Need for Standardization of Tilt-Table Test in Evaluation of syncope
I read with interest the recent article on head-upright tilt-table testing in evaluation of vasovagally mediated syncope by Grubb et a1.l They used the upright tilt-table test for 30 minutes with or without the use of intravenous isoproterenol. Head-upright tilt-table testing has been used for many years to provoke vasovagal syncope in susceptible persons through maximal venous pooling. l-l1 However, the length of tilting has differed widely among the different reports, varying from 5 to 60 minutes (Table I). TABLE I Variations of Duration of Tilting Repotted by Different Authors Authors
Duration
Kenny et al2 (1986) Waxman et al3 (1989) Almquist et al4 (1989) Fitzpatrick & Sutton5 (1989) Strasberg et al6 (1989) Raviele et al7 (1990) Grubbetale(1991) Calkins et aI9 (1991) Braunwaldlo (1992) Kapoor & Brantll (1992) Grubb et al1 (1992)
60 min. 5-15 min. 10 min. 45 min. 60 min. 60 min. 30 min. lo-20 min. 5-10 min. 15 min. 30 min.
Becauseof the possibility of a delayed response to tilting which has been reported,5 a longer duration than 5 to 15 minutes, reported by someinvestigators,3*9J0seemsto be required. In any case, in order to obtain comparable results among various study groups, it is about time that the length of time for tilting be standardized. Tsung0. cheng,MD
dycardia and hypotension by isoprotereno1 and upright posture in patients with unexplained syncope. N Engl J Med 1989; 320:346-351. 5. Fitzpatrick A, Sutton R. Tilting towards a diagnosis in recurrent unexplained syncope. Lancet 1989;1:658-660. 6. Strasberg B, Rechavia E, Sagie A, Kusniec J, Mager A, Sclarovsky S, Agmon J. The bead-up tilt table test in patients with syncope of unknown origin. Am Heart J 1989;118:923-927. 7. Raviele A, Gasparini G, DiPede F, Delise P, Bonso A, Piccolo E. Usefulness of head-up tilt test in evaluating patients with syncope of unknown origin and negative electrophysiologic study. Am J Cardiol 1990;65:1322-1327. 8. Grubb BP, Temesy-Armos P, Hahn H, Elliott L. Utility of upright tilt-table testing in the evaluation and management of syncope of unknown origin. Am J Med 1991;90:6-10. 9. Calkins H, Kadish A, Souza J, Rosenheck S, Morady F. Comparison of responses to isoproterenol and epinephrine during head-up tilt in suspected vasodepressor syncope. Am J Cardiol 1991; 67:207-209. 10. Braunwald E. Heart Disease. A Textbook of Cardiovascular Medicine. 4th ed. Philadelphia: WB Saunders, 1992:883. 11. Kapoor ‘WN, Brant N. Evaluation of syncope by upright tilt testing with isoproterenol. A nonspecific test. Ann Intern Med 1992;116:358-363.
