In patients presenting with STEMI, infarct size can be limited by early myocardial reperfusion via primary PCI, thereby preserving left ventricular systolic function and improving clinical outcome. However, the full benefits of myocardial reperfusion may be limited by the dramatic ionic and metabolic disturbances that can induce myocardial stunning, no-reflow phenomenon, RA, or lethal reperfusion injury [10,11,12,13,14]. Consequently, reperfusion may paradoxically enhance myocardial injury, finally contributing to 50% of the final MI size .
Reperfusion injury results from several complex and interdependent mechanisms that involve altered myocardial metabolism with the production of ROS, mishandling of intracellular calcium, microvascular and endothelial cell dysfunction, platelet, neutrophil, and complement activation .
Arrhythmias occurring during the ischemia/reperfusion period may be due to ischemia, no-reflow after opening of an IRA, or due to reperfusion injury leading to RA. The underlying mechanism of each differs although the type of arrhythmia may be indistinguishable. Unlike ischemic arrhythmias which are usually reentrant in nature, RA operate mainly through non-reentrant mechanisms such as abnormal or enhanced automaticity and triggered activity due to afterdepolarizations occurring as a result of intracellular calcium overload leading to spontaneous calcium oscillations [2, 16].
Previous studies using retrospective registry data showed a high incidence of arrhythmias following intervention, with new-onset AF ranging from 6 to 28%, non-sustained VT in 7–13%, high-degree AV block in 5–10%, sinus bradycardia in 7–16%, sinus arrest (≥ 5 s) in 5%, sustained VT in 3–6%, and VF in 3–6% .
In another study on 503 patients with STEMI, the arrhythmias and conduction disturbances occurring from arrival at the catheterization laboratory to 90 min after primary PCI were registered. The most common arrhythmias observed during primary PCI were AIVR in 42%, sinus bradycardia in 28%, and non-sustained VT in 26% .
Studies on RA in patients during the first 24 h after reperfusion using thrombolytic treatment revealed a prevalence of ventricular premature complexes and couplets of nearly 100%. Ninety percent of patients had an average of eight runs of AIVR per hour per patient, and VT in 23% of the patients had an average of two runs per hour per patient during the first 24 h after reperfusion .
Mehta et al.  published data on the incidence of major arrhythmia (VT and VF) in 5745 patients treated with primary PCI in the APEX AMI trial. They found that VT/VF occurred in 5.7% of patients, usually before catheterization was completed (64%).
In other studies, ventricular arrhythmias requiring electrical counter-shock, including VF and rapid sustained VT, occurred in 1.5 to 2.9% of patients undergoing percutaneous transluminal coronary angioplasty (PTCA) [21,22,23].
Different factors may explain the differences in the incidence of RA including differences in the time frame used for defining RA which ranged from 90 min  up to 48 h , as well as how reperfusion was achieved and how rapid was this done.
The earlier the revascularization therapy is initiated and the more rapidly the reperfusion is achieved, the more is the frequency of RA. Therefore, RA was more common in pre-hospital thrombolysis compared to in-hospital lytic therapy, as shown in a study on 5469 patients that was conducted by the European Myocardial Infarction Project Group . Furthermore, primary PCI is more often associated with RA compared to lytic therapy in acute MI, as proved in a randomized clinical study .
The widespread availability of revascularization therapy and the increased use of beta-blockers have decreased the incidence of sustained VT and VF occurring within 48 h of the onset of an acute coronary syndrome (ACS) over the past decade .
An advantage of the current study is that the arrhythmias occurred immediately after opening of IRA and resumption of flow, with the patient monitored in the cathlab, in a setting and time frame consistent with the occurrence of RA and not induced by ischemia.
Some of the RA are self-limited and do not need any intervention; however, others are sustained and are managed either pharmacologically or electrically (DC cardioversion or pacemaker) based on the type of arrhythmia.
In our study, six patients developed RA in the form of VT or SVT during the primary PCI procedure after restoring flow in the IRA. In case 1, the patient developed VT with hemodynamic instability, and while preparing for DC cardioversion, the operator decided to re-inflate the balloon at the site of the lesion for 1 min as a possible way to terminate the RA, and the VT was actually terminated and did not recur. In case 3, while VT was also successfully terminated by balloon re-inflation, the arrhythmia recurred again on balloon deflation. Re-inflating the balloon again for 1 min terminated the arrhythmia which did not recur. The success rate of this cost-free technique was 100% in all six patients (Table 2), and the effect was immediate within the 1-min balloon inflation. None of the patients needed DC cardioversion or anti-arrhythmic drugs for management of the acute arrhythmia obviating the patient from the possible pain and skin burns associated with the cardioversion and the possible side effects of medications.
In concordance with our results, although on a different type of arrhythmia, Grech and Ramsdale , in their single case report on a patient who developed AIVR following successful right coronary artery recanalization by primary PTCA, could achieve sinus rhythm on re-inflating the PTCA balloon. With each balloon deflation, idioventricular rhythm developed again with associated hypotension. A 100-mg intravenous bolus of lignocaine did not restore sinus rhythm, which spontaneously returned 20 min after the last balloon deflation.
Our results may be a clinical parallel to an experimental study on isolated Langendorff-perfused rat hearts which demonstrated that postconditioning by a single brief episode of global ischemia can effectively terminate persistent reperfusion-induced VF and convert it into a normal rhythm. Regular beating was maintained by all postconditioned hearts during the subsequent reperfusion. However, these experimental data were only done on reperfusion-induced VF .
Previous attempts to minimize reperfusion injury using mechanical ischemic postconditioning in which brief, intermittent episodes of inflation and deflation were done by angioplasty balloon starting within 1 min after reperfusion [6,7,8,9] demonstrated in several small-sized studies to be efficacious during the primary PCI procedure to further improve the prognosis of STEMI beyond myocardial reperfusion [28,29,30,31].
To our knowledge, this is the first report which shows the capability of balloon re-inflation in terminating RA in the form of VT (with pulse) and SVT during primary PCI after successful reperfusion. The mechanism of successful termination may be through temporary interruption of reperfusion, giving a chance for the accompanying electrical and biochemical chaos to ease, leading to reduction of oxygen free radicals, modulation of calcium overload, and correction of acidosis .
The present case study is not without limitations. First, a significant limitation is the relatively small number of patients included, and being a single-center study. However, these case reports, which are to our knowledge reported for the first time, should be considered hypothesis-generating and encourage larger-scale studies. Second, some of the RA are self-limited, and it is possible that even without balloon inflation some of these arrhythmias would have been spontaneously terminated. However, the time relation of balloon deflation and occurrence of arrhythmias and re-inflation and disappearance of the arrhythmia in a controlled cathlab setting favors the effect of balloon inflation on the termination of arrhythmias. A third limitation is that the technique of balloon re-inflation to terminate RA was used in only specific types of RA and was not attempted in the others.