Table 1.
Authors | Species | Characteristics | Key findings |
---|---|---|---|
Brembilla-Perrot et al. [96] | Human | Patients aged >70 years versus younger | Decreased AF inducibility due to increased atrial ERP |
Centurión et al. [89] |
Human | Patients with paroxysmal AF during sinus rhythm aged >60 years versus younger | Greater mean number of abnormal right atrial electrograms defined as ≥100 msec duration and, or showing eight fragmented deflections |
Roberts-Thomson et al. [87] | Human | Patients aged >60 years versus younger | Greater number of complex fractionated electrograms |
Sakabe et al. [94] | Human | Patients without a history of AF or structural heart disease | No relationship between age and inducibility of AF |
| |||
Calcium mishandling | |||
| |||
El-Armouche et al. [99] | Human | Western blotting used to assess phosphorylation levels of Ca handling proteins in right atrial appendage | Hyperphosphorylation of phospholamban could be contributory to leaky ryanodine receptors and thus abnormal calcium handling in chronic AF patients |
Hove-Madsen et al. [97] | Human | Age > 66 years | Higher calcium spark frequency and higher incidence of spontaneous calcium waves in comparison to patients with sinus rhythm |
Ono et al. [88] | Rats | Old versus young rats | Glycolytic inhibition has been shown to result in spontaneous AF due to calcium mishandling and early after depolarisation-induced triggered activity |
Wongcharoen et al. [90] | Rabbits | Responses of pulmonary vein tissues to rapamycin, FK-506, and ouabain in young and aged rabbits | Increased pulmonary vein arrhythmogenesis secondary to ryanodine receptor dysfunction-resultant calcium mis-handling |
| |||
Atrial ERP | |||
| |||
Kistler et al. [100] | Human | Electrophysiological and electroanatomical studies in 3 age groups (≥60 years, 31–59 years, and ≤30 years) | Age-associated electrical and structural remodeling (regional conduction slowing, increase in atrial ERP, impaired sinus node function, conduction delay at crista terminalis, and areas of low voltage) |
Brembilla-Perot et al. [96] | Human | 734 patients (age 16–85 years, mean 61 ± 15 years) | Increased atrial ERP and age >70 years independently predicted reduced AF inducibility |
Brorson and Olsson [101] | Human | Right atrial monophasic action potentials recorded in 40 healthy males | No age correlation |
Anyukhovsky et al. [92] | Dogs | Young versus old canine atrial | Age-related differences in action potential contour, decreased I CaL, and slower conduction of early premature beats |
Huang et al. [106] | Rats | Adult, middle aged versus aged rats | Age-associated prolongation of the monophasic action potential (mAP) and ERP in the right atrium, but a decrease in mAP and ERP in the left atrium, suggesting a potential reentrant mechanism for AF |
Kojodjojo et al. [107] | Humans | Most study subjects suffered from atrioventricular reentrant arrhythmias, syncope, or palpitations and hence these atria were not “healthy” | No change in left atrial ERP with ageing |
Michelucci et al. [105] | Humans | 17 normal subjects (age range 17–78 years) | Age-related increase in right atrial ERP |
Su et al. [103] | Rats | Adults versus aged rats | In response to muscarinic stimulation, ageing-related prolongation of atrial maximum diastolic potential but not of APD |
Toda [102] | Rabbit | Rabbit ages varied from 2–360 days old | Age-related prolongation of APD |
| |||
Ion channel remodelling in ageing and AF | |||
| |||
I CaL Anyukhovsky et al. [92] | Canine atria | Reduced I CaL | |
I
Na Baba et al. [108] |
Canine atria | (i) Peak current unchanged at low stimulation frequencies but reduced at stimulation frequencies relevant to AF |
|
Wu et al. [110] | Rabbit atria | (ii) Decreased in hyperlipidemic aged rabbits | |
I to Dun et al. [109] | Canine atrium | Increased in the left atrium | |
I KAch Su et al. [103] | Rat | Indirect evidence of increase [104] |