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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3695_Библиотеки_им_академика_М_И_Перельмана
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CASE REPORTS IN CARDIOLOGY
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Figure 1 Diagram showing the usual location of carcinoid plaques in patients
with carcinoid heart disease. CS = coronary sinus ostium; I = innominate vein;
IVC=inferior vena cava; LA=left atrium; LV=left ventricle; MV=mitral valve;
RA=right atrium; RV=right ventricle; SVC=superior vena cava; TV=tricuspid
valve. Reproduced with permission from the authors (Ross EM and Roberts WC)
and the publisher (Elsevier).
(Figure2). At age 66 (2012), she underwent left breast lumpectomy for conrmed
cancer and received radiation to that breast and to the left axillary region. At age
67, peripheral edema, abdominal swelling, and weight gain appeared and each
progressively worsened over a 6-month period during which time she gained
40 pounds. Examination in August 2013 conrmed the presence of anasarca.
Facial ushing, diarrhea or labile blood pressure, if present, was not recorded.
Aprecordial murmur was described as absent. An electrocardiogram now showed
total 12-lead QRS of 51mm; incomplete right bundle branch block and atrial
premature complexes (Figure2). Echocardiogram disclosed both pulmonic and
tricuspid valve regurgitation, thickening of both valvular leaets, immobility of
the tricuspid valve leaets, severe dilatation of both right sided chambers, and no
dilatation of the left-sided chambers (Figure3). Cardiac catheterization disclosed
the following pressures in mm Hg: pulmonary artery, 30/10; right ventricle,
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CASE 1636 CLUES TO DIAGNOSING CARCINOID HEART DISEASE
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Figure 2 Electrocardiograms of the described patient at age 57 (December2001)
(upper) showing total 12-lead QRS voltage to be 158mm (measured with normal
[10mm] standardization [10mm = 1 mV]). Electrocardiogram from same patient
11years later at age 66 (2012) (lower) with right-sided heart failure showing total
12-lead QRS voltage to be 51mm, the presence of incomplete right bundle branch
block, and atrial premature complexes.
Figure 3 Transesophageal echocardiographic 4-chamber view showing right ventricular volume overload pattern with dilated right ventricle (RV) and right atrium
(RA) and paradoxical ventricular septal motion. Left ventricle (LV) and left atrium
(LA) are of normal size and there was no atrial septal defect (left). Three-dimensional
short-axis view of the right atrium (RA), right ventricle (RV) and aortic valve (AV).
The tricuspid leaets (arrows) are shortened, thickened and immobile, consistent
with carcinoid heart disease (right).
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Figure 4 Computed tomographic image of the abdomen showing enlarged liver
with innumerable masses.
43/18; right atrial mean 18 with V wave 25 and pulmonary arterial wedge mean
8. The cardiac index was 1.4 L/min/m
2
. The left ventricular ejection fraction was
approximately 60%. Coronary angiography disclosed insignicant narrowing
(<30% diameter reduction).
In September 2013, the pulmonic valve was replaced with a homograft and
the tricuspid valve, with a bioprosthesis (Edwards, Magna Ease). The tricuspid
valve leaets and chordae were sclerotic. Early postoperatively, excessive bleeding
necessitated reexploration. Computed tomographic examination of the heart during
the postoperative period disclosed an enlarged liver (23cm in greatest dimension)
containing innumerable masses (Figure4) and “focal thickening of the cecum and
terminal ileum.” During the entire 10-day post-operative period, the patient never
awoke and had fatal multi-organ “failure”.
Examination of the operatively-excised thickened pulmonic valve and of a
portion of the thickened right atrial wall disclosed classic changes of carcinoid heart
disease (Figure5). Necropsy was not performed.
DISCUSSION
The patient described had some clinical features suggesting the presence of
carcinoid heart disease. These features included severe isolated right-sided heart
failure (anasarca), thickened pulmonic and tricuspid valve leaets with severe
regurgitation of both valves and some stenosis of the pulmonic valve, the absence of
left-sided heart disease, the absence of pulmonary disease including the absence of
pulmonary hypertension, the presence of extremely low total 12-lead QRS voltage
on electrocardiogram, and, the clincher, the presence of classic superimposed
bromuscular tissue on the operatively excised pulmonic valve cusps and on the
mural endocardium of the right atrium (which was biopsied).
1–6
A major clue to diagnosis was the echocardiogram which showed severe rightsided dilatation unassociated with any left-sided dilatation or atrial septal defect.
Additionally, both tricuspid and pulmonic valve leaets were thickened and the
tricuspid leaets immobile, something not seen in patients with cor pulmonale.
