Interventions for Adult Structural Heart Disease



Interventions for Adult Structural Heart Disease


Hong Jun (Francisco) Yun, MD

Stanley J. Chetcuti, MD



PERCUTANEOUS REPAIR OF PARAVALVULAR LEAKS

Because of an aging population, the burden of valvular heart disease is increasing. With the advent of transcatheter therapies, more patients are being referred for transcatheter aortic valve replacement (TAVR) and valve-in-valve (VIV) procedures besides the >100,000 surgical valve procedures performed annually in the United States.1 Paravalvular leak (PVL) is not an uncommon complication of mechanical or bioprosthetic surgical valves, occurring in 2% to 17% of all cases.2 At least moderate PVL has been reported in 22% of cases in patients undergoing TAVR with the Edwards Sapien or the Medtronic CoreValve.3 PVL is related to an abnormal gap between the outer edge of the prosthetic valve and the native valve annulus leading to turbulent flow. Although many patients with mild PVL remain asymptomatic, signs of more severe PVL include heart failure, LV enlargement, and hemolytic anemia. The occurrence of PVL is an important factor for TAVR devices, as the development of at least moderate PVL has been associated with impaired survival.4 Traditional therapy for the management of PVL has been open surgery, but the growth of safe, minimally invasive percutaneous techniques with experienced operators has obviated the need for surgery in many cases (FIGURES 22.1, 22.2 and 22.3).


PERCUTANEOUS CLOSURE OF VENTRICULAR SEPTAL DEFECTS

Ventricular septal defects (VSDs) are one of the most common congenital heart lesions and occur in ˜50% of all patients with congenital heart disease.4 Although most small defects close spontaneously within the first 2 years, undiagnosed and untreated defects may persist into adulthood. The natural history of untreated VSDs is related to the size of the defect. Patients may present with a murmur, endocarditis, heart failure, or pulmonary hypertension. Acquired VSDs, iatrogenic, traumatic, or postmyocardial infarction (MI), are much less common. VSDs complicating an acute myocardial infarction are a rare event, occurring in 0.17% of patients in the era of percutaneous coronary intervention (PCI) reperfusion therapy.5 Although the presentation may be insidious, patients with post-MI VSD can become acutely ill and develop cardiogenic shock. Thus, early identification is crucial because mechanical repair is the only effective treatment and mortality rates can approach 100% in patients who are treated medically.6 Although surgery has been the mainstay for VSD closure, transcatheter approaches have been demonstrated as viable alternatives since the first percutaneous VSD closure was performed in 1987 using the Rashkind double-umbrella device.7 Currently, the Amplatzer Muscular VSD Occluder is the most commonly used percutaneous device and has been associated with low mortality and high success rates, ranging from 93% to 100% (FIGURES 22.4, 22.5, 22.6 and 22.7).8







FIGURE 22.1 Cardiac CT angiography shows a #23 St Jude mechanical aortic valve with a severe PVL. There is irregular pooling of contrast and a path of contrast continuity around the mechanical aortic valve prosthesis concerning for a PVL.






FIGURE 22.2 Percutaneous repair of an aortic PVL using Amplatzer VSD Occluder Devices (St Jude Medical, St Paul, MN) under TEE and fluoroscopic guidance. A, TEE shows a bileaflet tilting-disc mechanical aortic valve with dehiscence and severe paravalvular aortic regurgitation. B, Three guide wires are advanced through the paravalvular space and into the left ventricle. C, One 4 mm and three 6 mm Amplatzer VSD Occluder devices are deployed with no residual paravalvular regurgitation. TEE and fluoroscopy show stability of the devices and a normally functioning mechanical valve with no impingement of leaflet excursion. D, 3D TEE shows the 4 VSD Occluder devices in the paravalvular space.







FIGURE 22.3 Step-by-step approach to transfemoral PVL closure using Amplatzer VSD Occluder devices. Severe aortic PVL closure via a retrograde transfemoral approach in a 32-year-old man with bicuspid aortic valve and prior valve sparing ascending aorta replacement and aortic valve repair followed by 2 subsequent AVRs (last with a 23 mm St Jude mechanical valve). A, A 6 FR AL1 catheter is used to cross the PVL using a J tipped guide wire and a 6 FR pigtail catheter is advanced into the left ventricle (image Video 22.1). B, Through the pigtail catheter, a J tipped Rosen wire is advanced into the left ventricle (image Video 22.2). C and D, 6 FR 90 cm Shuttle Sheath is then advanced into the LV to allow direct passage of 3 additional J tipped Rosen wires through the paravalvular space into the ventricle (image Video 22.3). E, Using a 5 FR Amplatzer TorqVue 180 Delivery System, a 4 mm VSD Occluder is positioned within the PVL and confirmed by TEE (image Videos 22.4 and 22.5). F-I, Three additional 6 mm VSD Occluder devices are positioned in the paravalvular space using the corresponding guide wires (image Video 22.6). A fifth J tipped Rosen wire is advanced into the left ventricle to maintain access of the paravalvular space. J, Once appropriate position of the occluding devices and reduction of the PVL is verified by fluoroscopy and TEE, the Rosen wire is removed and the VSD Occluder devices are deployed (image Video 22.7).







