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Sumario Vol. 43 - Nº 1 Enero - Marzo 2014


Usefulness of echocardiography in cardiac transplant patients

Carlos Secotaro

Centro Médico Palmares - Centro Medico La Barraca.
(5519) Mendoza, Argentina.
Email 1 - Email 2

Recibido el17-ENE-14 – ACEPTADO después de revisión el 26-FEBRERO-2014.
The author declare not having a conflict of interest.
Rev Fed Arg Cardiol. 2014; 43(1): 6-13


Print version Imprimir sólo la columna central

 

SUMMARY
Heart transplant is an option for patients with terminal heart failure. Despite the lack of donors, it is an increasingly frequent worldwide therapy. With the advent of new surgical techniques, conservation of the implant, a better preparation of the patient, but above all a more effective immunosuppressive therapy, survival improved. The causes of morbidity and mortality of the transplanted patients vary according to the time when the implant is made. Echocardiogram has demonstratedbeing useful in the majority of the causes of morbidity and mortality in heart transplants. We summarize the echocardiographic findings arising due to the transplanted heart's functional and anatomical peculiarities, to deal with the characteristics which are found in the different pathologies.
Key words: Heart transplant. Echocardiogram. Rejection.

 

 

INTRODUCTION
Heart transplant (HT) is an option for patients with terminal Heart Failure [1]. In spite of the shortage of donors, it is a therapy increasingly more frequent in all the world [2].

With the advent of new surgical techniques, of implant preservation, better preparation of the patient (mechanical assistance devices for the left ventricle); but mainly with a more effective immunosuppression therapy [3,4], survival has been improved [1]. The causes for morbi-mortality of the transplanted patient vary according to the time when the analysis of the implant is made, so we have:

  • During the intraoperative period, implant dysfunction and hyperacute rejection prevail.
  • During the first post-HT 7 days, there is still implant and dysfunction persisting and bleeding appears.
  • During the second week and until the first year acute rejection and infections by immunocompromise prevail.
  • After the first year, neoplastic disease appears, but the main cause of morbi-mortality is vasculopathy of the transplant or chronic rejection, which at 5 years already affects 22% of the patients [1].

The echocardiogram has shown to be useful in most of the causes of morbi-mortality in HT [5,2]. Next, we will analyze the echocardiographic findings that are presented due to the anatomic and functional features of the transplanted heart, to later deal with the characteristics that are found in the different pathologies.

 

PHYSIOLOGICAL FINDINGS

Background
There are two surgical techniques that are used in orthotopic HT [1]: the standard technique described by Lower and Shumway, also known as biatrial, and the bicaval technique. These two techniques differentiate essentially by the sutures at atrial level. In the Biatrial one, suturing is made at the level of the body of the atria, while in the Bicaval one, it is made in the outlet of the two cavae and in the outlets of the pulmonary veins.

The Bicaval technique presents advantages as to the atrial function of the implant, lower presence of thrombi in the Left Atrium [6,7,8], as well as ventricular function (cardiac index) in the first days; however, it does not represent a lower mortality [9], possibly because of a greater time of extracorporeal circulation, among other drawbacks.

Depending on the technique used, the findings will be different (Figures 1-4).


Figure 1. Biatrial technique. Atrial cuff ready for implant.

Figure 2
. Biatrial technique. Sutures after implant.
   
Figure 3. Bicaval technique. Pre-implant cuffs.
Figure 4. Bicaval technique. Sutures after implant.

 

ANATOMICAL AND FUNCTIONAL FINDINGS

Left atrium
With the biatrial technique, a dilatation of it is observed, traditionally described as “hourglass”, where the narrow part of the clock corresponds to the suturing line between the two atrial portions, the one of the implant and the receiving one. Depending on the previous size of the native atrium and the receiving one, the suturing line will be farther or closer to the mitral valve plane. If the implanted atrium predominates, the global size will be closer to normal; and if the receiving atrium predominates, the size will be larger, in some cases even reaching 60 mm, a fact that may not necessarily affect sinus rhythm.

This anatomical variability determines a functional variability manifest in transmitral Doppler. At times, the A wave is not found; at times, the A wave is “embryonic”, although a normal A wave may be found too. Besides, the relation between the E wave and the A wave could be erratic. These findings make the evaluation of the diastolic function of the left ventricle difficult, with this being on the foundations of early detection of acute rejection.

