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_3590_Библиотеки_им_академика_М_И_Перельмана
.pdf
20—TRANSCATHETER CLOSURE OF PMI, IATROGENIC, AND VSDs 245
https://t.me/medicina_free
deterioration irrespective of the shunt closure in a dying patient.
1
Failure to implant the device is
relatively uncommon and was only reported in 1 out of the 18 patients who had transcatheter
closure of PMI-VSD in a case series from the Mayo Clinic.
1
This is comparable to data from
Landzberg and colleagues, who also reported failure to implant the device in 1 out of 18 patients
undergoing transcatheter closure of PMI-VSD using a clamshell double umbrella and the
CardioSEAL.
9
The failure to close the shunt even after proper device implantation can occur in about 15%
to 35% of cases and tends to be higher with PMI-VSD compared with other types of VSDs.
1,10
This complication can be prevented, or at least reduced, by appropriate device sizing and meticulous device deployment using echocardiography guidance. Quantitative assessment of residual
left-to-right shunting should be performed using angiography and the Fick method, and a decision should be made whether a second device can safely be deployed to treat residual shunt.
Clinical deterioration and death despite successful shunt closure can sometimes occur after device
closure of PMI-VSD, especially when the procedure is performed during the acute phase.
1,9,11
This outcome can be prevented by appropriate patient selection and perhaps delaying the procedure beyond the acute phase, if possible. Other potential acute procedural complications include
device embolization (particularly in apical PMI-VSD, where there may be inadequate tissue or
ongoing necrosis proximal to the device), heart block (especially in pmVSD or patients with
preceding conduction defect), new valvular regurgitation, and cardiac perforation. Late complications
include hemolysis requiring blood transfusion and endocarditis.
Summary and Take-home Messages
l
Transcatheter closure of VSDs is a less invasive treatment option for patients with suitable
anatomy for device closure and those who are considered high-risk candidates for surgical
therapy.
l
First, the VSD is crossed and an A-V “rail” from the femoral artery to the internal jugular
vein is established.
l
Based on the combination of angiographic and echocardiographic data, a muscular or PMI-
VSD occluder (as appropriate) that is 2 or 3 mm larger than the maximum diameter is
inserted across the VSD.
l
Potential acute procedural complications include device embolization, heart block, new
valvular regurgitation, and cardiac perforation. Late complications include hemolysis
requiring blood transfusion and endocarditis.
References
1. Egbe AC, Poterucha JT, Rihal CS, et al. Transcatheter closure of postmyocardial infarction, iatrogenic, and
postoperative ventricular septal defects: The Mayo Clinic experience. Catheter Cardiovasc Interv.
2015;86:1264-1270.
2. Holzer R, Balzer D, Amin Z, et al. Transcatheter closure of postinfarction ventricular septal defects using
the new Amplatzer muscular VSD occluder: Results of a U.S. registry. Catheter Cardiovasc Interv.
2004;61:196-201.
3. Killen DA, Piehler JM, Borkon AM, Gorton ME, Reed WA. Early repair of postinfarction ventricular
septal rupture. Ann Thorac Surg. 1997;63:138-142.
4. Menon V, Slater JN, White HD, Sleeper LA, Cocke T, Hochman JS. Acute myocardial infarction com-
plicated by systemic hypoperfusion without hypotension: Report of the SHOCK trial registry. Am J Med.
2000;108:374-380.
5. Pedra CA, Pontes SC Jr., Pedra SR, et al. Percutaneous closure of postoperative and post-traumatic ven-
tricular septal defects. J Invasive Cardiol. 2007;19:491-495.
246 5—VENTRICULAR SEPTAL INTERVENTIONS
https://t.me/medicina_free
6. Holzer R, Balzer D, Cao QL, Lock K, Hijazi ZM, Amplatzer Muscular Ventricular Septal Defect I.
Device closure of muscular ventricular septal defects using the Amplatzer muscular ventricular septal
defect occluder: Immediate and mid-term results of a U.S. registry. J Am Coll Cardiol. 2004;43:1257-1263.
7. Carminati M, Butera G, Chessa M, Drago M, Negura D, Piazza L. Transcatheter closure of congenital
ventricular septal defect with Amplatzer septal occluders. Am J Cardiol. 2005;96:52L-58L.
