- Email: [email protected]
Glyceryl trinitrate reversal of post-sumatriptan coronary artery narrowing
excretion are clearly needed, in view of the prevalence of microalbuminuria in essential hypertension (25%).’ The study population was heterogeneous in terms of their renal function at entry and the various antihypertensive drugs they received. Diuretics and angiotensin-convertingenzyme inhibitors, for example, might have disparate effects on renal function. Hence, difference subgroups might have different outcomes. It therefore remains a challenge to identify early those hypertensives who might go on to develop renal failure, and to identify the drug class that best prevents it. Bernard
Cheung
Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong
Jacobsen FK, Christensen CK, Morgansen CE, Heilskov NSC. Evaluation of kidney function after meals. Lancet 1980; i: 319. 2 Shemesh O, Golbetz H, Kriss JP, Myers BD. Limitations of creatinine as a filtration marker in glomerulopathic patients. Kidney Int 1985; 28: 1
830-38. 3
Mimin A, Ribstein J, DuCailer G. Is microalbuminaria: a marker of early intrarenal vascular dysfunction in essential hypertension?
Hypertension 1994;
23
(part II): 1018-21.
Glyceryl trinitrate reversal coronary artery narrowing
of
post-sumatriptan
who received sumatriptan. 15 of 27 evaluable coronary segments showed reduced lumen diameters in the five patients who received placebo; the magnitude of reduction was similar to that seen in patients receiving sumatriptan. The placebo group results are not further discussed in this letter. In two of the seven patients receiving sumatriptan (7 segments) lumen diameter did not decrease 30 min after dosing (data not shown). In the remaining five patients, 18 of 24 evaluable coronary segments had reduced lumen diameters 30 min after sumatriptan. The table summarises the changes in the mean (integrated average) lumen diameter and the responses to intracoronary GTN. Dilation to at least 95% of baseline lumen diameter was noted in 14 of the 18 segments after GTN. For brevity the table shows data for just one segment (LAD) in patients A-E. These results, obtained in a clinical research setting, show that intracoronary GTN reverses coronary artery constriction in patients receiving sumatriptan under the conditions of this study. This is an important observation. Although we would expect oral GTN to produce similar results, this route of administration has yet to be studied in this context.
patients
*James Palmer, Robert Feldman, G B John Mancini, Mark Zimmerman Glaxo Research Institute, *Research Triangle Park, North Carolina, USA; Ocala, Florida; and Vancouver, British Columbia, Canada
SIR—Sumatriptan, a selective 5HT1D agonist for the treatment of migraine, may cause coronary vasospasm in patients with a history of coronary artery disease (CAD), who are known to be susceptible to coronary artery vasospasm, and, rarely, in those without a history suggestive of CAD. Two angiography studies in twenty patients with CAD or suspected CAD have shown clinically insignificant reductions
in
mean
coronary
artery
subcutaneous administration of either or sumatriptan placebo. Patients eligible for this study did not have a history of migraine headache and were being evaluated for suspected CAD; all sixteen patients enrolled in the study had at least one coronary artery segment with 50% or more stenosis. Angiography was done immediately before and at 15 and 30 min after subcutaneous sumatriptan (6 mg) or placebo. After the 30 min angiogram intracoronary GTN
after
(100 jLig)
was
given,
and
a
fourth
angiogram
was
obtained about 5 min later. All angiograms were evaluated quantitatively’ under blinded conditions. Angiograms were suitable for evaluation of lumen diameter changes (from baseline to the 30 min and postGTN study) for 31 coronary segments in seven of the eleven
*Only LAD data shown (mid in patients A and E, proximal in patients B-D). t% reversal (post-GTN/base!!ne) shown in parentheses. Table: Changes in lumen diameter 30 min after sumatriptan and then 5 min after GTN
1366
2
diameter
unaccompanied by electrocardiographic changes or anginal symptoms after intravenous or subcutaneous sumatriptan.I,2 Notably, coronary vasospasm was not observed in a 53-yearold female migraine patient with clinical signs suggestive of myocardial ischaemia who self-injected sumatriptan immediately before diagnostic coronary arteriography.3 Results from a Glaxo sponsored study provided uncontrolled data on the effect of intracoronary glyceryl trinitrate (GTN) on coronary arteries with reduced lumen diameters
1
3 4
MacIntyre PD, Bhargava B, Hogg KJ, Gemmill JD, Hillis WS. The effect of i.v. sumatriptan, a selective 5-HT1-receptor agonist, on central haemodynamics and the coronary circulation. Br J Clin Pharmacol 1992; 34: 541-46. MacIntyre PD, Bhargava B, Hogg KJ, Gemmill JD, Hillis WS. Effect of subcutaneous sumatriptan, a selective 5HT1 agonist, on the systemic, pulmonary, and coronary circulation. Circulation 1993; 87: 501-05. Evers S, Husstedt I-W, Enbergs A. Coronary angiography in migraine patient after subcutaneous sumatriptan. Lancet 1995; 345: 198. Mancim GBJ, Simon SB, McGillem MJ, LeFree MT, Friedman HZ, Vogel RA. Automated quantitative coronary artenography: morphologic and physiologic validation. Circulation 1987; 75: 452-60.
