Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3737_Библиотеки_им_академика_М_И_Перельмана
.pdf
222
https://t.me/med1917
(class III) [2, 57]
thickness≥3cm or<1.7cm [2, 57]
larger than mass removed by myectomy (6 +/− 4g)
[75]
cases with necrosis conned to R side of septum,
• Should not be performed in patients <21years old
• Discouraged in patients younger than 40 [2, 57]
• Discouraged in patients with septal
• Muscle necrosis induced by ASA (16 +/− 7g) is
• Variability of treatment effect (up to 25% of ASA
sparing anterior basal septum and LVOTO) [3]
• Higher reoperation rate than SM (10%) [76]
bypass
• Necessitates median sternotomy, cardiopulmonary
intervention has become favored approach for
• Decreasing familiarity worldwide as percutaneous
D. B. Loriaux et al.
majority of patients [65]
travel to center of excellence [77]
• Surgical expertise for procedure often necessitates
• Higher frequency of post- operative bleeding
• Longer post-operative LOS [68, 72]
• 2–3× Higher mean cost of hospitalization (40–50k)
[72]
• Safety; procedural mortality <1% [74]
• Long-term survival=general population [74]
• Less invasive
• Shorter procedural time
• Shorter post-operative LOS [73]
• Any procedural complication: 23.2% [72]
• Convert to open surgical procedure: 2% [72]
• RBBB (60%) [3]
• Intraprocedural CHB: 39.6% [71]
• Post-op PPM: 8–17% [72, 73]
Alcohol septal
ablation
Procedure Overview of complications Advantages Disadvantages
Table 9 Summary of outcomes and complications for septal reduction therapies
number of myectomies performed annually [4]
• Lower healthcare cost (15–20k) [72]
• Rising prevalence, now greatly outnumbering
(1.7%) [71]
• PPM placed beyond 30days post-discharge
[72]
• Hemorrhage requiring transfusion: 1.4%
• Pericardial complications: <0.5% [72]
• CVA/TIA: <0.5% [72]
• Safety; procedural mortality <1% [77, 78]
• DVT/PE: <0.5% [72]
• Need for repeat ablation: 17% [71]
• Any procedural complication: 30% [72]
Surgical
obstruction by operating surgeon allows more
tailored resection to distribution of septal
thickening [77]
• Long-term survival=general population [77]
• Direct visualization of outow tract
[72]
• Hemorrhage requiring transfusion: 5.4%
• LBBB (50%) [73]
• Post-op PPM: 8–10% [65, 72, 73]
myectomy
surgical lesions if needed [77]
• Permits concomitant correction of other
(4.3%) [71]
• PPM placed beyond 30days post-discharge
• Pericardial complications: 0.2% [72]
patients receiving medical management [74]
• Survival advantage over symptomatic HCM
• DVT/PE: 1.5% [72]
relative to septal ablation [73]
• Lower likelihood of requiring permanent PPM
• No post-operative intramyocardial scar [77]
• Less myocardium affected (6–10 g) [4]
• Lower reoperation rate than ASA (1–2%) [76]
• Infection: 3.3% [72]
• Pressure ulcer: 0.6% [72]
Comparison of complications, advantages, and disadvantages of common septal reduction therapies
ASA alcohol septal ablation, CHB complete heart block, CVA cerebrovascular accident, DVT deep vein thrombus, HCM hypertrophic cardiomyopathy, LBBB left bundle branch
block, LOS hospital length of stay, PE pulmonary embolism, PPM permanent pacemaker, RBBB right bundle branch block, SM surgical myectomy
Alcohol Septal Ablation intheManagement ofHypertrophic Obstructive Cardiomyopathy (HOCM)
https://t.me/med1917
223
Chapter Review Questions
1. What patient characteristics would favor surgical myectomy over alcohol septal ablation?
A. Age<21years
B. Baseline RBBB
C. Septal thickness>3cm
D. Prior median sternotomy
E. SAM
F. A and C
G. B and D
H. All of the above
Answer: F
Explanation: Alcohol septal ablation
should not be performed in patients less than
21years of age [57]. Alcohol septal ablation is
discouraged in patients younger than 40years
of age, those with extreme septal thickness
(≥30 mm), or those with septal thickness<17mm [2, 73]. The presence of SAM in
the absence of intrinsic mitral valve pathology
does not favor surgical myectomy. Surgical
myectomy is favored over septal ablation
when mitral regurgitation is secondary to primary mitral valve disease requiring concomitant MV repair or replacement.
