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Postpartum myocardial infarction treated with percutaneous transluminal coronary angioplasty
September
6 14
Brief Communications
American
Our patient demonstrated yet another radionuclide feature of hemorrhagic pericardial effusion-the presence of pseudoakinesis, the term we applied to the RNV image of akinesis in an area other than the infarcted area. This pseudoakinesis reflected direct communication (caused by free wall rupture) between the LV cavity and the pericardial space. The local accumulation of labeled blood outside the heart produced the image of pseudoakinesis. It must be recognized that the lowest limits of detectability of pericardial bleeding using RNV are not presently known. Therefore it is possible that small amounts of bleeding may go undetected. In addition, the specificity of our finding is not yet known.The finding of pseudoakinesis during postMI cardiac function studies may be related to other causes such as lack of consistency in assigning involved segments when alternative techniques such as two-dimensional echocardiography and RNV are used. Our report should direct attention to the diagnostic significance of the RNV image of pseudoakinesis. An awareness of this RNV finding may allow early recognition of incomplete heart rupture and hence lead to immediate intervention. REFERENCES
1. Balakumaran K, Verbaan CJ, Essed CE, Nauta J, Bos E, Haalebos MMP, Penn 0, Simmoons ML, Hugenholtz PG. Ventricular free wall rupture: sudden, subacute, slow, sealed and stabilized varieties. Eur Heart J 1984:5:282-S. 2. Uren RF, McLaughlin AF, Cormack J. Cardiac tamponade: accurate diagnosis by radionuclide angiography. Aust N Z J Med 1980;10:414-20. 3. Bateman TM, Czer LSC, Gray RJ, Kass RM, Raymond MJ, Garcia EV. Chaux A. Matloff JM. Berman DS. Detection of occult pericaridial hemorrhage early after open-heart surgery using technetium-99m red blood cell radionuclide ventriculography. AM HEART J 1984;108:1198-206. 4. Bateman TM. Czer LSC. Kass RM. Ravmond MJ. Chaux A. Matloff JM, Berman Ds, Gray RJ: Cardiac causes of shock early after open-heart surgery: etiologic classification by radionuclide ventriculography. Circulation 1985;71:1153-61.
Postpartum myocardial infarction treated with percutaneous transluminal coronary angioplasty Michael C. Giudici, MD, Andre K. Artis, Richard R. Webel, MD, and Martin A. Alpert, MD. Columbia, MO.
MD,
Postpartum myocardial infarction (MI) is exceedingly rare. A 1979 review by Beary et al.’ reported only 11 cases, and few have been added since that time. We report herein the first case of acute revascularization by percutaneous From the Department of Medicine, University of Missouri Health Sciences Center, Columbia. Reprint requests: Michael C. Giudici, MD, St. Luke’s Regional Heart Center, 1230 East Rusholme, Suite 305, Davenport. IA 52803. 4/4/13977
Heart
1989 Journal
transluminal coronary angioplasty (PTCA) in postpartum MI. The patient was a 41-year-old postpartum white woman with no risk factors for coronary artery disease and no previous cardiac history. The pregnancy and delivery were uncomplicated. Her only medication was bromocriptine given to suppress lactation. On the eleventh day postpartum, she had a sudden onset of left-sided “achy” chest pain without radiation or associated symptoms. She presented to our emergency room 1 hour later, where her electrocardiogram (ECG) demonstrated precordial ST segment elevation consistent with acute anterior subepicardial injury. Her physical examination and chest x-ray films were unremarkable. She was treated with intravenous nitroglycerin, sublingual nifedipine, and intravenous heparin, which reduced the intensity of but did not eliminate her chest pain. She was immediately taken to the cardiac catheterization laboratory where coronary angiography revealed a total occlusion of the mid left anterior descending coronary artery (LAD) (Fig. 1, A). PTCA of the LAD was then performed with a 2.5 mm Simpson-Roberts balloon dilatation catheter (Advanced Cardiovascular Systems, Inc.. Santa Clara, Calif.) and an 0.018 inch high torque floppy guide wire. This produced a widely patent vessel (Fig. 1, H). Left ventriculography after PTCA showed anterolateral akinesis with apical dyskinesis. An early creatine kinase peak and accelerated idioventricular rhythm on the monitor