In the patients in whom the Bicaval technique was used, a virtually normal anatomy is found, with functionality also being preserved.

Right atrium
In the usual technique, there is also dilatation observed with the suturing line, with no changes of functional significance occurring.

Left ventricle
The systolic and diastolic diameters are preserved, as well as fractional shortening and ejection fraction measured by different methods [10]. The wall thicknesses could be normal or slightly increased. In most patients, septal asynchrony is observed, because of the lack of biventricular interaction after pericardiotomy, although in some patients, contraction is uniform. Usually, over the last days of the first week, when post-HT ventricular dysfunction has yielded, and acute rejection still does not occur, a full echocardiogram is made, emphasizing LV function, which will be taken as “basal” for future comparisons. As previously said, in some patients with far transplant, a Left Ventricular Mass is observed as significantly greater than the one mentioned as normal for the age and body surface. For some authors, this hypertrophy is related to the use of cyclosporine and the presence of hypertension [11,12,13].

Right ventricle
Tricuspid valve, pulmonary systolic pressure, pulmonary capillary pressure.
In literature, the transplanted Right Ventricle (RV) has been described as with preserved shape and size [5]. In most of the presented papers [11,14,15,10] mild dilatation is verified, accompanied by also mild tricuspid valve insufficiency. Pulmonary pressures are within the normal upper limit, or there is mild pulmonary hypertension that does not harm the functional state of the patient. These changes also manifest during exercise [2,16]. It is important to try to differentiate this mild to moderate residual regurgitation, from that produced by a rejection that is from moderate to severe; the latter has an unfavorable prognosis [17,18].

In non-transplanted patients, it is possible to make an estimation of the Pulmonary Capillary Pressure analyzing the data of the Flow of Mitral filling with a good correlation, but it was not demonstrated for transplanted patients [19].

Aortic valve and aortic artery
Most of the patients have a normal valve or with minimal fibrosis, attributed to the ischemic period, with normal valvular function. An insufficiency in a minimal or mild degree (13%) has also been described, with no hemodynamic importance, which although it may not disappear, it does not advance over time [20]. Rarely, it is possible to see from a transthoracic window the suture in the aortic root, which is visualized as an image of increased density, that usually does not produce a significant narrowness, although this has been published in some reports [21]; other complications that may occur are dissection or pseudo-infectious aneurysm [22].

Mitral valve
Up to 55% of incidence of mild mitral valve insufficiency has been described in the first post-transplant week, with a 34% of patients mild mitral valve insufficiency remaining in the far post-transplant period [20,14]. These changes may be due to the changes produced by the time of ischemia and also the anatomical modifications produced by edema and the line of suture on the annulus and mitral subvalvular apparatus. It is important to differentiate the previous existence of mitral valve insufficiency with the one appearing as a consequence of rejection.

RV outflow tract, pulmonary valve and pulmonary artery
In the patients receiving a domino transplant (implant of a heart with hypertrophic RV secondary to pulmonary hypertension), usually a transient subvalvular gradient is observed, although at times significant, which disappears after the first week. Just as with the aortic valve, the pulmonary echogram is usually normal or with minimal fibrosis, at times accompanied by a minimal or mild insufficiency without hemodynamic importance.

Pericardium
In the pericardial cavity of the transplanted patient, there might be air in the first hours of the post-operative period, preventing the transthoracic echocardiographic evaluation; this is very frequent and it could be explained by the mismatch between the implanted organ and the residual pericardial cavity of the original cardiomegaly.

Before this situation, some authors advocated performing an early transesophageal echo, 30 minutes after leaving the pump, evaluating the ventricular function that allows them to predict the need to use inotropic agents [23]; but most accept leaving transesophageal echo for cases in which it is absolutely necessary, as for instance the suspicion of mediastinal hematoma [23] or technically difficult diagnoses from the transthoracic view, as coronary-cardiac fistulae [24].

Another possibility is the presence of mild to moderate pericardial effusion (40% of transplanted patients), very rarely with tamponade [25], this effusion is also the consequence of organ-cavity mismatch. The follow-up of it is important, as it normally evolves into total or partial reabsorption, at times with aspect of organization.
Two pathological circumstances should be differentiated:

  • Bleeding characterized by a rapid evolution, and the presence of tamponade.
  • And effusion by acute rejection that usually appears after the first week.