2. A patient with baseline LBBB is undergoing
alcohol septal ablation. What is the approximate likelihood that this patient will require
permanent pacemaker placement prior to hospital discharge?
A. <5%
B. 10%
C. 25%
D. 33%
E. ≥50%
Answer: E
Explanation: The prevalence of complete
heart block following ASA is 15–20%
(Table7). The prevalence of RBBB following
ASA is approximately 60% (Table9) [3]. For
patients with pre-existing LBBB undergoing
ASA, the likelihood of requiring a permanent
pacemaker post-procedurally is greater than
50%.
3. For the patient with suspected HCM who has
inadequate windows on chest wall echocardiogram, the best diagnostic study would be:
A. Cardiac CT
B. TEE
C. CMR
D. Coronary angiography with right heart
catheterization
E. B or C
Answer: C
Explanation: Comprehensive transtho-
racic echocardiography plays the primary role
in establishing the diagnosis of HCM. For
patients suspected to have HCM in whom
TTE is inconclusive, CMR imaging carries a
Class I indication for diagnostic clarication
(Fig.9) [2, 21].
4. For which of the following patients with
symptomatic HCM would a stress echocardiogram be indicated?
A.
a
B.
b
224
c
d
https://t.me/med1917
D. B. Loriaux et al.
C.
be measured. Which of the following imaging
studies would be the most appropriate diagnostic test for this patient?
A. Cardiac CT
B. Transesophageal echocardiogram
C. Cardiac MRI
D. Cardiac SPECT
E. Left and right heart catheterization
Answer: C
Explanation: CMR is indicated for diag-
nostic clarication in cases of suspected
obstructive HCM when transthoracic echocardiography is inconclusive (Class I, LOE
D.
B-NR) [2].
References
1. Eugene Braunwald DLM, Zipes DP, Libby P, Bonow
RO, editors. Braunwald’s heart disease: a textbook
of cardiovascular medicine, vol. 11. Philadelphia:
Elsevier/Saunders; 2015.
2. Ommen SR, etal. 2020 AHA/ACC guideline for the
diagnosis and treatment of patients with hypertrophic
cardiomyopathy: a report of the American College of
Answer: B
Explanation: LVOT gradients can be
dynamic and may be missed on resting echocardiography for up to 50% of patients with
obstructive physiology [79]. Stress echocardiography can be most helpful for patients
where the presence or severity of LVOTO is
uncertain after resting echocardiography.
Choice B is the only option above showing a
non-diagnostic LVOT gradient; stress echocardiography could be considered for this
patient.
5. A 55year-old woman with past medical history of severe COPD and morbid obesity presents to the Emergency Department after a
syncopal event. Her physical examination is
notable for a harsh systolic murmur heard
along the left sternal border. A transthoracic
echocardiogram is ordered and notable for
severe left ventricular hypertrophy (septal
wall thickness 2.1 cm). Due to limited windows, a gradient across the LVOT could not
Cardiology/American Heart Association joint committee on clinical practice guidelines. J Am Coll
Cardiol. 2020;76(25):e159–240.
3. Douglas JS Jr. Current state of the roles of alcohol
septal ablation and surgical myectomy in the treatment of hypertrophic obstructive cardiomyopathy.
Cardiovasc Diagn Ther. 2020;10(1):36–44.
4. Gimeno JR, Tomé MT, McKenna WJ.Alcohol septal
ablation in hypertrophic cardiomyopathy: an opportunity to be taken. Revista Española de Cardiología
(English Edition). 2012;65(4):314–8.
5. Matsuda J, et al. Relationship between procedural
right bundle branch block and 1-year outcome after
alcohol septal ablation for hypertrophic obstructive cardiomyopathy—a retrospective study. Circ J.
2021;85(9):1481–91.