following PTCA suggested successful revascularization. The patient remained asymptomatic until 24 hours later, when she again developed ischemic chest pain and precordial ST elevation on the ECG. She underwent emergency repeat catheterization, which revealed a subtotal occlusion in the proximal LAD (Fig. 2, A). Repeat PTCA was performed, restoring good flow with residual thrombus present (Fig. 2, B). Intravenous heparin therapy was continued (partial thromboplastin time 2.5 times control) when, 48 hours later, she developed her third episode of chest pain and precordial ST segment elevation. It was elected to treat this episode medically, and her pain resolved with intravenous nitroglycerin, morphine sulfate, and sublingual nifedipine. Elective cardiac catheterization was performed on the sixth hospital day. Left ventriculography suggested slight improvement in anterolateral wall motion. Coronary angiography revealed a large dissection of the LAD with the appearance of a false lumen (Fig. 3, A and B). Her course after her third episode of chest pain was unremarkable and she was discharged home on the ninth hospital day. This is the first reported attempt at revascularization during an acute postpartum MI. The cause of our patient’s initial occlusion and subsequent reocclusions after each initially successful angioplasty likely relates to the pathophysiology of the postpartum MI. Etiologic factors could include coronary atherosclerosis, coronary artery spasm, coronary artery thromboembolism, or primary coronary artery dissection. Coronary atherosclerosis, while uncommon in young females, was present in three of five women studied angiographically in the review by Beary et al.,’ and should be considered as a possible cause of postpartum MI.
Volume Number
11% 3
Brief Communications
615
Fig. 1. Left coronary angiograms.A, Right anterior oblique view demonstrating a total occlusionof the mid LAD furrow). B, Cranial left anterior oblique view post PTCA. The LAD is patent and an intimal flap is present in the mid to distal portion of the vessel (arrow).
2. Left coronary angiograms.A, Left anterior oblique view pre PTCA showsthat a large filling defect is present in the proximal LAD (arrow). B, Post PTCA the vesselis again widely patent (right anterior oblique view). Fig.
Coronary artery spasm,whether spontaneous?or induced by bromocriptine,3 has been postulated to causepostpartum MI. However, conclusive evidence linking the two is lacking. Thromboembolic diseasein pregnancy and the puerperium is well described.4During pregnancy, most clotting factors increaseto an averageof 1.8times the level in nonpregnant women.Despite an increasein both fibrinogen and plasminogenduring gestation, the spontaneous fibrinolytic activity is strikingly diminished. While venous
thromboembolismpredominates in this setting, it is conceivable that de novo coronary thrombosis might alsooccur. Postpartum coronary artery dissection accounts for more than one third of all primary coronary artery dissections in women.” Most of these dissections involve the proximal or mid LAD. Dissectionof the circumflex or right coronary arteries is uncommon. In pregnancy, muscular arteries undergo a marked transformation. Elastic fibers
6 16
Brief Chmmunications
American
September 1989 Heart Journal
tologic coronary artery abnormalities in such individuals. While the rationale exists for the useof emergencyPTC’A in acute MI due to coronary atherosclerosis,the presence of a hypercoagulablestate and the lossof normal structural integrity of the coronary arteries suggestthat PTCA will he of limited usefulnessin the managementof postpartum MI. REFERENCES
1.
BearyJF, SummerWR, Bulkley BH. Postpartum myocardial infarction:a rareoccurrenceof uncertainetiology.AmJ Car-
diol 1979;43:158-61. 2. Bornstein A, et al. Acute myocardial infarction in a thirty-six year old postpartum female. Angiology 1984;35:591-4. 3. Iffy L, Tentlove W, Frisoli G. Acute myocardial infarction in the puerperium in patients receiving bromocriptine. Am .I ObstetGynecol 1986;155:371-2. Bell WR. Hematologic abnormalities in pregnancy. Med Clin North Am 1977;61:165-91. Smith JC. Dissecting aneurysms of coronary arteries. Arch Path01 Lab Med 1975;99:117-21. Menalo-Estrella P, Barker AE. Histopathologic findings in
humanaortic mediaassociated with pregnancy.Arch Pathol Lab
Med
1967;83:336-41.
