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Hyperventilation-induced coronary vasospasm refractory to intracoronary nitroglycerin
Volume 119
Number
Brief Communications
4
957
Fig. 2. Right coronary arteriography demonstrating coronary ectasia and (A) large clot at 48 hours (ar-
rows), (B) significant resolution of clot at day 7 (arrows), and (C) complete resolution on day 40.
pirin, and subsequent oral anticoagulation resulted in complete resolution of this thrombus. A similar case report has demonstrated reperfusion with intracoronary streptokinase. 1~ Aspirin therapy has been effective in preventing thrombosis in coronary aneurysms in children with Kawasaki disease 11 and may be useful in patients with asymptomatic coronary artery ectasia.
ectasia:incidence and results of coronary bypass surgery. AM HEARTJ 1978;96:309-15. 10. Theron HD, Kleynhans PH, Marx JD, Marks DS. Successful coronary reperfusion with intracoronary streptokinase in a patient with coronary ectasia. S Afr Med J 1987;72:502-3. 11. Kato H, Kolke S, Yokoyama T. Kawasaki disease:effect of treatment on coronary artery involvement. Pediatrics 1979; 63:175-9.
REFERENCES
HyperventUation-induced coronary vasospasm refractory to intracoronary nitroglycerin
1. Vermani R, Robinowitz M, Atkinson JB, Forman MB, Silver MD, McAllister HA. Acquired coronary arterial aneurysms. Hum Pathol 1986;17:575-83. 2. Markis JE, Joffe CD, Cohn PF, Feen DJ, Hermon MJ, Gorlin R. Clinical significance of coronary arterial ectasia. Am J Cardiol 1976;37:217-22. 3. Hartnell GG, Parnell BM, Pride RB. Coronary artery ectasia. Its prevalence and significance in 4,993 patients. Br Heart J 1985;54:392-5. 4. Swaye PS, Fisher LD, Litwin P. Aneurysmal coronary artery disease. Circulation 1983;67:134-8. 5. Daoud AS, Pankin D, Tulgan H, Florentin RA. Aneurysms of the coronary artery--report of ten cases and review of the literature. Am J Cardiol 1963;11:228-37. 6. Munro J, Cotran RS. The pathogenesis of atherosclerosis: atherogenesis and inflammation. Lab Invest 1988;58:249-61. 7. Badimon L, Badimon JJ, Galvez A, Chesebro JH, Fuster V. Influence of arterial damage and wall shear rate on platelet deposition. Arteriosclerosis 1986;6:312-20. 8. Bove AA, Vlietstra RD. Spasm in ectatic coronary arteries. Mayo Clin Proc 1985;60:822-6. 9. Aintablian A, Hamby RK, Hoffman I, Kramer RJ. Coronary
Stefano Ghio, MD, Luigi Angoli, MD, Ezio Bramucci, MD, Stefano de Servi, MD, and Giuseppe Specchia, MD. Pavia, Italy
In 1980 Buxton et al. 1 described five patients who had ergonovine-induced coronary vasospasm refractory to sublingual or intravenous nitrogliceryn; direct intracoronary administration of the d r u g was recommended by the From the Divisionedi Cardiologia,PoliclinicoS. Matteo. Reprintrequests: StefanoGhio,MD, Divisionedi Cardiologia,PoliclinicoS. Matteo, 27100-Pavia,Italy. 4/4/18634
958
Brie[ Communications
April 1990 ]
A m e r i c a n Heart J o . . . .
Fig. 1. Left coronary artery in control conditions (A), 3 minutes after hyperventilation (B), after nitroglycerin infusion (C), and after successful PTCA (D). Arrows indicate the proximal LAD stenosis.
