying structural heart disease, valvular regurgitation, and cardiac (atrial) enlargement.
  • A slight inc in LA size can result from AF, even in the absence of MR.
  • ECG exercise test if horse is used for performance and cardioversion is not an option or could not be attained.
  • Suspected AF duration should be determined b/c it affects Px for conversion and likelihood of recurrence.
  • AF induces time-dependent electrical and structural remodeling within the atria, factors known to promote its persistence.
  • Significant LA enlargement –> dec chance of conversion and inc risk of recurrence.
  • AF + CHF/PHT –> grave Px; horse should be retired.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

37
Q

Describe treatment options for atrial fibrillation in horses.

A
  • Cardioversion is recommended when the average maximal HR during exercise at an intensity at or slightly exceeding the horse’s normal activities >220 bpm.
  • Treatment is also recommended when concurrent VA are observed as may rarely –> SCD.
  • If AF persists beyond 48 hours without spont conv, prompt tx is recommended to deter progressive atrial remodeling.
  • Should only be performed in a controlled setting with continuous (ECG) monitoring, regardless of tx method.
    1. Quinidine sulfate:
  • Indications: lone AF, AF with mild LA enlargement, and comorbidities in which GA or TVEC are not options.
  • Contradictions: rapid ventricular response to AF and complex ventricular ectopy owing to the proarrhythmic effect of quinidine and risk of polymorphic VT.
  • Risk of adverse drug effects necessitates monitoring and sometime discontinuation or admin of other drug e.g. digoxin to control ventricular response rate.
    2. TVEC:
  • Involves a timed shock delivery on the R-wave.
  • Indications: lone AF, AF with mild LA enlargement, and horses either intolerant of or unresponsive to quinidine treatment or horses in which quinidine is contraindicated.
  • Risks: GA, or rarely, dev of a fatal arrhythmia.
  • Immediate recurrence of AF (IRAF) within the first 24 hours after cardioversion, is more likely than with quinidine cardioversion. Pretreatment with antiarrhythmic
    drugs before TVEC or during and after anesthesia might
    minimize the likelihood of IRAF.
  • In the long term, recurrence rates after TVEC and quinidine cardioversion are believed to be similar.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

38
Q

Describe recommended post-cardioversion treatment of horses with prior atrial fibrillation.

A
  • Recurrent atrial arrhythmias can be obs in some horses following successful cardioversion ID via 24h ECG.
  • The optimal timing of this exam, the influence of APCs on long-term Px, and the best approach to management of recurrent atrial ectopy are unknown.
  • Complete echo: LV function should return to normal within 3 days; LA within days to weeks if AF was longstanding.
  • Persistent LA contractile dysfunction can be caused by AF-induced atrial remodeling or underlying primary cardiomyopathy and might portend recurrent AF.
  • Drugs known to predispose to ectopic impulse formation should be avoided, including furosemide, supplements containing sodium bicarbonate, and thyroid hormones.
  • Rest is enforced until atrial electrical and contractile function has normalised or nearly so e.g. short-duration paroxysmal AD –> 1wk, long-standing –> at least 1mo.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

39
Q

What is the likelihood of recurrence of atrial fibrillation following cardioversion?

A
  • Recurrent rate lowest (about 15%) with lone AF of recent onset (≤1 month).
  • Higher in horses with underlying cardiac disease, especially chronic valvular regurgitation with atrial enlargement.
  • High number of PACs or runs of atrial tachycardia are more likely to experience recurrent AF.
  • Persistent LA mechanical dysfunction thought to indicate irreversible atrial remodelling and might –> poorer Px.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

40
Q

List key recommendations for evaluation and management of horses with atrial fibrillation.

A
  • Select the most appropriate method of cardioversion based on risk factors for pharmacoversion or TVEC.
  • Perform a continuous 24-hour ECG and ideally evaluate LA function after cardioversion.
  • Return to training within 1 week with paroxysmal AF or short-duration lone AF if normal after cardioversion; rest horses with long-standing AF for 4–6 weeks.
  • Avoid furosemide, supplements containing sodium bicarbonate, and thyroid hormones after cardioversion.
  • Supplement oral potassium chloride to horses administered furosemide before racing or demonstrating low fractional excretion of potassium.
  • Horses should be cardioverted or retired when the exercising HR during sustained maximal exercise exceeds 220 beats/min or if concurrent VA are detected during exercise or with SNS stimulation.
  • Horses with persistent AF should only be ridden or driven by an informed adult and limited to an exercise level considered relatively safe based on an exercising ECG.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

41
Q

Describe premature atrial complexes in horses.

A
  • PACs are usually detected during auscultation as premature beats interrupting an otherwise regular rhythm.
  • Can be difficult to differentiate from marked sinus arrhythmia.
  • Uncommon cause for poor performance.
  • The greatest concern relates to their potential to incite atrial flutter and AF.
  • ECG:
    • Ectopic, premature atrial activation (P0) usually with changes in normal P-wave morphology.
    • PACs can be conducted with a variable P0-R interval or blocked at the AV node.
    • PACs are easily missed when buried in the ST segment or T wave, especially at higher HR.
    • QRS is generally normal, but ventricular conduction can be aberrant –> wider, taller or bizarre QRS complexes with secondary ST segment and T wave changes.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

42
Q

List key recommendations for evaluation and management of horses with premature atrial complexes.

