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Vasovagal reactions after heart transplantation
Division of C~rdiok~gy Em Angeles, Catiforn~a
refore, noue had any e wever, the two patients
5YlO48
e~t~ve~y~ and normal c I. Krucoff MW, Green CR, Satler LF, et a!. Non-invasive detection of coronary artery patency using continuous ST-segment monitoring. Am I Cardiol 1986;57:916-22. 2. CafiiRM, O’Neill W, Stack RS, et a!. Failure of simpleclinicat measurements to predict perfusion status after intravenous tiuombolysis. Ann fntem Med 3988;3083658-62. 3. Karagounis L, Sorenson S, Menfore RL, Moreno F. Anderson IL. Does thrombolysis in myocardiai infarction (TIMI) perfusion grade 2 represeut a mostly patent or a mostly occluded artery? Enzyma:ic and electrocardiographic evidence form the TEAM-2 study. J Am Co11Cardiol 1992;19:1-10. 4. Gibson MC, Cannon CP, Plana RN, et al. Consequences of TfMf grade 2 vs 3 flow at 90 minutes following thrombulysis [abstnct]. J Am Cob Cardiol 1993;ZfSuppplA:348~. 5. Lincoff AM, Ellis SG. Galeana A, et al. %scoronary artery with TIM grade 2 How “patent”? Outcome in the Tbrombolysis and Angioplasty in Myocardial Infarction {TAMI)trial k&tract]. Circulation 1992;86Suppl 1:8-26-k 6. Kennedy JW, Ritchie J, Davis KB, et al. The Western Washington randomized trial of intracoronary streptokinase in acute myoeardial infarction. N EmglJ Med 39653312: 1073-8. 7. Crines CL, Top01 EJ, Bates RR, et al. Infarct-vessel status after intravenous tissue plasminogen activator and acute coronary angioplasty: prediction of clinical outcome. Am &art J 1988;lEl-7. 8. Vogt A, von Essen R, Tebbe U, Feuerer W, Appel KF. Neuhaus RF. Impact ofearly perfusion status of the infarct-related artery on short term mortality after thrombolysis in acute myucardiaf infarction: retrospective analysis of four German multicenter studies. f Am Call Cardiol 1993;21:l391-5.
vation. Thus, our findings confirm those of ~~tz~a~~~~et al., demo~st~ti~g that vasodepressor reactions can occur after transting that left ventricular vagai tors of this responsein humans. of vagal rei~~e~atio~ with
tiarn.
Regional Cardiorhoracic Cenentre Freeman Hospiral Newcastle upon Tyne NE7 7DN, England. hired
Althoughthere have been isolated repotis of so-called vasovagal syncope after heart transplantation,the report by Fitzpatricket ali. (1) provides the fust systematic evidence that ?~~sp~antrecipients remain susceptible to ortbostatic stress. The authors imply on the nction testing that this may result from wagal 0 patientsbut failed to explain the mechanism in 4 of fO on this basis. Although there is good evidence for sympatheticreinnervation after transplantation(L&3),the evidence for vagalreinnervationwas previouslylimited.The authorspropose vagal reinnervation on the basis of two observations: 1) partial normalizationof donor heart rate responseto vagalimaneuvers,and 2) donor bradycardia during vasodepressorreactions. head-uptilt-inducedvasodepressorreactions28 f er transplantation in 6 of 17 long-term transplant ding 2 with donor bradycardia. Assessment of reinnervation status was performed in all patients, and included measurementof heart rate responseto deep breathing,the VaEsalva maneuver, exercise testing and injectionof tyramine into the coronary artery supplyingthe sinus node. Parasympathetictesting was performed with an esophagealelectrode in situ to detect recipient atrial activity, and electrocardiogramswere recorded speed of 100mrnls, ahowingPP intervals to be measure 25 ms and therefore heart rate variation to be calculatedto within 2 beatslminat heart rates of sMO beats/mm. Valsalvaratios were calculatedas the ratio of the donor PP interval at the time of the
Kingdom
1. Fitzpatrick AP. Banner N, Cheng A. Yacouh hf. Sutton R. Vasovagaf reactions may occur after onhotopic heart transplantation. J Am Coil Cardiol 1993:21:1132-7. 2. Schwaiger M. Hutchins GD, Kafff V. et al. Evidence for regional catecbohmine uptake and storage sites in the transplanted heart by positron emission tomography. 5 C.io Invert 1991;~?z1681-!%
3. Wilson RF, Christensen BV. Ohari MT. Simon A, White CW, Laxson QD. Evidence far structural sympathetic reinnervation after orthotopic cardiac transpfantatioa in humans. Circulation 1991:83:1210-20. 4. Ewing DJ. Clarke BF. Diagnosis and management of diabetic autonomic ncumpathy. Br Med I 1982;285:916-8. 5. W&in BG. Sundbf G. Sympathetic outflow to muscles during wasovagal syucope. J Auton Nerv Syst 1982;6:287-91.
