CASE REPORT

Heart Vessels (2005) 20:37–38 © Springer-Verlag 2005DOI 10.1007/s00380-004-0764-x

Yoko Ueno · Atsushi Takagi · Masatoshi KawanaHiroshi Kasanuki

Pulmonary hypertension during epileptic seizure with evidence of increasedangiotensin II in pulmonary artery

Received: September 27, 2003 / Accepted: December 29, 2003

onstrated high pulmonary arterial pressure (PAP) of 52/17mmHg. His systemic pressure was in the normal range,and urinary volume was decreased. Thus, a human atrialNa-diuretic polypeptide (carperitide) was administered,and PAP normalized immediately. Three days after admis-sion, he developed repeated epileptic attacks, and the PAPfollowing the frequent seizures reached 70/24mmHg. Dur-ing each seizure, PAP followed by systemic blood pressureincreased without a significant change in heart rate (Fig. 1).Epinephrine, norepinephrine, serotonin, and endothelin Ilevels did not change from the baseline levels (epinephrine0.18 vs 0.19ng/ml, norepinephrine 0.99 vs 1.1ng/ml, seroto-nin 13.9 vs 17.3ng/ml, endothelin I 1.2 vs 1.2pg/ml, respec-tively). Only the plasma level of angiotensin II (ATII)increased in a pulmonary arterial blood sample during theseizure (102.0 vs 53.0pg/ml). Spike waves on an electroen-cephalogram and a low plasma phenytoin concentration(9.7µg/ml) indicated insufficiency of the antiepileptic drug.After complete suppression of the seizures by increasing theoral phenytoin, heart failure was well controlled with orallosartan potassium, an ATII receptor antagonist.

Discussion

It seems essential to minimize the neuropathologicsequellae to epileptic seizures in managing patients with ahistory of epilepsy. Status epilepticus has been thought toraise both systemic and pulmonary pressure by elevatingcatecholamines.2 In our case, pulmonary hypertension pro-ceeded to systemic hypertension without increases in cat-echolamine during the seizure. To our knowledge, this is thefirst report that documents this phenomenon as well asincreased plasma ATII, a strong vasoconstricting peptide,3

in the pulmonary circulation during seizure. The baselinelevel of ATII was similar to the value reported in chronichypoxic lung diseases.4 Despite questions as to whether ornot this ATII increment can raise the PAP, and from wherethe ATII was released, our finding is interesting as it furtherinvestigates the neuropathologic pathway by which epilep-

Y. Ueno · A. Takagi (*) · M. Kawana · H. KasanukiDepartment of Cardiology, Tokyo Women’s Medical University,8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, JapanTel. �81-3-3353-8111; Fax �81-3-3356-0441e-mail: atakagi@attglobal.net

Abstract We experienced a 78-year-old man in whom tran-sient pulmonary hypertension was documented during epi-leptic seizure. A Swan-Ganz catheter demonstrated thatpulmonary arterial pressure rose immediately after theinitiation of the seizure, which was followed by systemichypertension. The plasma level of angiotensin II increasedin pulmonary circulation during the seizures; however, cat-echolamines did not change from the baseline. The patientresponded well to treatment with an antiepileptic drug andlosartan potassium.

Key words Epileptic seizure · Pulmonary hypertension ·Angiotensin II

Case report

Epilepsy in elderly patients is an increasing challenge as thepopulation grows, and patients with cardiovascular disor-ders often develop lifetime epilepsy.1 However, it is notclinically well recognized that epileptic seizure exacerbatesheart failure in patients with cardiovascular disease. Weexperienced a patient in whom transient pulmonary hyper-tension (PH) was documented during frequent epilepticseizures.

The patient was a 78-year-old man who underwent mi-tral valve replacement and pacemaker implantation for mi-tral stenosis with sick sinus syndrome at the age of 64. Hehad been on oral phenytoin, 200mg per day, since he hadhad the first seizure. On admission, he was in exertionaldyspnea with peripheral edema. Chest X-ray showed cardi-omegaly and pleural effusion. A Swan-Ganz catheter dem-

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Fig. 1. Swan-Ganz record during the seizure. Pulmonary pressure roseimmediately after the initiation of the seizure, which was followed bysystemic hypertension 1min later

tic seizures cause pulmonary hypertension. This case alsosuggests the possible impact of ATII receptor blockade onthe treatment of heart failure in patients with epileptic sei-zures.5 Further investigations are required to clarify the roleof ATII in pulmonary vasculature during seizures.

References

1. Li X, Breteler MM, de Bruyne MC, Meinardi H, Hauser WA,Hofman A (1997) Vascular determinants of epilepsy: theRotterdam Study. Epilepsia 38:1216–1220

2. Benowitz NL, Simon RP, Copeland JR (1986) Status epilepticus:divergence of sympathetic activity and cardiovascular response.Ann Neurol 19:197–199

3. Lipworth BJ, Dagg KD (1994) Vasoconstrictor effects of angio-tensin II on the pulmonary vascular bed. Chest 105:1360–1364

4. Peacock AJ, Matthews A (1992) Transpulmonary angiotensin IIformation and pulmonary haemodynamics in stable hypoxic lungdisease: the effect of captopril. Respir Med 86:21–26

5. Kiely DG, Cargill RI, Lipworth BJ (1995) Acute hypoxic pulmonaryvasoconstriction in man is attenuated by type I angiotensin II recep-tor blockade. Cardiovasc Res 30:875–880