*2.2.2 Pleuritic/pericardial involvement*

As discussed above, pneumothorax, pneumopericardium, hydropneumothorax, and pericardial effusion can produce delayed symptoms of pleural or pericardial pain leading to chest pain. This is typically due to a break in the continuity of the pleural or pericardial membrane secondary to lead perforation. It could be secondary to micro or macro perforations [43–45]. Nevertheless, patient symptoms of chest pain have to be evaluated very carefully and investigated accordingly. Simple chest X-ray and transthoracic echocardiogram would be sufficient in most cases [46]. Use of a CT chest could result in overreading lead perforation due to the presence of artifacts [47]. If there is any clinical suspicion for lead dislodgment, in most cases, lead revision would take care of the chest pain immediately.

### *2.2.3 Stress cardiomyopathy*

Patients may develop stress cardiomyopathy/Takotsubo cardiomyopathy, in the postoperative period. Clinically, they may present with chest pain, shortness of breath, new onset arrhythmias, and positive troponins. Transthoracic echocardiogram will show apical ballooning and basal septal sparing [48]. Cardiac catheterization can confirm the absence of any major obstructive coronary artery disease. Even though the pathophysiology of the stress cardiomyopathy is evident, etiology of stress cardiomyopathy in the setting of pacemaker implantation is not very clear. This could be secondary to the stress events which led to the device implantation, medications used for sedation, pacing induced dyssynchrony, and/or due to the stress of the surgical procedure itself [49–51].

### *2.2.4 Diaphragmatic pacing*

In a small percent of the population, it is possible that patients may have diaphragmatic pacing due to direct capture of the phrenic nerve [52]. This can be interpreted as chest discomfort/hiccups, manifesting predominantly in certain position [53]. For a CRT device, the coronary sinus lead would be placed into the posterolateral or lateral branches which would abut the lateral wall of the left ventricle [54, 55]. The left phrenic nerve runs very close toward the lateral border of the left ventricle. Hence, this lead could be pacing the phrenic nerve and producing diaphragmatic contractions. Usually, during lead placement, high output pacing will be performed from the coronary sinus lead to rule out any phrenic nerve capture. However, secondary to displacement of the leads, it is possible that the leads can move and capture the phrenic nerve leading on to diaphragmatic contractions [56]. The right ventricular lead typically does not produce diaphragmatic pacing except in the following situations: (1) perforation of the right ventricle and migration of the lead inferiorly to produce direct capture of the diaphragm; (2) extreme RV dilation to the extent that the lateral border of the cardiac silhouette is situated near the right ventricular apex [57]. These situations require lead revision. On the other hand, the right-sided phrenic nerve travels along the lateral border of the right atrium, distant from the right atrial appendage, and can lead to diaphragmatic pacing if the right atrial lead becomes dislodged and captures the right phrenic nerve [58, 59].