6. Maron MS, Rowin EJ, Maron BJ. How to image
hypertrophic cardiomyopathy. Circ Cardiovasc
Imaging. 2017;10(7):e005372.
7. Soor GS, etal. Hypertrophic cardiomyopathy: current
understanding and treatment objectives. J Clin Pathol.
2009;62(3):226–35.
8. Valente AM, etal. Comparison of echocardiographic
and cardiac magnetic resonance imaging in hypertrophic cardiomyopathy sarcomere mutation carriers
without left ventricular hypertrophy. Circ Cardiovasc
Genet. 2013;6(3):230–7.
9. Germans T, et al. Structural abnormalities of the
inferoseptal left ventricular wall detected by cardiac magnetic resonance imaging in carriers of
Alcohol Septal Ablation intheManagement ofHypertrophic Obstructive Cardiomyopathy (HOCM)
https://t.me/med1917
225
hypertrophic cardiomyopathy mutations. J Am Coll
Cardiol. 2006;48(12):2518–23.
10. Brouwer WP, et al. Multiple myocardial crypts on
modied long-axis view are a specic nding in prehypertrophic HCM mutation carriers. Eur Heart J
Cardiovasc Imaging. 2012;13(4):292–7.
11. Maron MS, et al. Prevalence, clinical signicance,
and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy. Circulation.
2008;118(15):1541–9.
12. Weinsaft JW, etal. LV thrombus detection by routine
echocardiography: insights into performance characteristics using delayed enhancement CMR. JACC
Cardiovasc Imaging. 2011;4(7):702–12.
13. Authors/Task Force Members, etal. 2014 ESC guidelines on diagnosis and management of hypertrophic
cardiomyopathy: the task force for the diagnosis and
Management of Hypertrophic Cardiomyopathy of the
European Society of Cardiology (ESC). Eur Heart J.
2014;35(39):2733–79.
14. Prinz C, et al. Myocardial brosis severity on cardiac magnetic resonance imaging predicts sustained
arrhythmic events in hypertrophic cardiomyopathy.
Can J Cardiol. 2013;29(3):358–63.
15. Bruder O, et al. Myocardial scar visualized by
cardiovascular magnetic resonance imaging predicts major adverse events in patients with hypertrophic cardiomyopathy. J Am Coll Cardiol.
2010;56(11):875–87.
16. O'Hanlon R, etal. Prognostic signicance of myocardial brosis in hypertrophic cardiomyopathy. J Am
Coll Cardiol. 2010;56(11):867–74.
17. Rubinshtein R, etal. Characteristics and clinical signicance of late gadolinium enhancement by contrastenhanced magnetic resonance imaging in patients
with hypertrophic cardiomyopathy. Circ Heart Fail.
2010;3(1):51–8.
18. Adabag AS, et al. Occurrence and frequency of
arrhythmias in hypertrophic cardiomyopathy in
relation to delayed enhancement on cardiovascular magnetic resonance. J Am Coll Cardiol.
2008;51(14):1369–74.
19. Maron MS, etal. Clinical prole and signicance of
delayed enhancement in hypertrophic cardiomyopathy. Circ Heart Fail. 2008;1(3):184–91.
20. Semsarian C, etal. New perspectives on the prevalence of hypertrophic cardiomyopathy. J Am Coll
Cardiol. 2015;65(12):1249–54.
21. Maron BJ, etal. Diagnosis and evaluation of hypertrophic cardiomyopathy: JACC state-of-the-art review. J
Am Coll Cardiol. 2022;79(4):372–89.
22. Seidman JG, Seidman C.The genetic basis for cardiomyopathy: from mutation identication to mechanistic paradigms. Cell. 2001;104(4):557–67.
23. Teare D. Asymmetrical hypertrophy of the heart in
young adults. Br Heart J. 1958;20(1):1–8.
24. Geisterfer-Lowrance AAT, et al. A molecular basis
for familial hypertrophic cardiomyopathy: a β cardiac
myosin heavy chain gene missense mutation. Cell.
1990;62(5):999–1006.
25. Coats CJ, Hollman A.Hypertrophic cardiomyopathy:
lessons from history. Heart. 2008;94(10):1258–63.
