Aortic Valve Disease

Front matter

IntechOpen Series Cardiology and Cardiovascular Medicine, Volume 1 Aortic Valve Disease Recent Advances Edited by P. Syamasundar Rao Edited by P. Syamasundar Rao Over the last 50 years, remarkable developments in the diagnosis and management of aortic valve disease have occurred. This book, Aortic Valve Disease - Recent Advances , addresses several aspects of diagnosis and management of aortic valve disease. It reviews several topics, namely, pathology of the aortic valve and ascending aorta, transcatheter aortic valve replacement techniques, management of aortic stenosis and aortic insufficiency (congenital and acquired) both by catheter-based and surgical techniques, complications associated with these procedures including the use of cerebral embolic protection devices, management of aortic valve disease in patients who also have atrial fibrillation, surgical therapy of bicuspid aortic valve syndrome, and patient perspective.

Published in London, UK © 2024 IntechOpen © Sashkinw / iStock ISBN 978-1-83769-153-1 Kaan Kırali , Cardiology and Cardiovascular Medicine Series Editor ISSN 3033-361X Aortic Valve Disease - Recent Advances

Aortic Valve Disease - Recent Advances Edited by P . Syamasundar Rao Published in London, United Kingdom

Section 1 Introduction

Chapter 1 Introductory Chapter: Aortic Valve Disease – Recent Advances P . Syamasundar Rao 1. Introduction The title of the book “ Aortic Valve Disease” was selected with the intent to discuss etiologic, diagnostic, and therapeutic aspects of aortic valve disease with a focus on recent advances. Selected clinicians and investigators were invited to submit chapter proposals, once received, suitable proposals were accepted. The purpose of this chapter is to introduce the subject, describe the normal anatomy of the aortic valve apparatus, review the prevalence of different types of aortic valve diseases, and address topics not adequately dealt with in the other chapters in the book. Several advances in the understanding of the anatomy of the aortic valve, the development of investigative tests to diagnose and quantitate the magnitude of aortic valve disease, and multiple modalities to treat the aortic valve disease have occurred over the last five decades. The objective of this book was to bring some of these advances to the attention of the reader. While surgical therapy of aortic valve disease has been in vogue since the early 1950s, catheter-based interventional techniques introduced in the early 1980s became initial management options at many institutions. This book will address the anatomy of the normal and diseased aortic valve; explore the utility of diagnostic tests such as echocardiogram, Doppler interrogation, magnetic resonance imaging, computed tomography, cardiac catheterization, and selective cine angiography; and review the relative usefulness of catheter-based vs. surgical techniques in addressing the aortic valve disease. Finally, a discussion of both short-term and long-term results of catheter interventional and surgical therapeutic modalities was included. 2. Normal anatomy of the aortic valve apparatus The functional unit of a normal aortic root is made up of three aortic sinuses of Valsalva. They are formed by the aortic wall and the aortic valve leaflets, which are attached to the corresponding sinus. This establishes three pocket-like spaces. They are divided by commissural spaces and interleaflet triangles, the so-called trigone [1, 2]. The sum of the zones of the valve leaflets is larger than the cross-sectional region of the aortic root and this in addition to valve leaflet tissue pliability permits for a competent valve closure during the diastolic phase and unhindered valve opening to allow forward flow during the systolic phase of the cardiac cycle. While tricuspid valve leaflets are the most common morphologic structure of the aortic valve, unicuspid, bicuspid, and quadricuspid morphologic variants are also seen, the later in aortic valve or truncal disease states.