Hemodynamic Effects of Nitroprusside on Valvular Aortic Stenosis
In their carefully performed study, Ikram et al1 showed increasedcardiac output and reduced left ventricular filling pressure in a subgroup of patients with valvular aortic stenosis. This subgroup was Washington,D.C. characterized as having more se10 April 1992 vere aortic stenosis and poorer left ventricular function. They conclude 1. Grubb BP, Temesy-Armos P, Moore J, that “the role of chronic vasodilator Wolfe D, Hahn H, Elliot L. Head-upright therapy should be evaluated in such tilt-table testing in evaluation and management of the malignant vasovagal syn- patients.” A word of caution should be drome. Am J Cardiol 1992;69:904-908. sounded about this conclusion. 2. Kenny RA, Ingram A, Bayliss J, Sutton R. Head-up tilt: a useful test for inves- Whereas nitroprusside is given by tigating unexplained syncope. Lancet infusion and is short-acting, allow1986;1:1352-1354. ing abrupt reduction or cessationof 3. Waxman MB, Yao L, Cameron DA, a vasodilator effect, such a possibilWald RW, Roseman J. Isoproterenol in- ity could not exist with chronic, duction of vasodepressor-type reaction in orally administered therapy. This is vasodepressor-prone persons. Am J Carimportant, becausethere may be a diol 1989;63:58-65. significant hazard from the use of 4. Almquist A, Goldenberg IF, Milstein S, Chen M-Y, Chen X, Hansen R, Gor- vasodilator therapy that the authors have not discussed. nick C, Benditt DG. Provocation of bra-
It has been demonstrated2-5that patients with significant aortic stenosis may have “used up” much of their coronary vascular reserveduring rest. In such patients, transmural myocardial perfusion is dependent on the diastolic coronary filling gradient. A reduction in diastolic blood pressure, coupled with shortening of diastole due to an increase in heart rate, could significantly reduce this index of myocardial perfusion. Although the authors do not report diastolic blood pressure levels, the significant reduction in mean blood pressure would likely be associated with a significant reduction in diastolic blood pressure. Heart rate also increased significantly in their patients. Whereas the demonstrated reduction of left ventricular enddiastolic pressure could favorably affect the coronary filling gradient, the net effect of these changes would need to be assessed. Moreover, a hemodynamic prediction of ischemia in aortic stenosis is possible2by calculation of the ratio of diastolic to systolic pressure time index. The authors’ data would probably allow calculation of such ratios, and it would be of interest to know these findings. On reviewing the details of their patients (presented in Table I), one notices that patient 21 in the Table had a heart rate increase of 48 beats/min, with a decrease of 26 mm Hg in mean blood pressure, an increase of 11 mm Hg in left ventricular systolic pressure, and minimal change of left ventricular end-diastolic pressure after nitroprusside. There was a minimal reduction of an already low cardiac index. It would seem that provocation of significant ischemia by nitroprusside in this patient was possible. Before a study of chronic vasodilator therapy is undertaken, it is necessaryto demonstrate which patients would be at risk of developing myocardial ischemia after achieving vasodilatation. Perhaps a preliminary testing with nitroprusside would allow this, but one has reservations as to whether it would be sufficiently reliable to prevent a possible dangerous consequenceof chronic vasodilator therapy in individual patients. READERS’ COMMENTS
1639
I read with interest the recent article on head-upright tilt-table testing in evaluation of vasovagally mediated syncope by Grubb et a1.l They used the upright tilt-table test for 30 minutes with or without the use of intravenous isoproterenol. Head-upright tilt-table testing has been used for many years to provoke vasovagal syncope in susceptible persons through maximal venous pooling. l-l1 However, the length of tilting has differed widely among the different reports, varying from 5 to 60 minutes (Table I). TABLE I Variations of Duration of Tilting Repotted by Different Authors Authors
Duration
Kenny et al2 (1986) Waxman et al3 (1989) Almquist et al4 (1989) Fitzpatrick & Sutton5 (1989) Strasberg et al6 (1989) Raviele et al7 (1990) Grubbetale(1991) Calkins et aI9 (1991) Braunwaldlo (1992) Kapoor & Brantll (1992) Grubb et al1 (1992)
60 min. 5-15 min. 10 min. 45 min. 60 min. 60 min. 30 min. lo-20 min. 5-10 min. 15 min. 30 min.
Becauseof the possibility of a delayed response to tilting which has been reported,5 a longer duration than 5 to 15 minutes, reported by someinvestigators,3*9J0seemsto be required. In any case, in order to obtain comparable results among various study groups, it is about time that the length of time for tilting be standardized. Tsung0. cheng,MD
dycardia and hypotension by isoprotereno1 and upright posture in patients with unexplained syncope. N Engl J Med 1989; 320:346-351. 5. Fitzpatrick A, Sutton R. Tilting towards a diagnosis in recurrent unexplained syncope. Lancet 1989;1:658-660. 6. Strasberg B, Rechavia E, Sagie A, Kusniec J, Mager A, Sclarovsky S, Agmon J. The bead-up tilt table test in patients with syncope of unknown origin. Am Heart J 1989;118:923-927. 7. Raviele A, Gasparini G, DiPede F, Delise P, Bonso A, Piccolo E. Usefulness of head-up tilt test in evaluating patients with syncope of unknown origin and negative electrophysiologic study. Am J Cardiol 1990;65:1322-1327. 8. Grubb BP, Temesy-Armos P, Hahn H, Elliott L. Utility of upright tilt-table testing in the evaluation and management of syncope of unknown origin. Am J Med 1991;90:6-10. 9. Calkins H, Kadish A, Souza J, Rosenheck S, Morady F. Comparison of responses to isoproterenol and epinephrine during head-up tilt in suspected vasodepressor syncope. Am J Cardiol 1991; 67:207-209. 10. Braunwald E. Heart Disease. A Textbook of Cardiovascular Medicine. 4th ed. Philadelphia: WB Saunders, 1992:883. 11. Kapoor ‘WN, Brant N. Evaluation of syncope by upright tilt testing with isoproterenol. A nonspecific test. Ann Intern Med 1992;116:358-363.
