- Email: [email protected]
Behavior of C-reactive protein levels in medically treated aortic dissection and intramural hematoma
Behavior of C-Reactive Protein Levels in Medically Treated Aortic Dissection and Intramural Hematoma Shinji Makita, MD, Atsushi Ohira, MD, Rintarou Tachieda, MD, Shigehiro Itoh, Yoshiteru Moriai, MD, Kunihiro Yoshioka, MD, Hiroyuki Niinuma, MD, Motoyuki Nakamura, MD, and Katsuhiko Hiramori, MD onservative management of aortic dissection and intramural hematoma not involving the ascending C aorta yields acceptable survival outcomes. How1–3
ever, a variety of aortic events can often arise during the follow-up phase.4 – 6 Although C-reactive protein (CRP) levels are inevitably elevated in patients with acute aortic dissection and intramural hematoma, variability exists among patients. However, few previous studies have investigated the behavior of CRP levels in these aortic disorders.7 The purpose of this prospective study was to assess the consequences of CRP levels on the course of aortic dissection and intramural hematoma, by means of comparison with findings from serial computed tomography (CT). •••
One hundred eight patients were diagnosed as having acute aortic dissection or intramural hematoma and admitted to our hospital from June 1997 to May 1999. Of these, 47 consecutive cases who presented within 24 hours (median 6 hours) of onset and were treated medically were initially enrolled in this prospective study. Four patients were excluded from this aggregate because of infectious diseases during the study in 3 cases and contraindication to the use of contrast material in 1 case. Data pertaining to the remaining 43 patients were analyzed: involvement of ascending aorta in 11 patients (type A) and no involvement in 32 patients (type B); there were 36 men and 7 women, average age 65.5 years old (range 42 to 84). Indication for medical treatment was based on the following criteria: (1) type B with descending aorta of ⬍55 mm in diameter, (2) type A with both ascending aorta of ⬍50 mm in diameter and no blood flow in false lumen of ascending aorta, and (3) patients without compromised organ perfusion, cardiac tamponade, aortic valve involvement, or aortic rupture. Diagnosis and disease classification was made on the basis of 2 imaging modalities: contrast-enhanced electron beam CT with contiguous slices of 6 mm thickness, and gadolinium-enhanced magnetic resonance imaging with a 1.5-T superconducting magnetic unit. Patients with typical aortic intimal flap were diagnosed as classic dissection (n ⫽ 13, including 4 patients with type A). Aortic dissection with thrombosed false lumen (n ⫽ 10, including 2 patients with type A) was defined by a large amount of intramural From the Departments of Internal Medicine II and Radiology, Iwate Medical University, Morioka, Japan. Dr. Makita’s address is: Department of Internal Medicine II, Iwate Medical University, 19-1 Uchimaru, Morioka 020-8505, Japan. E-mail: [email protected]. Manuscript received November 22, 1999; revised manuscript received and accepted January 27, 2000.
242
©2000 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 86 July 15, 2000
MD,
thrombus with intimal disruption (entry), as distinct from penetrating atherosclerotic ulcer.8 On the day of onset, the findings of hyperdense precontrast crescent in the aortic wall, no intimal flap, no intimal disruption, and no compressed aortic lumen, were considered diagnostic of intramural hematoma (n ⫽ 20, including 5 patients with type A). All participants were initially treated according to a single protocol as follows. During a 4- to 7-day stay in an intensive care unit, systolic blood pressure was maintained at ⬍130 mm Hg. Nicardipine hydrochloride was intravenously infused for the first 48 hours from onset, if appropriate. Thereafter, oral antihypertensive medications were administered in a fixed order. All patients underwent a uniform rehabilitation program that facilitated a stepwise restoration to normal daily life over a 3-week period. Contrast-enhanced electron beam CT was performed on the day of onset, after a few days, and thereafter at 1-week intervals for 4 to 5 weeks during hospitalization. Subsequent follow-up by electron beam CT was carried out at 3-month intervals after discharge (average 16 months). All tests consisted of early and delayed images, and changes in aortic condition were carefully evaluated by a specially trained radiologist and 2 physicians. In intramural hematoma and aortic dissection with thrombosed false lumen, 3 types of serious evolution of hematoma or thrombus were anticipated: (1) perceptible enlargement of localized contrast filling, suggesting secondary formed microdisruption of the intima9 or