Buspirone
treatment of Tourette’s
SiR-Treatment
of
syndrome
Tourette’s
syndrome is often unsatisfactory, although antipsychotic drugs such as haloperidol, pimozide, or risperidone improve tics despite an in deterioration drug-induced general expected functioning. [-3 There is some evidence that trans dermal nicotine may potentiate the therapeutic effects of haloperidol or even that it is effective alone.2 In a clinical trial of transdermal nicotine, one patient with Tourette’s syndrome (DSM-III-R 1987 criteria) had to be excluded because he had mild bronchial asthma (for which he used a salbutamol inhaler) and that was an exclusion criterion in the study. Buspirone is an anxiolytic/antidepressant which is a 5-HTIA partial agonist and a dopamine-D presynaptic terminal autoreceptor antagonist. There is some evidence that animal tic-like movements are blocked by buspirone and that 5-HT receptors may be involved in Tourette’s syndrome.3 We have therefore investigated the effects of buspirone on this patient, a 42-year-old man who had not responded to or tolerated other antipsychotic medications. The Yale global tic severity scale (maximum 50) was used for assessments, which were done from videotaped interviews, blind to medication status.2 Buspirone reduced the Yale score by 70%, and this effect was maintained during the 16 weeks of medication (table). Discontinuation of buspirone for 2 weeks resulted in an exacerbation, which suggests that the improvement had been
Cheung
Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong
Jacobsen FK, Christensen CK, Morgansen CE, Heilskov NSC. Evaluation of kidney function after meals. Lancet 1980; i: 319. 2 Shemesh O, Golbetz H, Kriss JP, Myers BD. Limitations of creatinine as a filtration marker in glomerulopathic patients. Kidney Int 1985; 28: 1
830-38. 3
Mimin A, Ribstein J, DuCailer G. Is microalbuminaria: a marker of early intrarenal vascular dysfunction in essential hypertension?
Hypertension 1994;
23
(part II): 1018-21.
Glyceryl trinitrate reversal coronary artery narrowing
of
post-sumatriptan
who received sumatriptan. 15 of 27 evaluable coronary segments showed reduced lumen diameters in the five patients who received placebo; the magnitude of reduction was similar to that seen in patients receiving sumatriptan. The placebo group results are not further discussed in this letter. In two of the seven patients receiving sumatriptan (7 segments) lumen diameter did not decrease 30 min after dosing (data not shown). In the remaining five patients, 18 of 24 evaluable coronary segments had reduced lumen diameters 30 min after sumatriptan. The table summarises the changes in the mean (integrated average) lumen diameter and the responses to intracoronary GTN. Dilation to at least 95% of baseline lumen diameter was noted in 14 of the 18 segments after GTN. For brevity the table shows data for just one segment (LAD) in patients A-E. These results, obtained in a clinical research setting, show that intracoronary GTN reverses coronary artery constriction in patients receiving sumatriptan under the conditions of this study. This is an important observation. Although we would expect oral GTN to produce similar results, this route of administration has yet to be studied in this context.