8. Chessa M, Carminati M, Cao QL, et al. Transcatheter closure of congenital and acquired muscular
ventricular septal defects using the Amplatzer device. J Invasive Cardiol. 2002;14:322-327.
9. Landzberg MJ, Lock JE. Transcatheter management of ventricular septal rupture after myocardial infarction. Semin Thorac Cardiovasc Surg. 1998;10:128-132.
10. Demkow M, Ruzyllo W, Kepka C, et al. Primary transcatheter closure of postinfarction ventricular
septal defects with the Amplatzer septal occluder: Immediate results and up-to 5 years follow-up. Euro-
Intervention. 2005;1:43-47.
11. Thiele H, Kaulfersch C, Daehnert I, et al. Immediate primary transcatheter closure of postinfarction
ventricular septal defects. Eur Heart J. 2009;30:81-88.
e1
https://t.me/medicina_free
Abstract: Ventricular septal defect (VSD) is an uncommon complication of myocardial infarction, and it is associated with high mortality if managed with medical therapy. Surgical closure of
VSD is also associated with high mortality, especially in the acute phase. Transcatheter therapy
provides a less invasive alternative to clinically stabilize these high-risk patients and potentially
reduce mortality. This chapter provides an overview of the indications and techniques for transcatheter closure of post–myocardial infarction VSD.
Keywords: Transcatheter; ventricular septal defect; myocardial infarction; heart failure
CHAPTER 21
https://t.me/medicina_free
Alcohol Septal Ablation for
Obstructive Hypertrophic
Cardiomyopathy
Thomas M. Waterbury Mackram F. Eleid
Background
Hypertrophic cardiomyopathy (HCM) is characterized by left ventricular hypertrophy not
explained by secondary causes, with a predisposition for outflow tract obstruction in some
patients. As the most commonly encountered genetic cardiac condition, HCM affects 1 out of
500 individuals in the general population with a myriad of morphologic variants and clinical
presentations.
variety of hemodynamic perturbations, including diastolic dysfunction, myocardial ischemia,
outflow obstruction, and mitral regurgitation. Left ventricular outflow tract (LVOT) obstruction, defined as a resting or provoked gradient over 30 mmHg, is present in over two-thirds of
patients with HCM.
anterior mitral leaflet abnormalities, and high ejection velocities of blood through the LVOT,
which in turn can pull or push the anterior mitral valve leaflet toward the muscular septum
(Fig. 21.1). This systolic anterior motion (SAM) leads to contact between the anterior mitral
valve leaflet and ventricular septum with consequent obstruction to blood flow and decrease in
forward stroke volume. In addition, mitral regurgitation may occur as a result of SAM
(Fig. 21.2). The degree of LVOT obstruction is a predictor of symptoms and heart failure in
patients with HOCM. Pharmacologic and invasive therapies are aimed at reducing symptomatic
LVOT obstruction in HOCM.
Medical therapy remains the first-line management strategy in patients with symptomatic HOCM. This predominantly involves the initiation of beta-blockers or calcium channel
blockers, which are effective at reducing LVOT obstruction through negative inotropic and
chronotropic properties. Disopyramide is an additional agent with negative inotropic effects
that can be used to improve symptoms. In select patients with refractory symptoms despite
medical therapy or those unable to tolerate pharmacologic titration, septal reduction therapy
may be required. Surgical septal myectomy, involving direct visualization and surgical resection of ventricular septal muscle, was previously the only available technique for invasive
septal reduction. However in the mid-1990s, the technique of transcatheter chemical septal
ablation was introduced as an alternative to surgery. Alcohol septal ablation (ASA) targets
relief of LVOT obstruction by creating a localized myocardial infarction in the basal septum
with resultant decreased contractility, and reduction in SAM. ASA has proven to be a safe
and effective strategy in clinical practice to reduce LVOT obstruction and improve symptoms in appropriate patients.
1
HCM can manifest with symptoms of dyspnea, chest pain, and syncope from a
1–2
Obstructive HCM (HOCM) results from narrowing of the LVOT,
247
248 5—VENTRICULAR SEPTAL INTERVENTIONS
https://t.me/medicina_free
Fig. 21.1 Schematic of left ventricular outflow tract obstruction and mitral regurgitation in obstructive
hypertrophic cardiomyopathy. (Used with permission of Mayo Foundation for Medical Education and
Research. All rights reserved.)