initial entry site, (2) abrupt expansion of the hematoma or thrombus, and (3) transition to classic dissection. These findings were designated as intramural events. Circulating CRP levels were measured daily until the initial peak had passed, and thereafter once or twice a week until discharge. The measurements were properly added when an abnormal change was found. Re-elevation of CRP levels was defined as an elevation of ⬎1.0 mg/dl after the initial peak level. CRP was measured by latex agglutination nephelometry with an assay sensitivity of 0.3 mg/dl and a normal range of ⬍0.6 mg/dl. The study protocol was approved by our hospital ethics committee, and informed consent was obtained from all subjects. Intergroup differences in the proportion of patients with CRP re-elevation were compared by chi-square test. The unpaired Student’s t test was used for comparison of CRP levels between the groups. Significance was set at p ⬍0.05. All values are expressed as mean ⫾ SD. In 9 of 20 patients with intramural hematoma, 0002-9149/00/$–see front matter PII S0002-9149(00)00869-9
TABLE I Factors Influencing Behavior of C-Reactive Protein (CRP) Levels in Patients With Intramural Hematoma and Aortic Dissection With Thrombosed False Lumen Frequences of CRP Re-elevation Factors Presence of intramural event Increase in aortic diameter Involvement of ascending aorta ⬍64 yrs (median)
Factor (⫹) 14/16 2/2 3/7 11/16
(88%) (100%) (43%) (69%)
Factor (⫺) 0/14 12/28 11/23 3/14
(0%) (43%) (48%) (21%)
intramural events were found during follow-up: enlargement of newly occurring localized contrast filling (7 patients), hematoma expansion with recurrent back pain on day 14 (1 patient), and transition to classic dissection on day 21 (1 patient). In contrast, 7 of 10 patients with aortic dissection with thrombosed false lumen had intramural events: enlargement of initial localized contrast filling (4 patients) and enlargement of newly occurring localized contrast filling (3 patients). All 16 intramural events were confirmed by electron beam CT. Ten of the 14 patients with enlarged localized contrast filling progressed to localized aortic dissection or saccular aneurysm on subsequent follow-up after discharge. In patients with classic dissection, organ malperfusion by obliteration of the true aortic lumen developed in 2 cases. Both underwent emergency surgical aortic intimal fenestration; 1 had visceral ischemia on day 14 and the other had bilateral renal ischemia on day 31. Another 2 patients showed gradual thrombosis in the false lumen without any organ malperfusion. As shown in the Table I, although CRP re-elevation was found in 14 of the 16 patients (88%) with intramural hematoma and aortic dissection with thrombosed false lumen and intramural events, none of the 14 patients without events had re-elevation of CRP levels (p ⬍0.01). CRP levels after 3 weeks were significantly higher in patients with intramural events than in those without (5.5 ⫾ 5.4 vs 1.4 ⫾ 1.3 mg/dl, p ⬍0.01). An increase in aortic diameter during intervals of electron beam computed tomographic testing during hospitalization and involvement of the ascending aorta had no effect on CRP levels. In a comparison by age with division around the median of 64 years, frequency of CRP re-elevation in the younger patients was significantly higher than that in the older patients (69% vs 21%, p ⬍0.05). However, there was no significant difference in CRP levels between the 2 age groups after 3 weeks. As shown in Figure 1, most of the patients with intramural hematoma and aortic dissection with thrombosed false lumen showed CRP levels within the normal range on the day of onset, and subsequently attained initial peak levels within 3 to 8 days (average 4.2). Initial peak levels in patients with intramural events were significantly higher than in patients without events (16.8 ⫾ 6.3 vs 12.4 ⫾ 3.8 mg/dl, p ⬍0.05). In the latter group, CRP levels gradually decreased, and most had recovered to within the normal range within 3 to 4 weeks (Figure 1). In contrast, even after 5 weeks, CRP levels were still above the normal range
CRP Levels After 3 Weeks p Value
Factor (⫹)
⬍0.01 NS NS ⬍0.05
5.5 3.9 3.6 4.8
⫾ ⫾ ⫾ ⫾
5.4 0.7 3.0 5.6
Factor (⫺)
p Value
⫾ ⫾ ⫾ ⫾
⬍0.01 NS NS NS
1.4 3.7 3.7 2.3
1.3 4.6 4.9 1.9
FIGURE 1. Changes in CRP levels in patients with intramural hematoma and aortic dissection with thrombosed false lumen, without (A) or with (B) intramural events. Day 1 means day of onset. Black circles, time points of intramural event verified by electron beam CT. White circles, time points of CRP re-elevation. Horizontal line graphs, intervals of intramural event and CRP re-elevation. Isolated black circles (2), patients without CRP reelevation.