authors for the resolution of vasospasm. We have observed a case in which intracoronary nitroglycerin failed to reverse, or even worsened, hyperventilation-induced vasospasm. An emergency percutaneous angioplasty (PTCA) was necessary to restore anterograde blood flow. R.M. is a 42-year-old man who came under observation for stable effort angina after having suffered from an anterior non-Q wave myocardial infarction. Angiography revealed normal left ventricular function (ejection fraction --- 0.62) and a single 90% stenosis of the proximal left anterior descending artery (LAD). PTCA was performed with a good angiographic result. The patient remained symptom-free for 3 months, but then chest pain appeared again during moderate to strenuous exertion. Coronary angiography now revealed a 90 % constricted long and concentric lesion of the LAD at the site of the dilated lesion (Fig. 1, A). A hyperventilation test was performed in the catheterization laboratory after routine examination; 3 minutes after the end of the test the patient complained of chest discomfort, and ST segment elevation appeared in leads V1 to V4 (Fig. 2, B). Control coronary angiography showed a subtotal narrowing of the LAD (Fig. 1, B) with very slow distal run-off. Intracoronary nitroglycerin was administered (350 #g in rapid infusion) and was then repeated at a similar dosage after a few minutes. ST segment elevation was reduced (Fig. 2, C) but left coronary angiography still revealed complete occlusion of the LAD
despite marked dilation of all other segments of the left coronary artery (Fig. 1, C); right coronary angiography showed a good collateral circulation toward the LAD that was not present under control conditions (Fig. 3). Intracoronary administration of urokinase (300,000 international units)failed to reopen the vessel. Twenty minutes after the beginning of the episode, an emergency PTCA was attempted and the procedure proved successful (Fig. 1, D). Chest pain, ST segment elevation, and collateral circulation from the right coronary artery promptly disappeared with restoration of anterograde flow through the LAD artery. Previously published studies 2, 3 uniformly report the safety of the hyperventilation test and the rapid reversibility of spasm after the administration of nitrates; to our knowledge, no cases of refractory vasospasm induced by this test have been described. The possibility that the peculiar histologic characteristics of restenosis 4 might have been the cause of the hyperresponsiveness of the lesion to the vasoconstrictive stimulus cannot be excluded; however, no data in the literature substantiate this hypothesis. The observation of complete occlusion of the vessel immediately after the administration of nitroglycerin raises questions concerning the effect of intracoronary nitroglycerin in our patient. Experimental studies have demonstrated that compliant stenosis may increase in severity when vasodilation produces a pressure drop in the distal artery segment.
V o l u m e 119
Number 4
Brie/Communications
Fig. 2. Precordial leads V2, V3, and V4 in control conditions (A), 3 minutes after hyperventilation (B), after nitroglycerin infusion (C), and after successful PTCA (D).
Fig. 3. Right coronary artery in control conditions (A), during LAD occlusion showing collateral circulation toward the LAD (arrows) (B), and after PTCA (C).
959
960
April 1990 American Heart Journal
Brief Communications
Such mechanisms have been suspected to be operative in man also. 5 It is possible t h a t the vasodilation induced by the intracoronary injection of nitroglycerin (at the relatively high dosage we used) might have produced a pressure drop in the distal LAD artery facilitating the persistence of vasocostriction at the proximal LAD level. Finally, the possibility has to be considered t h a t clot formation superimposed upon the hyperventilation-induced vasospasm might have been the cause of the prolonged occlusion of the artery. Failure to reopen the vessel with the lytic t h e r a p y is not definitive evidence against thrombotic occlusion, and a case of coronary thrombosis following hyperventilation has previously been reportedfi
II
V4 200 mmHg
REFERENCES
1. Buxton A, Goldberg S, Hirshfeld JW, Wilson J, Mann T, Williams DO, Overlie P, Oliva P. Refractory ergonovineinduced coronary vasospasrn: importance of intracoronary nitroclycerin. Am J Cardiol 1980;46:329-34. 2. Yasue H, Nagao M, Omote S, Takirawa A, Miwa K, Tanaka S. Coronary arterial spasm and Prinzmetal's variant form of angina induced by hyperventilation and tris buffer infusion. Circulation 1978;58:56-62. 3. Girotti LA, Crosatto JR, Messuti H, Kaski JC, Dyszel E, Rivas CA, Araujo LI, Vetulli H, Rosenbaum MB. The hyperventilation test as a method for developing successful therapy in Prinzmetal's angina. Am J Cardiol 1982;49:834-41. 4. Chesebro JH, Lam JYT, Badimon L, Fuster V. Restenosis after arterial angioplasty: a hemorrheologic response to injury. Am J Cardiol 1987;60:10B-16B. 5. Bove A, Wliestra RE. Paradoxical angina after nitroglycerin. Another variant. N Engl d Med 1982;306:484-5. 6. Wright CM, Engler R, Maisel A. Coronary thrombosis precipitated by hyperventilation-induced vasospasm. AM HEART J 1988;116:867-9.
Transient pulsus alternans during acute myocardial ischemia and its resolution following/~-adrenergic blockade Michael C. Giudici, MD, and Michael P. Savage, MD.
Philadelphia, Pa.
