Abstract Paroxysmal Supraventricular Tachycardia (PSVT) is the most common type of sustained tachycardia in healthy adults. It is generally believed that thromboembolic events are extremely low in patients with PSVT. Therefore, currently anticoagulant therapy is not a conventional therapy in those patients. Herein, we reported two patients with PSVT who had no stroke risk factors suffered from acute thromboembolic stroke.
It is widely acknowledged that atrial fibrillation is an independent predictor of thromboembolic stroke , and that Paroxysmal supraventricular tachycardia (PSVT) is not associated with throm-boembolic stroke. Therefore, anticoagulant therapy seems to have little clinical significance in patients with PSVT. However, here we reported two cases of acute thromboembolic stroke in young PSVT patients.
Case one: A 28-year-old male patient with 2-year-history of untreated PSVT was admitted to cardiovascular department in our hospital for a persistent palpitation suddenly started 3 days ago. Electrocardiogram (ECG) after the hospitalization was shown as a narrow QRS complex tachycardia with a pulse frequency of 168/min (Fig.1). The patient was received intravenous injection of propafenone 70 mg immediately after PSVT was confirmed. However, it could not terminate PSVT. Cardioversion was successfully realized by a following intravenous injection with adenosine 20 mg. The patient has no a history of any other arrhythmia or heart problems. The blood routine test and coagulation function were normal and echocardiography showed left atrial diameter (LAD) was 33 mm (reference values < 35 mm). However, a sudden left limb weakness was found at 16 hours after termination of PSVT by the patient. An emergency cranial magnetic resonance (MRI+MRA) was done and it showed an acute cerebral infarction in right frontal lobe, parietal lobe and temporal lobe and occlusion of right anterior cerebral artery (Fig.2). The patient was received peripheral intravenous Urokinase (150 U) thrombolytic therapy immediately. The above symptom was disappeared ten days later. Transthoracic echocardiography (TTE) did not show thrombus in left atrium. Three months after the patients receiving oral warfarin for anticoagulant, the PSVT of the patient was confirmed as a concealed left atrioventricular accessory pathway by intracardiac electrophysiology (EPS) and the patient was received radiofrequency catheter ablation (RFCA) successfully.
Case two: A 48-year-old male patient with 10-year-hisptory of PSVT was admitted to cardiovascular department in our hospital for a persistent palpitation suddenly started 10 days ago. Propafenone 150 mg was taken orally at the onset of palpitation by the patient himself. However, the palpitation could not be terminated. Electrocardiogram (ECG) after the hospitalization was shown as a narrow QRS complex tachycardia with a pulse frequency of 179/min (Fig.3). Cardioversion was successfully realized by an intravenous injection with adenosine 20 mg. The blood routine test and coagulation function were also normal. The past medical history was negative. However, 24 hours later, a sudden occurrence of slurred speech and felt left limb weakness was found in the patient. An emergency MRI+MRA was shown as acute cerebral infarction of left parietal lobe, temporal lobe and occipital cortex and occlusion of the left anterior cerebral artery (Fig.4). The patient was transferred to Neurological Intensive Care Unit and was received peripheral intravenous rt-PA (recombinant tissue type plasminogen activator) thrombolytic therapy immediately. The symptoms were disappeared completely two weeks later. Left atrial thrombus was not confirmed by transesophageal echocardiography. Three months later the patient received EPS and RFCA, which confirmed a concealed left atrioventricular accessory pathway.
Discussion It is generally thought anticoagulant therapy need not to be used in patients with PSVT for thrombus event is extremely rare .
Wang et al. has reported a case of a 15-year-old girl with PSVT lasted for 5 days. Several antiarrhythmic drugs could not terminated PSVT, then electrical cardioversion to sinus rhythm. But 30 hours later, the patient attacked acute stroke. This patient was young and no risk factors of thrombosis. The author speculated that PSVT lasted for a long time then resulted in thrombus formation in left atrium. In the case of paroxysmal tachycardia termination, the atrium contractility increased and resulted in thrombosis shedding.
Themostcom-Brembilla-Perrot et al.  observed patients have PSVT induced by oesophagea lead, following up 6 month ∼ 5 years, 14% of patients have stroke. Several studies reported high incidence of AF in patients with PSVT, 12% of these patients would develop atrial ﬁbrillation during a 1-year follow-up period , while the induction of atrial fibrillation in a patient studied for PSVT has no significance. PSVT increased thrombus risk when paroxysmal tachycardia degenerated into atrial fibrillation. For two cases, the patients had no stroke risk factors, suffered from acute thromboembolic stroke the tachycardia lasted several days might be responsible for the development of atrial myopathy and a risk of thrombus formation.
The two patients were young and have no any other stroke risk factors, except PSVT lasting for a long time. There were the possibility that the patients have unrecognized atrial fibrillation, this predisposed them to have the stroke. In our opinion, the patient should rule out thrombus in left atrium before terminating PSVT by echocardiogram. Whether these patients should receive anticoagulation therapy remain to be further studied.
In conclusion, anticoagulation therapy might be important in long-lasting PSVT patients. However, further studies are still warranted to assess the significance of anticoagulation therapy in PSVT patients, especially in long-lasting ones.
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