Cirrhotic Cardiomyopathy (CCM)
1️⃣ Definition
Cirrhotic cardiomyopathy (CCM) is a chronic cardiac dysfunction seen in patients with advanced liver cirrhosis, characterized by:
- Impaired cardiac contractile response to stress
- Diastolic dysfunction
- Electrophysiological abnormalities (especially QT prolongation)
- In the absence of intrinsic heart disease
It is a functional, stress-induced cardiomyopathy that becomes clinically apparent during:
- Sepsis
- TIPS insertion
- Liver transplantation
- Major surgery
- GI bleeding
2️⃣ Why It Matters in ICU
For you (critical care focus), CCM is important because:
- Cirrhotics may appear hemodynamically stable at rest
- Under stress → acute LV failure
- Major cause of:
- Post-TIPS heart failure
- Post-liver transplant cardiovascular collapse
- Hepatorenal syndrome worsening
- Poor septic shock outcomes
3️⃣ Pathophysiology
Cirrhosis → hyperdynamic circulation → chronic neurohormonal stimulation → myocardial remodeling.
Stepwise Mechanism
1. Hyperdynamic Circulation
- ↓ SVR (splanchnic vasodilation via NO)
- ↑ CO at rest
- ↓ Effective arterial blood volume
2. Chronic Neurohormonal Activation
- RAAS activation
- Sympathetic overactivity
- Vasopressin release
3. Myocardial Changes
- β-adrenergic receptor downregulation
- Impaired calcium signaling
4️⃣ Structural & Functional Changes
A. Systolic Dysfunction (Stress-Induced)
- EF may be normal at rest
- Blunted response to:
- Dobutamine
- Exercise
- Surgery
B. Diastolic Dysfunction (Early Finding)
- Impaired relaxation
- Increased LV stiffness
- E/A reversal
- Prolonged deceleration time
C. Electrophysiological Abnormalities
- QT prolongation (30–60% cases)
- Chronotropic incompetence
- Atrial arrhythmias
- Rare torsades
5️⃣ Diagnostic Criteria
Updated criteria (2019 consensus):
A. Systolic Dysfunction
One of:
- EF < 50%
- Global longitudinal strain (GLS) < 18%
- Blunted contractile response to stress
B. Diastolic Dysfunction
≥ 3 of:
- E/e′ > 14
- e′ < 7 cm/s
- LA volume index > 34 mL/m²
- TR velocity > 2.8 m/s
C. Supportive Findings
- QTc prolongation
- Elevated BNP
- Elevated troponin
Why Does QT Prolongation Occur in Cirrhotic Cardiomyopathy?
First – What Does QT Represent?
QT interval = total duration of ventricular depolarization + repolarization
- QRS → depolarization
- ST + T → repolarization
- QTc (corrected QT) normally:
- Men < 440 ms
- Women < 460 ms
- Dangerous ≥ 500 ms
QT prolongation = delayed ventricular repolarization
Repolarization depends mainly on potassium efflux currents (especially IKr and IKs).
In cirrhosis → these potassium currents are impaired → action potential duration increases → QT prolongs.
6️⃣ Clinical Presentation
Often Silent at Rest, but all these factors precipitate it therefore do screening ECHO in all these
|
Trigger |
Presentation |
|
Sepsis |
Sudden LV failure |
|
TIPS |
Pulmonary edema |
|
Liver transplant |
Intraoperative shock |
|
GI bleed |
Acute pulmonary edema |
|
Large fluid resuscitation |
Decompensation |
7️⃣ Biomarkers in CCM
|
Marker |
Significance |
|
BNP |
Elevated even without HF |
|
Troponin |
Mild elevation common |
|
NT-proBNP |
Correlates with severity |
|
QTc |
Prognostic marker |
8️⃣ Hemodynamic Pattern
Typical cirrhotic patient:
- High CO
- Low SVR
- Low MAP
- Normal/low filling pressures
When CCM manifests:
- ↓ Cardiac output under stress
- ↑ LVEDP
- Pulmonary edema
9️⃣ CCM vs Alcoholic Cardiomyopathy
|
Feature |
CCM |
Alcoholic CM |
|
Etiology |
Cirrhosis-related |
Direct ethanol toxicity |
|
EF at rest |
Usually normal |
Reduced |
|
Reversibility |
Improves after transplant |
Partial |
|
LV dilation |
Mild |
Marked |
🔟 Impact During TIPS
TIPS → sudden ↑ preload → unmask latent LV dysfunction → acute pulmonary edema.
High-risk predictors before TIPS:
- Diastolic dysfunction
- Elevated BNP
- QT prolongation
- Older age
11️⃣ During Liver Transplant
Phases:
- Pre-anhepatic – hyperdynamic
- Anhepatic – decreased preload
- Reperfusion – massive hemodynamic stress
CCM patients:
- Cannot augment cardiac output
- Risk of post-reperfusion syndrome
- Vasoplegia + myocardial depression
12️⃣ Management (Guideline-Oriented)
There is no specific therapy for CCM.
A. General Principles
- Treat cirrhosis
- Avoid volume overload
- Monitor QT interval
- Correct electrolytes
B. ICU Management
1️⃣ Septic Shock in Cirrhosis
- Norepinephrine = first line
- Vasopressin adjunct
- Dobutamine if low cardiac output
2️⃣ Acute LV Failure
- Loop diuretics
- Non-invasive ventilation
- Cautious vasodilators
3️⃣ Arrhythmia
- Correct K+, Mg++
- Avoid QT-prolonging drugs
13️⃣ Beta Blockers – Friend or Foe?
Non-selective beta blockers (NSBBs) like:
- Propranolol
- Carvedilol
Used for portal hypertension.
But:
- May worsen chronotropic incompetence
- Can precipitate hypotension in advanced cirrhosis
Use cautiously in refractory ascites or shock.
14️⃣ Reversibility
The only definitive treatment:
Liver Transplantation
After transplant:
- QT normalizes
- Diastolic function improves
- Systolic response improves
However:
- Severe pre-existing CCM → perioperative mortality ↑
15️⃣ Prognosis
Worse outcomes associated with:
- Elevated BNP
- QTc > 500 ms
- Severe diastolic dysfunction
- Child-Pugh C
- MELD > 25