 

PATHOLOGICAL FINDINGS

Bleeding
It manifests by significant pericardial effusion and with a rapid progression in the first post-operative hours or after some procedure that may potentially produce bleeding, as for example withdrawing pacemaker leads or pulmonary artery catheter.

Implant dysfunction
RV dysfunction or pulmonary hypertension
It constitutes 50% of all cardiac complications and 19% of early deaths after transplantation [26]. It occurs when a normal right ventricle (implant) is exposed to pulmonary hypertension.

It usually goes through a series of stages:

  • First stage: dilatation and hypocontractility of the right ventricle, that usually yields with low pulmonary pressures.
  • Second stage: the contractility of the right ventricle starts recovering with high pulmonary pressures.
  • Third stage: good RV contractility with nearly normal pulmonary pressures persisting with mild RV dilatation.

Global dysfunction
It occurs during the first hours and it lasts until the first week. The causes are:

1. Pre-implant:

Edema derived from ischemia time from the explant to the implant, incomplete preservation by cardioplegic solution, previous dysfunction by the state of the donor: for example, patients with central nervous system injury.

2. Post-implant:

Lesion by ischemia-reperfusion that occurs once the aortic clamp is released during the operation.
The echocardiographic findings are the increase in wall thickness with ventricular function impairment and different degrees of dilatation that with therapy will improve. There is a period, around the end of the first week, in which it will be impossible to distinguish echocardiographically between graft dysfunction and the onset of acute rejection.

Rejection
The detection of the rejection constitutes one of the most significant challenges of transplantology, in which area the echocardiogram has a significant role.

There are several types of rejection [1]:

  • Hyperacute rejection:
    • Mediated by preexisting antibodies, against the implant, usually during the operation, immediately after declamping, it produces thrombosis with ischemia that leads to the loss of the implant. The echocardiogram is not useful unless within the operation.
  • Vascular humoral rejection:
    • Lesion mediated by slow immune response, that produces endothelial lesion. It appears within the first months. The diagnosis is by immunofluorescence in biopsy. It is treated with plasmapheresis and cyclophosphamide. The role of echo has been little studied. This rejection is infrequent.
  • Acute cellular rejection:
    • Lesion mediated by cells, that occurs after the first week and it is the most frequent during the first year, although it may appear far from the transplant [27]. It is the first cause of death during the first year.

The gold standard in acute rejection standard is transjugular or transfemoral endomyocardial biopsy, which in most cases is guided by transthoracic echo with few complications [28,29], even in the patients with heterotopic transplant [30]. So they are supplementary methods and essential foundations to manage patients.

The International Society of Heart and Lung Transplantation (ISHLT) in 2004, made a classification or score of biopsy results [31] (Table 1).

0 DEGREE

No rejection

 

1R DEGREE

Mild

Interstitial or perivascular infiltrates with a focus of myocytic impairment.

2R DEGREE

Moderate

2 or more infiltrates with myocytic impairment.

3R DEGREE

Severe

Diffuse infiltrate, multifocal impairment, with or without edema, bleeding or vasculitis.

Table 1. Degrees of acute cellular rejection according to the ISHLT

The ISHLT [32] suggests making biopsies according to the requirements of the patient or scheduled according to the outline proposed in Table 2.

Biopsies 1,2,3,4 and 5

Weekly

Biopsies 6,7 and 8

Every 2 weeks

Biopsies 9 and 10

Every 3 weeks

Biopsies 11,12 and 13

Every 4 weeks

Biopsies during the first year

Every 5 or 6 weeks

Table 2. Recommendations by the ISHLT to perform
scheduled biopsies during the first year.

Chronic rejection:

    • It is the first cause of death after the first year. It consists of accelerated coronary artery disease, by multifactorial causes where the followingconverge: immune response, reperfusion injury, cytomegalovirus infection and classical cardiovascular risk factors. The echocardiogram as we will see, has a significant role to detect it.

 

DETECTION OF ACUTE REJECTION
In the past, rejection was diagnosed with clinical signs as cardiomegaly and pump failure; this made its diagnosis late and caused irreversible sequelae.

As we see, acute rejection presents as a wide spectrum that ranges from minimum cell changes that can only be detected by biopsy, up to gross macroscopic changes with edema and cell lesion that entail functional disorders and clear clinical manifestations. Rejection 1 is not given clinical significance and the significance of rejection 2 is being discussed [2], so that echocardiography has two fundamental roles in early detection of rejection: one, to detect signs of rejection, not as early as biopsy, but yes in the period of clinical usefulness before changes that could be irreversible occur, and the second, as we said to guide the performance of the biopsy.