26. Morrow AG, etal. Operative treatment in idiopathic
hypertrophic subaortic stenosis. Techniques, and
the results of preoperative and postoperative clinical and hemodynamic assessments. Circulation.
1968;37(4):589–96.
27. Sigwart U. Non-surgical myocardial reduction for
hypertrophic obstructive cardiomyopathy. Lancet.
1995;346(8969):211–4.
28. Knight C, et al. Nonsurgical septal reduction for
hypertrophic obstructive cardiomyopathy: outcome in the rst series of patients. Circulation.
1997;95(8):2075–81.
29. Maron BJ, Nishimura RA. Surgical septal myectomy versus alcohol septal ablation: assessing
the status of the controversy in 2014. Circulation.
2014;130(18):1617–24.
30. Veselka J, et al. Long-term clinical outcome after
alcohol septal ablation for obstructive hypertrophic
cardiomyopathy: results from the Euro-ASA registry.
Eur Heart J. 2016;37(19):1517–23.
31. Durand E, etal. Non-surgical septal myocardial reduction by coil embolization for hypertrophic obstructive
cardiomyopathy: early and 6 months follow-up. Eur
Heart J. 2008;29(3):348–55.
32. Greenbaum AB, etal. Transcatheter myotomy to treat
hypertrophic cardiomyopathy and enable transcatheter mitral valve replacement: rst-in-human report
of septal scoring along the midline endocardium. Circ
Cardiovasc Interv. 2022;15(6):e012106.
33. Hardarson T, et al. Prognosis and mortality of
hypertrophic obstructive cardiomyopathy. Lancet.
1973;302(7844):1462–7.
34. Mandes L, et al. The role of echocardiography for
diagnosis and prognostic stratication in hypertrophic
cardiomyopathy. J Echocardiogr. 2020;18(3):137–48.
35. Marian AJ, Braunwald E.Hypertrophic cardiomyopathy: genetics, pathogenesis, clinical manifestations,
diagnosis, and therapy. Circ Res. 2017;121(7):749–70.
36. Maron MS, et al. Hypertrophic cardiomyopathy is
predominantly a disease of left ventricular outow
tract obstruction. Circulation. 2006;114(21):2232–9.
37. Adawi S, etal. Echocardiographic Brockenbrough–
Braunwald–Morrow sign. Eur J Echocardiogr.
2011;12(3):E12.
38. Brockenbrough EC, Braunwald E, Morrow AG. A
hemodynamic technic for the detection of hypertrophic
subaortic stenosis. Circulation. 1961;23(2):189–94.
39. Dybro AM, et al. Randomized trial of metoprolol in
patients with obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol. 2021;78(25):2505–17.
40. Bonow RO, etal. Effects of verapamil on left ventricular systolic function and diastolic lling in patients
with hypertrophic cardiomyopathy. Circulation.
1981;64(4):787–96.
41. Delatycki MB, Corben LA. Clinical features of
Friedreich ataxia. J Child Neurol. 2012;27(9):1133–7.
42. Calore C, et al. Abstract 15703: Hypertrophic
cardiomyopathy with normal ECG: clinical
226
https://t.me/med1917
D. B. Loriaux et al.
meaning and prognostic implications. Circulation.
2018;124:A15703.
43. O'Hanlon R, Assomull RG, Prasad SK. Use of cardiovascular magnetic resonance for diagnosis and
management in hypertrophic cardiomyopathy. Curr
Cardiol Rep. 2007;9(1):51–6.
44. Olivotto I, etal. Assessment and signicance of left
ventricular mass by cardiovascular magnetic resonance in hypertrophic cardiomyopathy. J Am Coll
Cardiol. 2008;52(7):559–66.
45. Spiewak M, etal. Comparison between maximal left
ventricular wall thickness and left ventricular mass in
patients with hypertrophic cardiomyopathy. Kardiol
Pol. 2010;68(7):6.
46. Schulz-Menger J, etal. Left ventricular outow tract
planimetry by cardiovascular magnetic resonance differentiates obstructive from non-obstructive hypertrophic cardiomyopathy. J Cardiovasc Magn Reson.
2006;8(5):741–6.
