Developmental sequelae of fixed-rate ventricular pacing in the immature canine heart: An electrophysiologic, hemodynamic, and histopathologic evaluation

Karpawich, Peter P.; Justice, Cheryl D.; Cavitt, Dianne L.; Chang, Chung Ho

doi:10.1016/s0002-8703(05)80237-6

Cited by 152 publications

(85 citation statements)

References 22 publications

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“…Previous animal studies have shown that ventricular pacing can cause myofibrillar cellular disarray, dystrophic calcifications, prominent subendocardial Purkinje cells and an increase in variable-sized, disorganized mitochondria. 8 Thus, one possible mechanism is that ventricular pacing-induced histologic changes are associated with persistent left ventricular dysfunction in takotsubo cardiomyopathy. It was recently demonstrated that ventricular pacing can cause left ventricular mechanical dyssynchrony and subsequent remodeling, 9 so another possibility is ventricular pacing-induced mechanical dyssynchrony.…”

Section: Discussionmentioning

confidence: 99%

Persistent Left Ventricular Dysfunction in Takotsubo Cardiomyopathy After Pacemaker Implantation

Kurisu

Inoue

Kawagoe

et al. 2006

Circ J

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novel cardiac syndrome comprising transient left ventricular dysfunction with chest symptoms, electrocardiographic (ECG) changes and minimal myocardial enzymatic release has been gradually recognized worldwide [1][2][3][4][5] and is known as takotsubo cardiomyopathy in Japan because the end-systolic left ventriculogram resembles a "takotsubo", which is a pot used for trapping octopuses. Patients with takotsubo cardiomyopathy have a favorable prognosis in general, because the left ventricular dysfunction is usually transient.We report 2 cases of takotsubo cardiomyopathy associated with pacemaker implantation that presented as persistent left ventricular dysfunction even during the convalescent stage. Case Reports Case 1An 89-year-old woman with hypertension and left hemiparesis was admitted to hospital with dizziness. She was conscious, her blood pressure was 130/70 mmHg, and pulse rate was 38 beats/min. Her hematological test results were normal, and chest X-ray showed no pulmonary edema or cardiac enlargement.A 12-lead ECG showed sinus rhythm and complete atrioventricular block at a rate of 38 beats/min (Fig 1), and echocardiography showed normal left ventricular function (ejection fraction =62%). Next day, she received a dualchamber pacemaker under local anesthesia. The pulse generator was located in the left pectoral region, and the 52-cm and 58-cm bipolar leads were positioned in the low right atrial septum and mid right ventricular septum, respectively. No complications occurred during the operation.She had chest discomfort 10 min after the operation, and her ECG showed significant ST-segment elevation in leads I, aVL and V2-6. Emergency coronary angiography showed Circulation Journal Vol. 70, May 2006 no significant coronary artery disease, but left ventriculography showed akinesia of the mid-to-distal portion of the left ventricular chamber (ejection fraction =38%) (Fig 2). We diagnosed takotsubo cardiomyopathy. She had congestive heart failure that required intravenous furosemide. Creatine phosphokinase increased to 613 IU/L 20 h after the operation.Follow-up echocardiography 2 months later showed persistent akinesia of the mid-to-distal portion of the left ventricular chamber. Serial ECG showed resolution of the ST-segment elevation, but there was not deep T wave inversion under ventricular pacing. Case 2A 77-year-old woman with hypertension and diabetes was admitted to hospital with dyspnea on effort. She was conscious, her blood pressure was 140/80 mmHg, and pulse rate was 30 beats/min. Her hematological test results were normal, and chest X-ray showed no pulmonary edema or cardiac enlargement.A 12-lead ECG showed sinus rhythm and complete atrioventricular block at a rate of 30 beats/min (Fig 3), and echocardiography showed normal left ventricular function (ejection fraction =75%) (Fig 4). She also received a dualchamber pacemaker under local anesthesia, with the pulse generator located in the left pectoral region and the 52-cm and 58-cm bipolar leads positioned in the right atrial appendage and ri...

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Section: Discussionmentioning

confidence: 99%

Persistent Left Ventricular Dysfunction in Takotsubo Cardiomyopathy After Pacemaker Implantation

Kurisu

Inoue

Kawagoe

et al. 2006

Circ J

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“…46 In addition, LV cavity volume increases with longer duration of RVA pacing and LBBB. Dystrophic calcifications, disorganized mitochondria, and myofibrillar cellular disarray 47 have been described with RVA pacing, especially in immature hearts.…”