in all but 3 of the patients with intramural events. In 14 patients with CRP re-elevation, the time difference of re-elevation from initial confirmation of event was 1.7 ⫾ 4.5 days (range ⫺7 to 7). These 2 phenomena were considered to be closely associated (Figure 1). Although 2 patients with events did not have CRP re-elevation, 1 did show an increase of 5.1 mg/dl after 3 weeks; however, no specific abnormality was detected in the other subject. In the patients with classic dissection, 4 of 13 patients showed CRP re-elevation; 2 of these patients had a gradual thrombosis in false lumen and 1 patient had renal malperfusion. No cause could be identified in the remaining patient (Figure 2). BRIEF REPORTS
243
instability of intramural thrombus or hematoma, defined as enlargement of localized contrast filling, transition to classic dissection, or expansion of hematoma in the aortic wall. In classic dissection, the abnormal behavior of CRP levels could be partly explained by gradual thrombosis in false lumen. The evaluation of CRP levels may serve as a useful marker for early and noninvasive detection of aortic events and for conservative management in patients with acute aortic dissection and intramural hematoma. FIGURE 2. Changes in CRP levels in patients with classic dissection. Black arrows, CRP re-elevation (on the second peak) in patients with progression of thrombosis in false lumen. White arrow, CRP re-elevation (on the second peak) without definite aortic event. Black squares, 2 patients who underwent surgical intimal fenestration for organ malperfusion on the day of surgery.
•••
This study revealed re-elevation or retarded recovery of CRP levels in a proportion of patients with aortic dissection or intramural hematoma. Especially in cases with intramural hematoma and aortic dissection with thrombosed false lumen, such abnormal behavior of CRP levels corresponded with intramural events. In conclusion, re-elevation and retarded recovery of CRP levels were considered to reflect an
1. Schor JS, Yerlioglu ME, Galla JD, Lansman SL, Ergin MA, Griepp RB.
Selective management of acute type B aortic dissection: long-term follow-up. Ann Thorac Surg 1996;61:1339 –1341. 2. Vilacosta I, San Roman JA, Ferreiros J, Aragoncillo P, Mendez R, Castillo JA, Rollan MJ, Batlle E, Peral V, Sanchez-Harguindey L. Natural history and serial morphology of aortic intramural hematoma: a novel variant of aortic dissection. Am Heart J 1997;134:495–507. 3. Robbins RC, McManus RP, Mitchell RS, Latter DR, Moon MR, Olinger GN, Miller DC. Management of patients with intramural hematoma of the thoracic aorta. Circulation 1993;88:II1–10. 4. Mohr-Kahaly S, Erbel R, Kearney P, Puth M, Meyer J. Aortic intramural hemorrhage visualized by transesophageal echocardiography: findings and prognostic implications. J Am Coll Cardiol 1994;23:658 – 664. 5. Nienaber CA, von Kodolitsch Y, Petersen B, Loose R, Helmchen U, Haverich A, Spielmann RP. Intramural hemorrhage of the thoracic aorta; diagnostic and therapeutic implications. Circulation 1995;92:1465–1472. 6. Ide K, Uchida H, Otsuji H, Nishimine K, Tsushima J, Ohishi H, Kitamura S. Acute aortic dissection with intramural hematoma: possibility of transition to classic dissection or aneurysm. J Thorac Imaging 1996;11:46 –52. 7. Hara K, Yamaguchi T, Wanibuchi Y, Kurokawa K. The role of medical treatment of distal type aortic dissection. Int J Cardiol 1991;32:231–240. 8. Kazerooni EL, Bree RL, Williams DM. Penetrating atherosclerotic ulcers in the descending thoracic aorta: evaluation with CT and distinction from aortic dissection. Radiology 1992;183:759 –765. 9. Williams MP, Farrow R. Atypical patterns in the CT diagnosis of aortic dissection. Clin Radiol 1994;49:686 – 689.