The echocardiogram also suggested the absence of pulmonary hypertension, a
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CASE 1636 CLUES TO DIAGNOSING CARCINOID HEART DISEASE
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Figure 5 Histologic section of wall of right atrium (top, lower left) and pulmonic
valve cusp (lower right). Carcinoid plaque (stained green) is superimposed on the
mural endocardium of the right atrium and on the cusp and endocardium of the
pulmonic valve. Movat stains: x20 (upper); x100 (lower left); x40 (lower right).
requirement for the presence of cor pulmonale. And, most important, there was no
evidence of any pulmonary disease.
Because the patient had received radiation a year earlier for cancer of the left
breast, the thickening of the right-sided valves was attributed clinically to the
radiation-induced heart valve disease. An earlier study, however, had suggested that
signicant cardiac valve thickening secondary to radiation takes years as a rule to
occur after completion of the radiation therapy.
our patient was no more than 1year. Moreover, the radiation was limited to the left
breast and axilla, yet only the right-sided heart valves were involved, a pattern more
consistent with carcinoid heart disease than radiation injury.
Hemodynamic clues that carcinoid heart disease was the cause of the isolated
right-sided heart failure was the pressure gradient—albeit small (13mm Hg)—across
7
The interval between the 2 events in
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the pulmonic valve. Such gradients across this valve do not occur in patients with
cor pulmonale. The normal pulmonary arterial wedge pressure and the normal left
ventricular end-diastolic pressures in the presence of the very elevated right atrial
mean and right ventricular end-diastolic pressures rule out constrictive pericarditis
as the cause of the isolated rightsided heart failure.
The extremely low QRS voltage on electrocardiogram ts the picture of carcinoid
heart disease. Roberts and colleagues
8
studied total 12-lead QRS voltage in 11
different cardiac conditions (aortic stenosis, pure aortic regurgitation, pure mitral
regurgitation, hypertrophic cardiomyopathy, idiopathic dilated cardiomyopathy,
amyloid heart disease, cardiac adiposity and the carcinoid syndrome among others)
and found that the 19 patients with carcinoid heart disease had the lowest 12-lead
QRS voltage (mean 105) except for the 30 patients with cardiac amyloidosis who
had a total 12-lead mean QRS voltage of 104mm (measured with normal [10mm]
standardization [10mm=1mV]). Our patient near the end of life preoperatively had
a total 12-lead QRS voltage of 51mm!
And nally, the nding by computed tomography of multiple masses in the
liver occurs in nearly 100% of patients with the carcinoid syndrome with or without
carci noid heart disea se.
of the breast occurs in only about 20%.
4
In contrast, metast asis to the liver of a patient with carcinoma
9–13
The superimposed bromuscular tissue
devoid of elastic bers on the mural endocardium of right atrium and similar
tissue superimposed on the pulmonic valve cusps is diagnostic of carcinoid heart
disease.
1–6
DISCLOSURES
There are no conicts of interest for any author.
REFERENCES
1. Roberts WC, Sjoerdsma A. The cardiac disease associated with the carcinoid
syndrome (carcinoid heart disease). Am J Med 1964;36:5–34.
2. Roberts WC, Mason DT, Wright LD Jr. The non-distensible right atrium of carci-
noid disease of the heart. Am J Clin Pathol 1965;44:627–631.
3. Ferrans VJ, Roberts WC. The carcinoid endocardial plaque. An ultrastructural
study. Hum Pathol 1976;7:387–409.
4. Ross EM, Roberts WC. The carcinoid syndrome: comparison of 21 necropsy
subjects with carcinoid heart disease to 15 necropsy subjects without carcinoid
heart disease. Am J Med 1985;79:339–354.
5. Roberts WC. Aunique heart disease associated with a unique cancer: carcinoid
heart disease. Am J Cardiol 1997;80:251–256.
6. Roberts WC, Varughese CA, Ko JM, Grayburn PA, Hebeler RF Jr, Burton EC.
Carcinoid heart disease without the carcinoid syndrome but with quadrivalvular regurgitation and unsuccessful operative intervention. Am J Cardiol
2011;107:788 –792.
7. Brosius FC 3rd, Waller BF, Roberts WC. Radiation heart disease. Analysis of 16
young (aged 15 to 33years) necropsy patients who received over 3,500 rads to the
heart. Am J Med 1981;70:519–530.
8. Roberts WC, Filardo G, Ko JM, Siegel RJ, Dollar AL, Ross EM, Shirani J.
Comparison of total 12-lead QRS voltage in a variety of cardiac conditions and its
usefulness in predicting increased cardiac mass. Am J Cardiol 2013;112:904–909.
