Can Severe Critical Illness Cause Left Ventricular Hypertrophy?
Yes, severe critical illness can cause left ventricular hypertrophy (LVH), though the mechanisms differ from traditional causes and the presentation is often regional rather than global.
Evidence from Critical Illness Populations
Chronic critical illness, particularly in infants with chronic lung disease, directly causes LVH through multiple pathophysiologic mechanisms. 1
Mechanisms in Critically Ill Patients
The pathogenesis of LVH in severe critical illness involves several interconnected factors:
Metabolic stress from chronic hypoxemia, hypercarbia, and acidosis increases cardiac output and stimulates the renin-angiotensin system, elevating afterload 1
Increased intrathoracic pressure changes during mechanical ventilation create more negative inspiratory pressures that directly increase left ventricular afterload and contribute to hypertrophy 1
Myocardial scarring can result from prolonged metabolic derangements in critical illness 1
Systemic hypertension frequently develops in critically ill patients (particularly those with chronic lung disease), which independently contributes to LVH 1, 2
Clinical Patterns and Significance
Regional wall motion abnormalities are more common than global hypokinesia in acute critical illness, occurring in approximately 13% of ICU patients without underlying cardiac disease 3. This pattern differs from traditional causes of LVH:
In chronic critical illness (such as prolonged mechanical ventilation >60 days), patients who developed LVH had higher rates of late unexpected sudden death compared to those without LVH 1
LV posterior wall thickness correlates directly with severity of chronic lung disease 1
The hypertrophy can elevate left atrial pressure, potentially worsening pulmonary edema and disease severity 1
Mortality Impact
Critical illness-associated LV dysfunction carries significant mortality risk:
Crude 30-day mortality is 33% in ICU patients with LV dysfunction from non-cardiac causes versus 18% in those with normal LV function 3
At 90 days, mortality increases to 44% versus 22%, remaining significant even after risk adjustment (OR 2.40) 3
Clinical Approach
Screening Recommendations
Serial echocardiograms are necessary to monitor the degree of hypertrophy and myocardial function in critically ill patients 1:
Echocardiography is superior to ECG for detecting LVH, as ECG screening alone frequently misses hypertrophy documented by echo or autopsy 1
Doppler and M-mode echocardiography should assess LV posterior wall thickness and flow velocities 1
Evaluation for Reversible Causes
When LVH is identified in critical illness, screen for:
Left-to-right shunting via patent ductus arteriosus or large systemic-to-pulmonary collateral vessels using echocardiography 1
Medication effects, particularly corticosteroids which can induce hypertension in critically ill patients 1
Important Caveats
The contribution of LVH to clinical outcomes in critical illness remains incompletely understood, as these patients often have prolonged exposure to multiple pharmaceutical agents that may confound the relationship 1
Regional wall motion abnormalities in acute critical illness are frequently reversible, unlike chronic hypertrophy 3
A single identifiable cause is usually not found; the etiology is typically multifactorial involving hemodynamic, metabolic, and mechanical factors 1