3. Prevalence 3.1 Congenital valvar AS The incidence of congenital valvar aortic stenosis (AS) is 5–6% of all congenital heart defects (CHDs). Given the prevalence of CHDs in 0.8% of live births [3, 4], the population prevalence of AS is estimated to be 0.5–0.6% (5 to 6 per 1000) of live births. AS’ s occurrence is more frequent in males than in females. 3.2 Bicuspid aortic valve The prevalence of bicuspid aortic valve is generally thought to be 1–2% of population [5, 6]. More recent studies indicated a slightly lower prevalence. A study that reviewed echocardiograms of 24,265 subjects with a gender distribution of 47% males and 53% females revealed a 0.6% prevalence of bicuspid aortic valves [7]. Screening echocardiograms of 1742 teenage athletes with male preponderance (67% male and 33% female) revealed a 0.5% incidence of bicuspid aortic valves [7]. In another study of 2273 competitive athletes, aged 8–60 years, bicuspid aortic valves were present in 2.5% [8], higher than seen in the previous study. An echocardiogram of 1075 neonates revealed a prevalence of 0.46%; there was a higher (0.71%) prevalence in male babies than in female infants (0.19%) [9]. Studies do confirm a high level of accuracy of echocardiography in diagnosing bicuspid aortic valve [10]. Variations from 0.5 to 2.5% in the prevalence of bicuspid aortic valve appear to be related to the types of study cohorts selected in each study. 3.3 Calcific AS In a study published in 2013, the prevalence of calcific AS in the elderly has ranged between 2.8 and 4.6% [11]. In a more recent study examining the global epidemiology of valvular heart disease, calcific AS among adults is age-dependent, older the subject, and more frequent, is its prevalence; the highest is in the older adults: 1000 per 100,000 (1%) in 75–79 year-olds and 1400 per 100,000 (1.4%) in 80–85 year-olds [12]. These prevalences are lower than those described in the above study [11]. There was nearly an equal gender distribution [12]. By contrast, rheumatic heart disease is more common in low-income countries with prevalence rates of 400–500 per 100,000 with similar distribution among all adult age groups [12]. The gender distribution of rheumatic heart disease is also similar in all age groups [12]. 3.4 Aortic insufficiency In the Framingham heart study involving 1696 men and 1893 women aged 54 ± 10 years, the prevalence of aortic insufficiency (AI) was found to be 13% in men and 8.5% in women; the subjects were assessed by echocardiography [13]. 3.5 Ascending aortic aneurysm The prevalence of ascending aortic aneurysms is 5 per 100,000 patient-years; this is based on population-based studies [14].

Introductory Chapter: Aortic V alve Disease – Recent Advances DOI: http://dx.doi.org/10.5772/intechopen.112887 4. Clinical features 4.1 AS in the pediatric patient Most children with valvar AS are asymptomatic and the AS is usually detected because of a cardiac murmur heard on routine auscultation [15–17]. Patients with severe AS may exhibit symptoms such as dyspnea, easy fatigability, or chest pain. Syncope may be a presenting complaint in some children with very severe AS. On physical examination, the left ventricular impulse is increased (left ventricular heave) in all but mild cases. A thrill may be felt at the right upper sternal border and/or in the supra-sternal notch. The first heart sound is usually normal. The second heart sound is also normal unless the AS is extremely severe when there may be a paradoxical splitting of the second heart sound. An ejection systolic click is heard best at the apex and left mid and right upper sternal borders and the click does not vary with respiration. An ejection systolic murmur of grade II–V/VI intensity is heard best at the right upper sternal border with radiation into both carotid arteries. The arterial pulses are usually normal. 4.2 Critical AS in neonates The term critical AS is used to describe very severe aortic valve stenosis who have high peak systolic pressure gradients across the aortic valve, signs and symptoms of congestive heart failure (CHF) are present, and/or a ductal-dependent systemic circulation exists. The pressure gradient across the aortic valve may not be high in some babies because of poor left ventricular function.

They usually present during the first 24–48 hours after birth with symptoms of tachypnea, respiratory distress, cyanosis, pallor, lethargy, metabolic acidosis, and oliguria. Physical examination reveals signs of CHF and poor pulses in all four extremities. Ejection systolic click at the apex and ejection systolic murmur at the right upper sternal border may be heard, but not as prominent as non-critical AS patients. 4.3 Mild, moderate, and severe AS in the adult The clinical features are essentially like those seen in pediatric patients described above, although, the findings are less discernable in obese adult subjects. 4.4 Calcific AS in the elderly Patients with milder forms of calcific AS are asymptomatic and are usually detected because of a cardiac murmur heard on routine physical examination or by an echocardiographic study performed for an unrelated reason. Moderate to severe forms may present with symptoms of dyspnea on exertion or exercise intolerance. Rarely, the presenting symptoms such as syncope, chest pain, or signs of CHF may appear. Physical examination reveals increased left ventricular impulse; slow upstroke of the pulse (pulsus tardus) and small pulse volume (pulsus parvus), both are better perceived in carotid than in radial and brachial pulses; ejection systolic click at the apex, unless the aortic valve is immobile because of marked calcification; soft aortic component of the second heart sound; and an ejection systolic murmur, heard at the right upper sternal border, radiating to the carotid arteries. Higher grades of the murmur (grade IV) and late peaking in systole suggest more severe obstruction.

