Page 275 - fbkCardioDiabetes_2017

Diabetic Dysrhythmias 251

products; AGEs) interact with their receptors (RAGE)
and upregulate the connective tissue growth factor
(CGTF). This system (AGERAGE) may start or contrib-
ute to atrial fibrosis in diabetic patients via stimula-
tion of connective tissue growth factor in the atrial
myocardium .
9
Several clinical and electrophysiological studies have
demonstrated DCAN to play significant role in the
10
genesis of AF .
Atrial electrical structure is also affected in diabetic
patients. Shortened atrial effective refractory period
(AERP), increased dispersion of AERP, inter and intra
atrial conduction time, which are the key elements of
atrial electrical remodelling have been documented.
11
Chao et al analyzed the detailed three dimensional
electro anatomic mapping of 228 patients who has
DM or abnormal glucose metabolism (AGM) and un-
derwent AF ablation for the first time. Results showed
that biatrial voltage measurements in DM and AGM Figure 1 : Potential pathophysiological mechanisms
group were significantly lower than control group. of atrial fibrillation in DM
Furthermore these patients also had increased re-
currence rate of AF in the follow up period. The rela- Diabetes and ventricular arrhythmias
tionship between the degree of control of hypergly- High incidence and extent of atherosclerotic heart
caemia and the incidence of AF is not clear. While disease in DM leads to high incidence of VA and SCD
fluctuations in the blood glucose level rather than the inevitably . Although this close relationship between
15
long-term hyperglycemic environment has been im- VA, SCDs and DM is mostly based on the extent of
plicated for the increase in the incidence of AF in di- coronary artery disease, non coronary atherosclerotic
12
abetic patients another clinical study failed to show processes like diabetic cardiomyopathy DCAN, mi-
any correlation between glucose levels, insulin levels, crovascular disease, ventricular structural and elec-
HbA1c levels and AF onset in DM patients . Fatemi et trical changes may play a role in this phenomenon
16
13
14
al prospectively evaluated the affect of intense gly- (Figure 2).
cemic control on incidence of AF in diabetic patients. A ventricular repolarization anomaly, which is reflect-
Interestingly, they failed to present any association ed by QTc interval prolongation, is associated with
between incident AF and intense therapy comparing high risk of VA. There are several studies showing,
to standard therapy group. However, their choice of marked QTc prolongation in diabetic patients . An-
17
periodic electrocardiographic testing instead of event other strong predictor of VA, microvolt T wave al-
recorders might alter the results in terms of missing ternans (TWA) measurement, has been found to be
the paroxysmal AF episodes occurring any time be- often abnormal in DM . Every 1% rise in HbA1c levels
18
sides the time of ECG taken in the clinic.
is linked with 13 fold higher risk of having TWA and
Overall, DM seems to be acting a pivotal role in gen- suboptimal glycemic control is linked with higher risk
eration and maintenance of AF in diabetic patients. of spontaneous VA independent of QTc interval dura-
Specific structural, electrical and electromechanical tion. There are studies to suggest that diabetic myo-
alterations in diabetic heart might create fertile sub- cardium is vulnerable for electrical instability and can
strate for the development of AF. On the other hand, be independent from the scarred myocardium areas
acute hypo or hyperglycemia changes in electrolyte from previous ischemic cardiac damages 15,17 .
levels or acid base status and autonomic system dis-
tortions may be trigger mechanisms for the arrhyth-
mia (Figure 1). It is clear that there are still knowledge
gaps about the relationship between AF and DM that
warrant further studies.

Cardio Diabetes Medicine