47. Vogel-Claussen J, et al. Cardiac MRI evaluation of
hypertrophic cardiomyopathy: left ventricular outow tract/aortic valve diameter ratio predicts severity of LVOT obstruction. J Magn Reson Imaging.
2012;36(3):598–603.
48. Huang L, etal. MRI native T1 and T2 mapping of
myocardial segments in hypertrophic cardiomyopathy: tissue remodeling manifested prior to structure
changes. Br J Radiol. 2019;92(1104):20190634.
49. van Dockum WG, et al. Myocardial infarction after
percutaneous transluminal septal myocardial ablation
in hypertrophic obstructive cardiomyopathy: evaluation by contrast-enhanced magnetic resonance imaging. J Am Coll Cardiol. 2004;43(1):27–34.
50. Henry WL, etal. Mechanism of left ventricular outow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic
subaortic stenosis). Am J Cardiol. 1975;35(3):337–45.
51. Levine RA, et al. Papillary muscle displacement
causes systolic anterior motion of the mitral valve.
Experimental validation and insights into the
mechanism of subaortic obstruction. Circulation.
1995;91(4):1189–95.
52. Shah PM, Taylor RD, Wong M. Abnormal mitral
valve coaptation in hypertrophic obstructive cardiomyopathy: proposed role in systolic anterior motion
of mitral valve. Am J Cardiol. 1981;48(2):258–62.
53. Maron MS, etal. Mitral valve abnormalities identied by cardiovascular magnetic resonance represent
a primary phenotypic expression of hypertrophic cardiomyopathy. Circulation. 2011;124(1):40–7.
54. Balaram SK, etal. Role of mitral valve plication in
the surgical management of hypertrophic cardiomyopathy. Ann Thorac Surg. 2012;94(6):1990–7.
55. Shah AA, Glower DD, Gaca JG. Trans-aortic Aleri
stitch at the time of septal myectomy for hypertrophic obstructive cardiomyopathy. J Card Surg.
2016;31(8):503–6.
56. Sherrid MV, et al. The mitral valve in obstructive
hypertrophic cardiomyopathy: a test in context. J Am
Coll Cardiol. 2016;67(15):1846–58.
57. Gersh BJ, et al. 2011 ACCF/AHA guideline for
the diagnosis and treatment of hypertrophic cardiomyopathy: a report of the American College of
Cardiology Foundation/American Heart Association
task force on practice guidelines. Circulation.
2011;124(24):e783–831.
58. Hong JH, etal. Mitral regurgitation in patients with
hypertrophic obstructive cardiomyopathy: implications for concomitant valve procedures. J Am Coll
Cardiol. 2016;68(14):1497–504.
59. Butzner M, etal. Stable rates of obstructive hypertrophic cardiomyopathy in a contemporary era. Front
Cardiovasc Med. 2021;8:765876.
60. Fifer MA. Controversies in cardiovascular medicine. Most fully informed patients choose septal ablation over septal myectomy. Circulation.
2007;116(2):207–16.
61. Spoladore R, etal. Pharmacological treatment options
for hypertrophic cardiomyopathy: high time for evidence. Eur Heart J. 2012;33(14):1724–33.
62. Braunwald E, Ebert PA. Hemodynamic alterations in idiopathic hypertrophic subaortic stenosis
induced by sympathomimetic drugs*. Am J Cardiol.
1962;10(4):489–95.
63. Desai MY, et al. Myosin inhibition in patients with
obstructive hypertrophic cardiomyopathy referred
for septal reduction therapy. J Am Coll Cardiol.
2022;80(2):95–108.
64. Spirito P, Rossi J, Maron BJ.Alcohol septal ablation:
in which patients and why? Ann Cardiothorac Surg.
2017;6(4):369–75.
65. Kim LK, etal. Hospital volume outcomes after septal
myectomy and alcohol septal ablation for treatment
of obstructive hypertrophic cardiomyopathy: US
Nationwide inpatient database, 2003–2011. JAMA
Cardiol. 2016;1(3):324–32.
66. Sorajja P, et al. Outcome of alcohol septal ablation for obstructive hypertrophic cardiomyopathy.
Circulation. 2008;118(2):131–9.