4.5 Aortic insufficiency Most patients with mild to moderate AI are asymptomatic and are detected because of a cardiac murmur. Severe AI patients present with symptoms of easy fatigability, dyspnea on exertion, or chest pain. On physical examination, while the peripheral pulses are normal in mild AI, they are increased and “bounding” in patients with moderate and severe AI. The pulse pressure is increased secondary to increased systolic blood pressure with a concurrent decrease in diastolic pressure. Peripheral signs of AI such as water-hammer pulse (rapid increase and decrease of pulse when palpating the forearm), Corrigan’ s pulse (strikingly augmented carotid pulses), Duroziez’ s murmur [bruits both in systole and diastole auscultated in the femoral artery region while it is partially occluded], pistol shot sounds (systolic and diastolic vibrations of the arterial wall—Traube’ s sign), and Quinke’ s pulse (flushing and blanching alternatively of the capillary beds of the tips of finger) are seen in subjects with moderate to severe AI; however, these signs do not inevitably categorize that the AI is severe. The left ventricular impulse is prominent to hyperdynamic. The diastolic thrill of AI is rarely felt. In general, there are no abnormal cardiac sounds. If the AI is due to a bicuspid aortic valve, an aortic systolic click is auscultated. A systolic ejection murmur is heard at the upper right or at mid-left sternal borders; this may be related to the increased volume of blood that has to be pumped back via the aortic valve.

Alternatively, the systolic component may be due to associated aortic valve stenosis. An early diastolic decrescendo murmur is auscultated at the right upper and left mid sternal borders. The murmur has a high pitch and is heard better with the diaphragm than the bell of the stethoscope. The murmur begins with the aortic component of the 2nd sound and is better heard when the patient sits up, leans forward, and holds the breath at end-expiration. It may transmit inferiorly to the left lower sternal border. An Austin-Flint type of mid-diastolic murmur may be appreciated at the apex. 5. Echocardiographic diagnosis 5.1 Congenital AS in the pediatric patient Echocardiographic studies are very useful in the diagnosis of the type of AS (valvar, sub-valvar, and supra-valvar), in characterizing the aortic valve morphology, and in quantitating the degree of obstruction. 5.1.1 Types of AS Obstruction of the left ventricular outflow tract may be seen at valvar (Figure 1), sub-valvar (subaortic membranous stenosis [Figure 2] and hypertrophic cardiomyopathy [Figure 3]), and supra-valvar (Figure 4) locations [15–17]. Examples are shown in Figures 1–4. 5.1.2 Characterization of aortic valve morphology The normal aortic valve is tricuspid as shown in Figure 5. In congenital AS, most commonly, the aortic valve is bicuspid (Figures 6 and 7), The aortic valve leaflets are thickened (Figures 1A, B and 7A, B) and dome during systole (Figures 1B and 7C) in most patients.

Introductory Chapter: Aortic V alve Disease – Recent Advances DOI: http://dx.doi.org/10.5772/intechopen.112887 5.1.3 Quantification of the degree of obstruction The flow velocity magnitude across the aortic valve, measured by Doppler, is increased (Figures 7E and 8C) which is used to calculate the systolic pressure gradient across the aortic valve by a modified Bernoulli equation: = 2Peak instantaneous gradient 4V (1) Where V is the peak Doppler velocity across the aortic valve in meters/sec. The Doppler velocity measurements are made in parasternal, suprasternal notch, and apical views. Most important, however, is to achieve a close alignment of the Doppler signal to the aortic flow . It should be understood that the Doppler peak Figure 1.

Echocardiographic frames from precordial long axis view of the left ventricle (L V) demonstrating valvar AS. Note the thickened and domed aortic valve (A V). Ao, aorta; LA, left atrium; L V , left ventricle. Reproduced from reference [17].

Figure 2.