Fig. 21.2 Echocardiographic assessment of hypertrophic obstructive cardiomyopathy. (A) Transthoracic
apical long-axis view demonstrating systolic anterior motion of the mitral valve with septal contact. (B) Color
flow Doppler demonstrating turbulent LVOT flow and posteriorly directed mitral regurgitation jet. LA, Left
atrium; LV, left ventricle.
21—ALCOHOL SEPTAL ABLATION FOR OBSTRUCTIVE HYPERTROPHIC CARDIOMYOPATHY 249
https://t.me/medicina_free
AHA Guidelines
When surgery is contraindicated or the risk is considered unacceptable because of serious
comorbidities or advanced age, ASA can be beneficial in eligible adult patients with
HCM with LVOT obstruction and severe drug-refractory symptoms (usually New York
Heart Association [NYHA] functional classes III or IV).
ASA, when performed in experienced centers, may be considered an alternative to surgical
myectomy for eligible adult patients with HCM with severe drug-refractory symptoms
and LVOT obstruction when, after a balanced and thorough discussion, the patient
expresses a preference for septal ablation.
From Gersh BJ, Maron BJ, Bonow RO, et al. ACCF/AHA guideline for the diagnosis and treatment of hypertrophic
cardiomyopathy. Circulation. 2011;124:e783-e831.
IIa B
IIb B
ASA INDICATIONS AND PATIENT SELECTION
Septal reduction therapy is indicated in patients with HOCM who have severe (NYHA functional class III or IV) symptoms that limit quality of life despite optimization of medical
therapy. Additionally, patients should have severe LVOT obstruction, defined as a gradient
50 mmHg at rest or with provocative maneuvers, in addition to SAM.
preferred in older patients or in those with more extensive comorbidities for whom surgery is
deemed high risk. Excessive septal hypertrophy can decrease the efficacy of ASA, and therefore
the degree of septal thickness should be considered in patient selection. Generally in patients
with a septum thickness over 30 mm, surgical myectomy should be considered. Myectomy may
also be indicated in patients with coexisting valve disease or coronary atherosclerosis requiring
surgery.
Careful interrogation of the mitral valve by echocardiography should be performed before
ASA, as patients with primary abnormalities of the mitral valve, such as anomalous papillary
muscle insertion or cleft, may be better served by surgical intervention. The typical jet of mitral
regurgitation in HCM will direct posteriorly. Any other direction, central or anterior, should raise
a concern that there is something unusual, such as a single papillary muscle or predominant
midventricular obstruction.
In addition, the level of outflow tract obstruction is important. Patients with basal hypertrophy and obstruction with favorable septal artery anatomy are optimal candidates for ASA. Conversely, those with midcavity obstruction may require extended surgical myectomy for adequate
hemodynamic improvement and symptom relief.
Finally, patient preference should be incorporated into the selection process after an informed
discussion regarding risks, benefits, and current understanding of long-term outcomes between
ASA and surgical myectomy. ASA interventions should be performed in high-volume cardiac
catheterization laboratories by operators experienced with the procedure.
2–3
ASA is generally
CORONARY ANATOMY
The success and degree of symptom relief after ASA in patients with HOCM ultimately depend on
the septal coronary anatomy and correct identification of the vessel(s) supplying the myocardial region of interest. Coronary angiography is used to identify the branch most likely to supply the septal
distribution targeted for intervention. Angiography should include injections of both right and left
systems, as septal branches can occasionally originate from the right coronary artery, ramus, or branch
250 5—VENTRICULAR SEPTAL INTERVENTIONS
Baseline Postablation
https://t.me/medicina_free
Fig. 21.3 Septal perforator localization on coronary angiography. (A) Right anterior oblique view. (B) Left
anterior oblique view; first septal perforator (arrow).
from the left main. In most cases the first or second septal branch will arise from the left anterior
descending (LAD). Right anterior oblique (RAO) angiography images are useful to determine size,
course, and suitability of the septal branch for wiring and alcohol ablation. Left anterior oblique views
are crucial to ensure that the branch vessel indeed supplies the ventricular septum rather than coursing to the lateral wall (Fig. 21.3). Septal branches that course deeper into the ventricular septum will
result in a larger area of myocardium for ablation and likely enhance the hemodynamic improvement
from ASA. In septal perforator vessels that have diameter .2 mm and multiple branches, a subbranch for ablation should be selected to avoid ablation outside of the target region.