As with any progressive diffuse cardiac pathology, acute rejection also manifests first functionally by altering diastole and finally the systole.

So early detection efforts for rejection are made looking for indicators of diastolic function alteration.

In Figure 5, the time relation between the different factors at play.

Figure 5. Correlation between degrees of rejection
in biopsy and implant alterations.

 

Acute rejection. Echocardiographic findings

  • As late echocardiographic findings, we find anatomical alterations in:

Left ventricle
Increase in wall thicknesses with increase in left ventricular mass [5]. It is important to compare previous studies, since maybe the changes may not be as significant in the beginning and thus, normal values may not be exceeded. Another aspect to be considered is that using cyclosporine decreases edema as a manifestation of rejection [2]. The differential diagnosis should be made with Hypertrophy by hypertension that these patients frequently present. Increase in diastolic and systolic diameters, with a significant drop in ejection fraction in the last stages.

Mitral valve
Presence of a new mitral valve insufficiency or an increase in the preexisting one.

Right ventricle
Increase in dilatation.

Tricuspid valve and pulmonary systolic pressure
Greater degree of tricuspid valve insufficiency and increase in ventricular-atrial gradient with increase in pulmonary systolic pressure.

Pericardium
Appearance of new effusion, progressive over several days. Sometimes, it is early in regard to other structural alterations.

It is necessary to know the findings described, although late; but it is clear that we should aim at making an early recognition of rejection.

  • As early echocardiographic findings we find:

Different attempts have been made to identify a diastolic parameter that alters early in acute rejection. In general, rejection alters diastole as any diffuse process. If we take transmitral flow and its alterations as diastolic function worsens, we move from a normal filling to a filling of the relaxation alteration type, to a restrictive filling, going through the pseudo-normalcy stage [33]. This worsening process then has in transmitral measurements, a behavior of a J curve (Figure 6).

Figure 6. Correlation between diastolic function
worsening and E/A ratio in transmitral Doppler.

 

This has consequences:
It is impossible to distinguish with transmitral flow values, between normalcy and pseudo-normalcy.

With an isolated value in any measurement, as for instance isovolumetric relaxation time (IVRT), pressure half time (PHT), E/A ratio, and so on, it is not possible to know whether there is worsening or improvement.

This has originated a certain confusion described in literature [34], where for example, some authors take as indicator of rejection, IVRT and PHT shortening and for instance, others their increase. This lead to searching other parameters with a more “linear” relation with worsening, such as: color flow propagation velocity, the use of spectral Tissue Doppler imaging (TDI), trying to obtain estimations of hemodynamic variables as end of diastole pressure by Doppler echo, relating: mitral E wave with E’ wave by TDI of mitral annulus [35], that are also valuable in transplanted patients [36].

Besides, there are other changes in transplanted patients that make interpretation difficult, such as:
It is difficult to evaluate mitral fluxometry because the atrial component is very variable. The tendency to tachycardia produces a change to the right in the curve and basal values with a tendency to a restrictive pattern [37].

There are frequent changes in the load conditions that also have an influence.

With so many variables at play, it is understandable that results may be dissimilar. For example:
Fábregas et al, evaluating TDI in different regions of the left ventricle in two groups according to a significant rejection or not (IIIA), did not find differences although other authors did find them [38].

A mitral annulus TDI study in patients with and without significant acute rejection, found that an A’ wave by TDI lower than 8.7 cm/sec has 82% sensibility and 53% specificity to detect rejection, which yields, with a cutoff value of A’ greater than 9 cm/sec, a significant negative predictive value [37].

It is difficult to evaluate the A’ wave by TDI and this difficulty is based on the surgical technique used.

A TDI study of inferior side, showed a significant decrease in peak relaxation velocity (E’) in patients with moderate rejection. Taking as cutoff value, an E’ velocity lower than 0.16 cm/sec, the sensibility was 76%, the specificity was 88%, and the negative predictive value 92% [39].

Fauchier L. et al, made standard measurements of diastolic function and ventricular mass and change relations in regard to the last study in patients with and without rejection, finding as the single value with statistical significance, the percentage of pressure half time (PHT) variation; thus, a decrease in PHT of 15% yields a 29% sensibility and 81% specificity to detect rejection, with a 78% negative predictive value [40].