Echocardiogram in parasternal long axis (A) and apical five-chamber (B) projections demonstrating the subaortic membrane (SAM). The position of the aortic valve (A V) is shown. Continuous wave and color Doppler studies demonstrated elevated Doppler flow velocity across SAM but are not shown in these echo frames. LA, left atrium; L V , left ventricle. Reproduced from reference [18].

instantaneous gradient does not accurately reflect the true peak-to-peak systolic pressure gradient obtained in the cardiac catheterization laboratory because of the pressure recovery phenomenon [19]. Consequently, applicable corrections to account for pressure recovery should be made during the calculations of the pressure gradient. Turbulent flow is also demonstrated by color flow Doppler (Figures 7D and 8B). Figure 4.

Echo-Doppler studies in parasternal long axis (A and B) and subcostal (C and D) projections illustrating supra-valvar AS. Note that the stenosis is above the aortic valve as shown with arrows. Color flow imaging shows turbulence in Doppler flow signal as pointed out with arrows (B and D). An increased Doppler flow velocity was recorded superior to the aortic valve but is not illustrated in the above echo frames. LA, left atrium; L V , left ventricle. Reproduced from reference [18].

Figure 3.

Echocardiograms in parasternal long (A) and short (B) axis projections illustrating severe thickening of the inter-ventricular septum (arrows), suggestive of hypertrophic cardiomyopathy. Continuous wave and color Doppler studies demonstrated elevated Doppler flow velocity across the left ventricular outflow tract at the level of thickened inter-ventricular septum. Ao, aorta; LA, left atrium; L V , left ventricle. Modified from reference [17].

Introductory Chapter: Aortic V alve Disease – Recent Advances DOI: http://dx.doi.org/10.5772/intechopen.112887 The echo-Doppler studies in pediatric patients are sufficiently accurate such that there is generally no need for other imaging studies such as magnetic resonance imaging (MRI) and computed tomography (CT). 5.1.4 Other echocardiographic features Annular hypoplasia and dysplasia of aortic valve leaflets have also been seen, mostly in neonates and young babies.

Left ventricular internal dimension (L VID) in diastole is usually normal for age. However, L VID may be increased in patients with long-standing and severe AS. Such left ventricular enlargements are more common in neonates with critical AS. Hypertrophy of the left ventricular musculature in a concentric manner is seen which is mostly proportionate to the severity of obstruction. The left ventricular shortening fraction may be increased, usually proportional to the degree of narrowing. However, in neonates with critical AS and patients with heart failure, it may be decreased. Poststenotic dilatation of the aorta (Ao) is observed in most patients; the degree of such dilatation is not related to the degree of aortic valve obstruction [16–18]. Figure 5.

Selected echo images in parasternal short axis view demonstrating normal tricuspid aortic valve in closed (A) and open (B) positions. LA, left atrium; RA, right atrium; RV , right ventricle. Figure 6.

Selected echo images in parasternal short axis view demonstrating normal tricuspid aortic valve (A), bicuspid aortic valve with vertical (B) and horizontal (C) commissures. The arrows point to the respective aortic valve leaflets.

Figure 8.

Echo-Doppler studies of a patient with severe AS illustrating an aortic valve (A V) which is thick and domed (A). Color flow imaging demonstrates turbulent flow with a narrow jet (NJ) at the A V (arrow) (B). The Doppler velocity via the A V is high (>6 m/s) (C), suggesting very severe AS; the calculated peak instantaneous gradient is 148 mmHg with a mean of 75 mmHg. The patient has a bicuspid A V which is not demonstrated in these echo frames. Ao, ascending aorta; LA, left atrium; L V , left ventricle. Reproduced from reference [18]. Figure 7.

Echo images illustrating a thick (A) and bicuspid (B) aortic valve (BA V) with doming of the aortic valve (A V) (C) pointed out by arrows. Color flow Doppler demonstrates turbulent flow (TF) at the aortic valve (arrow) (D). The Doppler velocity across the A V is low (<2 m/s) (E), suggesting trivial AS with a bicuspid aortic valve. LA, left atrium; L V , left ventricle. Reproduced from reference [18].