INVASIVE HEMODYNAMIC ASSESSMENT
Invasive hemodynamic assessment for LVOT obstruction in patients with HOCM ideally involves simultaneous measurement of left ventricular and ascending aorta pressures
LV
Ao
Fig. 21.4 Hemodynamic tracings of aortic (Ao) and left ventricular (LV) pressure at baseline and after
alcohol septal ablation. At baseline, a resting gradient of 50 mmHg and post-premature ventricular contrac-
tion gradient of 200 mmHg are present. After ablation there is no evidence of residual obstruction.
300
200
100
o
4
(Fig. 21.4).
21—ALCOHOL SEPTAL ABLATION FOR OBSTRUCTIVE HYPERTROPHIC CARDIOMYOPATHY 251
https://t.me/medicina_free
This can be accomplished with a transseptal approach with subsequent advancement of a balloon-tipped catheter with side holes through the mitral valve and into the LVOT. This approach
is useful to avoid catheter entrapment within the dynamic left ventricle. A separate pigtail catheter can be advanced retrograde through arterial access into the ascending aorta for simultaneous
pressure assessment.
Alternatively, a multipurpose catheter can be advanced retrogradely across the aortic valve into
the left ventricle. Through this, a high-fidelity tip manometer pressure wire can be inserted to the
distal end of the catheter and then “unsheathed” by withdrawing the multipurpose catheter across
the aortic valve while leaving the pressure wire in the left ventricle. Before withdrawing the catheter, the high-fidelity pressure wire needs to be calibrated to the fluid-filled pressure tracing. This
technique avoids catheter entrapment and allows enhanced assessment of dynamic LVOT
obstruction without the need for transseptal puncture.
Temporary Pacemaker Insertion
ASA carries a high risk of right bundle branch block and additional conduction abnormalities, so
appropriate preparation with transvenous pacing backup is necessary, particularly in patients with
underlying left bundle branch block (LBBB), wide QRS, or those undergoing repeat ablation. In
patients who do not already have a permanent pacemaker system, a temporary transvenous pacemaker lead should be placed before septal ablation. This is best accomplished through right internal
jugular venous access with advancement of the lead to the right ventricular septum.
ASA Technique and Tips
Femoral or radial arterial access can be obtained through standard techniques. A 6F sheath is usually adequate for guide catheter and equipment insertion. A guiding catheter is advanced into the
ascending aorta, and the left main coronary artery is engaged. A 6F Judkins left or XB guiding
catheter has been our general approach to achieve adequate support for the procedure. Standard
procedural anticoagulation with IV heparin should be administered before guidewire insertion. An
over-the-wire balloon is selected that will be slightly larger than the diameter of the septal perforator branch (e.g., 1.5 or 2.0 mm) to ensure it will be occlusive when inflated. A 0.014-inch hydrophilic coronary guidewire with two 45-degree bends is then advanced through an over-the-wire
balloon and the guiding catheter into the proximal LAD artery.
In the RAO view, the appropriate septal artery branch is identified and the guidewire is
advanced into the target vessel. The angle of the septal artery coursing off the LAD may impede
wire advancement into the branch vessel. Once the wire is positioned to the most distal point in
the septal perforator, the over-the-wire balloon is advanced into a location proximal to the
desired ablation region. The balloon is then inflated to low pressure (3 to 5 atmospheres). To
ensure that the balloon is occlusive in the septal artery to prevent reflux of alcohol into the LAD,
a contrast injection of the left coronary system is performed (Fig. 21.5). The guidewire can then
be removed, leaving the inflated over-the-wire balloon in place. Nondiluted contrast is then
injected through the balloon catheter under fluoroscopy to confirm target artery course, lack of
collaterals or reflux, and ensure that there is no vessel dissection. Simultaneous transthoracic
echocardiography with use of microbubble contrast should also be used to confirm that the selected septal vessel supplies the targeted area of septal myocardium (best seen in the apical longaxis view) and confirm that there is no enhancement of the papillary muscles (best seen in the
parasternal short-axis view) (Fig. 21.6).
