Dilated cardiomyopathy (DCM) is defined by ventricular chamber enlargement and impaired systolic function, typically of the left ventricle but often involving both ventricles in advanced stages. It occurs in the absence of coronary artery disease, hypertension, or valvular pathology sufficient to explain the dysfunction. DCM accounts for nearly 30–40% of all cardiomyopathies and remains the leading cause of heart transplantation worldwide.
From the anesthesiologist’s perspective, DCM is not merely a cardiac diagnosis but a dynamic physiologic problem — the ventricle is chronically overstretched, the neurohormonal system is maladaptively activated, and the myocardium is metabolically exhausted. Each anesthetic drug and physiologic perturbation can either stabilize or destabilize this precarious balance.
Patients with DCM may present for non-cardiac surgery, often with compensated heart failure that can easily decompensate under anesthesia.
Intraoperative circulatory collapse is a constant threat due to limited myocardial reserve.
Arrhythmias, pulmonary congestion, and hypotension are common perioperative complications.
Reduced cardiac output limits oxygen delivery during surgical stress.
RAAS activation makes patients preload-sensitive yet fluid-intolerant.
Downregulated β-adrenergic receptors blunt response to indirect sympathomimetics.
Altered myocardial compliance increases risk of pulmonary edema with small fluid shifts.
The anesthesiologist’s task is to:
Preserve contractility and avoid myocardial depression.
Maintain adequate but not excessive preload.
Prevent abrupt afterload reductions.
Control heart rate and rhythm.
Provide sufficient oxygen delivery and tissue perfusion.
DCM therefore demands a pathophysiology-guided approach, where molecular understanding translates directly into clinical decisions on induction, ventilation, fluids, and vasoactive drugs.
References
Bozkurt B, Colvin M, Cook J, Cooper LT, Deswal A, Fonarow GC, et al. Current diagnostic and treatment strategies for specific dilated cardiomyopathies: a scientific statement from the American Heart Association. Circulation. 2016;134(23):e579–e646.
Pinto YM, Elliott PM, Arbustini E, Adler Y, Anastasakis A, Böhm M, et al. Proposal for a revised definition of dilated cardiomyopathy, hypokinetic non-dilated cardiomyopathy, and its implications for clinical practice: a position statement of the ESC Working Group on Myocardial and Pericardial Diseases. Eur Heart J. 2016;37(23):1850–1858.
Understanding the pathophysiological cascade in DCM is the foundation of safe anesthesia. The disease evolves through interconnected mechanisms: myocyte injury, neurohormonal activation, and structural remodeling — all of which directly alter anesthetic responses.
Mechanism:
Loss of contractile myocytes through apoptosis and replacement fibrosis reduces effective contractile units. Surviving myocytes hypertrophy and elongate, leading to ventricular dilation
