Pacemaker-Induced Cardiomyopathy: Causes and Detection

Pacemaker-induced cardiomyopathy (PICM) is a complication of long-term right ventricular pacing that can lead to heart failure symptoms. While pacemakers are essential for managing bradycardia and conduction disorders, their impact on cardiac function can sometimes be detrimental. Early recognition of PICM is crucial for optimizing treatment and preventing further deterioration.

Mechanisms of Ventricular Dyssynchrony

Prolonged right ventricular (RV) pacing disrupts the heart’s natural electrical conduction, causing ventricular dyssynchrony—an uncoordinated contraction of the left and right ventricles. Unlike the His-Purkinje system, which ensures rapid and synchronous activation, RV pacing primarily depolarizes the right ventricle first, delaying left ventricular (LV) activation. This altered sequence mimics a left bundle branch block (LBBB) pattern, prolonging the QRS duration and impairing contraction efficiency.

Asynchronous contraction reduces systolic function by creating regional disparities in myocardial workload. The septal wall contracts early, while the lateral LV wall lags, leading to inefficient energy transfer, increased wall stress, and impaired stroke volume. Over time, these inefficiencies contribute to declining cardiac output and heart failure symptoms in susceptible individuals.

Beyond impaired contraction, ventricular dyssynchrony affects diastolic function. Delayed LV lateral wall activation prolongs relaxation, disrupting ventricular filling and increasing left atrial pressures, which can lead to pulmonary venous congestion. Dyssynchronous contraction also alters myocardial perfusion patterns, with some regions experiencing prolonged systolic contraction while others enter diastole prematurely. This mismatch in oxygen demand and supply may contribute to progressive ventricular remodeling.

Hemodynamic Effects

Right ventricular pacing alters electrical activation, significantly impacting cardiac hemodynamics. The delayed LV activation disrupts coordinated contraction, reducing systolic efficiency and increasing myocardial energy expenditure. This inefficiency results in decreased stroke volume and cardiac output, contributing to fatigue, exercise intolerance, and worsening heart failure symptoms. Studies have shown that chronic RV pacing leads to a measurable decline in left ventricular ejection fraction (LVEF), with some patients developing PICM due to prolonged hemodynamic stress.

Beyond systolic dysfunction, RV pacing impairs diastolic filling. Desynchronized LV contraction prolongs relaxation, increasing left atrial pressure and promoting pulmonary congestion. Elevated left atrial pressures can cause dyspnea and orthopnea, particularly in those with preexisting diastolic dysfunction. A study in Circulation: Arrhythmia and Electrophysiology found that chronic RV pacing increases left atrial volume index, suggesting that persistent dyssynchrony contributes to progressive remodeling and worsening hemodynamics.

Altered ventricular contraction also affects myocardial blood flow. The asynchronous activation pattern forces some myocardial regions to remain contracted while others enter diastole prematurely, leading to uneven coronary perfusion. This mismatch in oxygen supply and demand may contribute to subendocardial ischemia, even in patients without coronary artery disease. Research in JACC: Clinical Electrophysiology has shown that RV pacing reduces coronary flow reserve, further impacting myocardial perfusion efficiency. Over time, these disturbances may accelerate structural remodeling and functional decline.

Structural Changes in the Heart

Prolonged RV pacing induces progressive cardiac remodeling, particularly in the left ventricle. The altered contraction sequence forces the myocardium to adapt to an abnormal workload distribution, triggering structural modifications that impair function. One of the most notable changes is LV dilation, which arises from chronic mechanical inefficiencies. As the LV struggles to compensate, wall stress increases, leading to chamber enlargement and reduced systolic performance.

This maladaptive remodeling is accompanied by interstitial fibrosis, driven by sustained mechanical strain and neurohormonal activation. Excess collagen deposition stiffens the ventricular walls, impairing both contraction and relaxation. Fibrotic changes are particularly pronounced in the lateral and posterior LV segments, where delayed activation prolongs mechanical stress. Cardiac MRI with late gadolinium enhancement has confirmed fibrosis in patients with chronic pacing, correlating it with worsening ventricular function.

In addition to fibrosis, RV pacing disrupts myocardial fiber orientation. The natural helical arrangement of cardiomyocytes optimizes the twisting motion of the ventricle during systole, but dyssynchronous activation interferes with this movement, reducing contractile efficiency. Studies using diffusion tensor imaging have documented alterations in myocardial fiber architecture in patients with long-term pacing, providing insight into the structural underpinnings of pacing-induced dysfunction.

Clinical Indicators

Patients with PICM often present with subtle but progressive symptoms that can be mistaken for other forms of heart failure. Initially, mild exertional dyspnea and fatigue may occur, but as the hemodynamic burden increases, symptoms such as lower extremity edema, paroxysmal nocturnal dyspnea, and reduced exercise tolerance become more pronounced. These manifestations are often overlooked in pacemaker-dependent patients, delaying diagnosis.

A decline in LVEF is a key indicator of PICM. A reduction of more than 10% from baseline, particularly when LVEF falls below 40%, suggests pacing-induced dysfunction. This decline is often detected during routine echocardiographic follow-ups, highlighting the importance of regular imaging in pacemaker recipients. Additionally, elevated brain natriuretic peptide (BNP) or N-terminal proBNP (NT-proBNP) levels may signal worsening myocardial stress and serve as biochemical markers of disease progression.

Diagnostic Imaging Approaches

Identifying PICM requires multiple imaging modalities to assess ventricular function, mechanical dyssynchrony, and structural remodeling. Echocardiography remains the primary tool for initial evaluation, offering a non-invasive means to quantify LVEF and detect myocardial motion abnormalities. Speckle-tracking echocardiography, which measures global longitudinal strain (GLS), provides additional insights into subclinical dysfunction before overt reductions in LVEF appear. A progressive decline in GLS has been documented in patients with chronic RV pacing, highlighting its role as an early marker of myocardial impairment.

Cardiac MRI offers superior tissue characterization, particularly for detecting fibrosis and myocardial scarring. Late gadolinium enhancement (LGE) imaging identifies fibrotic regions linked to prolonged mechanical stress, correlating with worsening ventricular compliance and contractility. In some cases, nuclear imaging techniques such as single-photon emission computed tomography (SPECT) or positron emission tomography (PET) may assess myocardial perfusion abnormalities related to dyssynchronous contraction. These advanced imaging approaches help differentiate PICM from other cardiomyopathies, guiding treatment decisions for patients with progressive functional decline.

Common Risk Factors

Several factors influence the likelihood of developing PICM, with prolonged RV pacing being the most significant. Patients who are pacemaker-dependent or have a high percentage of ventricular pacing—typically exceeding 40%—face an increased risk of LV dysfunction. A study in Heart Rhythm found that individuals with pacing burdens above 50% were significantly more likely to experience LVEF deterioration over time.

Preexisting cardiac conditions also play a role. Patients with borderline LV function or mild systolic dysfunction at implantation are more prone to further decline. Similarly, those with conduction disorders such as LBBB or intraventricular conduction delays may be more vulnerable to the detrimental effects of dyssynchronous pacing. Emerging research suggests genetic predisposition may also contribute to differential outcomes among patients with similar pacing burdens.