Pacing On Mechanical Remodeling

Cardiac myocytes are known to adapt to changes in hemody-namic load. Ventricular remodeling refers to changes in left ventricular geometry, mass, or volume in response to myocar-dial injury or alterations in load (e.g., hypertension). The extent of left ventricular dilation or remodeling in both ischemic and nonischemic cardiomyopathy is a strong predictor of both morbidity and mortality. Angiotensin-converting enzyme inhibitors and p-adrenergic blockers inhibit left ventricular remodeling and improve survival in patients with left ventricular dysfunction. It has been reported that chronic asynchronous electrical activation, such as chronic pacing or left bundle branch block, in the heart induces redistribution of cardiac mass (29).

Further, chronic right ventricular apical pacing may adversely alter cellular growth, especially among the young, on the cellular and subcellular levels, potentially contributing to the diminished function observed clinically (30). It has also been shown that such pacing may increase myocardial perfusion defects and regional wall motion abnormalities, reduce left ventricular ejection fractions, or cause diastolic dysfunction (31,32).

Short-term right ventricular apical pacing has been associated with both impaired left ventricular pump function and relaxation. Long-term right ventricular apical pacing may result in permanent impairment of left ventricular function. In 24 young patients (average age 19 years), Tantengco et al. (31) demonstrated that left ventricular function was significantly lower than for age-matched controls after right ventricular apical pacing for 10 years.

In contrast, biventricular pacing resulted in reverse remodeling in patients with congestive heart failure. Lau et al. (33) demonstrated that 3 months of biventricular pacing was associated with reduced left ventricular end-systolic and end-dias-tolic volumes by 33 and 24%, respectively. This was consistent with published data from the MIRACLE study (16). It has also been reported that chronic biventricular pacing may be associated with changes in QRS axis without concomitant changes in QRS duration or lead dislocation (34), suggesting possible electrical remodeling induced by such pacing.

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