- Email: [email protected]
Spontaneous coronary artery dissection in a pregnant woman
Spontaneous Coronary Artery Dissection in a Pregnant Woman Ronald S. McKechnie, MD, Devang Patel, MD, Daniel T. Eitzman, MD, Sanjay Rajagopalan, MD, and Thippeswamy H. Murthy, MD Division of Cardiology, Department of Internal Medicine, University of Michigan Hospitals, Ann Arbor, Michigan
BACKGROUND: Spontaneous coronary dissection is a rare condition occurring more often in women, with a higher frequency during the peripartum period. No specific etiology has been defined to describe this uncommon, yet often fatal phenomenon. CASE: A young woman presented at 36 weeks of a noncomplicated pregnancy with recent onset of diaphoresis, dyspnea, and tingling substernal chest discomfort. Upon evaluation, she developed cardiovascular collapse and ventricular fibrillation requiring aggressive resuscitative measures, eventually leading to extracorporeal membrane oxygenation. Right coronary artery dissection was ultimately diagnosed and treated with intracoronary angioplasty and stent placement. CONCLUSION: Spontaneous coronary dissection must be considered when evaluating a patient with a similar clinical presentation, given its overall mortality of more than 50% at presentation, particularly in the peripartum period. (Obstet Gynecol 2001;98:899 –902. © 2001 by the American College of Obstetricians and Gynecologists.)
Spontaneous coronary dissection is a rare condition occurring more often in women, with a higher frequency during the peripartum or postpartum period. Clinical presentation usually appears with sudden collapse and death or with a severe ischemic syndrome. CASE A young gravid woman presented at 36 weeks of a noncomplicated pregnancy with recent onset of diaphoresis, dyspnea, and tingling substernal chest discomfort radiating to both arms. The patient had no risk factors for coronary artery disease, family history of sudden death, or any other systemic illnesses. Upon Address reprint requests to: Thippeswamy H. Murthy, MD, Section of Cardiology, Washington Hospital Center, 110 Irving Street NW, Room 1094, Washington, DC 20010-2975; E-mail: thippeswamy. [email protected].
initial evaluation, she developed a tonic-clonic seizure with subsequent onset of hemodynamic collapse requiring emergent cesarean delivery. Immediate cardiovascular monitoring revealed ventricular fibrillation, and resuscitation efforts were performed including antiarrhythmic medications, multiple defibrillatory shocks, and catecholamine support without significant improvement. Rescue implementation of extracorporeal membrane oxygenation (ECMO) was initiated for cardiopulmonary support. Electrocardiogram (Figure 1) and transesophageal echocardiogram revealed evidence of inferoposterior and lateral infarction with diminished overall left ventricular function with an ejection fraction of less than 10%. After hemodynamic stabilization with ECMO, emergent cardiac catheterization revealed proximal dissection of the right coronary artery (Figure 2). Angioplasty and six consecutive, intracoronary stents were placed, resulting in normal coronary flow within the right coronary artery (Figure 3). Subsequent removal of ECMO support was achieved 3 days later, and repeat echocardiogram upon hospital discharge revealed an improved left ventricular function at 40 – 45% with persistent akinetic inferoposterior segments. Both the patient and child were ultimately discharged alive and well from the hospital approximately 2 weeks later.