A
  • A continuous 24-hour ECG is recom to assess freq PACs.
  • Horses with occasional PACs that are overdriven during exercise and those with occasional PACs during exercise are considered as safe to ride or drive as their age-matched peers.
  • Underlying causes should be sought.
  • The risk for AF should be appreciated.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

43
Q

Describe ventricular premature complexes and ventricular tachycardia in horses.

A
  • Auscultation: characterised by premature beats interrupting an otherwise regular rhythm, usually followed by a compensatory pause.
  • VT: abnormal rhythm caused by 3 or more repetitive or linked PVCs; ausc: rapid, usually regular rhythm, with variable intensity and often booming heart sounds.
  • Because of intermittent aortic valve opening, the rhythm can sound irregular on ausc; an intermittent pulse deficit could be present; abnormal jugular pulses are freq obs.
  • ECG: PVCs are charac by premature ventricular activation without an assoc P wave, QRS typically wide and bizarre and followed by a large T wave of opposite polarity.
  • The complexity of a ventricular arrhythmia is presumed to relate to the risk of hypotension and SCD because of VF.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

44
Q

Safety is of primary concern in recommended whether or not horses with ventricular arrhythmia can be exercised. What information can be used to try and assess safety and prognosis in horses with ventricular premature complexes and ventricular tachycardia.

A
  • Hx of collapse raises great concern in a horse w PVCs.
  • Similarly ventricular ectopy in assoc with important structural heart disease (and cardiomegaly) poses another long-term safety concern (perform exercising ECGs).
  • Detection of systemic hypotension during a documented run of VT is another indication of a serious arrhythmia.
  • In the absence of CSx or serious structural heart dz, the risk of ventricular ectopy is usually defined by ECG charac incl the morphology, timing, and rate of the ectopic activity.
  • The following are features of complex or potentially “malignant” VA:
    • Multiform or polymorphic QRS morphology.
    • Short coupling intervals (especially R-on-T timing).
    • Sustained VT.
    • Rapid ventricular rate (exceeding 120 beats/min).
    • Repetitive ectopic activity (couplets, VT).
  • Polymorphic VT can be observed with diffuse myocardial disease or with drug toxicity (quinidine toxicosis) and induces both hemodynamic and electrical instability.
  • Occasional monomorphic PVCs overdriven with exercise or only detected in the immediate postexercise period are not usually a cause for poor performance.
  • A wide range of VA occur during and immediately after intense exercise in normally performing horses.
  • PVCs during exercise are a cause for concern; their relationship with poor performance is uncertain.
  • VA can be assoc with medical or surgical disorders and often resolve with correction of the underlying problem.
  • A clinical laboratory profile, including plasma or serum cardiac troponin I (cTnI) concentration should be obtained.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

45
Q

List key recommendations for evaluation and management of horses with ventricular premature complexes and ventricular tachycardia.

A
  • Underlying causes should be sought & managed if poss.
  • Horses with occasional PVCs at rest or during exercise or with sustained AIVR that is overdriven by exercise can be ridden or driven with caution by an informed adult.
  • Horses with sustained monomorphic VT should be rested and treated. NSR should be present for at least 4 weeks before re-evaluation is performed.
  • A continuous 24-hour ECG is indicated before returning the horse to work. If normal, an exercising ECG should be performed, followed by another exercising ECG once the
    horse has returned to full work.
  • Horses affected by a single episode generally have a favourable prognosis, but on occasion monomorphic VT
    can recur.
  • Horses with symptomatic or complex VA should be rested and treated. Follow-up examinations are similar as for horses with sustained monomorphic VT although the safety of these horses remains uncertain. These horses should only be ridden or driven by an informed adult.
  • Rigorous athletic work is not recommended for horses that showed VA in the setting of moderate or severe structural heart disease, incl echo lesions suspected to indicate myocardial fibrosis and moderate to severe AR.
  • For horses with a history of VT that remain in work follow-up 24-hour and exercising ECGs should be performed at least annually.

Ref: ACVIM Consensus Statement (2014) - Heart Dz.

46
Q

Cardiac troponin I (cTnI) is frequently used for diagnosis of myocardial damage in horses. In people cTnT is preferred. What is the advantage of cTnT over cTnI? Is it an indicator of myocardial damage in horses?

A
  • Different cardiac troponin I (cTnI) assays give different results. Only 1 manufacturer has marketed troponin T (cTnT) assays. Therefore, cTnT often is preferred for detection of myocardial infarction in human patients.
  • Despite large quantitative differences, cTnI and cTnT are both useful for detection of myocardial damage in horses.

Ref: J. Vet. Intern. Med. 2015; 29(1):348-354.