FIGURE 22.4 Post-MI VSD with residual defect after surgical repair. Computed tomography image showing postsurgical changes at the cardiac apex with at least 1 cm residual ventricular septal defect along the inferoapical septum.






FIGURE 22.5 A, Amplatzer Muscular VSD Occluder. It is a self-expanding, double-disc device made of nitinol and interwoven polyester to promote occlusion and tissue ingrowth. It has a 7 mm waist length to accommodate the muscular ventricular septal wall. B, The device comes in a variety of sizes (4-18 mm at the waist, corresponding to disc diameters of 9-26 mm). A, device size at the waist. B, length of the proximal disc. C, length of the waist. The Amplatzer Muscular VSD Occluder is implanted with either a 45° or a 180° Amplatzer TorqVue Delivery System accommodating 5-9 F access vessels.







FIGURE 22.6 Transesophageal echocardiography images of an inferoapical VSD, measuring 1.0 to 1.3 mm. A and B, Left-to-right shunting is seen on color Doppler before intervention. C, TEE images after VSD closure reveal no evidence of shunt on color Doppler.






FIGURE 22.7 Fluoroscopic views of an apical VSD closure in a 59-year-old patient who underwent VSD repair after a STEMI and had a residual VSD with left-to-right shunting (Qp:Qs was measured at 1.8:1). A, Left ventricular angiography shows a large apical VSD (image Video 22.8). B, A JR4 catheter is used to direct a J tipped wire through the VSD and the wire is then snared through the right internal jugular vein sheath, thus creating an arteriovenous loop formed by externalizing the J tipped wire through the VSD (image Video 22.9). C, Using a venous approach, the Amplatzer VSD Occluder device is advanced through the VSD and the left ventricular disc is deployed. D, The right ventricular disc is semi-deployed. E, Left ventricular angiography shows appropriate position of the left disc and trivial residual shunt (image Video 22.10). F, The right disc is then fully deployed and the device is released (image Video 22.11)



PERCUTANEOUS CLOSURE OF PATENT FORAMEN OVALE

The foramen ovale is an important structure during fetal development and facilitates flow of oxygenated blood from the right atrium to the left atrium. At birth, most people have functional closure of the foramen ovale by apposition of the septum primum on the left against the septum secundum on the right. The prevalence of a patent foramen ovale (PFO) is very common and has been estimated to be 25% in autopsy and community-based transesophageal echocardiography (TEE) studies.9,10 Most of them are asymptomatic, but PFOs have been associated with cryptogenic strokes, platypnea-orthodeoxia syndrome, decompression sickness, and migraines. The main indication for percutaneous PFO closure is to prevent recurrent cryptogenic strokes, particularly in young patients if there is no other cause of stroke after extensive evaluation. In 2014, the American Heart Association guidelines concluded that the evidence did not support routine PFO closure for secondary stroke prevention and this was reiterated by the American Academy of Neurology in 2016.11,12 Recently, extended follow-up from the RESPECT trial along with 2, new randomized clinical trials, REDUCE and CLOSE, strongly suggest that PFO closure reduces the risk of recurrent stroke in young, carefully selected patients with cryptogenic stroke, when no alternative etiology of stroke is present. Although the annual risk of stroke recurrence is low and the absolute benefit of closure is modest, cumulative lifetime risk reduction is likely meaningful in young patients.13,14,15 At this time, the 2 most commonly used percutaneous devices are the Amplatzer PFO Occluder (St Jude Medical, St Paul, MN) and the Gore Helex or Cardioform Septal Occluders (WL Gore & Associates, Flagstaff, AZ) (FIGURES 22.8, 22.9, 22.10 and 22.11).


PERCUTANEOUS CLOSURE OF PATENT DUCTUS ARTERIOSUS

The ductus arteriosus is a persistent, vascular connection between the left pulmonary artery near its origin and the aorta, just distal to the left subclavian artery. It is a fetal structure that spontaneously closes after delivery in more than 95% of full-term infants during the first 72 hours of life, completing the conversion of the fetal circulation to the normal postnatal circulation. It can be isolated or may be present in association with other forms of congenital heart disease. Clinical manifestations of persistent patent ductus arteriosus (PDA) are related to the degree of left-to-right shunting. Significant and prolonged aortopulmonary shunting may result in LV dilation and ultimately left-sided heart failure. Left untreated, large left-to-right shunts may additionally lead to irreversible pulmonary hypertension and progress to Eisenmenger physiology with right-to-left shunting at the level of the PDA.16 The ACC/AHA Task Force on Practice Guidelines recommend routine follow-up for patients with a small PDA without evidence of left-sided heart volume overload. Closure of the PDA, through either a transcatheter or surgical approach, is recommended in patients with left atrial and/or left ventricular enlargement, or in the presence of a net left-to-right shunt, or a history of endarteritis.16 Since the first surgical closure of a PDA by Gross and Hubbard in 1939, and

later transcatheter closure by Portsmann in 1967, there have been significant advances in device development, making transcatheter closure the preferred approach in contemporary practice. The Amplatzer Occluders are the most commonly used device to treat moderate to large PDAs. Coil embolization has also been successfully used to close PDAs of 2 mm or smaller at the narrowest portion (FIGURES 22.12, 22.13 and 22.14).

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May 3, 2019 | Posted by in CARDIOLOGY | Comments Off on Interventions for Adult Structural Heart Disease

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