67. El Masry H, Breall JA. Alcohol septal ablation for
hypertrophic obstructive cardiomyopathy. Curr
Cardiol Rev. 2008;4(3):193–7.
68. Geske JB, Gersh BJ.Myectomy versus alcohol septal
ablation: experience remains key. JACC Cardiovasc
Interv. 2014;7(11):1235–6.
69. Veselka J, Tomasov P, Zemanek D.Long-term effects
of varying alcohol dosing in percutaneous septal ablation for obstructive hypertrophic cardiomyopathy: a
randomized study with a follow-up up to 11 years.
Can J Cardiol. 2011;27(6):763–7.
70. Wells S, etal. Clinical prole of nonresponders to surgical myectomy with obstructive hypertrophic cardiomyopathy. Am J Med. 2018;131(6):e235–9.
71. Batzner A, etal. Survival after alcohol septal ablation
in patients with hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol. 2018;72(24):3087–94.
72. Panaich SS, et al. Results of ventricular septal
myectomy and hypertrophic cardiomyopathy (from
Nationwide inpatient sample [1998–2010]). Am J
Cardiol. 2014;114(9):1390–5.
Alcohol Septal Ablation intheManagement ofHypertrophic Obstructive Cardiomyopathy (HOCM)
https://t.me/med1917
227
73. Nguyen A, et al. Surgical myectomy versus alcohol
septal ablation for obstructive hypertrophic cardiomyopathy: a propensity score-matched cohort. J Thorac
Cardiovasc Surg. 2019;157(1):306–315 e3.
74. Ommen SR, etal. Long-term effects of surgical septal myectomy on survival in patients with obstructive
hypertrophic cardiomyopathy. J Am Coll Cardiol.
2005;46(3):470–6.
75. Valeti US, etal. Comparison of surgical septal myectomy and alcohol septal ablation with cardiac magnetic resonance imaging in patients with hypertrophic
obstructive cardiomyopathy. J Am Coll Cardiol.
2007;49(3):350–7.
76. Cho YH, etal. Residual and recurrent gradients after
septal myectomy for hypertrophic cardiomyopathy-
mechanisms of obstruction and outcomes of reoperation. J Thorac Cardiovasc Surg. 2014;148(3):909–15.
77. Maron BJ.Controversies in cardiovascular medicine.
Surgical myectomy remains the primary treatment
option for severely symptomatic patients with obstructive hypertrophic cardiomyopathy. Circulation.
2007;116(2):196–206.
78. Rastegar H, etal. Results of surgical septal myectomy for obstructive hypertrophic cardiomyopathy: the tufts experience. Ann Cardiothorac Surg.
2017;6(4):353–63.
79. Woo A, et al. Clinical and echocardiographic determinants of long-term survival after surgical myectomy in obstructive hypertrophic cardiomyopathy.
Circulation. 2005;111(16):2033–41.
Percutaneous Closure
https://t.me/med1917
ofPost- myocardial Infarction
Ventricular Septal Rupture
JessicaRaviv andBarryLove
Abstract
Ventricular septal rupture is a rare sequala of
myocardial infarction typically appearing in
the rst week after the initial ischemic insult.
Early revascularization strategies have
reduced the incidence of post-myocardial
infarction ventricular septal defect (PMIVSD) to less than 1% of all myocardial infarctions however if they occur, the mortality
remains high. Surgical closure of PMI-VSD
carries a signicant mortality risk and high
chance of incomplete closure as the friable
margins of the defect do not hold sutures well.
Transcatheter closure of PMI-VSD was rst
reported in 1998. Results for primary transcatheter closure of PMI-VSD for large defects
associated with shock remain poor. Better outcomes for later close of smaller defects or
those who have residual VSD after attempted
surgical closure fare better. In this section, we
will describe a case of PMI-VSD and the strategies of transcatheter PMI-VSD closure.