COMMENT Primary dissection of a coronary artery during pregnancy or the puerperium is a rare, yet potentially fatal entity in otherwise healthy individuals. Since the first case of pregnancy-related dissection was reported in 1931, recent review of the medical literature suggests a mean age of 33, mean parity of 2.7, and mean time span to event of 20 days postpartum in 31 additional patients.1,2 Given its overall mortality of more than 50% at presentation, this diagnosis must be considered when evaluating a patient with a similar clinical presentation, especially given the good prognosis (85%) in those patients surviving the acute event.3 Early coronary angiography should be performed to aid in the choice of immediate medical or surgical intervention. Coronary dissection involves the left anterior descending artery in approximately 80% of cases and the right coronary artery in most others.4 However, the etiology of spontaneous coronary dissection in gravid patients remains unclear. Furthermore, no coronary risk factors or connective tissue disorders have been identified as independent risk factors for dissection. Theories regarding the etiology include a pregnancyinduced degeneration of collagen in conjunction with the
VOL. 98, NO. 5, PART 2, NOVEMBER 2001 © 2001 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
0029-7844/01/$20.00 PII S0029-7844(01)01563-0
899
Figure 1. Twelve lead electrocardiogram showing 3– 4 mm of ST segment elevation in leads II, III, aVF, and V6 with Q waves consistent with acute inferolateral myocardial infarction. McKechnie. Spontaneous Coronary Dissection. Obstet Gynecol 2001.
Figure 3. Completely patent right coronary artery (see arrowheads) after successful angioplasty and placement of six consecutive intracoronary stents (not visible). McKechnie. Spontaneous Coronary Dissection. Obstet Gynecol 2001.
900
McKechnie et al
Spontaneous Coronary Dissection
OBSTETRICS & GYNECOLOGY
Figure 2. Selective injection of the right coronary artery showing an abrupt, complete proximal occlusion (closed arrow) with a dissection flap (open arrow). McKechnie. Spontaneous Coronary Dissection. Obstet Gynecol 2001.
hemodynamic stresses of pregnancy, a primary rupture of the vasa vasorum into the medial wall, or a medial eosinophilic angiitis (although potentially a secondary reaction rather than primary lesion).5,6 Common histologic findings consist of a dissection, often in the outer third of the media or between the media and the adventitia with a large hematoma compressing the true lumen. Cystic medial necrosis, intimal tears, and infiltration of eosinophilic granulocytes have also been observed. The most likely explanation seems to involve induction of morphologic changes of the arterial wall by hormonal influences or connective tissue alterations during or shortly after pregnancy. Successful management of this disease has incorporated medical management, percutaneous coronary angioplasty, intracoronary stent placement, surgical bypass of the affected coronary artery, ventricular assist devices, and heart transplant in select cases.7 Our combination of management, including ECMO support and angioplasty with intracoronary stent placement, represents a unique,
VOL. 98, NO. 5, PART 2, NOVEMBER 2001
successful pathway in a potentially fatal situation as described in one case elsewhere.8 REFERENCES 1. Pretty HC. Dissecting aneurysm of a coronary artery in a woman aged 42. Br Med J 1931;1:667. 2. Engelman DT, Thayer J, Derossi J, Scheinerman J, Brown S. Pregnancy related coronary artery dissection: A case report and collective review. Conn Med 1993;57:135–9. 3. DeMaio SJ, Kinsella SH, Silverman ME. Clinical course and long term prognosis of spontaneous coronary artery dissection. Am J Cardiol 1989;64:471– 4. 4. Kearney P, Singh H, Hutter J, Khan S, Lee G, Lucey J. Spontaneous coronary artery dissection: A report of three cases and review of the literature. Postgrad Med J 1993;69: 940 –5. 5. Robinowitz M, Virmani R, McAllister HA. Spontaneous coronary artery dissection and eosinophilic inflammation: A cause and effect relationship? Am J Med 1982;72:923– 8. 6. Bonnet J, Aumailley M, Thomas D, Grosgogeat Y, Broustet JP, Bricaud H. Spontaneous coronary artery dissection:
McKechnie et al
Spontaneous Coronary Dissection
901
Case report and evidence for a defect in collagen metabolism. Eur Heart J 1986;7:904 –9. 7. Togni M, Amann FW, Follath F. Spontaneous multivessel coronary artery dissection in a pregnant woman treated successfully with stent implantation. Am J Med 1999;107: 407– 8.
