Because infections can reduce QOL by interfering with daily activities, requiring patients to take additional medications or necessitating a return to the hospital, the reduced infection
Trang 1chanical failure of the device contributed
impor-tantly to the low 2-year survival rate of 23% The
device employeddthe HeartMate XVEdrequires
a large percutaneous line, which can become
a conduit for bacterial and fungal infection
Malnutrition was identified in these patients as
a predisposing factor to infection and other
complications Factors contributing to
postoper-ative malnutrition include early satiety, nausea, or
both from the bulk of the implanted device;
chronic inflammation associated with HF and
the device; and severe and often-underdiagnosed
preoperative debilitation[15]
Because these pumps are large, a substantial
pump pocket must be formed around them, and the
blood that collects in this pump pocket can be
a culture medium for bacteria The axial flow
devices, on the other hand, are much smaller than
conventional LVADs Furthermore, the Jarvik
2000 is implanted within the left ventricle,
elimi-nating the need for a pump pocket altogether One
study has shown that the Jarvik 2000 is associated
with a lower infection rate than a conventional
LVAD [7] Additionally, the 26 patients in the
authors’ previously published clinical study
experi-enced no significant device-related infections[10]
Because infections can reduce QOL by interfering
with daily activities, requiring patients to take
additional medications or necessitating a return
to the hospital, the reduced infection rate
associ-ated with the Jarvik 2000 may enable the device
to enhance QOL to a greater extent than
conven-tional LVADs
Mechanical failure of the LVAD was the second
most frequent cause of death in the REMATCH
trial’s device group The findings of inflow-valve
failure and late erosions of the outflow graft
resulting from kinking have already led to
modifi-cations in the device’s design Malfunction of the
mechanical parts, such as rupture of the lining,
motor failure, and wear on the bearings, also limits
the durability of the device Device failure limited
use of the HeartMate XVE to 2 years or less New
devices have longer life spans, however; the Jarvik
2000 is expected to last 5 years
One study suggests that patients survive longer
after heart transplantation if they were supported
by HeartMate XVE LVADs than if they did not
have LVAD support during the waiting period
[16] However, patients supported by conventional
LVADs also have greater cognitive impairment
and are more likely to be unemployed 1 year after
heart transplantation[17]
and reliability of the Jarvik device and the frequency of medical problems in outpatients with these pumps There were no readmissions for technical reasons, and the pump never failed QOL improved and was not adversely affected by the need to monitor or maintain the LVAS[18] Cardiac support with an LVAD can signifi-cantly improve symptoms of HF and, in some cases, lead to complete recovery[19–22] Signs of improvement in LVAD-supported patients in-clude decreased levels of epinephrine, norepineph-rine, angiotensin II, and arginine vasopressin, as well as interleukin-6, interleukin-8, and tissue necrosis factor-alpha [23–25] Additionally, long-term LVAD support reduces collagen content and myocyte size in the myocardium and im-proves contractility and response to b-adrenergic stimulation, suggesting that prolonged cardiac unloading with the LVAD promotes reverse re-modeling[26,27]
However, patient selection is important be-cause LVAD support does not produce complete recovery in all patients who have HF [28] The degree of irreversible myocardial damage at the time of LVAD implantation as well as the quality
of medical management after implantation are important determinants of outcome after LVAD implantation[29]
Symptomatic relief with cardiac resynchronization therapy placement
In patients who have advanced HF and a pro-longed QRS interval, CRT has been shown to improve symptoms and hemodynamics, increase exercise tolerance, and decrease the risk of death from any cause[30–33] In the Multicenter InSync Randomized Clinical Evaluation (MIRACLE) study, CRT resulted in clinical improvement in patients who had moderate-to-severe HF (LVEF
!35%) and an intraventricular conduction delay (QRS interval O130 msec)[33] After 6 months, the 228 CRT patients could walk farther in 6 min-utes and had greater endurance on the treadmill during exercise testing than the 225 patients in the control group The CRT patients also had
a greater decrease in LVEF, less need for hospital-ization and intravenous medications, and greater improvement in NYHA class and QOL However,
4 of the CRT patients had refractory hypotension, bradycardia, or asystole, and 2 of them died during implantation Two other patients had
Trang 2Should Patients who have Persistent Severe Symptoms Receive a Left Ventricular Assist Device or Cardiac Resynchronization Therapy as the Next Step?