Keywords
Myocardial infarction · Post-myocardial
infarction ventricular septal defect
J. Raviv · B. Love (*)
Icahn School of Medicine at Mount Sinai, Mount
Sinai Medical Center, NY, New York, USA
e-mail: Jessica.raviv@mssm.edu;
Barry.love@mssm.edu
Complications of myocardial infarction ·
Acquired ventricular septal defect · Device
closure
Abbreviations
CO Cardiac output
ECMO Extracorporeal membrane oxyge nation
ELSO Extracorporeal life support
LV Left ventricle
MI Myocardial infarction
PMI-VSD Post-myocardial infarction ventricu-
lar septal defect
RCA Right coronary artery
RV Right ventricle
SVR Systemic vascular resistance
TEE Transesophageal echocardiography
TTE Transthoracic echocardiography
VSD Ventricular septal defect
Test your learning and check your under-
standing of this book’s contents: use the
“Springer Nature Flashcards” app to
access questions using ▶ https://sn.pub/
ambACS.
To use the app, please follow the instruc-
tions in the chapter “Transcatheter
Aortic Valve Replacement.”
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
A. M. Kelsey et al. (eds.), Cardiac Imaging in Structural Heart Disease Interventions,
https://doi.org/10.1007/978-3-031-50740-3_8
229
230
https://t.me/med1917
Learning Objectives
1. Be able to suspect post-myocardial infarction
ventricular septal defect by symptoms and
clinical signs.
2. Diagnose PMI-VSD by transthoracic and/or
transesophageal echocardiography.
3. Understand the high mortality of PMI-VSD
when accompanied by shock.
4. Be able to calculate a pulmonary to systemic
ow ratio (Qp/Qs) by oximetry
measurements.
5. Appreciate bridging strategies including medical therapy, intraaortic balloon pump,
impella, ECMO.
6. Appreciate the advantages and disadvantages
of surgical and transcatheter treatment options
for closure of PMI-VSD.
J. Raviv and B. Love
Case Study
A 55 year old woman with poorly controlled diabetes, active smoker, history of
prior strokes with residual aphasia, and paroxysmal atrial brillation presented with
inferior ST elevation MI after 3 days of
chest pain. She was found to have a subtotal
occlusion of a dominant right coronary
artery and had successful percutaneous coronary intervention (Fig. 1). Despite successful PCI, her clinical condition worsened
with progressive shortness of breath and
orthopnea. Physical examination revealed a
2/6 holosystolic murmur at the left sternal
border. An echocardiogram was obtained
showing a basal ventricular septal rupture.
She was transferred for management.
Fig. 1 Selective right coronary angiography showing subtotal mid and total distal RCA occlusion (arrows). Post-PCI
ow has been reestablished with perfusion of the posterior descending coronary artery
Percutaneous Closure ofPost-myocardial Infarction Ventricular Septal Rupture
https://t.me/med1917
231
Background andDenitions
Post-myocardial infarction septal rupture (PMIVSD) occurs days to weeks after myocardial
infarction of a coronary territory supplying the
ventricular septum. With better reperfusion strategies for acute myocardial infarction, the incidence of PMI-VSD has decreased and now is
encountered in less than 1% of all myocardial
infarctions [1]. When PMI-VSD occurs, it typically leads to symptoms of heart failure and low
cardiac output as the left ventricular blood is
shunted through the VSD to the pulmonary artery
and back to the left ventricle. Physical examination will reveal a holosystolic murmur that may
be mistaken for mitral regurgitation. Septal
infarction at the margins of the heart may also
lead to cardiac pseudoaneurysm. Infarction of the
LAD territory usually leads to PMI-VSD in the
mid-septum to apex whereas infarctions in the
posterior descending territory tend to lead to
more basal-mid VSDs.
Diagnosis of the VSD is usually made by
transthoracic echocardiogram with color
Doppler interrogation of the septum in multiple
views. Transesophageal echocardiogram can be
additionally helpful in obtaining additional
views and is used for guiding transcatheter closure. The VSD itself is often serpiginous through
the infarcted septum. The extent of the VSD is
often underestimated as the margins of the hole
itself are surrounded by necrotic tissue that is not
stable enough to hold sutures or devices. The
extent of LV damage may be underestimated as
the LV free-wall function will usually appear
hyperdynamic and the overall EF may appear
quite good in the face of low afterload with much
of the cardiac output being diverted though the
VSD to the low-resistance pulmonary system.