Left Atrial Kinetic Energy in AL Amyloidosis: Can It Detect Early Dysfunction? Laura Murphy,
MD,
and Rodney H. Falk,
L amyloidosis (formerly known as primary amyloidosis) is characterized by extracellular infiltraA tion of various organs by a proteinaceous material derived from monoclonal light chain fragments.1 Clinical evidence of cardiac involvement occurs in 30% to 50% of patients, resulting in congestive heart failure with predominant diastolic dysfunction.2 The Doppler features of restrictive physiology have been well described and include a shortened transmitral E-wave deceleration time associated with a decreased peak A-wave velocity.3 Cardiac infiltration in AL amyloidosis occurs in all 4 chambers, raising the possibility that atrial systolic dysfunction may play a role in the diminished A wave seen in patients with more adFrom the Section of Cardiology, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts. Dr. Falk’s address is: Boston Medical Center, Boston University School of Medicine, 88 East Newton Street, Boston, Massachusetts 02118. E-mail: [email protected]. Manuscript received September 17, 1999; revised manuscript received and accepted February 7, 2000.
244
©2000 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 86 July 15, 2000
MD
vanced disease.4 Because atrial function may be more vulnerable than ventricular function to minor structural changes, it is possible that the decreased A-wave velocity in some patients is due to primary atrial failure caused by amyloid infiltration. Left atrial function has been assessed by the left atrial stroke work index calculated from invasively assessed parameters.5,6 Recently, left atrial stroke work has been shown to correlate well with noninvasively derived left atrial kinetic energy.7 We postulated that, if early left atrial dysfunction is present in AL amyloidosis, it should be identified by this sensitive index of left atrial function. •••
The echocardiograms of 10 patients with echocardiographic features of cardiac AL amyloidosis and biopsy-proved AL amyloid were selected at random from the Boston University Amyloid Research and Clinical Center echocardiographic database. Ten agematched AL amyloid, biopsy-proved patients with no 0002-9149/00/$–see front matter PII S0002-9149(00)00870-5
ever, a variety of aortic events can often arise during the follow-up phase.4 – 6 Although C-reactive protein (CRP) levels are inevitably elevated in patients with acute aortic dissection and intramural hematoma, variability exists among patients. However, few previous studies have investigated the behavior of CRP levels in these aortic disorders.7 The purpose of this prospective study was to assess the consequences of CRP levels on the course of aortic dissection and intramural hematoma, by means of comparison with findings from serial computed tomography (CT). •••
One hundred eight patients were diagnosed as having acute aortic dissection or intramural hematoma and admitted to our hospital from June 1997 to May 1999. Of these, 47 consecutive cases who presented within 24 hours (median 6 hours) of onset and were treated medically were initially enrolled in this prospective study. Four patients were excluded from this aggregate because of infectious diseases during the study in 3 cases and contraindication to the use of contrast material in 1 case. Data pertaining to the remaining 43 patients were analyzed: involvement of ascending aorta in 11 patients (type A) and no involvement in 32 patients (type B); there were 36 men and 7 women, average age 65.5 years old (range 42 to 84). Indication for medical treatment was based on the following criteria: (1) type B with descending aorta of ⬍55 mm in diameter, (2) type A with both ascending aorta of ⬍50 mm in diameter and no blood flow in false lumen of ascending aorta, and (3) patients without compromised organ perfusion, cardiac tamponade, aortic valve involvement, or aortic rupture. Diagnosis and disease classification was made on the basis of 2 imaging modalities: contrast-enhanced electron beam CT with contiguous slices of 6 mm thickness, and gadolinium-enhanced magnetic resonance imaging with a 1.5-T superconducting magnetic unit. Patients with typical aortic intimal flap were diagnosed as classic dissection (n ⫽ 13, including 4 patients with type A). Aortic dissection with thrombosed false lumen (n ⫽ 10, including 2 patients with type A) was defined by a large amount of intramural From the Departments of Internal Medicine II and Radiology, Iwate Medical University, Morioka, Japan. Dr. Makita’s address is: Department of Internal Medicine II, Iwate Medical University, 19-1 Uchimaru, Morioka 020-8505, Japan. E-mail: [email protected]. Manuscript received November 22, 1999; revised manuscript received and accepted January 27, 2000.