Dipyridamole-induced negative U waves: Scintigraphic evidence of severe anterior myocardial ischemia Michele Galli, MD, Enzo Bosimini, MD, Andrea Campi, MD,* and Luigi Tavazzi, MD. Veruno and Novara, Italy
6 3. Right anterior oblique(A) and left anterior oblique views of the left coronary artery showinga large dissection (arrows) of the proximal and mid LAD. Fig. (B)
lose their normal corrugation, reticular fibers fragment, there is a decreasein acid mucopolysaccharide ground substance,and smoothmusclehypertrophy and hyperplasiaoccur.6Thesechangeshave beenattributed primarily to progesteroneexcessand may be exacerbated at the time of delivery by the releaseof relaxin. Such biochemical and histologic abnormalitiesmay predisposeto coronary artery dissection. While all of the aforementioned pathogenic mechanismsmay contribute to coronary occlusion, the precisecauseof the initial occlusion in this patient is unclear. Whether coronary artery dissectionoccurredde novo or resulted from PTCA also is uncertain; however, it is likely that coronary artery dissectioncontributed to subsequent coronary artery occlusions. It is reasonable to speculatethat postpartum patients undergoingPTCA may beat increasedrisk for coronary artery dissectiondueto the presenceof the previously discussedbiochemical and his-
Among the electrocardiographicsignsof transient myocardial ischemia,negative U wavesin the precordial leadshave beenreported to bevery specificfor coronary artery disease and to be almost hallmark of left anterior descending (LAD) coronary stenosis’or spasm.2Although the mechanism of U wave negativity remains unclear,3 recently Yamakado et a1.4postulated that myocardial ischemiaassociated with transient negative U wavescould be lesssevere than that associatedwith ST segmentelevation or depression. We report the caseof a patient with both spontaneous and dipyridamole-induced negative U waves and the scintigraphic evidence of severe anterior myocardial ischemia causingsuch an electrocardiographic (ECG) finding. A previously well 34-year-old man was admitted to a nearby hospital becauseof prolonged chest pain with ECG evidenceof ST segmentelevation in precordial leadsVs to Vs. Pain promptly ceasedand the ECG reverted to normal
From Clinica de1 Lavoro Foundation, Institute of Care and Research, Division of Cardiology, Veruno Medical Center, Veruno (No); and Hemodynamic Laboratory,* Ospedale della Carita’, Novara. Reprint requests: Michele Galli, MD, Cardiology Division, Centro Medico. Veruno (No), 28010 Italy. 4/4/139’76
6 14
Brief Communications
American
Our patient demonstrated yet another radionuclide feature of hemorrhagic pericardial effusion-the presence of pseudoakinesis, the term we applied to the RNV image of akinesis in an area other than the infarcted area. This pseudoakinesis reflected direct communication (caused by free wall rupture) between the LV cavity and the pericardial space. The local accumulation of labeled blood outside the heart produced the image of pseudoakinesis. It must be recognized that the lowest limits of detectability of pericardial bleeding using RNV are not presently known. Therefore it is possible that small amounts of bleeding may go undetected. In addition, the specificity of our finding is not yet known.The finding of pseudoakinesis during postMI cardiac function studies may be related to other causes such as lack of consistency in assigning involved segments when alternative techniques such as two-dimensional echocardiography and RNV are used. Our report should direct attention to the diagnostic significance of the RNV image of pseudoakinesis. An awareness of this RNV finding may allow early recognition of incomplete heart rupture and hence lead to immediate intervention. REFERENCES
1. Balakumaran K, Verbaan CJ, Essed CE, Nauta J, Bos E, Haalebos MMP, Penn 0, Simmoons ML, Hugenholtz PG. Ventricular free wall rupture: sudden, subacute, slow, sealed and stabilized varieties. Eur Heart J 1984:5:282-S. 2. Uren RF, McLaughlin AF, Cormack J. Cardiac tamponade: accurate diagnosis by radionuclide angiography. Aust N Z J Med 1980;10:414-20. 3. Bateman TM, Czer LSC, Gray RJ, Kass RM, Raymond MJ, Garcia EV. Chaux A. Matloff JM. Berman DS. Detection of occult pericaridial hemorrhage early after open-heart surgery using technetium-99m red blood cell radionuclide ventriculography. AM HEART J 1984;108:1198-206. 4. Bateman TM. Czer LSC. Kass RM. Ravmond MJ. Chaux A. Matloff JM, Berman Ds, Gray RJ: Cardiac causes of shock early after open-heart surgery: etiologic classification by radionuclide ventriculography. Circulation 1985;71:1153-61.