9. Van Walsum GAM, de Ridder JAM, Verhoef C, Bosscha K, van Gulik TM,
Hesselink EJ, Ruers TJM, van den Tol MP, Nagtegaal ID, Brouwers M, van
Hillegersberg R, Porte RJ, Rijken AM, Strobbe LJA, de Wilt JHW. Resection of
liver metastases in patients with breast cancer: survival and prognostic factors.
EJSO 2012;38:910–917.
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CASE 1636 CLUES TO DIAGNOSING CARCINOID HEART DISEASE
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10. Mariani P, Servois V, Rycke YD, Bennett SP, Feron JG, Alumbarak MM, Reyal F,
Baranger B, Pierga JY, Salmon RJ. Liver metastases from breast cancer: surgical
resection or not? Acase-matched control study in highly selected patients. EJSO
2013;39:1377–1383.
11. Kim JY, Park JS, Lee SA, Kim JK, Jeong J, Yoon DS, Lee HD. Does liver resection
provide long-term survival benets for breast cancer patients with liver metastasis? Asingle hospital experience. Yonsei Med J 2014;55:558–562.
12. Cummings MC, Simpson PT, Reid LE, Jayanthan J, Skerman J, Song S, McCart
Reed AE, Kutasovic JR, Morey AL, Marquart L, O’Rourke P, Lakhani SR.
Metastatic progression of breast cancer: insights from 50 years of autopsies. J
Pathol 2014;232:23–31.
13. Elsberger B, Roxburgh CS, Horgan PG. Is there a role for surgical resections of
hepatic breast cancer metastases? Hepatogastroenterology 2014;61:181–186.
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Case 1723 The Mitral Valve 16 Months After
Operative Insertion of the Alfieri Stitch
Samreen Fathima, MD, Shelley A. Hall, MD, Paul A. Grayburn, MD,
and William C. Roberts, MD*
We describe considerable brous thickening of the mitral leaets 16 months
after insertion of an Aleri stitch in a previously anatomically normal but
functionally regurgitant mitral valve. Whether this type of mitral thickening
will occur after percutaneous insertion of the mitral clip for pure mitral
regurgitation remains to be determined. © 2018 Elsevier Inc. All rights reserved.
(Am J Cardiol 2019;123:695–696)
1
In the early 1990s, Aleri et al
Stitch,” a bowtie procedure or edge-to-edge mitral valve repair for patients with
pure mitral regurgitation. The operation usually decreased the severity of the
mitral regurgitation and it usually reduced the pulmonary arterial pressure.
The procedure, however, was not without complications, a major one being the
conversion of the previous mitral regurgitation to mitral stenosis. Subsequently, of
course, percutaneous transcatheter mitral valve repair has proved to be effective and
has replaced the operative approach.
“the stitch” has been found.
“the stitch” operatively inserted months earlier.
introduced what became known as “The Aleri
2–5
6
The present report describes another patient who had
Only 1 published photo late after insertion of
CASE DESCRIPTION
A 19-year-old man, who was born in January1998, had heart failure (HF) shortly after
birth. The degree of HF waxed and waned during the next 15 or so years. By June2016
(age 17), the HF had reached the point that a left ventricular assist device was inserted
and at the same procedure an Aleri st itch was placed on the m itral leaet s to decreas e
the degree of functional mitral regurgitation. Neither the left ventricular assist device
nor the Aleri stitch proved to be benecial. The patient gained 40 pounds during
the next several months because of worsening HF. An echocardiogram 6 months
before the heart transplant showed mild mitral regurgitation, thickening of the distal
third of the mitral leaets, severe dilatation of both ventricular cavities, and severe
tricuspid valve regurgitation (Figure 1). Echocardiographic ndings before and
after placement of the Aleri stitch are summarized in Table1. In October2017 (age
18), heart transplantation was performed. Examination of the native heart showed
it to be typical of idiopathic dilated cardiomyopathy. It weighed 330 g. The mitral
leaets, which had been anatomically normal at the time of insertion of the Aleri
stitch, were now quite thickened by brous tissue, particularly in their distal halves
(Figure2). When contacted in November2018, 13 months after the heart transplant,
the patient was asymptomatic and working.
Baylor Scott & White Heart and Vascular Institute, the Departments of Pathology and
Internal Medicine (Division of Cardiology), Baylor University Medical Center, Dallas, Texas.
Manuscript received August7, 2018; revised manuscript received and accepted November12,
2018.