242
©2000 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 86 July 15, 2000
MD,
thrombus with intimal disruption (entry), as distinct from penetrating atherosclerotic ulcer.8 On the day of onset, the findings of hyperdense precontrast crescent in the aortic wall, no intimal flap, no intimal disruption, and no compressed aortic lumen, were considered diagnostic of intramural hematoma (n ⫽ 20, including 5 patients with type A). All participants were initially treated according to a single protocol as follows. During a 4- to 7-day stay in an intensive care unit, systolic blood pressure was maintained at ⬍130 mm Hg. Nicardipine hydrochloride was intravenously infused for the first 48 hours from onset, if appropriate. Thereafter, oral antihypertensive medications were administered in a fixed order. All patients underwent a uniform rehabilitation program that facilitated a stepwise restoration to normal daily life over a 3-week period. Contrast-enhanced electron beam CT was performed on the day of onset, after a few days, and thereafter at 1-week intervals for 4 to 5 weeks during hospitalization. Subsequent follow-up by electron beam CT was carried out at 3-month intervals after discharge (average 16 months). All tests consisted of early and delayed images, and changes in aortic condition were carefully evaluated by a specially trained radiologist and 2 physicians. In intramural hematoma and aortic dissection with thrombosed false lumen, 3 types of serious evolution of hematoma or thrombus were anticipated: (1) perceptible enlargement of localized contrast filling, suggesting secondary formed microdisruption of the intima9 or initial entry site, (2) abrupt expansion of the hematoma or thrombus, and (3) transition to classic dissection. These findings were designated as intramural events. Circulating CRP levels were measured daily until the initial peak had passed, and thereafter once or twice a week until discharge. The measurements were properly added when an abnormal change was found. Re-elevation of CRP levels was defined as an elevation of ⬎1.0 mg/dl after the initial peak level. CRP was measured by latex agglutination nephelometry with an assay sensitivity of 0.3 mg/dl and a normal range of ⬍0.6 mg/dl. The study protocol was approved by our hospital ethics committee, and informed consent was obtained from all subjects. Intergroup differences in the proportion of patients with CRP re-elevation were compared by chi-square test. The unpaired Student’s t test was used for comparison of CRP levels between the groups. Significance was set at p ⬍0.05. All values are expressed as mean ⫾ SD. In 9 of 20 patients with intramural hematoma, 0002-9149/00/$–see front matter PII S0002-9149(00)00869-9
TABLE I Factors Influencing Behavior of C-Reactive Protein (CRP) Levels in Patients With Intramural Hematoma and Aortic Dissection With Thrombosed False Lumen Frequences of CRP Re-elevation Factors Presence of intramural event Increase in aortic diameter Involvement of ascending aorta ⬍64 yrs (median)
Factor (⫹) 14/16 2/2 3/7 11/16
(88%) (100%) (43%) (69%)
Factor (⫺) 0/14 12/28 11/23 3/14
(0%) (43%) (48%) (21%)
intramural events were found during follow-up: enlargement of newly occurring localized contrast filling (7 patients), hematoma expansion with recurrent back pain on day 14 (1 patient), and transition to classic dissection on day 21 (1 patient). In contrast, 7 of 10 patients with aortic dissection with thrombosed false lumen had intramural events: enlargement of initial localized contrast filling (4 patients) and enlargement of newly occurring localized contrast filling (3 patients). All 16 intramural events were confirmed by electron beam CT. Ten of the 14 patients with enlarged localized contrast filling progressed to localized aortic dissection or saccular aneurysm on subsequent follow-up after discharge. In patients with classic dissection, organ malperfusion by obliteration of the true aortic lumen developed in 2 cases. Both underwent