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(Stroke. 1997;28:1461-1463.)
© 1997 American Heart Association, Inc.
Articles |
99mTc-HMPAO Brain SPECT Imaging in a Case of Repeated Syncopal Episodes Associated With Smoking
From the Departments of Neurology and Cardiovascular Disease (H.O.), Masuda Red Cross Hospital, Shimane, Japan.
Correspondence to Hitoshi Fukuda, MD, Department of Neurology, Masuda Red Cross Hospital, I103-1, Otoyoshi, Masuda, Shimane, 698, Japan.
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Abstract |
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Background We report here a rare case of repeated syncopal episodes associated with smoking and findings of 99mTc–hexamethylpropyleneamine oxime (HMPAO) brain single-photon emission CT (SPECT) imaging.
Case Description A 77-year-old man had four syncopal episodes during a half-month period. All four occurred when he stood up and walked immediately after smoking a cigarette, and syncope did not occur after cessation of smoking. Although upright testing revealed orthostatic hypotension, the patient did not complain of fainting on standing alone. Compared with brain SPECT in the supine position, perfusion was decreased in the posterior circulation structures after the subject smoked a cigarette or chewed nicotine gum.
Conclusions The combination of cerebral vasoconstriction due to smoking and orthostatic hypotension probably decreased cerebral blood flow in this patient, resulting in syncope.
Key Words: cerebral blood flow • cigarette smoking • syncope • tomography, emission computed
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Introduction |
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Although information on the acute effects of smoking on CBF is limited, some previous studies1 2 have shown a decrease in CBF and that acute smoking can induce cerebral vasoconstriction. However, smoking does not usually cause syncope in chronic smokers. We report here a patient who had several syncopal episodes immediately after smoking; 99mTc-HMPAO brain SPECT images revealed hypoperfusion in the posterior circulation during the smoking of a cigarette or chewing of nicotine gum.
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Case Report |
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The patient was a 77-year-old man who was admitted to our hospital on August 31, 1996, for determination of the etiology of repeated episodes of loss of consciousness. He had previously been diagnosed with gout, alcoholic hepatitis, chronic renal failure, hypertension, and left ventricular hypertrophy. He had taken medicine since age 67 years: 2 mg benidipine HCl, 20 mg furosemide, 0.5 µg alfacalcidol, 200 mg allopurinol, and 60 mg diltiazem HCl by daily oral administration; diltiazem HCl was discontinued on August 31. He had no history of fainting on standing alone or of stroke and had smoked cigarettes since age 17 years. He had recently been smoking about 20 filtered cigarettes (containing 1.3 mg nicotine and 14 mg tar per cigarette) per day.
The patient lost consciousness on standing immediately after smoking a cigarette on August 17 and 23. The third episode of loss of consciousness occurred in our hospital on September 2. In that episode, when he stood up and walked immediately after smoking a cigarette, the patient complained of dizziness and motor weakness of the lower extremities and then fainted with fecal incontinence. He suffered no convulsions. His blood pressure was 202/80 mm Hg; heart rate was 80 bpm and regular, and the electrocardiogram revealed no arrhythmia. He regained consciousness within 1 minute. Aspirin, 100 mg PO daily, was added to his medication on September 3. Another fainting episode occurred on September 6, under the same conditions as the third attack. We suspected that smoking was associated with his fainting and forbade him from smoking. He suffered no further episodes of loss of consciousness. Extensive laboratory examination was performed at the times of the episodes. Complete blood count, electrolyte levels, liver function tests, glucose level, and results of blood gas analysis were all normal, but blood urea nitrogen and creatinine were elevated at 29 and 2.4 mg/dL, respectively. Upright tests revealed orthostatic hypotension with no complications. Blood pressure, heart rate, and plasma norepinephrine levels were 144/70 mm Hg, 62 bpm, and 0.80 ng/mL, respectively, in the supine position and 96/60 mm Hg, 84 bpm, and 1.3 ng/mL, respectively, with the patient upright. Twenty-four-hour electrocardiographic recording revealed only insignificant extrasystoles. An echocardiogram revealed mild aortic regurgitation but normal left ventricular function with an ejection fraction of 80%. The electroencephalogram was normal. Brain MRI revealed moderate periventricular hyperintensity on T2-weighted imaging, with old asymptomatic lacunar infarcts in the basal ganglia and cerebral atrophy. MRA revealed multiple stenotic changes of intracranial and extracranial arteries. Although MRA did not show a flow signal of the right vertebral artery, the left vertebral artery and basilar artery were almost normal. Severe stenosis at the origin of the right internal carotid artery was suspected because of a signal defect 1 cm in length on MRA.