Section: Isovolumic Contraction (Ic) and Relaxation (Ir) (A) Onset Omentioning

confidence: 99%

Ventricular Pump Function and Pacing

Sweeney

Prinzen

2008

Circ: Arrhythmia and Electrophysiology

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O ptimal cardiac pump function depends on ordered mechanical events that are orchestrated by electrical timing. This electromechanical coupling occurs at multiple anatomic levels: within atria, between atria and ventricles, between ventricles, and especially within the left ventricle (LV). Such disruptions to proper electrical timing result in disordered mechanical events (desynchronization, or "dyssynchrony"), can occur spontaneously or be induced in isolation or in various combinations at any level, and degrade cardiac pump function. These disruptions to normal mechanical ordering occur because of fixed or functional conduction blocks and can be generated by myocardial disease or can be induced by cardiac pacing. The adverse effects of disruption of proper electromechanical coupling at all levels with particular attention to the effects of ventricular conduction delay due to conventional (usually right ventricular apical, RVA) pacing and left bundle-branch block (LBBB) are discussed later. Subsequently, remedies for prevention or treatment are discussed along the same lines. Consequences of Uncoupling atVarious Levels Uncoupling at the Atrial LevelThe right atrium and left atrium are activated nearly simultaneously (within 50 to 80 ms) during sinus rhythm. Preferential sites of interatrial conduction exist at the posteriorsuperior interatrial septum (Bachmann's bundle region), fossa ovalis, and coronary sinus ostium. 1,2 Significant interatrial conduction delays (up to 200 ms or greater) can occur in myopathic atria. Similar conduction delays can be also be induced, or exacerbated, by right atrial pacing. Delayed left atrial contraction can disrupt optimal left-sided atrioventricular (AV) coupling. Severe atrial decoupling and delayed left atrial contraction reverses the left-sided AV contraction sequence, resulting in atrial transport block. 3 This causes increased left atrial pressures, retrograde flow in the pulmonary veins, and counterphysiological neurohormonal responses termed "pseudopacemaker syndrome." 4 -6 Uncoupling at Atrioventricular LevelOptimal AV coupling contributes to ventricular pump function. The normal AV interval results in atrial contraction just before the pre-ejection (isovolumic) period of ventricular contraction that maximizes LV filling (LV end-diastolic pressure, or preload) and cardiac output by the Starling mechanism. This optimal timing relationship maximizes diastolic filling time, reduces diastolic mitral regurgitation (MR), and maintains mean left atrium pressure at low levels. Delayed AV coupling due to conduction delay in the AV node displaces atrial contraction earlier in diastole, which may occur immediately after or even within the preceding ventricular contraction. Atrial contraction before completion of venous return reduces preload and contractile force. A late diastolic LVϾleft atrium pressure gradient may occur, causing diastolic MR and partial closure of the mitral valve, which shortens diastolic filling time. Delayed AV coupling may be worsened or induced by atrial...

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“…This result in decreased systolic and diastolic ventricular function, [26][27] and some studies have even indicated that chronic pacing in the apex of the right ventricle might be harmful to left ventricular function. [28][29][30] Despite of the fact that we demonstrated lower stroke volume index, cardiac index, end diastolic volume, early diastolic function ratio, left cardiac work index, and higher thoracic fluid index, systemic vascular resistance index on dual-chamber pacemaker compared to single-chamber pacemaker, all parameters result that measured were within normal limit. We attempt to find weather atrial pacing in dual-chamber group enhanced hemodynamic outcome, which atrial pacing supposed to be physiological.…”

Section: Discussionmentioning

confidence: 55%

A novel non invasive measurement of hemodynamic parameters: Comparison of single-chamber ventricular and dual-chamber pacemaker

Pardede¹,

Yuniadi²

2008

Med J Indones

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AbstrakKami melakukan studi untuk menganalisis parameter hemodinamik pada pacu jantung jenis satu kamar ventrikel dibandingkan dengan jenis dua kamar secara non-invasif dengan thoracic electrical bioimpedance (Physio Flow™ dual-chamber pacemaker: 92% (10.2-187.7%) vs. 100.6% (48.7-403.2%); p=0.006. Systemic parameters assessment revealed significantly higher left cardiac work index in single-chamber group than dual-chamber group 4.9 kg.m/m² (2.8-7.6 kg.m/m²) vs. 4.3 kg.m/m² (2.9-7.2

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Developmental sequelae of fixed-rate ventricular pacing in the immature canine heart: An electrophysiologic, hemodynamic, and histopathologic evaluation

Cited by 152 publications

References 22 publications

Persistent Left Ventricular Dysfunction in Takotsubo Cardiomyopathy After Pacemaker Implantation

Persistent Left Ventricular Dysfunction in Takotsubo Cardiomyopathy After Pacemaker Implantation

Ventricular Pump Function and Pacing

A novel non invasive measurement of hemodynamic parameters: Comparison of single-chamber ventricular and dual-chamber pacemaker

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