Pulsus alternans is a pulse p a t t e r n characterized by a regular r h y t h m in which there is alternating attenuation of the height of systolic arterial pressure. 1 This phenomenon is usually observed in the setting of severe left ventricular dysfunction a n d / o r critical aortic stenosis. In this report, we describe a p a t i e n t who developed transient pulsus alternans during acute myocardial ischemia that p r o m p t l y resolved after intravenous fl:adrenergic blockade and sublingual nitroglycerin. From the Division of Cardiology, Department of Medicine, Thomas Jefferson University Hospital. Reprint requests: Michael P. Savage, MD, Cardiac Catheterization Laboratory, Room 5611-D, N.H., Thomas Jefferson University Hospital, 111 S. l l t h Street, Philadelphia, PA 19107. 4/4/18660
0 Fig. 1. Baseline electrocardiographic and hemodynamic recordings. Simultaneous left ventricular and central arterial pressures demonstrate a 55 m m Hg peak-to-peak systolic gradient across the aortic valve.
W.R. is a 77-year-old white m a n with a 20-year history of a heart murmur. In the month prior to admission, he developed episodic dyspnea, angina, and syncope during exertion. There were no symptoms at rest. Physical examination revealed a regular pulse at 80 beats/min and blood pressure of 150/64 m m Hg. There was no jugular venous distention. Carotid upstokes were normal. The lungs were clear. Cardiac examination d e m o n s t r a t e d a laterally displaced left ventricular apical impulse, an absent A2, and an $4 gallop. A grade I I I / V I late peaking, systolic ejection m u r m u r was present throughout the precordium and radiated to the neck. Electrocardiography revealed normal sinus rhythm, left ventricular hypertrophy, and an ageindeterminate diaphragmatic myocardial infarction. Echocardiography demonstrated left ventricular hypertrop h y and mild dilatation with anterior and apical hypokinesis. The aortic valve leaflets were severely thickened and restricted in motion. Fig. I shows the baseline/eft ventricular and central arterial pressures at the time of cardiac catheterization. Aortic pressure was 150/90 mm Hg and left ventricular pressure was 205/15 m m Hg. Using the Gorlin equation, the calculated aortic valve area was 0.6 cm 2. Cardiac output and cardiac index were 4.5 L/min and 2.6 L / m i n / m 2, respectively, by the Fick method. Left ventriculography was not performed. Coronary arteriography re-
Number
Brief Communications
4
957
Fig. 2. Right coronary arteriography demonstrating coronary ectasia and (A) large clot at 48 hours (ar-
rows), (B) significant resolution of clot at day 7 (arrows), and (C) complete resolution on day 40.
pirin, and subsequent oral anticoagulation resulted in complete resolution of this thrombus. A similar case report has demonstrated reperfusion with intracoronary streptokinase. 1~ Aspirin therapy has been effective in preventing thrombosis in coronary aneurysms in children with Kawasaki disease 11 and may be useful in patients with asymptomatic coronary artery ectasia.
ectasia:incidence and results of coronary bypass surgery. AM HEARTJ 1978;96:309-15. 10. Theron HD, Kleynhans PH, Marx JD, Marks DS. Successful coronary reperfusion with intracoronary streptokinase in a patient with coronary ectasia. S Afr Med J 1987;72:502-3. 11. Kato H, Kolke S, Yokoyama T. Kawasaki disease:effect of treatment on coronary artery involvement. Pediatrics 1979; 63:175-9.
