Dilated Cardiomyopathy, presented by Dr. Onur İskefli

Dr. Veteriner Hekim Onur İskefli: Dilate Kardiyomiyopati

In this blog post, we have compiled the key highlights from the session titled “Dilated Cardiomyopathy”, presented by Dr. Onur İskefli, held as part of VetSummit 2025: New Horizons in Veterinary Clinical Sciences, sponsored by the Kito Healthy Pet Nutrition Ecosystem. We would like to thank our speaker for the presentation.

Dilated Cardiomyopathy in Dogs: It Starts Quietly, Then One Day It Knocks With Syncope

Some diseases appear to happen “suddenly” in the clinic, but in reality they have been building for years. Dilated cardiomyopathy (DCM) in dogs is exactly that kind of process. It is typically associated with medium-to-large breeds as a “genetic fate,” but we now know the issue is not purely genetic. Diet, medications, endocrine diseases—many different pathways can open the door to the same clinical picture.

In the 7th session of New Horizons in Veterinary Clinical Sciences, Dr. Onur İskefli explained DCM in a practical, field-oriented way. Two key messages stood out:

  • “The most critical thing in DCM is early detection. Once clinical signs appear, you are already in a completely different phase.”
  • “If you see syncope in a patient, you cannot move forward without an ECG.”

1) What Is DCM? A Disease of “Loss of Contractile Power”

Dilated cardiomyopathy is a disease of the heart muscle. The basic problem is:

  • The heart chambers enlarge (especially the left ventricle and left atrium).
  • The walls become thinner.
  • Contraction (systolic function) decreases significantly.

In other words, the heart becomes larger but not stronger; it becomes weaker as it dilates.

2) The Cause Is Not One: Genetics + Nutrition + Secondary Factors

The speaker challenged the classic “purely genetic disease” assumption. Genetics still play a major role:

  • Breeds such as Dobermans and Boxers have clear predispositions.
  • Several genetic variants have been identified.

However, other important contributors exist in real-life practice:

Nutritional causes

  • Taurine deficiency is one of the most critical factors.
  • Well known in cats since the 1990s, which is why taurine is routinely added to cat foods.
  • In dogs, the risk also increases with certain diets.
  • Carnitine deficiency (especially in Spaniel-type breeds) may trigger DCM.

Drug-related and toxic causes

  • Cardiotoxic chemotherapy agents such as doxorubicin can directly cause DCM.
  • These patients must be monitored cardiologically before and after treatment.

Secondary / endocrine-related pathways

  • Conditions such as hyperadrenocorticism and pheochromocytoma can create chronic catecholamine overload, gradually damaging the myocardium and leading to DCM.

In summary:

“Sometimes DCM is fate, sometimes it is an incorrect diet, and sometimes it is the final stage of another disease.”

3) Phases: The Gap Between the Occult Stage and the Clinical Stage

Clinical management of DCM is impossible without understanding its phases. The speaker explained this clearly by comparing it to the ACVIM mitral valve staging system:

Occult phase (asymptomatic)

  • The breed is at risk but shows no clinical signs.
  • Or arrhythmias are present on ECG/Holter without systolic dysfunction.

At this stage:

  • monitoring is the priority, not medication.
  • annual echocardiography and, ideally, Holter screening are recommended.

Overt phase (symptomatic)

Clinical signs are now present:

  • heart failure, arrhythmias, syncope, etc.

At this stage, treatment becomes more aggressive and quality of life becomes the main goal.

4) Clinical Signs: How Does DCM Reveal Itself?

DCM typically presents in two ways:

Signs of left-sided heart failure

  • cough
  • exercise intolerance
  • tachypnea

If both left and right sides are affected

  • ascites (abdominal fluid accumulation), in addition to the above signs

Arrhythmias (the most critical alarm signal)

  • ventricular premature complexes (VPCs)
  • atrial fibrillation
  • ventricular tachycardia → may progress to fibrillation

The speaker emphasized an important clinical reflex:

“If you see syncope, do an ECG first.”

Many fainting episodes have a potentially fatal arrhythmia in the background.

5) The Cough Issue: “Heart Patients Cough” Is Not Always True

This was one of the most educational parts of the talk.

The main mechanism of cardiac cough:

  • the left atrium enlarges
  • it compresses the left main bronchus
  • coughing begins

However, pulmonary edema does not always cause cough, because:

  • cough receptors are concentrated in the upper airways
  • there are very few in the alveoli

If edema is mainly alveolar, the patient may have severe dyspnea without coughing.