In the first years of the 21st century, there are promising methods rising for an early echocardiographic finding of rejection, some semiquantitative scores, using the TEI index, using microbubbles marked with ICAM-1, acoustic quantification, and acoustic video densitometry, which were finally not implemented as a routine practice [41-50].

Before this scenario, the solution seems to lie in:

  • Comparing multiple parameters in the same patient, trying to obtain matching information. For example: incipient effusion, small increase in IVRT and pulmonary systolic pressure.
  • Comparison of all parameters with previous studies with report and previous video available.
  • The studies should be made by the observer proper, to try to prevent interobserver mistakes.
  • Using novel technologies already available as Speckle Tracking Echocardiography, seem promising in the early detection of acute cellular rejection [51,52].

 

CHRONIC REJECTION DETECTION
Chronic rejection is the main limitation of survival in transplanted patients in the long run; this pathology also known as transplant coronary artery vasculopathy (CAV) presents an incidence as high as 10% per year [53].

Pathophysiologically, it has immunologic and non-immunologic components that produce endothelial impairment with muscle proliferation and intimal thickening that is observed during the first post-transplant year [54].

The clinical diagnosis of CAV is difficult by the denervation and its symptoms are late, presenting with dyspnea and pump failure signs, with indistinguishable findings of dilated cardiomyopathy being found in echo. So, early diagnosis should be made by screening. Most centers made a yearly coronary angiography. This is a very specific method, but not so sensitive.

The most sensitive method is intravascular ultrasound (IVUS), since it reaches the wall thickness, the place where hyperplasia occurs. This method also has limitations, such as: only large epicardial arteries are seen, the cost of the transducer and a limited single useful life, risks proper of an invasive producer.

Using stress echo with dobutamine (DSE) has been proposed as screening of patients with chronic rejection [55,56,57], even in children [58]. The mechanism by which regional anomalies occur in transplanted patients with CAV is an increase in chronotropism and a decrease in diastolic pressure, which produces an increase in oxygen consumption and a decrease in perfusion [59]. The report is made with information about wall motion score index (WMSI) where 1 is normal and >1 is abnormal. As well as WMSI ≥1.5 at two years, there is 51% of cardiac events [57]. Globally, the sensibility is between 79-95% and specificity 55-95%, with a negative predictive value of 91-92%. It is also valuable to make serial studies, since they make the existence of transient disorders evident, which are not correlated to subsequent cardiac events [60].

Stress echo with dobutamine has also shown to be useful in patients with myocardial dysfunction induced by brain death, where patients with low response to low doses of dobutamine after transplant are seen to improve contractility [61,62].

Investigation studies on coronary flow reserve have been made, with dissimilar results to separate lesions discovered in IVUS [63,64], possible due to endothelial dysfunction in these patients not being homogeneous and coronary reserve differing from one artery to another [65,32]. So, more results are needed with these new techniques.


Cardiac infections in transplanted patients [31]
Cardiac infectious involvement in transplanted patients is hard to diagnose. Further, clinical symptoms, physical examination and several imaging studies are usually late and unclear. The infections occur by opportunistic germs such as candida fungi, aspergillus, toxoplasma and cytomegalovirus. Or else, as a consequence of a iatrogenic rupture of the skin barrier (infections by staphylococcus of central venous catheters). In transplanted patients, pathogens may come from the implanted organ, as for instance cytomegalovirus. The typical signs and symptoms of an infectious process could be absent and congestive heart failure be the most clear manifestation of cardiac infection. Failure could be caused by infectious endocarditis, myocarditis or pericarditis.

In endocarditis, echocardiogram should be used as a screening method, since 10 to 20% of infections do not have valve vegetations and in turn, thrombi could be found or images that are useless, so first hemocultures and serological studies should be a first resource.

The findings in myocarditis could be similar to those of vascular rejection, with differential diagnosis constituting a dilemma in which endomyocardial biopsy may help and be very useful.

In pericarditis, effusion may also be difficult to differentiate from effusion by acute rejection.

 

ACKNOWLEDGEMENTS
To Dr. Salvador Mangione†, for his help with the illustrations of the review.