REFERENCES
HyperventUation-induced coronary vasospasm refractory to intracoronary nitroglycerin
1. Vermani R, Robinowitz M, Atkinson JB, Forman MB, Silver MD, McAllister HA. Acquired coronary arterial aneurysms. Hum Pathol 1986;17:575-83. 2. Markis JE, Joffe CD, Cohn PF, Feen DJ, Hermon MJ, Gorlin R. Clinical significance of coronary arterial ectasia. Am J Cardiol 1976;37:217-22. 3. Hartnell GG, Parnell BM, Pride RB. Coronary artery ectasia. Its prevalence and significance in 4,993 patients. Br Heart J 1985;54:392-5. 4. Swaye PS, Fisher LD, Litwin P. Aneurysmal coronary artery disease. Circulation 1983;67:134-8. 5. Daoud AS, Pankin D, Tulgan H, Florentin RA. Aneurysms of the coronary artery--report of ten cases and review of the literature. Am J Cardiol 1963;11:228-37. 6. Munro J, Cotran RS. The pathogenesis of atherosclerosis: atherogenesis and inflammation. Lab Invest 1988;58:249-61. 7. Badimon L, Badimon JJ, Galvez A, Chesebro JH, Fuster V. Influence of arterial damage and wall shear rate on platelet deposition. Arteriosclerosis 1986;6:312-20. 8. Bove AA, Vlietstra RD. Spasm in ectatic coronary arteries. Mayo Clin Proc 1985;60:822-6. 9. Aintablian A, Hamby RK, Hoffman I, Kramer RJ. Coronary
Stefano Ghio, MD, Luigi Angoli, MD, Ezio Bramucci, MD, Stefano de Servi, MD, and Giuseppe Specchia, MD. Pavia, Italy
In 1980 Buxton et al. 1 described five patients who had ergonovine-induced coronary vasospasm refractory to sublingual or intravenous nitrogliceryn; direct intracoronary administration of the d r u g was recommended by the From the Divisionedi Cardiologia,PoliclinicoS. Matteo. Reprintrequests: StefanoGhio,MD, Divisionedi Cardiologia,PoliclinicoS. Matteo, 27100-Pavia,Italy. 4/4/18634
958
Brie[ Communications
April 1990 ]
A m e r i c a n Heart J o . . . .
Fig. 1. Left coronary artery in control conditions (A), 3 minutes after hyperventilation (B), after nitroglycerin infusion (C), and after successful PTCA (D). Arrows indicate the proximal LAD stenosis.
authors for the resolution of vasospasm. We have observed a case in which intracoronary nitroglycerin failed to reverse, or even worsened, hyperventilation-induced vasospasm. An emergency percutaneous angioplasty (PTCA) was necessary to restore anterograde blood flow. R.M. is a 42-year-old man who came under observation for stable effort angina after having suffered from an anterior non-Q wave myocardial infarction. Angiography revealed normal left ventricular function (ejection fraction --- 0.62) and a single 90% stenosis of the proximal left anterior descending artery (LAD). PTCA was performed with a good angiographic result. The patient remained symptom-free for 3 months, but then chest pain appeared again during moderate to strenuous exertion. Coronary angiography now revealed a 90 % constricted long and concentric lesion of the LAD at the site of the dilated lesion (Fig. 1, A). A hyperventilation test was performed in the catheterization laboratory after routine examination; 3 minutes after the end of the test the patient complained of chest discomfort, and ST segment elevation appeared in leads V1 to V4 (Fig. 2, B). Control coronary angiography showed a subtotal narrowing of the LAD (Fig. 1, B) with very slow distal run-off. Intracoronary nitroglycerin was administered (350 #g in rapid infusion) and was then repeated at a similar dosage after a few minutes. ST segment elevation was reduced (Fig. 2, C) but left coronary angiography still revealed complete occlusion of the LAD
despite marked dilation of all other segments of the left coronary artery (Fig. 1, C); right coronary angiography showed a good collateral circulation toward the LAD that was not present under control conditions (Fig. 3). Intracoronary administration of urokinase (300,000 international units)failed to reopen the vessel. Twenty minutes after the beginning of the episode, an emergency PTCA was attempted and the procedure proved successful (Fig. 1, D). Chest pain, ST segment elevation, and collateral circulation from the right coronary artery promptly disappeared with restoration of anterograde flow through the LAD artery. Previously published studies 2, 3 uniformly report the safety of the hyperventilation test and the rapid reversibility of spasm after the administration of nitrates; to our knowledge, no cases of refractory vasospasm induced by this test have been described. The possibility that the peculiar histologic characteristics of restenosis 4 might have been the cause of the hyperresponsiveness of the lesion to the vasoconstrictive stimulus cannot be excluded; however, no data in the literature substantiate this hypothesis. The observation of complete occlusion of the vessel immediately after the administration of nitroglycerin raises questions concerning the effect of intracoronary nitroglycerin in our patient. Experimental studies have demonstrated that compliant stenosis may increase in severity when vasodilation produces a pressure drop in the distal artery segment.
V o l u m e 119
Number 4
Brie/Communications
Fig. 2. Precordial leads V2, V3, and V4 in control conditions (A), 3 minutes after hyperventilation (B), after nitroglycerin infusion (C), and after successful PTCA (D).
Fig. 3. Right coronary artery in control conditions (A), during LAD occlusion showing collateral circulation toward the LAD (arrows) (B), and after PTCA (C).