*
Corresponding author: Tel: (214) 820–7911; fax: (214) 820–7533.
E-mail address: William.Roberts1@bswhealth.org (W.C. Roberts).
266 DOI: 10.1201/9781003409281-56
CASE 1723 THE MITRAL VALVE 16 MONTHS AFTER OPERATIVE INSERTION OF THE ALFIERI STITCH
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Figure 1 Echocardiographic images after insertion of a left ventricular assist
device (LVAD) and Aleri stitch. (A) Parasternal long-axis view showing thickened
mitral leaets with restricted diastolic excursion (small arrows). Both ventricular
cavities and the left atrium are dilated (left ventricle at end-diastole=6.2cm, and
at peak systole=5.9cm). The LVAD cannula is seen at lower left (large arrow). (B)
Parasternal short-axis view showing Aleri stitch (arrow) with double orice mitral
valve. (C) Mean transmitral gradient is 3mm Hg by continuous wave Doppler.
DISCUSSION
Described in this report is considerable brous thickening of the mitral leaets after
insertion of an Aleri stitch 16 months earlier. Today, the Aleri stitch operation
is infrequently performed but the insertion of the mitral clip by the percutaneous
route is now frequently performed.
cause the leaets to thicken and potentially convert an occasional patient from pure
mitral regurgitation to mitral stenosis remains to be seen.
DISCLOSURES
The investigators have no conicts of interest to disclose.
2–4
Whether the percutaneous approach will also
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Figure 2 Photographs of the heart of patient described. (A). Cross section of the
ventricles at the level of tricuspid and mitral valves showing the ventricular aspect
of the Aleri stitch. (B) Aclose-up of the mitral valves from the ventricular aspect.
(C) View of the tricuspid and mitral valves after “deroong” the atrial walls. The
quantity of adipose tissue in the atrioventricular sulci is excessive.
Table 1: Echocardiographic data before and after placement of the Aleri stitch
Variable
Peak velocity in early diastolic transmitral ow (m/s) 1.8 1.1 1.0
Decel time (m/s) 230 89 282
Mean gradient (mm Hg) 0 6 3
Mitral regurgitation (0–3+) 3+ 1+ 3+
Left ventricular internal diameter end diastole (mm) 83 74 62
Left ventricular posterior wall, peak systole (mm) 69 – 59
Left ventricular posterior wall, end diastole (mm) 7 8 6
Left ventricular ejection fraction (%) 37 34 10
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Pre-OP
(days) Post-OP (days)
–10 +1 +330
CASE 1723 THE MITRAL VALVE 16 MONTHS AFTER OPERATIVE INSERTION OF THE ALFIERI STITCH
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REFERENCES
1. Aleri O, Maisano F, De Bonis M, Stefano PL, Torracca L, Oppizzi M, La Canna G.
The double-orice technique in mitral valve repair: a simple solution for complex
problems. J Thorac Cardiovasc Surg 2001;122:674–681.
2. Feldman T, Kar S, Rinaldi M, Fail P, Hermiller J, Smalling R. Percutaneous mitral
repair with the MitraClip system: safety and midterm durability in the initial
EVEREST (endovascular valve edge-to-edge repair study) cohort. J Am Coll Cardiol
2009;54:686–694.
3. Maisano F, La Canna G, Colombo A, Aleri O. The evolution from surgery to per-
cutaneous mitral valve interventions: the role of the edge-to-edge technique. J Am
Coll Cardiol 2011;58:2174–2182.
4. Feldman T, Foster E, Glower DD, Glower DG, Kar S, Rinaldi MJ, Fail PS, Smalling
RW, Siegel R, Rose GA, Engeron E, Loghin C, Trento A, Skipper ER, Fudge T,
Letsou GV, Massaro JM, Mauri L. EVEREST II Investigators. Percutaneous repair
or surgery for mitral regurgitation. N Engl J Med 2011;364:1395–1406.
5. Stone GW, Lindenfeld JA, Abraham WT, Kar S, Lim DS, Mishell JM, Whisenant B,
Grayburn PA, Rinaldi M, Kapadia SR, Rajagopal V, Sarembock IJ, Brieke A, Marx
SO, Cohen DJ, Weissman NJ, Mack MJ, for the COAPT Investigators. Transcatheter
mitral-valve repair in patients with heart failure. N Engl J Med 2018;379:2307–2318.
6. Privitera S, Butany J, Cusimano RJ, Silversides C, Ross H, Leask R. Aleri mitral
valve repair clinical outcome and pathology. Circulation 2002;106:173–174.
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