emergency surgical aortic intimal fenestration; 1 had visceral ischemia on day 14 and the other had bilateral renal ischemia on day 31. Another 2 patients showed gradual thrombosis in the false lumen without any organ malperfusion. As shown in the Table I, although CRP re-elevation was found in 14 of the 16 patients (88%) with intramural hematoma and aortic dissection with thrombosed false lumen and intramural events, none of the 14 patients without events had re-elevation of CRP levels (p ⬍0.01). CRP levels after 3 weeks were significantly higher in patients with intramural events than in those without (5.5 ⫾ 5.4 vs 1.4 ⫾ 1.3 mg/dl, p ⬍0.01). An increase in aortic diameter during intervals of electron beam computed tomographic testing during hospitalization and involvement of the ascending aorta had no effect on CRP levels. In a comparison by age with division around the median of 64 years, frequency of CRP re-elevation in the younger patients was significantly higher than that in the older patients (69% vs 21%, p ⬍0.05). However, there was no significant difference in CRP levels between the 2 age groups after 3 weeks. As shown in Figure 1, most of the patients with intramural hematoma and aortic dissection with thrombosed false lumen showed CRP levels within the normal range on the day of onset, and subsequently attained initial peak levels within 3 to 8 days (average 4.2). Initial peak levels in patients with intramural events were significantly higher than in patients without events (16.8 ⫾ 6.3 vs 12.4 ⫾ 3.8 mg/dl, p ⬍0.05). In the latter group, CRP levels gradually decreased, and most had recovered to within the normal range within 3 to 4 weeks (Figure 1). In contrast, even after 5 weeks, CRP levels were still above the normal range
CRP Levels After 3 Weeks p Value
Factor (⫹)
⬍0.01 NS NS ⬍0.05
5.5 3.9 3.6 4.8
⫾ ⫾ ⫾ ⫾
5.4 0.7 3.0 5.6
Factor (⫺)
p Value
⫾ ⫾ ⫾ ⫾
⬍0.01 NS NS NS
1.4 3.7 3.7 2.3
1.3 4.6 4.9 1.9
FIGURE 1. Changes in CRP levels in patients with intramural hematoma and aortic dissection with thrombosed false lumen, without (A) or with (B) intramural events. Day 1 means day of onset. Black circles, time points of intramural event verified by electron beam CT. White circles, time points of CRP re-elevation. Horizontal line graphs, intervals of intramural event and CRP re-elevation. Isolated black circles (2), patients without CRP reelevation.
in all but 3 of the patients with intramural events. In 14 patients with CRP re-elevation, the time difference of re-elevation from initial confirmation of event was 1.7 ⫾ 4.5 days (range ⫺7 to 7). These 2 phenomena were considered to be closely associated (Figure 1). Although 2 patients with events did not have CRP re-elevation, 1 did show an increase of 5.1 mg/dl after 3 weeks; however, no specific abnormality was detected in the other subject. In the patients with classic dissection, 4 of 13 patients showed CRP re-elevation; 2 of these patients had a gradual thrombosis in false lumen and 1 patient had renal malperfusion. No cause could be identified in the remaining patient (Figure 2). BRIEF REPORTS
243
instability of intramural thrombus or hematoma, defined as enlargement of localized contrast filling, transition to classic dissection, or expansion of hematoma in the aortic wall. In classic dissection, the abnormal behavior of CRP levels could be partly explained by gradual thrombosis in false lumen. The evaluation of CRP levels may serve as a useful marker for early and noninvasive detection of aortic events and for conservative management in patients with acute aortic dissection and intramural hematoma. FIGURE 2. Changes in CRP levels in patients with classic dissection. Black arrows, CRP re-elevation (on the second peak) in patients with progression of thrombosis in false lumen. White arrow, CRP re-elevation (on the second peak) without definite aortic event. Black squares, 2 patients who underwent surgical intimal fenestration for organ malperfusion on the day of surgery.