959
960
April 1990 American Heart Journal
Brief Communications
Such mechanisms have been suspected to be operative in man also. 5 It is possible t h a t the vasodilation induced by the intracoronary injection of nitroglycerin (at the relatively high dosage we used) might have produced a pressure drop in the distal LAD artery facilitating the persistence of vasocostriction at the proximal LAD level. Finally, the possibility has to be considered t h a t clot formation superimposed upon the hyperventilation-induced vasospasm might have been the cause of the prolonged occlusion of the artery. Failure to reopen the vessel with the lytic t h e r a p y is not definitive evidence against thrombotic occlusion, and a case of coronary thrombosis following hyperventilation has previously been reportedfi
II
V4 200 mmHg
REFERENCES
1. Buxton A, Goldberg S, Hirshfeld JW, Wilson J, Mann T, Williams DO, Overlie P, Oliva P. Refractory ergonovineinduced coronary vasospasrn: importance of intracoronary nitroclycerin. Am J Cardiol 1980;46:329-34. 2. Yasue H, Nagao M, Omote S, Takirawa A, Miwa K, Tanaka S. Coronary arterial spasm and Prinzmetal's variant form of angina induced by hyperventilation and tris buffer infusion. Circulation 1978;58:56-62. 3. Girotti LA, Crosatto JR, Messuti H, Kaski JC, Dyszel E, Rivas CA, Araujo LI, Vetulli H, Rosenbaum MB. The hyperventilation test as a method for developing successful therapy in Prinzmetal's angina. Am J Cardiol 1982;49:834-41. 4. Chesebro JH, Lam JYT, Badimon L, Fuster V. Restenosis after arterial angioplasty: a hemorrheologic response to injury. Am J Cardiol 1987;60:10B-16B. 5. Bove A, Wliestra RE. Paradoxical angina after nitroglycerin. Another variant. N Engl d Med 1982;306:484-5. 6. Wright CM, Engler R, Maisel A. Coronary thrombosis precipitated by hyperventilation-induced vasospasm. AM HEART J 1988;116:867-9.
Transient pulsus alternans during acute myocardial ischemia and its resolution following/~-adrenergic blockade Michael C. Giudici, MD, and Michael P. Savage, MD.
Philadelphia, Pa.
Pulsus alternans is a pulse p a t t e r n characterized by a regular r h y t h m in which there is alternating attenuation of the height of systolic arterial pressure. 1 This phenomenon is usually observed in the setting of severe left ventricular dysfunction a n d / o r critical aortic stenosis. In this report, we describe a p a t i e n t who developed transient pulsus alternans during acute myocardial ischemia that p r o m p t l y resolved after intravenous fl:adrenergic blockade and sublingual nitroglycerin. From the Division of Cardiology, Department of Medicine, Thomas Jefferson University Hospital. Reprint requests: Michael P. Savage, MD, Cardiac Catheterization Laboratory, Room 5611-D, N.H., Thomas Jefferson University Hospital, 111 S. l l t h Street, Philadelphia, PA 19107. 4/4/18660
0 Fig. 1. Baseline electrocardiographic and hemodynamic recordings. Simultaneous left ventricular and central arterial pressures demonstrate a 55 m m Hg peak-to-peak systolic gradient across the aortic valve.
W.R. is a 77-year-old white m a n with a 20-year history of a heart murmur. In the month prior to admission, he developed episodic dyspnea, angina, and syncope during exertion. There were no symptoms at rest. Physical examination revealed a regular pulse at 80 beats/min and blood pressure of 150/64 m m Hg. There was no jugular venous distention. Carotid upstokes were normal. The lungs were clear. Cardiac examination d e m o n s t r a t e d a laterally displaced left ventricular apical impulse, an absent A2, and an $4 gallop. A grade I I I / V I late peaking, systolic ejection m u r m u r was present throughout the precordium and radiated to the neck. Electrocardiography revealed normal sinus rhythm, left ventricular hypertrophy, and an ageindeterminate diaphragmatic myocardial infarction. Echocardiography demonstrated left ventricular hypertrop h y and mild dilatation with anterior and apical hypokinesis. The aortic valve leaflets were severely thickened and restricted in motion. Fig. I shows the baseline/eft ventricular and central arterial pressures at the time of cardiac catheterization. Aortic pressure was 150/90 mm Hg and left ventricular pressure was 205/15 m m Hg. Using the Gorlin equation, the calculated aortic valve area was 0.6 cm 2. Cardiac output and cardiac index were 4.5 L/min and 2.6 L / m i n / m 2, respectively, by the Fick method. Left ventriculography was not performed. Coronary arteriography re-