Postpartum myocardial infarction treated with percutaneous transluminal coronary angioplasty Michael C. Giudici, MD, Andre K. Artis, Richard R. Webel, MD, and Martin A. Alpert, MD. Columbia, MO.
MD,
Postpartum myocardial infarction (MI) is exceedingly rare. A 1979 review by Beary et al.’ reported only 11 cases, and few have been added since that time. We report herein the first case of acute revascularization by percutaneous From the Department of Medicine, University of Missouri Health Sciences Center, Columbia. Reprint requests: Michael C. Giudici, MD, St. Luke’s Regional Heart Center, 1230 East Rusholme, Suite 305, Davenport. IA 52803. 4/4/13977
Heart
1989 Journal
transluminal coronary angioplasty (PTCA) in postpartum MI. The patient was a 41-year-old postpartum white woman with no risk factors for coronary artery disease and no previous cardiac history. The pregnancy and delivery were uncomplicated. Her only medication was bromocriptine given to suppress lactation. On the eleventh day postpartum, she had a sudden onset of left-sided “achy” chest pain without radiation or associated symptoms. She presented to our emergency room 1 hour later, where her electrocardiogram (ECG) demonstrated precordial ST segment elevation consistent with acute anterior subepicardial injury. Her physical examination and chest x-ray films were unremarkable. She was treated with intravenous nitroglycerin, sublingual nifedipine, and intravenous heparin, which reduced the intensity of but did not eliminate her chest pain. She was immediately taken to the cardiac catheterization laboratory where coronary angiography revealed a total occlusion of the mid left anterior descending coronary artery (LAD) (Fig. 1, A). PTCA of the LAD was then performed with a 2.5 mm Simpson-Roberts balloon dilatation catheter (Advanced Cardiovascular Systems, Inc.. Santa Clara, Calif.) and an 0.018 inch high torque floppy guide wire. This produced a widely patent vessel (Fig. 1, H). Left ventriculography after PTCA showed anterolateral akinesis with apical dyskinesis. An early creatine kinase peak and accelerated idioventricular rhythm on the monitor following PTCA suggested successful revascularization. The patient remained asymptomatic until 24 hours later, when she again developed ischemic chest pain and precordial ST elevation on the ECG. She underwent emergency repeat catheterization, which revealed a subtotal occlusion in the proximal LAD (Fig. 2, A). Repeat PTCA was performed, restoring good flow with residual thrombus present (Fig. 2, B). Intravenous heparin therapy was continued (partial thromboplastin time 2.5 times control) when, 48 hours later, she developed her third episode of chest pain and precordial ST segment elevation. It was elected to treat this episode medically, and her pain resolved with intravenous nitroglycerin, morphine sulfate, and sublingual nifedipine. Elective cardiac catheterization was performed on the sixth hospital day. Left ventriculography suggested slight improvement in anterolateral wall motion. Coronary angiography revealed a large dissection of the LAD with the appearance of a false lumen (Fig. 3, A and B). Her course after her third episode of chest pain was unremarkable and she was discharged home on the ninth hospital day. This is the first reported attempt at revascularization during an acute postpartum MI. The cause of our patient’s initial occlusion and subsequent reocclusions after each initially successful angioplasty likely relates to the pathophysiology of the postpartum MI. Etiologic factors could include coronary atherosclerosis, coronary artery spasm, coronary artery thromboembolism, or primary coronary artery dissection. Coronary atherosclerosis, while uncommon in young females, was present in three of five women studied angiographically in the review by Beary et al.,’ and should be considered as a possible cause of postpartum MI.
Volume Number
11% 3
Brief Communications
615
Fig. 1. Left coronary angiograms.A, Right anterior oblique view demonstrating a total occlusionof the mid LAD furrow). B, Cranial left anterior oblique view post PTCA. The LAD is patent and an intimal flap is present in the mid to distal portion of the vessel (arrow).
2. Left coronary angiograms.A, Left anterior oblique view pre PTCA showsthat a large filling defect is present in the proximal LAD (arrow). B, Post PTCA the vesselis again widely patent (right anterior oblique view). Fig.