 

BIBLIOGRAPHY

  1. Dressler DK. Heart Transplantation: a review. J TransplCoord1999; 9 (1): 25-32.
  2. Burgess M, Bhattacharyya A, Ray SG.Echocardiography after cardiac transplantation. J Am SocEchocardiogr2002; 15 (9): 917-25.
  3. Taylor DO,Barr ML, Meiser BM, et al. Suggested guidelines for the use of tacrolimus in cardiac transplant recipients. J Heart Lung Transpl2001; 20 (7): 734-8.
  4. Taylor D. Immunosuppresive therapies after heart transplantation: best, better and beyond. CurrOpinCardiol2000; 15 (2): 108-14.
  5. Otto C. Evaluation of the cardiac transplant patient. Textbook of clinical echocardiography.2000. 2nd Edit.
    6. Geny B, Piquard F, Petit H,et al. Atrial Systolic function after heart transplantation. Transpproc1998; 30 (6): 2835-6.
    7. Peteiro J1, Redondo F, Calviño R, et al. Differences in heart transplant physiology according to surgical technique. J ThoracCardiovascSurg1996; 112 (3): 584-9.
    8. Derumeaux G1, Habib G, Schleifer DM, et al. Standartorthotopic heart transplantation versus total orthotopic heart transplantation. Circulation 1995; 92 (9 Suppl): 196-201.
    9. Milano CA1, Shah AS, Van Trigt P, et al. Evaluation of early postoperative results after bicaval versus standart cardiac transplantation an review of the literature. Am Heart J 2000; 140 (5): 717-21.
    10. Wilhelmi M1, Pethig K, Wilhelmi M, et al. Heart transplantation: echocardiographic assessment of morphology and function after more than 10 years of follow-up. Ann. Thoracsurg2002; 74 (4): 1075-9.
    11. Gorcsan J 3rd, Snow FR, Paulsen W, etal. Echocardiographic profile of transplanted human heart in clinically well recipients. J Heart Lung Transplant1992; 11(1 pt1): 80-89.
    12. Bellenger N, Marcus NJ, Davies C, et al. Left ventricular function and mass after orthotopic heart tranplantation. J Heart Lung Transplant2000; 19 (5): 444-52.
    13. AntunesM, Spotnitz HM, Clark MB, et al. Long term function of human cardiac allograft assessed by two-dimensional echocardiography. J ThoracCardiovascSurg1989; 98 (2): 275-84.
    14. De Simone R, Lange R, Sack RU, et al.Atrioventricular valve insufficiency and atrial geometry after orthotopic heart transplantation. Ann ThoracSurg1995; 60 (6): 1686-93.
    15. Aziz T, Burgess MI, Rahman AN, et al. Risk factors for tricuspid valve regurgitation after orthotopic heart tranplantation. Ann ThoracSurg1999; 68 (4): 1247-51.
    16. Barbant S, Redberg RF, Tucker KJ, et al. Abnormal pulmonary artery pressure profile after cardiac transplantation: an exercise Doppler echocardiography study. Am Heart J1995; 129 (6): 1185-92.
    17. Hausen B, Albes JM; Rohde R, et al. Tricuspid valve regurgitation atributable to endomyocardial biopsies and rejection in heart transplantation. Ann ThoracSurg1995; 59 (5): 1134-40.
    18. Chan M, Giannetti N, Kato T, et al. Severe tricuspid regurgitation after heart transplantation. J Heart Lung Transplant2001; 20 (7): 709-17.
    19. Richards D, Guilliland Y, Bernal JA, et al. Mitral inflow and pulmonary venous doppler measurement do not predict pulmonary capillary wedge pressure in heart transplant recipients. Am Heart J1998; 135 (4): 641-6.
    20. Vaturi M, Aravot D, Ben-Gal T, et al. Natural history of left-sided valves after heart transplantation. TransplantProc2000; 32 (4): 735-6.
    21. Rose AG, Park SJ, Shumway SJ, et al. Acquired supravalvular aortic stenosis following heart transplantation:report of 2 cases. JHeart Lung Transplant2002; 21: 499-502.
    22. Vigano M, Rinaldi M, DÁrmini M, et al.The spectrum of aortic complications after heart transplantation. Ann ThoracSurg1999; 68 (1): 105-11.
    23. Kaye DM, Bergin P, Buckland M, et al. Value of postoperative assessment of cardiac allograft funtion by tranesophagealechocardigraphy. J Heart Lung Transplant1994; 13 (2): 165-72.
    24. Gascueña R, de Lombera F, Fernández S, et al. Left circunflex artery to left atrium fistulas detected by transesophageal echocardiography en heart transplant recipients. Echocardiography 2000; 17 (5): 443-5.