Introductory Chapter: Aortic V alve Disease – Recent Advances DOI: http://dx.doi.org/10.5772/intechopen.112887 5.2 Congenital AS in the young adults The echo-Doppler studies in young adults with congenital AS are similar to those described in the preceding section, although an occasional patient with poor acoustic windows may require trans-esophageal echo evaluation or other imaging studies. 5.3 Calcific AS in the elderly Like AS in the pediatric patient, echocardiographic studies are very useful in characterizing the aortic valve morphology, in quantitating the degree of obstruction, and in assessing left ventricular response to increased afterload. The aortic valve leaflets have increased echo density and decreased valve leaflet motion. It is frequently difficult to discern whether it is a tricuspid or bicuspid aortic valve. The Peak Doppler flow velocity is increased which is used to calculate the systolic pressure gradient across the aortic valve by a modified Bernoulli equation, as reviewed above in the section on “Congenital AS in the Pediatric Patient. ” Other disease entities such as hypertrophic cardiomyopathy, mitral valve disease, and CHDs are excluded by echo studies. Left ventricular hypertrophy is usually detected by echo evaluation. Left ventricular ejection fraction can be quantitated; in most cases, it is preserved until late in the disease. 5.4 Aortic insufficiency Echocardiographic, MRI, and CT features of AI were described in the chapter on “Transcatheter Therapies for Aortic Regurgitation – Where Are We in 2023?” by Shabbir and his associates and will not be repeated in this chapter. 6. Aortic valve surgery without valve replacement Most chapters in this book deal with surgical or transcatheter replacement of the aortic valve. Other forms of surgery such as commissurotomy, plastic repair of aortic valve, and Ross procedure have not been addressed. These will be reviewed briefly. 6.1 Commissurotomy Aortic valvotomy via aortotomy under cardiopulmonary bypass has been used with success [20]; however, most institutions currently use balloon aortic valvuloplasty as the initial treatment option. 6.2 Plastic repair of the aortic valve Neocuspidization (plastic repair of aortic valve) either into a bicuspid or tricuspid aortic valve, as the case may be, with or without prosthetic material (patient’ s native leaflet tissue, glutaraldehyde-treated autologous pericardium, non-treated autologous pericardium, expanded polytetrafluoroethylene (ePTFE) membrane, decellularized xenogenic tissue, glutaraldehyde-treated bovine pericardium, or untreated equine

Author details P . Syamasundar Rao Children’ s Heart Institute, Children’ s Memorial Hermann Hospital and McGovern Medical School, University of Texas Health Sciences Center at Houston, Houston, Texas, USA * Address all correspondence to: p.syamasundar.rao@uth.tmc.edu pericardium) and cusp augmentation to restore the aortic valve close to its normal structure and function has been used successfully [21–24]. 6.3 Ross procedure Aortic valve replacement with patient’ s own pulmonary valve and inserting a bioprosthetic valve in the pulmonary position [25, 26] has been used successfully to address severe AS cases both in neonates and older patients, although the risk of double valve disease exists [27]. © 2023 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Introductory Chapter: Aortic V alve Disease – Recent Advances DOI: http://dx.doi.org/10.5772/intechopen.112887 References [1] Angelini A, Ho SY , Anderson RH, et al. The morphology of the normal aortic valve as compared with the aortic valve having two leaflets. The Journal of Thoracic Cardiovasc Surgery. 1989;98:362-367 [2] McKay R, Smith A, Leung MP , Arnold R, Anderson RH. Morphology of the ventriculoaortic junction in critical aortic stenosis: Implications for hemodynamic function and clinical management. The Journal of Thoracic Cardiovasc Surgery. 1992;104:434-442 [3] Mitchell SC, Korones SB, Berendes HW . Congenital heart disease in 56,109 births. Incidence and natural history. Circulation. 1971;43:323-332.

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DOI: 10.1016/s0002-9149(98)01064-9 Erratum in: The American Journal of Cardiology. 1999;84:1143 [14] Gouveia e Melo R, Silva Duarte G, Lopes A, Alves M, Caldeira D, Fernandes e Fernandes R, et al. Incidence and prevalence of thoracic aortic aneurysms: A systematic review and meta-analysis of population-based studies. Seminars in Thoracic Cardiovascular Surgery. 2022;34:1-16 [15] Rao PS. Diagnosis and management of acyanotic heart disease: Part I-obstructive lesions. The Indian Journal of Pediatrics. 2005;72:496-502 [16] Singh GK, Rao PS. Left heart outflow obstructions. In: Crawford MH, DiMarco JP , Paulus WJ, editors. Cardiology. 3rd ed. Edinburgh, UK: Mosby Elsevier; 2010. pp. 1507-1518.

