In our study, the incidence of reperfusion arrhythmias detected in the first 48 hours did not differ significantly between the two treatment groups. 83.3% of patients in primary PCI group and 88.7% of the thrombolytic group, had at least one reperfusion arrhythmia. When the rates of different arrhythmia findings were examined separately, the ratio of sustained VT, nonsustained VT, VF, frequently VEA, and AV block was similar between the two groups. However AIVR and AF ratio were higher in the thrombolytic group.
The incidence of the development of AF in acute MI is about 5–10% and it is known that AF development in acute MI is usually due to impaired left ventricular function or poor reperfusion [5
]. Celik et al. reported that in patients who underwent PTCA, p dispersion was reduced, showing that successful reperfusion may reduce the likelihood of development of AF [6
]. On the contrary, the incidence of AF could increase in patients with poor reperfusion. The left ventricular functions in both groups of patients were normal in this study. Therefore, the cause of AF was thought to be residuel ischemia or poor reperfusion instead of impaired left ventricular functions. Unlike thrombolytic group, we observed significantly lower rates of AF in PTCA group. Six et al. investigated the predictive value of ventricular arryhtmias as an indicator of angiographic arterial patency after thrombolytic therapy. Among these, AIVR was the most sensitive and specific arrythmia in cases of successful reperfusion [7
]. In contrast, Bonnemeier et al. demonstrated that only 19 of 125 patients who were successfully treated with primary PCI exhibited AIVR which indicated a poor relationship between TIMI 2 or 3 flow and reperfusion arrhythmia and declared that AIVR may not be used as a reperfusion criteria [8
Terkelsen et al. mentioned that although AIVR does not meet criteria for reperfusion, it may be an indicator of more extensive myocardial damage and delayed microvascular reperfusion in a study of 503 patients who were treated by primary PTCA [9
]. In another study, Gibson et al. [10
] exhibited the development of VT and VF in 3491 patients with STEMI after thrombolytic therapy, and reported that cases who developed VT or VF had TIMI 0–2 flow.
The relationship between arterial patency rates demonstrated via coronary angiography (TIMI flow grades). The analysis of TIMI flows allows better understanding of the relationship between arterial patency rates and reperfusion arryhtmias.
In the primary PCI group, TIMI 3 patency was obtained in 83.3% of cases. There was no statistically significant relation between the presence of reperfusion arryhtmia and TIMI flow grades in primary PCI group although reperfusion arryhtmia was observed with a ratio of 82.2% in these patients with TIMI 3 flow.
42.3% and 38.1% of the patients who had received thrombolytic therapy had TIMI 3 and TIMI 2 flow, respectively. The incidence of reperfusion arryhthmia observed in the group of patients with TIMI 1 flow was significantly lower in thrombolytic therapy arm. On the other hand, there was no relationship between the presence of reperfusion arryhthmia and higher TIMI flow grades (TIMI 2 and TIMI 3) in the same group.
Wehrens et al. [11
] compared the electrocardiographic changes following reperfusion in AMI patients to whom thrombolytic therapy, primary PTCA, or rescue PTCA were performed. The researchers demonstrated that electrocardiographic changes as a noninvasive tool associated with reperfusion did not provide sufficient information to clinicians to distinguish TIMI 2 and 3 flows from each other after thrombolytic therapy. This result is compatible with our results. Gressin et al., investigated the relationship between ventricular arrhytmias and arterial patency by recording ventricular arrhytmias in the first 24 hours and examining the angiographic views in a group of patients with acute myocardial infarction treated with thrombolytic therapy [12
]. On the basis of ventricular arrhythmias detected; arryhtmia rates, in patients with TIMI 2 and 3 flow grades and in those without arterial patency (TIMI 0 or 1 flow grades), was found to be similar. These results suggest that some arrythmias may be due to different reasons such as ongoing ischemia or metabolic abnormalities. However, in another study, rates of sustained VT or AIVR occurring in the first 6 hours were found significantly higher in patients with arterial patency and these arrhytmias were defined as noninvasive indicators of early coronary reperfusion [13
]. But it must be emphasized that the results and assessment of this study were limited to the detection of arrythmias in the first 6 hours, which is different from previous studies.
Engelen et al. demonstrated that at least 97% of patients developed one ventricular reperfusion arrhythmia in a study group of 62 patients with acute anterior myocardial infarction who underwent primary PCI. Nonsustained VT, AIVR, and frequent VEA were the most frequently arrhythmias (similar to our findings) and ventricular arrhytmias were correlated with reduced and worsening left ventricular functions after the acute phase of myocardial infarction among this group of patients treated via primary PCI and concluded that reperfusion arrhythmias are noninvasive indicators of myocardial cell damage [14
4.1. Study Limitations
The main limitation of the present study resides in its retrospective design. Larger scale studies may provide additional information for clinical applications.