99mTc-HMPAO brain SPECT studies (Figure
) were
performed using a dual-head scintillation camera with a 3.2-mm
resolution in full width at half maximum (Hitachi RC-2600I). Image data
were collected in a 128x128 matrix using a low-energy fan-beam
collimator. Brain SPECT without nicotine administration was initiated
10 minutes after injection of 370 MBq 99mTc-HMPAO with a
20-mL saline flush into the antecubital vein of the patient in a
recumbent position. After the first SPECT study, the patient maintained
this position and smoked a filtered cigarette (0.1 mg nicotine and 1 mg
tar) of 2.5 cm in length; the second SPECT study was then initiated
after 555 MBq 99mTc-HMPAO was injected. On a different day,
another SPECT study was performed after the patient chewed nicotine
gum. 99mTc-HMPAO (740 MBq) was injected 15 minutes after
the patient chewed a piece of gum containing 2 mg nicotine for 30
minutes. Another SPECT study was performed to assess perfusion changes
with orthostasis. After 20 minutes in the recumbent position, the
patient stood up and received a bolus injection of 740 MBq
99mTc-HMPAO. He remained standing for another 10 minutes,
until initiation of SPECT imaging. Blood pressure and heart rate were
156/60 mm Hg and 60 bpm, respectively, in the supine position and
140/50 mm Hg and 66 bpm, respectively, in the upright position.
The patient's medications were not changed during the cerebral
perfusion studies.
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The concentration of 99mTc-HMPAO was decreased in the brain stem, cerebellum, occipital lobe, parietal lobe, and temporal lobe on brain SPECT after smoking compared with that in frontal lobe and basal ganglia. Although brain SPECT after the chewing of nicotine gum also showed hypoperfusion in the posterior circulation, the changes were smaller in magnitude than those in SPECT after the smoking. The findings of brain SPECT in the upright position did not differ from those in the supine position.
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Discussion |
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TopAbstractIntroductionCase ReportDiscussionReferences |
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The patient suffered four syncopal episodes within a half-month period. Although upright testing revealed orthostatic hypotension, he did not usually complain of fainting on standing alone. Plasma norepinephrine level and heart rate both increased on standing. The patient had no other neurological deficits indicative of multiple systems atrophy. Because all four syncopal attacks occurred when the patient stood up and walked immediately after smoking a cigarette and syncope did not occur after cessation of smoking, we suspected that cerebral vasoconstriction due to smoking and orthostatic hypotension together decreased CBF, causing syncope.
We studied cerebral perfusion with 99mTc-HMPAO brain SPECT in various conditions. Although the patient had orthostatic hypotension and stenosis of the right internal carotid artery, the findings of SPECT study on standing did not differ from those in the supine position. Smoking or chewing nicotine gum induced hypoperfusion, especially in the posterior cerebral circulation. Previous studies showed that smoking a single cigarette could produce a brief disturbance of coronary blood flow,3 4 digital blood flow,5 and CBF.1 2 It has been proposed that nicotine induces the release of adrenergic catecholamines and thus produces vasoconstriction and decreased regional blood flow. The findings of SPECT study after smoking or chewing nicotine gum probably revealed a decrease in CBF induced by nicotine, especially in the posterior circulation. Thus, the combination of orthostatic hypotension and smoking induced fainting in this patient.
Change in perfusion due to nicotine administration was more pronounced after the smoking of a cigarette containing 0.1 mg nicotine than after chewing nicotine gum containing 2 mg nicotine. Bounameaux et al5 reported that the maximum concentration of plasma nicotine was higher after the smoking of a cigarette containing 0.1 mg nicotine than after chewing nicotine gum containing 4 mg nicotine. Similarly, in our patient, plasma nicotine concentration was probably higher and the change in perfusion larger after he smoked a cigarette than after he chewed nicotine gum. Because the patient usually smoked cigarettes containing 1.3 mg nicotine, the decrease in CBF he experienced on smoking was probably severe in syncopal episodes.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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We thank Masanori Harada and Kazumi Takada of the Department of Radiology for technical support in performing brain SPECT imaging.
Received January 16, 1997; revision received April 17, 1997; accepted April 17, 1997.
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References |
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1. Cruickshank JM, Neil-Dwyer G, Dorrance DE, Hayes Y, Patel S. Acute effects of smoking on blood pressure and cerebral blood flow. J Hum Hypertens. 1989;3:443-449.[Medline] [Order article via Infotrieve]
2. Dorrance DE, Bullock PR, Bagley JS, Neil-Dwyer G. The response of intracranial vessels to cigarette smoking. In: Angerson WJ, Sheldon CD, Barbenel JC, Fisher AC, Gaylor JDS, eds. Blood Flow in the Brain. Oxford, UK: Clarendon Press; 1988:88-94.
3. Deanfield JE, Shea MJ, Wikson RA, Horlock P, de Landsheere CM, Selwyn AP. Direct effects of smoking on the heart: silent ischemic disturbances of coronary flow. Am J Cardiol. 1986;57:1005-1009.[Medline] [Order article via Infotrieve]
4.
Winniford MD, Wheelan KR, Kremers MS, Ugolini V, van
den Berg E Jr, Niggemann EH, Jansen DE, Hillis D.
Smoking-induced coronary vasoconstriction in patients with
atherosclerotic coronary artery disease: evidence for
adrenergically mediated alterations in coronary artery
tone. Circulation. 1986;73:662-667.
5. Bounameaux H, Griessen M, Benedet P, Krahenbuhl B, Deom A. Nicotine induced haemodynamic changes during cigarette smoking and nicotine gum chewing: a placebo controlled study in young healthy volunteers. Cardiovasc Res. 1988;22:154-158.[Medline] [Order article via Infotrieve]
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