Having carefully read the contributions of Unzué et al,1 we would like to add the following comments to ensure a greater understanding of the case.1
The assessment of cardiovascular symptoms in patients with a history of radiotherapy is complex and, given the low incidence of such cases, the evaluation should be individualized and aimed at ruling out possible cardiac sequelae of the radiotherapy.
Damage to the coronary arteries with the development of heart disease is one of the most common presentations in patients of this type, as reported in several earlier publications referred to previously. In the case of our patient, the presentation did not involve the classic symptoms that would suggest a coronary origin, and there was a low pretest probability of coronary artery disease. Likewise, the initial laboratory tests showed no elevation of biomarkers of myocardial injury, and the electrocardiogram revealed no evidence of dynamic changes indicative of ischemia.
Because there are no specific treatment protocols for these patients, during the hospital stay, we decided to perform tests that would progressively rule out possible cardiac mechanisms involved in the episodes of syncope, taking into consideration, to a certain extent, the risk associated with our patient's profession as a truck driver.
Concerning the electrophysiological study, as Unzué et al point out, the normal HV interval has a duration of 35ms to 55ms, and up to 60ms in the case of left bundle branch block. In our patient, who had right bundle branch block, an HV interval of 65ms cannot be considered normal. However, as the Wenckebach point was nearly normal and its location was suprahisian, and the predictive value of the progression of a baseline HV of less than 100ms to atrioventricular block is low, we decided to perform the study with procainamide, with a negative result, as reported in our earlier letter. Thus, at the time, there was no indication for permanent antibradycardia pacing.2–4
Due to the lack of specificity and low diagnostic yield of the initial tests, the decision was made to carry out exercise echocardiography to rule out ischemic heart disease (low pretest probability), while examining a possible dynamic obstruction in the left ventricular outflow tract due to valvular and subvalvular calcification detected on transthoracic echocardiography. During the test, there was no evidence of the usual symptoms suggestive of ischemia. The patient began to reproduce the symptoms that had led to his hospital admission, with a heart rate of 146 bpm, which was accompanied by the appearance of complete atrioventricular block at 45 bpm, with atrioventricular dissociation, which progressed to a 12-second asystole, the tracing of which is shown in Figure 2.1 Because of limited space, we provided only the tracing that we had considered most relevant.1
Subsequently, the decision was made to implant a permanent transvenous pacemaker. The choice of this approach was based on the belief that the causal mechanism was related to an infranodal block triggered by exercise.5
One month after discharge, the patient underwent cardiac catheterization because he had developed exertional dyspnea. The procedure revealed no obstructive coronary artery lesions. Spirometry confirmed the presence of GOLD stage II chronic obstructive pulmonary disease as the cause of the dyspnea.
Cardiac toxicity secondary to radiotherapy is usually difficult to demonstrate, and the diagnosis is reached after ruling out, to a reasonable extent, the most common causes of cardiac disease. In our patient, cardiac catheterization was not performed to assess the presence of coronary artery disease as the cause of the atrioventricular block because the initial tests and the absence of clinical signs of angina did not point in that direction, and because of the low pretest probability of coronary artery disease. However, its performance could have been an equally valid approach.