8. Ko WJ, Ho HN, Chu SH. Postpartum myocardial infarction rescued with an intraaortic balloon pump and extracorporeal membrane oxygenator. Int J Cardiol 1998;63:81– 4.
Optic Neuritis With Transient Total Blindness During Lactation
The differential diagnosis for lactation-associated blindness includes evaluation for mass lesions, infection, and autoimmune etiologies. Specifically, the diagnosis of bilateral optic neuritis requires a high index of suspicion for early multiple sclerosis.
Matthew G. Retzloff, MD, Erik J. Kobylarz, MD, PhD, and Cynthia Eaton, MD Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, and Departments of Obstetrics and Gynecology and Neurology, Darnall Community Hospital, Ft. Hood, Texas
BACKGROUND: Lactation-induced blindness is a rare but devastating puerperal complication. There are few reported cases and no consistent associated disease processes historically identified. This case illustrates lactation-associated optic neuritis as an early identifier of multiple sclerosis. CASE: A nulliparous woman underwent a term vaginal delivery complicated only by chorioamnionitis. She was treated with intravenous antibiotics, which included spontaneous bacterial endocarditis prophylaxis. Her postpartum course was uncomplicated, and she was discharged on postpartum day 2 with her infant. She was readmitted on postpartum day 16 completely blind. Evaluation revealed bilateral optic neuritis. Symptoms were initiated and exacerbated during nursing. Transitory waxing and waning of her visual deficits were noted after aggressive steroid therapy and discontinuing nursing. The patient was subsequently diagnosed with multiple sclerosis of relapsing-remitting type. CONCLUSION: Multiple sclerosis must be considered as an etiology for acute puerperal lactation-associated blindness when there is no clear anatomic or infectious cause. (Obstet Gynecol 2001;98:902– 4. © 2001 by the American College of Obstetricians and Gynecologists.) Address reprint requests to: Matthew G. Retzloff, MD, Harvard Medical School, Brigham and Women’s Hospital, 75 Francis Street, ASBI-3, Boston, MA 02115; E-mail: [email protected]. The opinions and assertions contained herein are the expressed views of the authors and are not to be construed as official or reflecting the opinions of the Department of Defense, the United States Air Force, or United States Army.
902
Received February 12, 2001. Received in revised form April 24, 2001. Accepted June 28, 2001.
CASE A nulliparous woman experienced an uncomplicated antepartum course and subsequently delivered a healthy term male infant vaginally. Chorioamnionitis was diagnosed intrapartum and was treated with intravenous antibiotics. There was no evidence of preeclampsia. She initiated breastfeeding immediately, and she noted subtle visual changes, a mild headache, and periorbital pain, which she attributed to expulsive efforts during the second stage of labor. She was subsequently discharged home after routine recovery with a healthy infant. Over the next 2 weeks, she noted a waxing and waning of her visual acuity, described as visual “blurring” with rings appearing around objects. She was readmitted on postpartum day 16 complaining of retro-orbital pain of 4 days’ duration culminating in complete blindness. She was afebrile and normotensive. Ophthalmologic examination confirmed no light perception, sluggish pupillary responses, moderate optic disk swelling bilaterally with normal vessels consistent with papillary edema. The neurologic examination was otherwise normal. Head computed tomography was without mass effect or other central nervous system (CNS) abnormality. Lumbar puncture revealed normal opening pressure, normal cerebrospinal fluid protein (29 mg/dL) and glucose (71 mg/dL), four white blood cells, and no red blood cells. There was no increase in immunoglobulin G synthesis or presence of oligoclonal bands. Antinuclear antibody, reactive plasma reagin, lyme titer, and angiotensin-converting enzyme levels were within normal limits. Magnetic resonance brain and orbit imaging with gadolinium revealed bilateral optic nerve enhancement extending posterior to the optic chiasm. Also, a 7 ⫻ 8 mm white matter lesion consistent with a demyelinating plaque was noted adjacent to the right lateral ventricle. Cervical spine magnetic resonance imaging and chest x-ray were normal. The diagnosis of bilateral optic neu-
VOL. 98, NO. 5, PART 2, NOVEMBER 2001 © 2001 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
0029-7844/01/$20.00 PII S0029-7844(01)01556-3
BACKGROUND: Spontaneous coronary dissection is a rare condition occurring more often in women, with a higher frequency during the peripartum period. No specific etiology has been defined to describe this uncommon, yet often fatal phenomenon. CASE: A young woman presented at 36 weeks of a noncomplicated pregnancy with recent onset of diaphoresis, dyspnea, and tingling substernal chest discomfort. Upon evaluation, she developed cardiovascular collapse and ventricular fibrillation requiring aggressive resuscitative measures, eventually leading to extracorporeal membrane oxygenation. Right coronary artery dissection was ultimately diagnosed and treated with intracoronary angioplasty and stent placement. CONCLUSION: Spontaneous coronary dissection must be considered when evaluating a patient with a similar clinical presentation, given its overall mortality of more than 50% at presentation, particularly in the peripartum period. (Obstet Gynecol 2001;98:899 –902. © 2001 by the American College of Obstetricians and Gynecologists.)