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Section 2 Pathology of the Aortic Valve and Ascending Aorta

Chapter 2 Acquired Aortic Valve Diseases (Current Status of the Problem) Abdumadjidov Khamidulla Amanullaevich and Urakov Shukhrat Tukhtaevich Abstract Acquired heart disease – the concept of “acquired heart disease” includes a variety of pathological conditions acquired during the life of the patient. The lion’ s share of these diseases are acquired heart defects. The significance of this problem is special for our region, since the incidence of rheumatic diseases and its complications in our Republic is still significant. However, in recent decades, statistical data on acquired defects, especially on aortic heart defects, have changed markedly. Thus, the prevalence of aortic heart disease among the elderly and senile is about 10.7%, significantly increasing for sclerotic lesions of the aortic valve – up to 25–48%. According to Euro Heart Survey on valvular heart disease, damage to the aortic valve was detected in 44.3% of patients with valvular heart disease (33.9% – aortic stenosis, 10.4% – aortic valve insufficiency. At the same time, aortic stenosis in 81.9% and insufficiency – in 50 .3% of patients were of degenerative origin. According to the statistics of our Republic, more than 400 patients with rheumatism per 100 thousand of the population are detected per year, of which, after an appropriate examination, in terms of the population of our Republic, more than 16,000 require surgical correction of acquired heart disease, which confirms the importance of discussing the problem for our healthcare.

Keywords: acquired heart defects, current data, research methods, treatment tactics, current of correction 1. Introduction Aim of chapter. In connection with the foregoing, we think that the discussion of modern data on aortic malformation of acquired genesis, namely, the modern idea of changing the etiology, frequency of occurrence, clinical picture, as well as diagnostic issues, including new modern highly informative research methods, determining the tactics of surgical treatment with analysis indications and contraindications to a particular method of treatment, respectively, is of great scientific and practical importance. Therefore, we once again decided to discuss the above issues regarding aortic heart disease of acquired origin.

1.1 Actuality The trend towards an increase in the general morbidity of the population with diseases of the circulatory system can be clearly seen [1, 2], both according to the results of world statistics, according to the results of the State Report on the state of health of the population of the Russian Federation (2002, 2003), and according to the Ministry of Health of Uzbekistan (2008). The number of open heart surgeries is increasing every year. Reconstructive operations on the aortic valve (A V) are in the center of attention of cardiac surgeons: in economically developed countries, this operation is already in second place in terms of frequency among all cardiac surgical interventions performed in the adult population. The reason for this is the changes that have taken place in the etiology of the formation of aortic valve disease and the change in the demographic structure of society itself. In developed countries, calcified aortic disease is the third most common nosological form after arterial hypertension and coronary heart disease [3].

Knowledge of the etiology of the process that led to aortic malformation can significantly influence both the surgical tactics and the protocol of postoperative treatment of patients and, as a result, the prognosis of the long-term period. Therefore, at all stages of treatment, one should strive to answer the question of the etiology of the primary process that caused valve dysfunction. Sometimes this answer can only be given by a surgeon who visually assesses the nature of the valve lesion already during the operation. In any case, elucidation of the etiology, even with a presumptive conclusion, is extremely important. 2. Etiology Assessing our own experience, published data of colleagues from other countries and Russian clinics, it should be emphasized that even today aortic malformations of rheumatic etiology dominate in cardiac surgery hospitals, although not as clearly as in the statistics of half a century ago. This figure does not exceed 30–40%. However, if we take into account that only during the period from 1993 to 1998 in Russia the frequency of cardiac rheumatism increased by 7 times [1, 2], then in the future we should again expect an increase in the number of patients with rheumatic valvular defects.

The etiology of pathological changes in AK from the moment of the first operations has changed several times. If at the beginning rheumatic lesions, endocarditis, syphilis and atherosclerosis prevailed; then at present, atherosclerotic (degenerative) and congenital malformations (mainly bicuspid aortic valve) of the aortic valve come to the fore. Such changes in the etiology could not but affect the course of the disease itself, the clinic of the defect and, accordingly, the development of a specific tactic for the introduction of such patients.