![GW Research Days 2016 - 2020](../../../../assets/md5images/9926fcc244b99fc84a4662e307127b44.jpg)
School of Medicine and Health Sciences Poster Presentations
Acute Pacing-Induced Cardiomyopathy
Poster Number
154
Document Type
Poster
Publication Date
3-2016
Abstract
The first pacemaker devices became available in the late 1960s and have since become the mainstay of therapy for patients with complete heart block (1). Since that time, pacemaker implantation has risen dramatically because of both the increase in clinical indications for pacemaker use and the aging of the population. This increased use has lowered the mortality rate and improved quality of life among patients with cardiac arrhythmia (2). Artificial pacing has been associated with detrimental effects on left ventricular function in patients who require right ventricular pacing such as patients with complete heart block (3). Several animal studies have shown that right ventricular pacing reduces tissue perfusion and increases norepinephrine release in myocardial muscles (4). This results in histological changes that include myofibrillar cellular disarray and dystrophic calcifications (5). After heart block was induced by ablation and pacemakers were subsequently implanted, such histological changes in animals’ hearts develop within 3–4 months. Therefore, this adverse clinical outcome has led to a phenomenon called pacing-induced cardiomyopathy (PICM). PICM is defined as a 10% reduction in the left ventricular ejection fraction (EF) over one year after pacemaker implantation, resulting in an EF of less than 50%. Other causes of cardiomyopathy should be excluded to diagnose patients with this condition (6). PICM has been reported in up to 9% of patients who have right ventricular pacing and 1% who have biventricular pacing (7). Patients with this condition usually present with symptoms of congestive systolic heart failure such as exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and lower extremity edema (8). A recent study revealed several factors that raise the risk of PICM such as male gender, a low EF, and a wide QRS (6). Our report describes a patient with a severe acute form of PICM and discusses the prevention and therapy of this condition.
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.
Open Access
1
Acute Pacing-Induced Cardiomyopathy
The first pacemaker devices became available in the late 1960s and have since become the mainstay of therapy for patients with complete heart block (1). Since that time, pacemaker implantation has risen dramatically because of both the increase in clinical indications for pacemaker use and the aging of the population. This increased use has lowered the mortality rate and improved quality of life among patients with cardiac arrhythmia (2). Artificial pacing has been associated with detrimental effects on left ventricular function in patients who require right ventricular pacing such as patients with complete heart block (3). Several animal studies have shown that right ventricular pacing reduces tissue perfusion and increases norepinephrine release in myocardial muscles (4). This results in histological changes that include myofibrillar cellular disarray and dystrophic calcifications (5). After heart block was induced by ablation and pacemakers were subsequently implanted, such histological changes in animals’ hearts develop within 3–4 months. Therefore, this adverse clinical outcome has led to a phenomenon called pacing-induced cardiomyopathy (PICM). PICM is defined as a 10% reduction in the left ventricular ejection fraction (EF) over one year after pacemaker implantation, resulting in an EF of less than 50%. Other causes of cardiomyopathy should be excluded to diagnose patients with this condition (6). PICM has been reported in up to 9% of patients who have right ventricular pacing and 1% who have biventricular pacing (7). Patients with this condition usually present with symptoms of congestive systolic heart failure such as exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and lower extremity edema (8). A recent study revealed several factors that raise the risk of PICM such as male gender, a low EF, and a wide QRS (6). Our report describes a patient with a severe acute form of PICM and discusses the prevention and therapy of this condition.
Comments
Presented at: GW Research Days 2016