The amount of ethanol needed for adequate septal ablation varies based on artery anatomy,
presence of collateral vessels, and septal width. A general rule of thumb is approximately 1 mL
of alcohol per centimeter of septal thickness. The alcohol should be injected extremely slowly
252 5—VENTRICULAR SEPTAL INTERVENTIONS
https://t.me/medicina_free
Fig. 21.5 Septal perforator cannulation to facilitate ablation. Right anterior oblique views demonstrating
(A) 0.014-inch guidewire positioned in the desired first septal perforator branch (arrow) and (B) selective
contrast injection of septal perforator through the inflated over-the-wire balloon (arrow).
Fig. 21.6 Echocardiographic guidance for alcohol septal ablation. (A) Apical long-axis view with micro-
bubble contrast identifying appropriate basal septal location for ablation (arrow). (B) Parasternal short-axis
view showing no involvement of papillary muscles (arrows).
through the balloon catheter using a 1-mL syringe, usually over a period of 5 to 10 minutes.
Analgesic medications may be necessary for patient discomfort during alcohol infusion. Patient
hemodynamics and telemetry should be monitored carefully during this step. Widening of the
QRS or new right bundle branch block may be seen in up to two-third of cases. ST-segment
elevation is also common during alcohol infusion. After infusion of ethanol, the balloon catheter should be flushed with saline slowly over an additional 5 minutes and left inflated for
several minutes. The coronary guidewire is then reinserted through the over-the-wire catheter
with subsequent balloon deflation and removal. Repeat coronary angiography should demonstrate absence of flow in the ablated septal perforator (Fig. 21.7). Hemodynamic assessment of
outflow obstruction can then be performed, with additional treatment of other septal branches
if needed. Successful ASA is generally defined by a greater than 50% reduction in the peak
LVOT gradient (see Fig. 21.4).
21—ALCOHOL SEPTAL ABLATION FOR OBSTRUCTIVE HYPERTROPHIC CARDIOMYOPATHY 253
https://t.me/medicina_free
Fig. 21.7 Post-ablation coronary angiography. (A) Right anterior oblique caudal view. (B) Left anterior
oblique cranial view; after ablation there is no longer flow in the first septal perforator (arrow).
Monitoring and Complications
After completion of the ASA procedure, patients at our institution are observed in the cardiac
intensive care unit overnight before transfer to a general telemetry service for continued monitoring. Ventricular arrhythmias are most common in the first 12 hours after ablation. Atrioventricular (AV ) block is the most frequently encountered rhythm abnormality postablation and is often
transient. Thus a temporary transvenous pacemaker wire is important in patients without a permanent pacemaker. If high-grade AV block occurs outside of the intraprocedural period, permanent pacemaker implantation is often required. In patients with preexisting LBBB, permanent
pacemaker implantation is needed in approximately 25% of cases.
The acute improvement in outflow obstruction observed after alcohol ablation is predominantly due to myocardial stunning. Over the first 1 to 2 days after the procedure, septal edema
may transiently worsen the LVOT gradient and can result in hemodynamic compromise if significant. This situation should be managed with beta-blockade, intravenous (IV) fluids, and
pure afterload vasopressor support, if needed, with phenylephrine. Other uncommon but potential complications include vascular access site bleeding, cardiac effusion, and tamponade, as well
as iatrogenic coronary artery dissection. Periprocedural mortality is estimated at 1%. Among 601
patients undergoing ASA at the Mayo Clinic from 1998 to 2006, procedural complications
included pacemaker implantation in 20%, tamponade in 3%, ventricular arrhythmia in 3%, and
death in 1.4%.
and slower infusion of alcohol, there has been a decrease in arrhythmic complications.
5
With more experience and improved techniques over time, including lower dose
6
Risks of Arrhythmias Postprocedure
Patients should be monitored for a minimum of 48-72 hours following septal ablation. Patients
with normal QRS morphology who do not develop heart block during the procedure require a
temporary pacemaker for only 24 hours and may be dismissed from the hospital at 74 hours
if no further heart block is observed.
procedure requiring pacing for more than the duration of alcohol infusion, we would usually
recommend a permanent pacemaker, even if they regain conduction after the procedure, due to
6
If a patient develops complete heart block during the
Соседние файлы в папке Библиотека им академика М.И. Перельмана