patients
*James Palmer, Robert Feldman, G B John Mancini, Mark Zimmerman Glaxo Research Institute, *Research Triangle Park, North Carolina, USA; Ocala, Florida; and Vancouver, British Columbia, Canada
SIR—Sumatriptan, a selective 5HT1D agonist for the treatment of migraine, may cause coronary vasospasm in patients with a history of coronary artery disease (CAD), who are known to be susceptible to coronary artery vasospasm, and, rarely, in those without a history suggestive of CAD. Two angiography studies in twenty patients with CAD or suspected CAD have shown clinically insignificant reductions
in
mean
coronary
artery
subcutaneous administration of either or sumatriptan placebo. Patients eligible for this study did not have a history of migraine headache and were being evaluated for suspected CAD; all sixteen patients enrolled in the study had at least one coronary artery segment with 50% or more stenosis. Angiography was done immediately before and at 15 and 30 min after subcutaneous sumatriptan (6 mg) or placebo. After the 30 min angiogram intracoronary GTN
after
(100 jLig)
was
given,
and
a
fourth
angiogram
was
obtained about 5 min later. All angiograms were evaluated quantitatively’ under blinded conditions. Angiograms were suitable for evaluation of lumen diameter changes (from baseline to the 30 min and postGTN study) for 31 coronary segments in seven of the eleven
*Only LAD data shown (mid in patients A and E, proximal in patients B-D). t% reversal (post-GTN/base!!ne) shown in parentheses. Table: Changes in lumen diameter 30 min after sumatriptan and then 5 min after GTN
1366
2
diameter
unaccompanied by electrocardiographic changes or anginal symptoms after intravenous or subcutaneous sumatriptan.I,2 Notably, coronary vasospasm was not observed in a 53-yearold female migraine patient with clinical signs suggestive of myocardial ischaemia who self-injected sumatriptan immediately before diagnostic coronary arteriography.3 Results from a Glaxo sponsored study provided uncontrolled data on the effect of intracoronary glyceryl trinitrate (GTN) on coronary arteries with reduced lumen diameters
1
3 4
MacIntyre PD, Bhargava B, Hogg KJ, Gemmill JD, Hillis WS. The effect of i.v. sumatriptan, a selective 5-HT1-receptor agonist, on central haemodynamics and the coronary circulation. Br J Clin Pharmacol 1992; 34: 541-46. MacIntyre PD, Bhargava B, Hogg KJ, Gemmill JD, Hillis WS. Effect of subcutaneous sumatriptan, a selective 5HT1 agonist, on the systemic, pulmonary, and coronary circulation. Circulation 1993; 87: 501-05. Evers S, Husstedt I-W, Enbergs A. Coronary angiography in migraine patient after subcutaneous sumatriptan. Lancet 1995; 345: 198. Mancim GBJ, Simon SB, McGillem MJ, LeFree MT, Friedman HZ, Vogel RA. Automated quantitative coronary artenography: morphologic and physiologic validation. Circulation 1987; 75: 452-60.
Buspirone
treatment of Tourette’s
SiR-Treatment
of
syndrome
Tourette’s
syndrome is often unsatisfactory, although antipsychotic drugs such as haloperidol, pimozide, or risperidone improve tics despite an in deterioration drug-induced general expected functioning. [-3 There is some evidence that trans dermal nicotine may potentiate the therapeutic effects of haloperidol or even that it is effective alone.2 In a clinical trial of transdermal nicotine, one patient with Tourette’s syndrome (DSM-III-R 1987 criteria) had to be excluded because he had mild bronchial asthma (for which he used a salbutamol inhaler) and that was an exclusion criterion in the study. Buspirone is an anxiolytic/antidepressant which is a 5-HTIA partial agonist and a dopamine-D presynaptic terminal autoreceptor antagonist. There is some evidence that animal tic-like movements are blocked by buspirone and that 5-HT receptors may be involved in Tourette’s syndrome.3 We have therefore investigated the effects of buspirone on this patient, a 42-year-old man who had not responded to or tolerated other antipsychotic medications. The Yale global tic severity scale (maximum 50) was used for assessments, which were done from videotaped interviews, blind to medication status.2 Buspirone reduced the Yale score by 70%, and this effect was maintained during the 16 weeks of medication (table). Discontinuation of buspirone for 2 weeks resulted in an exacerbation, which suggests that the improvement had been