•••
This study revealed re-elevation or retarded recovery of CRP levels in a proportion of patients with aortic dissection or intramural hematoma. Especially in cases with intramural hematoma and aortic dissection with thrombosed false lumen, such abnormal behavior of CRP levels corresponded with intramural events. In conclusion, re-elevation and retarded recovery of CRP levels were considered to reflect an
1. Schor JS, Yerlioglu ME, Galla JD, Lansman SL, Ergin MA, Griepp RB.
Selective management of acute type B aortic dissection: long-term follow-up. Ann Thorac Surg 1996;61:1339 –1341. 2. Vilacosta I, San Roman JA, Ferreiros J, Aragoncillo P, Mendez R, Castillo JA, Rollan MJ, Batlle E, Peral V, Sanchez-Harguindey L. Natural history and serial morphology of aortic intramural hematoma: a novel variant of aortic dissection. Am Heart J 1997;134:495–507. 3. Robbins RC, McManus RP, Mitchell RS, Latter DR, Moon MR, Olinger GN, Miller DC. Management of patients with intramural hematoma of the thoracic aorta. Circulation 1993;88:II1–10. 4. Mohr-Kahaly S, Erbel R, Kearney P, Puth M, Meyer J. Aortic intramural hemorrhage visualized by transesophageal echocardiography: findings and prognostic implications. J Am Coll Cardiol 1994;23:658 – 664. 5. Nienaber CA, von Kodolitsch Y, Petersen B, Loose R, Helmchen U, Haverich A, Spielmann RP. Intramural hemorrhage of the thoracic aorta; diagnostic and therapeutic implications. Circulation 1995;92:1465–1472. 6. Ide K, Uchida H, Otsuji H, Nishimine K, Tsushima J, Ohishi H, Kitamura S. Acute aortic dissection with intramural hematoma: possibility of transition to classic dissection or aneurysm. J Thorac Imaging 1996;11:46 –52. 7. Hara K, Yamaguchi T, Wanibuchi Y, Kurokawa K. The role of medical treatment of distal type aortic dissection. Int J Cardiol 1991;32:231–240. 8. Kazerooni EL, Bree RL, Williams DM. Penetrating atherosclerotic ulcers in the descending thoracic aorta: evaluation with CT and distinction from aortic dissection. Radiology 1992;183:759 –765. 9. Williams MP, Farrow R. Atypical patterns in the CT diagnosis of aortic dissection. Clin Radiol 1994;49:686 – 689.
Left Atrial Kinetic Energy in AL Amyloidosis: Can It Detect Early Dysfunction? Laura Murphy,
MD,
and Rodney H. Falk,
L amyloidosis (formerly known as primary amyloidosis) is characterized by extracellular infiltraA tion of various organs by a proteinaceous material derived from monoclonal light chain fragments.1 Clinical evidence of cardiac involvement occurs in 30% to 50% of patients, resulting in congestive heart failure with predominant diastolic dysfunction.2 The Doppler features of restrictive physiology have been well described and include a shortened transmitral E-wave deceleration time associated with a decreased peak A-wave velocity.3 Cardiac infiltration in AL amyloidosis occurs in all 4 chambers, raising the possibility that atrial systolic dysfunction may play a role in the diminished A wave seen in patients with more adFrom the Section of Cardiology, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts. Dr. Falk’s address is: Boston Medical Center, Boston University School of Medicine, 88 East Newton Street, Boston, Massachusetts 02118. E-mail: [email protected]. Manuscript received September 17, 1999; revised manuscript received and accepted February 7, 2000.
244
©2000 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 86 July 15, 2000
MD
vanced disease.4 Because atrial function may be more vulnerable than ventricular function to minor structural changes, it is possible that the decreased A-wave velocity in some patients is due to primary atrial failure caused by amyloid infiltration. Left atrial function has been assessed by the left atrial stroke work index calculated from invasively assessed parameters.5,6 Recently, left atrial stroke work has been shown to correlate well with noninvasively derived left atrial kinetic energy.7 We postulated that, if early left atrial dysfunction is present in AL amyloidosis, it should be identified by this sensitive index of left atrial function. •••
The echocardiograms of 10 patients with echocardiographic features of cardiac AL amyloidosis and biopsy-proved AL amyloid were selected at random from the Boston University Amyloid Research and Clinical Center echocardiographic database. Ten agematched AL amyloid, biopsy-proved patients with no 0002-9149/00/$–see front matter PII S0002-9149(00)00870-5