47
Q

The quantification of equine LV function is generally limited to short-axis M-mode measurements. However, LV deformation is 3D and consists of longitudinal shortening, circumferential shortening, and radial thickening. In human medicine, longitudinal motion is the best marker of subtle myocardial dysfunction. Can 2D speckle tracking be used to quantify equine LV longitudinal function?

A

Yes, 2DST is a reliable technique for measuring systolic LV longitudinal motion in healthy horses.

Ref: J. Vet. Intern. Med. 2011; 25(2):330-338.

48
Q

Myocarditis is thought to occur secondary to EIV infections in horses, but there is a lack of published evidence. In an experimental study of experimental infection of 29 horses was there evidence of myocardial damage, detectable by increases in plasma cTnI concentrations?

A
  • All EIV-infected ponies developed clinical signs and viral shedding.
  • One vaccinated pony and 2 unvaccinated ponies had cTnI greater than the reference range at 1 time point. At all other
    times, cTnI was
49
Q

Do echocardiographic changes occur in association with hypohydration in normal horses?

A
  • Hypohydration decreased LV internal diameter in systole and diastole, LA diameter and LV volume and inc septal wall thickness in diastole, free wall thickness in diastole, mean wall thickness and relative wall thickness.
  • Hypohydration produces changes in left ventricular and atrial size that could mask or promote the severity of cardiac disease. The thickened, ‘‘pseudohypertrophied’’ appearance of the left ventricle in hypohydrated horses could affect interpretation of echocardiographic variables that are applied to the prediction of athletic performance.
  • Echocardiography may prove a noninvasive method of monitoring volume status and response to fluid therapy in hypovolaemic horses.

Ref: J. Vet. Intern. Med. 2011; 25(3):563-569.

50
Q

What is the upper reference limit for cTnI in Standardbred racehorses? Do increases in plasma cTnI concentration occur 1–2 hours after a race.

A
  • The 95th and 99th percentile upper reference limits were
51
Q

CO measurement in critically ill people and small animals is performed to evaluate cardiac function and glocal oxygen delivery to tissues. Do transthoracic echocardiographic methods of measuring CO in standing adult horses compare to the lithium dilution CO (LiDCO) method?

A
  • The 4-chamber area-length, Simpson, bullet, and RVOT Doppler provided better agreement with lithium dilution than LVOT Doppler or cubic methods
  • These methods warrant further investigation for use in critically ill adult horses.

Ref: J. Vet. Intern. Med. 2013; 27(2):324–330.

52
Q

Can atrial fibrillation cycle length can be determined in horses with AF via intra-atrial ultrasound?
Are AFCL and atrial size are related to risk for recurrence of AF?

A
  • Atrial fibrillation cycle length could be determined in all horses.
  • Significant parameters to predict rAF were:
    i) The ratios of the p5AFCL to the LA sizes corrected to the size of AO.
    ii) LA sizes corrected to the size of AO.
  • Before TVEC, assessment of LA size and atrial electrophysiologic characteristics might help to identify horses at increased risk for AF recurrence.

Ref: J. Vet. Intern. Med. 2014; 28(2):624–629.

53
Q

What is the recurrence rate of atrial fibrillation following cardioversion? Can echocardiographic examination at 24 hours post-TVEC or quinidine conversion predict likelihood of recurrence?

A
  • AF recurred in 36/100 horses with a first AF episode and in 57/ 133 AF episodes overall.
  • Factors associated with recurrence in horses with a first episode were previous unsuccessful treatment attempt and mild or moderate mitral regurgitation.
  • When the last AF episode of all horses was included, previous AF and active left atrial fractional area change were significant predictors.
  • The only echocardiographic variable of left atrial function with significant prognostic value for recurrence was low active left atrial fractional area change.

Ref: J. Vet. Intern. Med. 2015; 29(3):946–953.

54
Q

Can flecainide terminate acutely induced AF of short duration (≥15 minutes) in horses? What are the effects of flecainide on right atrial effective refractory period, AF cycle length, and ventricular depolarization and repolarization?

A
  • Flecainide had clear antiarrhythmic properties in terminating acute pacing-induced AF, but showed no protective properties against immediate reinduction of AF.
  • Flecainide caused temporary prolongation in the ventricular repolarization, which may be a proarrhythmic effect.
    NB in a prior study sudden death occured in 1/2 horses treated for 7 days with flecainide.

Ref: J. Vet. Intern. Med. 2015; 29(1):339–347.

55
Q

Idiopathic haemorrhagic pericardial effusion has been reported as a precursor to epicardial lymphosarcoma in three cows. Describe the presentation and outcome of these cases.

A
  • Physical examination findings at initial presentation that were consistent with effusive pericardial disease and tamponade (muffled heart sounds, brisket oedema, mammary and jugular pulsation).
  • All had haemorrhagic pericardial effusion 10-14L.
  • Tx w dexmathasone and ceftiour. All discharged within one week.
  • Did well clinically for 7-19mo then either died or re-presented for same signs.
  • Necropsy: epicardial lymphosarcoma with no tumour extension to rest of heart/thorax.

Ref: J. Vet. Intern. Med. 2012;26(4):1069–1072.

LAIM: Cardiology (7 decks)

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