Symptomatic Pericarditis After Influenza Vaccination*

an arc originating in cardiac sensory receptors located principally in the left ventricle, particularly along the inferoposterior wall, but also along the base of the right ventricle.5 Stimulation of these receptors by stretch or chemical agents triggers impulses along nonmyelinated vagal afferents. The consequent increased parasympathetic and decreased sympathetic activity induce bradycardia, vasodilation, and hypotension. Such stimulation has been described in inferoposterior myocardial ischemia and infarction, coronary catheterization, exertional syncope with aortic stenosis, and vasovagal syncope induced by tilt table testing. In acute pulmonary embolism, the hyperadrenergic state results in increased contractility of an underfilled left ventricle. This, in turn, may stimulate Bezold-Jarisch ventricular receptors and increase vagal impulses, causing sinus and atrioventricular nodal slowing, peripheral vasodilation, and syncope. Such a mechanism is consistent with the findings noted on ambulatory ECG monitoring in this patient. The ischemic ECG changes, ie, ST-segment depression and T-wave inversion, were, in retrospect, consistent with those previously described in patients with acute pulmonary embolism. Early precordial T-wave inversion, which was present on the initial ECG, is a common clue to right heart strain and suggested the correct diagnosis. In several series of patients with acute pulmonary embolism, T-wave inversion and ST-segment depression were among the most common associated ECG abnormalities, which also included low QRS-complex voltage, an S1Q3T3 pattern (seen in this patient, Fig 1), right bundle branch block, and right axis deviation.6 This is the first known case report of documented, high-grade atrioventricular block in an ambulatory outpatient with pulmonary embolism and syncope. The use of a Holter monitor in this individual enabled exquisite sequential recording of ST-segment depression and high-grade heart block exactly concurrent with his symptoms, supporting a Bezold-Jarisch vasodepressor reflex as a pathogenic mechanism.