Spontaneous coronary dissection is a rare condition occurring more often in women, with a higher frequency during the peripartum or postpartum period. Clinical presentation usually appears with sudden collapse and death or with a severe ischemic syndrome. CASE A young gravid woman presented at 36 weeks of a noncomplicated pregnancy with recent onset of diaphoresis, dyspnea, and tingling substernal chest discomfort radiating to both arms. The patient had no risk factors for coronary artery disease, family history of sudden death, or any other systemic illnesses. Upon Address reprint requests to: Thippeswamy H. Murthy, MD, Section of Cardiology, Washington Hospital Center, 110 Irving Street NW, Room 1094, Washington, DC 20010-2975; E-mail: thippeswamy. [email protected].
initial evaluation, she developed a tonic-clonic seizure with subsequent onset of hemodynamic collapse requiring emergent cesarean delivery. Immediate cardiovascular monitoring revealed ventricular fibrillation, and resuscitation efforts were performed including antiarrhythmic medications, multiple defibrillatory shocks, and catecholamine support without significant improvement. Rescue implementation of extracorporeal membrane oxygenation (ECMO) was initiated for cardiopulmonary support. Electrocardiogram (Figure 1) and transesophageal echocardiogram revealed evidence of inferoposterior and lateral infarction with diminished overall left ventricular function with an ejection fraction of less than 10%. After hemodynamic stabilization with ECMO, emergent cardiac catheterization revealed proximal dissection of the right coronary artery (Figure 2). Angioplasty and six consecutive, intracoronary stents were placed, resulting in normal coronary flow within the right coronary artery (Figure 3). Subsequent removal of ECMO support was achieved 3 days later, and repeat echocardiogram upon hospital discharge revealed an improved left ventricular function at 40 – 45% with persistent akinetic inferoposterior segments. Both the patient and child were ultimately discharged alive and well from the hospital approximately 2 weeks later.
COMMENT Primary dissection of a coronary artery during pregnancy or the puerperium is a rare, yet potentially fatal entity in otherwise healthy individuals. Since the first case of pregnancy-related dissection was reported in 1931, recent review of the medical literature suggests a mean age of 33, mean parity of 2.7, and mean time span to event of 20 days postpartum in 31 additional patients.1,2 Given its overall mortality of more than 50% at presentation, this diagnosis must be considered when evaluating a patient with a similar clinical presentation, especially given the good prognosis (85%) in those patients surviving the acute event.3 Early coronary angiography should be performed to aid in the choice of immediate medical or surgical intervention. Coronary dissection involves the left anterior descending artery in approximately 80% of cases and the right coronary artery in most others.4 However, the etiology of spontaneous coronary dissection in gravid patients remains unclear. Furthermore, no coronary risk factors or connective tissue disorders have been identified as independent risk factors for dissection. Theories regarding the etiology include a pregnancyinduced degeneration of collagen in conjunction with the
VOL. 98, NO. 5, PART 2, NOVEMBER 2001 © 2001 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
0029-7844/01/$20.00 PII S0029-7844(01)01563-0
899
Figure 1. Twelve lead electrocardiogram showing 3– 4 mm of ST segment elevation in leads II, III, aVF, and V6 with Q waves consistent with acute inferolateral myocardial infarction. McKechnie. Spontaneous Coronary Dissection. Obstet Gynecol 2001.
