Complete heart block as presenting symptom of massive pulmonary embolism in an elderly patient.

A 68-year-old man presented to the emergency department due to recurrent episodes of syncope and shortness of breath during the previous two days. Her medical history included arterial hypertension and diabetes. She was not taking any negative chronotropic drugs but she referred a familial history of fatal pulmonary embolism and sudden cardiac death. At admission, blood pressure, pulse rate and peripheral oxygen saturation were 88/60 mmHg, 49 beats/min and 88%, respectively. ECG revealed a third-degree AV block (Figure 1A). Routine blood tests demonstrated an ultrasensitive cardiac troponin I (cTnI) of 225 ng/L (n.v. < 45 ng/L) and no evidences of electrolyte imbalances, while chest X-ray revealed no signs of heart failure. The woman required the placement of a temporary pacing but, after 4 h from the admission, she spontaneously recovered sinus rhythm remaining hemodynamically unstable (86/62 mmHg). A new ECG demonstrated sinus tachycardia, incomplete right bundle branch block (RBBB), S1Q3T3 pattern and Q waves in inferior and anteroseptal leads (Figure 1B). Considering the patient's familial history, previous laboratory findings and the McGinn and White pattern observed after the spontaneous recovery of sinus rhythm, further investigations were performed. D-dimer level and N-terminal pro–B-type natriuretic peptide levels resulted 15.2 µg/mL (normal value < 0.50 µg/L) and 2019 pg/mL (normal value < 300 pg/mL), respectively, while cTnI further increased (502 ng/L). Bedsides, transthoracic echocardiography demonstrated an enlarged-hypokinetic right ventricle and diastolic dyskinesia of the interventricular septum, while doppler-derived pulmonary artery systolic pressure was 38 mmHg. The strongly suspect of acute pulmonary embolism (PE) was confirmed by the computed tomography angiography which demonstrated the presence of endoluminal filling defects in both the right main and left lobar pulmonary arteries (Figure 2). The diagnosis of high-risk PE was made and the woman received systemic thrombolysis (recombinant tissue plasminogen activator: 100 mg over 2 h) with rapid improvement of symptoms and hemodynamic parameters. A subsequent electrophysiological study was performed to evaluate whether a placement of a definitive pacemaker could be necessary. However, since the anterograde and retrograde conductions were both maintained without any defects, the implantation of a definitive device was not considered necessary. Moreover, coronary angiography was performed to exclude an ischemic genesis of the complete heart block (CHB). The patient was discharged in good conditions under oral anticoagulation with rivaroxaban. CHB as presenting symptom of acute PE is very rare and its paroxysmal even more rare.[1] To the best of our knowledge, this is the first case of CHB in high-risk PE. Indeed, only another report has described the occurrence of a paroxysmal CHB but in a hemodynamic stable woman.[2] Moreover, unlike our case, previous investigations have demonstrated that generally the CHB occurred after the damage of the right bundle branch in patients with a previous left bundle branch block.[1] To date, the real pathogenetic mechanism underling the occurrence of CHB as presenting symptom of acute PE remains to be clarified.

Figure 1.

ECG results.

(A): Standard 12-lead ECG demonstrating a third-degree atrioventricular block; (B) ECG performed after the spontaneous recover of the sinus rhythm demonstrating sinus tachycardia, incomplete right bundle branch block, S1Q3T3 (McGinn and White's sign) and Q waves in both inferior and anteroseptal leads.

Figure 2.

Computed tomography angiography of the chest showing endovascular filling defects among the right main and left lobar pulmonary arteries (white arrows).