Introduction: Cough syncope is more frequent among middle-aged obese male subjects who associate obstructive pulmonary pathology. It is caused by an increase in intrathoracic pressure during a paroxysmal cough episode, causing a reduction in venous return and thus a diminished systemic and cerebral blood-flow. Other mechanisms such as hypoxia, an acute increase in cerebral vascular resistance or cardiac arrhythmias can also be involved in cough syncope pathogenesis.
Case presentation: We present the case of a 47 year old patient who experienced a syncope 2 days prior to admission, occurring after a paroxysmal dry cough episode, which led to a mild cranio-cerebral trauma. Our patient had been diagnosed 2 months before with grade II arterial hypertension (treated with perindopril and amlodipine) and severe obstructive sleep apnea under current continuous positive airway pressure (CPAP) therapy. Upon admission our patient was in a good general condition, with grade II abdominal obe-sity (BMI 35.9 kg/m², WC 123 cm), skin excoriations on the forehead and nasal pyramid, BP 130/85 mmHg. The electrocardiogram documented sinus rhythm 78/ min, QRS axis -15°, 1st degree A-V block, normal QRS morphology, negative T waves in DIII, V1 and flat-tenned T waves in aVF. Echocardiography showed a normal ejection fraction (58%), normal chamber size and volumes with no hemodynamically significant val-ve disease. ABPM recording showed partially controlled BP values under treatment (maximum BP 164/98 mmHg, average BP 132/83 mmHg), non-dipper cicarian profile. Holter monitoring showed sinus rhythm 39-147/min, 1 episode of atrial fibrillation that lasted 90 s, but no significant pauses >2 s. We completed our investigations with a Schellong test and a carotid sinus massage (both negative) in order to exclude orthostatic hypotension and a potential reflex syncope. The causality between the cough and the syncope is sustained by anamnesis (context of the syncope) but also by the disappearing of the dry cough and the absence of re-current syncopes after the switching the patient on an angiotensin receptor blocker instead of perindopril. According to the guidelines we initiated anticoagulant treatment (CHADS VASC score=1, class IIa indication) and chose a novel oral anticoagulant (IA). We chose propafenone for rhythm control along with a beta blocker for adequate rate control. Our patient should continue CPAP therapy (4-10.5 cmH20), and will undergo Holter ECG and cardio-respiratory polygraphy after 6 months.
Case particularity: T he hallmark of our case is the presence of cough syncope as a rare adverse effect of angiotensin converting enzyme inhibitors, being to our knowledge the third such case reported in scientific literature. Interestingly, our relatively young patient developed atrial fibrillation in the absence of left atrial dilation, probably favored by the presence of obstructive sleep apnea.