Figure 3. Completely patent right coronary artery (see arrowheads) after successful angioplasty and placement of six consecutive intracoronary stents (not visible). McKechnie. Spontaneous Coronary Dissection. Obstet Gynecol 2001.
900
McKechnie et al
Spontaneous Coronary Dissection
OBSTETRICS & GYNECOLOGY
Figure 2. Selective injection of the right coronary artery showing an abrupt, complete proximal occlusion (closed arrow) with a dissection flap (open arrow). McKechnie. Spontaneous Coronary Dissection. Obstet Gynecol 2001.
hemodynamic stresses of pregnancy, a primary rupture of the vasa vasorum into the medial wall, or a medial eosinophilic angiitis (although potentially a secondary reaction rather than primary lesion).5,6 Common histologic findings consist of a dissection, often in the outer third of the media or between the media and the adventitia with a large hematoma compressing the true lumen. Cystic medial necrosis, intimal tears, and infiltration of eosinophilic granulocytes have also been observed. The most likely explanation seems to involve induction of morphologic changes of the arterial wall by hormonal influences or connective tissue alterations during or shortly after pregnancy. Successful management of this disease has incorporated medical management, percutaneous coronary angioplasty, intracoronary stent placement, surgical bypass of the affected coronary artery, ventricular assist devices, and heart transplant in select cases.7 Our combination of management, including ECMO support and angioplasty with intracoronary stent placement, represents a unique,
VOL. 98, NO. 5, PART 2, NOVEMBER 2001
successful pathway in a potentially fatal situation as described in one case elsewhere.8 REFERENCES 1. Pretty HC. Dissecting aneurysm of a coronary artery in a woman aged 42. Br Med J 1931;1:667. 2. Engelman DT, Thayer J, Derossi J, Scheinerman J, Brown S. Pregnancy related coronary artery dissection: A case report and collective review. Conn Med 1993;57:135–9. 3. DeMaio SJ, Kinsella SH, Silverman ME. Clinical course and long term prognosis of spontaneous coronary artery dissection. Am J Cardiol 1989;64:471– 4. 4. Kearney P, Singh H, Hutter J, Khan S, Lee G, Lucey J. Spontaneous coronary artery dissection: A report of three cases and review of the literature. Postgrad Med J 1993;69: 940 –5. 5. Robinowitz M, Virmani R, McAllister HA. Spontaneous coronary artery dissection and eosinophilic inflammation: A cause and effect relationship? Am J Med 1982;72:923– 8. 6. Bonnet J, Aumailley M, Thomas D, Grosgogeat Y, Broustet JP, Bricaud H. Spontaneous coronary artery dissection:
McKechnie et al
Spontaneous Coronary Dissection
901
Case report and evidence for a defect in collagen metabolism. Eur Heart J 1986;7:904 –9. 7. Togni M, Amann FW, Follath F. Spontaneous multivessel coronary artery dissection in a pregnant woman treated successfully with stent implantation. Am J Med 1999;107: 407– 8.
8. Ko WJ, Ho HN, Chu SH. Postpartum myocardial infarction rescued with an intraaortic balloon pump and extracorporeal membrane oxygenator. Int J Cardiol 1998;63:81– 4.