    25. Vandenberg B, Mohanty PK, Craddock KJ, et al. Clinical significance of pericardial effusion after heart trasplantation. J Heart Transplant 1988; 7 (2): 128-34.
    26. Stobierska-Dzierzek B, Awad H, Michler RE, et al. The evolving management of acute rigth sided heart failure in cardiac transplant recipients. J Am CollCardiol2001; 38 (4):923-31.
    27. GradekW,D´Amico C, Smith AL, et al.Routine surveillance endomyocardial biopsy continues to detect significant rejection late after heart transplantation. J Heart Lung Transplant2000; 20 (5): 497-502.
    28. Sánchez J. Seguridad de la biopsia endomiocardicatransyugular del ventrículo derecho guiada por ecocardiografia bidimensional en pacientes post-transplante cardiaco. Rev Fed ArgCardiol1999; 28: 77-85.
    29. From AM, Maleszewski JJ, Rihal CS. Current status of endomyocardial biopsy. Mayo ClinProc2011; 86 (11):1095-1102.
    30. Grande AM, De Pieri G, Pederzolli C, et al. Echoguidedendomyocardial biopsy in heterotopic heart transplantation: Case report. J CardiovascSurg (Torino) 1998;39(2):223-5.
    31. Stewart S, Winters GL, Fishbein MC, et al. Revision of the 1990 formulation for the standarization of nomenclature in the diagnosis of heart rejection. J Heart Lung Transplant 2005; 24(11):1710.
    32. Costanzo MR, Dipchand A, Starling R, et al. The International Society of Heart and Lung Transplantation Guidelines for the care of heart transplant recipients.J Heart Lung Transplant 2010;29 (8): 914-56.
    33. Ommen SR. Echocardiographic assessment of diastolic function.CurrOpinCardiol2001; 16: 240-5.
    34.Ubilla M, Mastrobuoni S, Martín Arnau A, et al. Heart transplant. AnSistSanitNavar.2006;29 Suppl 2:63-78.
    35. Ommen SR, Nishimura RA, Appleton CP, et al. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures. Circulation 2000; 102 (15): 1788-94.
    36. Sundereswaran L, Nagueh SF, Vardan S, et al. Estimation of left and right ventricular filling pressures after heart transplantation by tissue Doppler imaging. Am J Cardiol1998; 82 (3): 352-7
    37. Stengel SM, AllemanY, Zimmerli M, et al. Doppler tissue imaging for assessing left ventricular diastolic dysfunction in heart transplant rejection. Heart 2001; 86 (4): 432-7
    38. Frábegas R, Crespo Leiro M, Muñiz J, et al. Usefulness of pulsed Doppler tissue imaging for noninvasive detection of cardiac after heart transplantation. TransplantProc1999; 31: 2545-7.
    39. Puleo JA, Aranda JM, Weston MW, et al. Noninvasive detection of allograft rejection in heart transplant recipients by use of Doppler tissue imaging. J Heart Lung Transplant1998; 17 (2): 176-84.
    40. Fauchier L1, Sirinelli A, Aupart M, et al. Performance of doppler echocardiography for diagnosis of acute mild or moderate cardiac allograft rejection. TransplantProc1997; 29 (5): 2442-5.
    41. Putzer G, Cooper D, Keehn C, et al. An improved echocardiographic rejection-surveillance strategy following pediatric heart transplantation. J Heart Lung Transplant2000; 19 (12): 1166-74.
    42. Tei C, Nishimura RA, Seward JB, et al. Noninvasive Doppler derived myocardial performance index: correlation with simultaneous measurement of cardiac catheterization measurements. J Am SocEchocardiogr1997; 10 (2): 169-78.
    43. Kang SM,Ha JW, Rim SJ, et al. Index of myocardial performance using doppler-derived param in the evaluation of left ventricular function in patients with HBP. Yonsei Med J 1998; 39 (5): 446-52.
    44. Tei C, Ling LH, Hodge DO, et al. New index of combined systolic and diastolic myocardial performance: a simple and reproducible measure of cardiac function. J Cardiol1995;26 (6): 357-66.
    45. Dujardin K, Tei C, Yeo TC, et al. Prognostic value of a Doppler index combining systolic and diastolic performance in idiopathic-dilated cardiomyopathy. Am J Cardiol1998; 82 (9): 1071-6.