Coronary artery spasm,whether spontaneous?or induced by bromocriptine,3 has been postulated to causepostpartum MI. However, conclusive evidence linking the two is lacking. Thromboembolic diseasein pregnancy and the puerperium is well described.4During pregnancy, most clotting factors increaseto an averageof 1.8times the level in nonpregnant women.Despite an increasein both fibrinogen and plasminogenduring gestation, the spontaneous fibrinolytic activity is strikingly diminished. While venous
thromboembolismpredominates in this setting, it is conceivable that de novo coronary thrombosis might alsooccur. Postpartum coronary artery dissection accounts for more than one third of all primary coronary artery dissections in women.” Most of these dissections involve the proximal or mid LAD. Dissectionof the circumflex or right coronary arteries is uncommon. In pregnancy, muscular arteries undergo a marked transformation. Elastic fibers
6 16
Brief Chmmunications
American
September 1989 Heart Journal
tologic coronary artery abnormalities in such individuals. While the rationale exists for the useof emergencyPTC’A in acute MI due to coronary atherosclerosis,the presence of a hypercoagulablestate and the lossof normal structural integrity of the coronary arteries suggestthat PTCA will he of limited usefulnessin the managementof postpartum MI. REFERENCES
1.
BearyJF, SummerWR, Bulkley BH. Postpartum myocardial infarction:a rareoccurrenceof uncertainetiology.AmJ Car-
diol 1979;43:158-61. 2. Bornstein A, et al. Acute myocardial infarction in a thirty-six year old postpartum female. Angiology 1984;35:591-4. 3. Iffy L, Tentlove W, Frisoli G. Acute myocardial infarction in the puerperium in patients receiving bromocriptine. Am .I ObstetGynecol 1986;155:371-2. Bell WR. Hematologic abnormalities in pregnancy. Med Clin North Am 1977;61:165-91. Smith JC. Dissecting aneurysms of coronary arteries. Arch Path01 Lab Med 1975;99:117-21. Menalo-Estrella P, Barker AE. Histopathologic findings in
humanaortic mediaassociated with pregnancy.Arch Pathol Lab
Med
1967;83:336-41.
Dipyridamole-induced negative U waves: Scintigraphic evidence of severe anterior myocardial ischemia Michele Galli, MD, Enzo Bosimini, MD, Andrea Campi, MD,* and Luigi Tavazzi, MD. Veruno and Novara, Italy
6 3. Right anterior oblique(A) and left anterior oblique views of the left coronary artery showinga large dissection (arrows) of the proximal and mid LAD. Fig. (B)
lose their normal corrugation, reticular fibers fragment, there is a decreasein acid mucopolysaccharide ground substance,and smoothmusclehypertrophy and hyperplasiaoccur.6Thesechangeshave beenattributed primarily to progesteroneexcessand may be exacerbated at the time of delivery by the releaseof relaxin. Such biochemical and histologic abnormalitiesmay predisposeto coronary artery dissection. While all of the aforementioned pathogenic mechanismsmay contribute to coronary occlusion, the precisecauseof the initial occlusion in this patient is unclear. Whether coronary artery dissectionoccurredde novo or resulted from PTCA also is uncertain; however, it is likely that coronary artery dissectioncontributed to subsequent coronary artery occlusions. It is reasonable to speculatethat postpartum patients undergoingPTCA may beat increasedrisk for coronary artery dissectiondueto the presenceof the previously discussedbiochemical and his-
Among the electrocardiographicsignsof transient myocardial ischemia,negative U wavesin the precordial leadshave beenreported to bevery specificfor coronary artery disease and to be almost hallmark of left anterior descending (LAD) coronary stenosis’or spasm.2Although the mechanism of U wave negativity remains unclear,3 recently Yamakado et a1.4postulated that myocardial ischemiaassociated with transient negative U wavescould be lesssevere than that associatedwith ST segmentelevation or depression. We report the caseof a patient with both spontaneous and dipyridamole-induced negative U waves and the scintigraphic evidence of severe anterior myocardial ischemia causingsuch an electrocardiographic (ECG) finding. A previously well 34-year-old man was admitted to a nearby hospital becauseof prolonged chest pain with ECG evidenceof ST segmentelevation in precordial leadsVs to Vs. Pain promptly ceasedand the ECG reverted to normal
From Clinica de1 Lavoro Foundation, Institute of Care and Research, Division of Cardiology, Veruno Medical Center, Veruno (No); and Hemodynamic Laboratory,* Ospedale della Carita’, Novara. Reprint requests: Michele Galli, MD, Cardiology Division, Centro Medico. Veruno (No), 28010 Italy. 4/4/139’76