Optic Neuritis With Transient Total Blindness During Lactation
The differential diagnosis for lactation-associated blindness includes evaluation for mass lesions, infection, and autoimmune etiologies. Specifically, the diagnosis of bilateral optic neuritis requires a high index of suspicion for early multiple sclerosis.
Matthew G. Retzloff, MD, Erik J. Kobylarz, MD, PhD, and Cynthia Eaton, MD Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, and Departments of Obstetrics and Gynecology and Neurology, Darnall Community Hospital, Ft. Hood, Texas
BACKGROUND: Lactation-induced blindness is a rare but devastating puerperal complication. There are few reported cases and no consistent associated disease processes historically identified. This case illustrates lactation-associated optic neuritis as an early identifier of multiple sclerosis. CASE: A nulliparous woman underwent a term vaginal delivery complicated only by chorioamnionitis. She was treated with intravenous antibiotics, which included spontaneous bacterial endocarditis prophylaxis. Her postpartum course was uncomplicated, and she was discharged on postpartum day 2 with her infant. She was readmitted on postpartum day 16 completely blind. Evaluation revealed bilateral optic neuritis. Symptoms were initiated and exacerbated during nursing. Transitory waxing and waning of her visual deficits were noted after aggressive steroid therapy and discontinuing nursing. The patient was subsequently diagnosed with multiple sclerosis of relapsing-remitting type. CONCLUSION: Multiple sclerosis must be considered as an etiology for acute puerperal lactation-associated blindness when there is no clear anatomic or infectious cause. (Obstet Gynecol 2001;98:902– 4. © 2001 by the American College of Obstetricians and Gynecologists.) Address reprint requests to: Matthew G. Retzloff, MD, Harvard Medical School, Brigham and Women’s Hospital, 75 Francis Street, ASBI-3, Boston, MA 02115; E-mail: [email protected]. The opinions and assertions contained herein are the expressed views of the authors and are not to be construed as official or reflecting the opinions of the Department of Defense, the United States Air Force, or United States Army.
902
Received February 12, 2001. Received in revised form April 24, 2001. Accepted June 28, 2001.
CASE A nulliparous woman experienced an uncomplicated antepartum course and subsequently delivered a healthy term male infant vaginally. Chorioamnionitis was diagnosed intrapartum and was treated with intravenous antibiotics. There was no evidence of preeclampsia. She initiated breastfeeding immediately, and she noted subtle visual changes, a mild headache, and periorbital pain, which she attributed to expulsive efforts during the second stage of labor. She was subsequently discharged home after routine recovery with a healthy infant. Over the next 2 weeks, she noted a waxing and waning of her visual acuity, described as visual “blurring” with rings appearing around objects. She was readmitted on postpartum day 16 complaining of retro-orbital pain of 4 days’ duration culminating in complete blindness. She was afebrile and normotensive. Ophthalmologic examination confirmed no light perception, sluggish pupillary responses, moderate optic disk swelling bilaterally with normal vessels consistent with papillary edema. The neurologic examination was otherwise normal. Head computed tomography was without mass effect or other central nervous system (CNS) abnormality. Lumbar puncture revealed normal opening pressure, normal cerebrospinal fluid protein (29 mg/dL) and glucose (71 mg/dL), four white blood cells, and no red blood cells. There was no increase in immunoglobulin G synthesis or presence of oligoclonal bands. Antinuclear antibody, reactive plasma reagin, lyme titer, and angiotensin-converting enzyme levels were within normal limits. Magnetic resonance brain and orbit imaging with gadolinium revealed bilateral optic nerve enhancement extending posterior to the optic chiasm. Also, a 7 ⫻ 8 mm white matter lesion consistent with a demyelinating plaque was noted adjacent to the right lateral ventricle. Cervical spine magnetic resonance imaging and chest x-ray were normal. The diagnosis of bilateral optic neu-
VOL. 98, NO. 5, PART 2, NOVEMBER 2001 © 2001 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
0029-7844/01/$20.00 PII S0029-7844(01)01556-3