Hemodynamic Effects of Nitroprusside on Valvular Aortic Stenosis
In their carefully performed study, Ikram et al1 showed increasedcardiac output and reduced left ventricular filling pressure in a subgroup of patients with valvular aortic stenosis. This subgroup was Washington,D.C. characterized as having more se10 April 1992 vere aortic stenosis and poorer left ventricular function. They conclude 1. Grubb BP, Temesy-Armos P, Moore J, that “the role of chronic vasodilator Wolfe D, Hahn H, Elliot L. Head-upright therapy should be evaluated in such tilt-table testing in evaluation and management of the malignant vasovagal syn- patients.” A word of caution should be drome. Am J Cardiol 1992;69:904-908. sounded about this conclusion. 2. Kenny RA, Ingram A, Bayliss J, Sutton R. Head-up tilt: a useful test for inves- Whereas nitroprusside is given by tigating unexplained syncope. Lancet infusion and is short-acting, allow1986;1:1352-1354. ing abrupt reduction or cessationof 3. Waxman MB, Yao L, Cameron DA, a vasodilator effect, such a possibilWald RW, Roseman J. Isoproterenol in- ity could not exist with chronic, duction of vasodepressor-type reaction in orally administered therapy. This is vasodepressor-prone persons. Am J Carimportant, becausethere may be a diol 1989;63:58-65. significant hazard from the use of 4. Almquist A, Goldenberg IF, Milstein S, Chen M-Y, Chen X, Hansen R, Gor- vasodilator therapy that the authors have not discussed. nick C, Benditt DG. Provocation of bra-
It has been demonstrated2-5that patients with significant aortic stenosis may have “used up” much of their coronary vascular reserveduring rest. In such patients, transmural myocardial perfusion is dependent on the diastolic coronary filling gradient. A reduction in diastolic blood pressure, coupled with shortening of diastole due to an increase in heart rate, could significantly reduce this index of myocardial perfusion. Although the authors do not report diastolic blood pressure levels, the significant reduction in mean blood pressure would likely be associated with a significant reduction in diastolic blood pressure. Heart rate also increased significantly in their patients. Whereas the demonstrated reduction of left ventricular enddiastolic pressure could favorably affect the coronary filling gradient, the net effect of these changes would need to be assessed. Moreover, a hemodynamic prediction of ischemia in aortic stenosis is possible2by calculation of the ratio of diastolic to systolic pressure time index. The authors’ data would probably allow calculation of such ratios, and it would be of interest to know these findings. On reviewing the details of their patients (presented in Table I), one notices that patient 21 in the Table had a heart rate increase of 48 beats/min, with a decrease of 26 mm Hg in mean blood pressure, an increase of 11 mm Hg in left ventricular systolic pressure, and minimal change of left ventricular end-diastolic pressure after nitroprusside. There was a minimal reduction of an already low cardiac index. It would seem that provocation of significant ischemia by nitroprusside in this patient was possible. Before a study of chronic vasodilator therapy is undertaken, it is necessaryto demonstrate which patients would be at risk of developing myocardial ischemia after achieving vasodilatation. Perhaps a preliminary testing with nitroprusside would allow this, but one has reservations as to whether it would be sufficiently reliable to prevent a possible dangerous consequenceof chronic vasodilator therapy in individual patients. READERS’ COMMENTS
1639