    46. Haque A, Otsuji Y, Yoshifuku S, et al. Effects of valve dysfunction on Doppler Tei index. J AmSocEchocardiogr2002; 15(9): 877-83.
    47. Weler G, Lu E, Csikari MM, et al. Ultrasound imaging of acute cardiac transplant rejection with microbubbles targeted to intercellular adhesion molecule-1. Circulation 2003; 108 (2): 218-24
    48. MoidlR, Chevtchik O, Simon P, et al. Noninvasive monitoring of peak filling rate with acoustic quantification echocardiography accurately detects acute cardiac allograft rejection. J Heart Lung Transplant1999; 18 (3): 194-201.
    49. Almenar L, Osa A, Miró V, et al. Utility of acoustic densitometry in graft rejection diagnosis in heart transplantation. TransplantProc1999; 31 (6): 2544.
    50. Ciliberto GR, Pingitore A, Mangiavacchi M, et al. The clinical value of blunting of cyclic gray scale level variation for the detection of acute cardiac rejection: a twodimensional, doppler and videodensitometric ultrasound study. J AmSocEchocadiogr1996; 9 (3): 306-13.
    51. Pieper G,Shah A, Harmann L, et al.Speckle-tracking 2-dimensional strain echocardiography: A new noninvasive imaging tool to evaluate acute rejection in cardiac transplantation. J Heart Lung Transplant 2010; 29 (9):1039-1046.
    52Cameli M, Lisi M, Righini FM, et al. Speckle tracking echocardiography as a new technique to evaluate right ventricular function in patients with left ventricular assist device therapy.J Heart Lung Transplant 2013; 32(4):424-30.
    53. Aranda JM Jr, Hill J. Cardiac transplant vasculopathy. Chest 2000; 118 (6):1792-1800.
    54. Kobashigawa J, Wener L, Johnson J, et al. Longitudinal study of vascular remodeling in coronary arteries after heart transplantation. J Heart Lung Tranplant2000; 19 (6): 546-50.
    55. Spes C, Klaus V, Mudra H, et al. Role of dobutamine stress echocardiography for diagnosis of cardiac allograft vasculopathy. Transplantproc1998; 30 (3): 904-6.
    56. Young JB. Allograft vasculopathy: diagnosing the nemesis of heart transplantation. Circulation 1999; 100 (5): 458-60.
    57. Akosah K, Mohanty PK. Role of dobutamine stress echocardiography in heart transplant patients. Chest 1998; 113 (3): 809-15.
    58. Di Filippo S, Semiond B, Roriz R, et al. Noninvasive detection of coronary artery disease by dobutamine stress ecocardiography in children after heart transplantation. J Heart Lung Transplant 2003; 22 (8): 876-82.
    59. Akosah K,Denlinger B, Mohanty PK., et al. Safety profile and hemodynamic responses to B-adrenergic stimulation by dobutamine in heart transplantation. Chest 1999; 116 (6): 1587-92.
    60. Akosah K, McDaniel S, Hanrahan JS, et al. Dobutamine stress echocardiography early after heart transplantation predict development of allograft coronary artery disease and outcome. J Am CollCardiol1998; 31 (7): 1607-14.
    61. Kono T, Nishina T, Morita H, et al. Usefulness of low-dose dobutamine stress echocardiography for evaluating reversibility of brain death-induced myocardial dysfunction. Am J Cardiol1999; 84 (5): 578-82.
    62. Palac RT, Sumner G, Laird R, et al.  Reversible myocardial dysfunction after traumatic brain injury: mechanism and implications for heart transplantation. ProgTranplant2003; 13 (1): 42-6.
    63. Preumont N,Berkenboom G, Vachiery J, et al. Early alterations of myocardial blood flow reserve in heart transplant recipients with angiographically normal coronary arteries. J Heart Lung Transplant 2000; 19 (6): 538-45.
    64. Spes CH,Klauss V, Rieber J, et al. Functional and morphological finding in heart transplant recipients with a normal coronary angiogram: an analysis by dobutamine stress echocardiography, intracoronary doppler and intravascular ultrasound. J Heart Lung Transplant1999; 18 (5): 391-8.
    65. Weis M,Peter-Wolf W, Mazzilli N, et al. Variations of segmental endothelium-dependent and endothelium-independent vasomotor tone after cardiac transplantation. Am Heart J 1997; 134 (2 Pt 1): 306-16.

Publication: March  2014

 
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