Cough becomes more likely once fluid reaches the bronchi, sometimes accompanied by pink frothy discharge.

Clinical takeaway:

Do not rule out heart disease because there is no cough, and do not assume edema simply because cough is present.

6) Diagnosis: Suspect With Radiographs, Confirm With Echocardiography

Physical examination is the foundation

The speaker strongly emphasized full-body clinical examination before advanced testing:

  • inspection
  • palpation
  • auscultation
  • respiratory rate, pulse quality, temperature

Without this, further testing becomes “imaging without knowing what you are looking for.”

ECG

Common findings:

  • sinus tachycardia
  • atrial fibrillation
  • ventricular premature complexes

In syncope cases, ECG is a life-saving first step.

Radiography

Generalized cardiomegaly can be seen, but this alone does not confirm DCM because:

  • pericardial effusion may create a similar appearance.

Echocardiography (the diagnostic key)

Echocardiographic criteria supporting DCM include:

  • normalized LVIDd > 1.7
  • sphericity index > 1.65
  • fractional shortening (FS) < 25%
  • ejection fraction (EF) < 45%
  • LA/Ao ≥ 1.6
  • EPSS > 7.7

With echo images, the speaker clearly demonstrated:

the ventricle is enlarged, walls are thin, and contraction is weak—like “an incomplete closure performed by hand.”

7) Nutritional DCM: The Grain-Free Diet Paradox

A growing issue in real-world practice:

a small-breed dog (for example, a Yorkshire Terrier) developing DCM after 10 years on a grain-free diet.

The mechanism:

grain-free diets often rely heavily on plant-based proteins (lentils, peas).

The methionine–taurine synthesis cycle may not be adequately supported.

Over time, nutritional DCM may develop.

Key warning:

“Even if the breed is not predisposed, diet history can still lead to DCM.”

8) Treatment: Management Based on Phase

Occult phase

  • do not start medication in asymptomatic at-risk patients
  • regular monitoring + avoid intense exercise
  • omega-3 may be recommended (evidence is limited but benefits are possible)

Arrhythmia present without systolic dysfunction

  • Holter monitoring is ideal; if not available, serial ECGs
  • antiarrhythmic therapy if needed
  • taurine/carnitine supplementation + dietary correction

Systolic dysfunction begins (preclinical stage similar to B2)

  • pimobendan becomes essential
  • based on the PROTECT study, it is emphasized to delay clinical signs

Clinical heart failure (Stage C)

Four core drugs form the backbone:

  • loop diuretic (furosemide)
  • ACE inhibitor
  • pimobendan
  • spironolactone

Arrhythmia-specific therapy:

  • atrial fibrillation: diltiazem / digoxin
  • VPCs: sotalol / mexiletine / amiodarone when necessary

Monitoring becomes essential:

  • electrolytes (K, Na, Mg)
  • renal function

Refractory advanced stage (Stage D)

  • torsemide (approximately 10 times stronger than furosemide)
  • hospital-based dobutamine / IV inotropes
  • close monitoring

9) Home Monitoring: Sleeping Respiratory Rate Saves Lives

The most valuable homework for owners:

sleeping respiratory rate.

  • over 30 breaths per minute = early edema alarm

If owners detect this early, the patient can often be stabilized as an outpatient before severe edema develops.

If not detected, the patient may arrive in emergency with 50–60 breaths per minute, requiring hospitalization.

10) Anxiety Management in Acute Cases: The Butorphanol Note

In acute pulmonary edema, the animal feels like it is suffocating and panics.

A practical point highlighted by the speaker:

Butorphanol is a good anxiolytic.

It has minimal cardiac effects and makes treatment much easier to manage.

Closing: The Most Important Thing in DCM Is Catching It Before Symptoms Appear

This session left three clear clinical messages:

1. DCM is not caused by a single factor. Diet history is extremely valuable for diagnosis.

2. A patient diagnosed in the occult phase will have a completely different life compared to one diagnosed in the symptomatic phase.

3. Syncope + arrhythmia risk = never skip ECG.

Heart disease can progress silently for years…

But one day, that silence turns into a patient that suddenly collapses in the clinic.

In that moment, your strongest tool is knowledge and clinical reflex.

“The heart may become enlarged, but if you are late, the game becomes much bigger.”

We will continue sharing key highlights from VetSummit 2025: New Horizons in Veterinary Clinical Sciences, sponsored by the Kito Healthy Pet Nutrition Ecosystem. See you in our upcoming content that will support your clinical practice.

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