Rumbergeret al. (I) provide left ventricular mass and v However, their implication after anterior infarctionwit dial mass represents the natural history of the healing process disregardsa possiblerole of therapy. Theypoint out that most of patient:; in the study were receiving beta-adrenoceptor b~~~~g agents and nitrates. These agents may sfgnihcant~~ inhibit myo~ardial hypertrophy (2-4). We agree that there are relatively few data
refore, noue had any e wever, the two patients
5YlO48
e~t~ve~y~ and normal c I. Krucoff MW, Green CR, Satler LF, et a!. Non-invasive detection of coronary artery patency using continuous ST-segment monitoring. Am I Cardiol 1986;57:916-22. 2. CafiiRM, O’Neill W, Stack RS, et a!. Failure of simpleclinicat measurements to predict perfusion status after intravenous tiuombolysis. Ann fntem Med 3988;3083658-62. 3. Karagounis L, Sorenson S, Menfore RL, Moreno F. Anderson IL. Does thrombolysis in myocardiai infarction (TIMI) perfusion grade 2 represeut a mostly patent or a mostly occluded artery? Enzyma:ic and electrocardiographic evidence form the TEAM-2 study. J Am Co11Cardiol 1992;19:1-10. 4. Gibson MC, Cannon CP, Plana RN, et al. Consequences of TfMf grade 2 vs 3 flow at 90 minutes following thrombulysis [abstnct]. J Am Cob Cardiol 1993;ZfSuppplA:348~. 5. Lincoff AM, Ellis SG. Galeana A, et al. %scoronary artery with TIM grade 2 How “patent”? Outcome in the Tbrombolysis and Angioplasty in Myocardial Infarction {TAMI)trial k&tract]. Circulation 1992;86Suppl 1:8-26-k 6. Kennedy JW, Ritchie J, Davis KB, et al. The Western Washington randomized trial of intracoronary streptokinase in acute myoeardial infarction. N EmglJ Med 39653312: 1073-8. 7. Crines CL, Top01 EJ, Bates RR, et al. Infarct-vessel status after intravenous tissue plasminogen activator and acute coronary angioplasty: prediction of clinical outcome. Am &art J 1988;lEl-7. 8. Vogt A, von Essen R, Tebbe U, Feuerer W, Appel KF. Neuhaus RF. Impact ofearly perfusion status of the infarct-related artery on short term mortality after thrombolysis in acute myucardiaf infarction: retrospective analysis of four German multicenter studies. f Am Call Cardiol 1993;21:l391-5.
vation. Thus, our findings confirm those of ~~tz~a~~~~et al., demo~st~ti~g that vasodepressor reactions can occur after transting that left ventricular vagai tors of this responsein humans. of vagal rei~~e~atio~ with
tiarn.
Regional Cardiorhoracic Cenentre Freeman Hospiral Newcastle upon Tyne NE7 7DN, England. hired
Althoughthere have been isolated repotis of so-called vasovagal syncope after heart transplantation,the report by Fitzpatricket ali. (1) provides the fust systematic evidence that ?~~sp~antrecipients remain susceptible to ortbostatic stress. The authors imply on the nction testing that this may result from wagal 0 patientsbut failed to explain the mechanism in 4 of fO on this basis. Although there is good evidence for sympatheticreinnervation after transplantation(L&3),the evidence for vagalreinnervationwas previouslylimited.The authorspropose vagal reinnervation on the basis of two observations: 1) partial normalizationof donor heart rate responseto vagalimaneuvers,and 2) donor bradycardia during vasodepressorreactions. head-uptilt-inducedvasodepressorreactions28 f er transplantation in 6 of 17 long-term transplant ding 2 with donor bradycardia. Assessment of reinnervation status was performed in all patients, and included measurementof heart rate responseto deep breathing,the VaEsalva maneuver, exercise testing and injectionof tyramine into the coronary artery supplyingthe sinus node. Parasympathetictesting was performed with an esophagealelectrode in situ to detect recipient atrial activity, and electrocardiogramswere recorded speed of 100mrnls, ahowingPP intervals to be measure 25 ms and therefore heart rate variation to be calculatedto within 2 beatslminat heart rates of sMO beats/mm. Valsalvaratios were calculatedas the ratio of the donor PP interval at the time of the
Kingdom
1. Fitzpatrick AP. Banner N, Cheng A. Yacouh hf. Sutton R. Vasovagaf reactions may occur after onhotopic heart transplantation. J Am Coil Cardiol 1993:21:1132-7. 2. Schwaiger M. Hutchins GD, Kafff V. et al. Evidence for regional catecbohmine uptake and storage sites in the transplanted heart by positron emission tomography. 5 C.io Invert 1991;~?z1681-!%
3. Wilson RF, Christensen BV. Ohari MT. Simon A, White CW, Laxson QD. Evidence far structural sympathetic reinnervation after orthotopic cardiac transpfantatioa in humans. Circulation 1991:83:1210-20. 4. Ewing DJ. Clarke BF. Diagnosis and management of diabetic autonomic ncumpathy. Br Med I 1982;285:916-8. 5. W&in BG. Sundbf G. Sympathetic outflow to muscles during wasovagal syucope. J Auton Nerv Syst 1982;6:287-91.
Rumbergeret al. (I) provide left ventricular mass and v However, their implication after anterior infarctionwit dial mass represents the natural history of the healing process disregardsa possiblerole of therapy. Theypoint out that most of patient:; in the study were receiving beta-adrenoceptor b~~~~g agents and nitrates. These agents may sfgnihcant~~ inhibit myo~ardial hypertrophy (2-4). We agree that there are relatively few data