As the pulmonary to systemic ow ratio (Qp/Qs)
increases, the systemic output falls and signs and
symptoms of shock emerge. Stabilization of
these patients prior to intervention is key as
“rushing” to do an intervention (surgical or
transcatheter) in the face of this deteriorating
clinical situation is invariably fatal. Placement of
an intraaortic balloon pump (IABP) and initiation of systemic afterload reduction as the blood
pressure allows will decrease the Qp/Qs and
increase systemic output. If more support is
needed, impella [2] ECMO [3] or other mechanical support can be contemplated but the chances
of salvage if that is required become increasingly
slim.
In a patient with a large PMI-VSD, the ratio of
pulmonary:systemic ow (Qp/Qs) can be calculated with the aid of a pulmonary artery catheter.
The formula is as follows:
Qp/Qs=Aortic sat (%) − Mixed venous sat
(%)/Pulmonary vein sat (%) − Pulmonary artery
sat (%).
The superior vena cava, SVC, saturation
obtained from the side port of an internal jugular
vein sheath is the best proxy for a mixed venous
saturation. The aortic saturation is the arterial
saturation obtained from an arterial line or pulse
oximeter. The pulmonary vein saturation is the
same as the aortic saturation as there is no signicant right to left shunt in this lesion, and the pulmonary artery saturation is obtained from the
pulmonary artery catheter. It is important to use a
co-oximeter to measure the saturation and not
use a blood gas machine that calculates an oxygen saturation as this may introduce considerable
error. Equally important is to do the Qp/Qs measurements on the lowest amount of oxygen that
produces an arterial saturation of 90–95%.
Higher inspired O2 leads to signicant dissolved
oxygen which may make the calculation less
accurate.
The method to estimate Qp/Qs by echocardiography is notoriously inaccurate and should
not be used.
In patients with signicant PMI-VSD and
shock, the Qp/Qs is usually >2:1.
Diagnosis andPre-procedural
Assessment
Transthoracic echocardiogram demonstrated a
basal PMI-VSD measuring about 1cm × 1.4cm
with left to right ow (Figs.2 and 3). The LV systolic function was normal (EF 55%) and the RV
function was moderately depressed. She was initially warm with good urine output and a loud
232
https://t.me/med1917
J. Raviv and B. Love
Fig. 2 Transthoracic echo (apical 4 chamber view) showing basal PMI-VSD and proximity to AV valves
holosystolic murmur was present. Her mentation
was normal. The lactate initially was 0.6mmol/L
with a creatinine of 2.5mg/dL however over the
course of the next 3days, her creatinine rose to
3.2 mg/dL and the lactate rose to 5.6 mmol/L
with corresponding decrease in urine output.
She was taken to the catheterization laboratory where a pulmonary artery catheter was
placed. The Qp/Qs was 2.8:1 (PA sat 83% SVC
61% Ao 95%) with a PA pressure of 42/15 (26)
and a wedge pressure of 16mmHg with a simultaneous blood pressure of 92/35 (70). An intraaortic balloon pump (IABP) was placed. In the rst
few hours, the lactate improved to 0.6mmol/L
and the Qp/Qs came down to 1.8:1. Over the next
3days with the addition of milrinone, her urine
output improved, and the creatinine normalized
to 1.3mg/dL.
Fig. 3 Transthoracic echo with color Doppler (modied
apical/parasternal) showing VSD with L to R ow
Heart Team Approach
andDiscussion
The patient had been stabilized with medical
management and IABP, but there continued to be
a signicant shunt. It had now been ~12 days
since the onset of chest pain.
Left unrepaired, PMI-VSD carried a mortality
of 90% within 2 months [4]. Surgical repair of
PMI-VSD itself however is not low risk. Mortality
has been reported between 19–60% [5]. A retrospective review of the STS database showed a
higher operative risk (54%) for those operated on
within 7days of the MI and a lower risk of mortality (18%) for those operated 8 days or more
after MI.However, this was a retrospective study
and it is likely that those who could wait were
also those who were less ill with a less extensive
Соседние файлы в папке Библиотека им академика М.И. Перельмана