Olga Khaleva, MD, Neil Hobson, MBBS, Andrew L Clark, MD
University of Hull, Castle Hill Hospital, Kingston-upon-Hull, UK
Many patients who have heart failure
experi-ence severe recurrent or persistent symptoms
despite standard pharmacologic treatment with
diuretics, ACE inhibitors or angiotensin receptor
blockers, aldosterone antagonists, and
beta-blockers[1–3] Careful review of standard
medica-tion may identify that the dose of one or more
components is not optimal and can be adjusted
for greater effect Finding the optimal dose and
combination of diuretics may be particularly
diffi-cult Excessive doses will cause hypotension, renal
dysfunction, and worsening symptoms
Insuffi-cient doses will also lead to worsening symptoms
Digoxin probably still has a role for the
manage-ment of advanced symptoms, especially when
the patient has atrial fibrillation, because
beta-blockers often do not adequately control
ventric-ular rate [4] Correction of anemia with iron
supplements when it is due to iron deficiency or
erythropoietin-stimulating peptides when not due
to specific haematinic deficiency may also improve
symptoms, although the data are not robust[5]
Withdrawal of nonsteroidal anti-inflammatory
drugs, including aspirin, also seems to reduce the
need for hospitalization for worsening heart
fail-ure[6,7] However, when standard pharmacologic
therapy has failed, surgical and device options
should be considered
Two substantial studies are underway to assess
the benefits of revascularization with or without
the benefits of surgical left ventricular remodeling [8–10] Currently there is no evidence that revas-cularization of patients who have heart failure and LVSD is safe or effective, even when a large amount of viable but hibernating myocardium is present We should obtain the first results of trials in 2007 Revascularization is not discussed further in this manuscript
The initial enthusiasm for skeletal myoblast and stem cell transplantation into the failing myocardium has been tempered by experience There is now considerable uncertainty whether this approach provides worthwhile benefits [11,12] Hopefully, refinements in the technologic approach might improve results
The two surgical technologies that have shown benefit on symptoms and survival are left ventricular assist devices (LVADs) and cardiac resynchronization therapy (CRT), with or without
a defibrillator function[3,13–15] The purpose of this manuscript is to describe the benefits of CRT and the gaps in our knowledge that are an impediment to clinical practice and may be ex-ploited by further research and then to compare that to what we know about LVADs However,
it should be clear from the outset that there is
a role for both in the management of advanced heart failure
Cardiac dyssynchrony Cardiac dyssynchrony is conceptually simple but rather difficult to define and measure on an individual patient basis[13] Indeed, it may not be
* Corresponding author University of Hull, Castle
Hill Hospital, Kingston-upon-Hull, HU 16 5JQ, UK.
E-mail address: j.g.cleland@hull.ac.uk (J Cleland).
1551-7136/07/$ - see front matter Ó 2007 Elsevier Inc All rights reserved.
Trang 3Does Myectomy Convey Survival Benefit
in Hypertrophic Cardiomyopathy?
Harry Rakowski, MD, FRCPC, FACC
University of Toronto, Toronto, ON, Canada
Hypertrophic cardiomyopathy (HCM) is
a complex disorder and concepts regarding this
condition have evolved considerably since its
modern description in the 1950s [1,2] Although
once perceived as a rare disease causing sudden
cardiac death (SCD) in young adults [2], HCM
is now recognized as a relatively common genetic
disorder affecting 1 in 500 individuals and
charac-terized by a wide spectrum of clinical
manifesta-tions[3,4] Dynamic left ventricular outflow tract
(LVOT) obstruction has been a prominent aspect
of HCM and, in the early years of the disease’s
recognition, its presence was inextricably linked
to the diagnosis of this condition [5,6] Patients
who have the obstructive form of HCM have
unique and distinguishing clinical and
hemody-namic features[4–6]
The dynamic LVOT obstruction of HCM has
generated much interest and controversy; its
existence, cause, diagnosis, treatment, and
prog-nosis have all provoked debate[3,4] Aside from
its hemodynamic effects, some investigators had
questioned the importance of obstruction and
re-garded it as a secondary finding in this disease
[7,8] Multiple echocardiographic and
hemody-namic studies support the view that LVOT
ob-struction is caused by systolic anterior motion
(SAM) of the anterior mitral leaflet, contact of
the mitral leaflet with the hypertrophied
interven-tricular septum, and consequent obstruction to
blood flow in the outflow tract during systole [3,4,9] LVOT obstruction is accompanied by mi-tral regurgitation [10,11], and these lesions are largely responsible for the disabling symptoms (eg, dyspnea, angina, presyncope, syncope) and hemodynamic abnormalities associated with obstructive HCM [3,4,6] The presence of an LVOT gradient measuring at least 30 mm Hg is generally accepted as the definition for obstructive HCM[3]
At the present time there is a general consensus that patients who have symptoms attributable to LVOT obstruction should receive treatment to diminish or abolish the LVOT gradient[3] Treat-ment options include medications (negative ino-tropic agents), dual chamber (DDD) permanent pacing, septal ethanol ablation (SEA), or surgical myectomy All of these therapies have variable ef-fects on reducing symptoms and on controlling the LVOT gradient[3,4] The longest experience has been with surgery, which was first performed
in this condition in the late 1950s [5] Because myectomy has consistently improved symptoms and LVOT obstruction, many investigators regard this procedure as the optimum treatment of ob-structive HCM[3,12] Myectomy remains contro-versial, however, because it is unclear if there is
a survival advantage with myectomy compared with conservative management or compared with other available therapies [3,8]
Because recent studies demonstrate that LVOT obstruction is associated with a worsened prog-nosis[13,14]and because there are different treat-ment options for obstructive HCM, it is important to evaluate the risks and benefits of myectomy, especially in its impact on survival
In this article we review the clinical course of
* Corresponding author Division of Cardiology,
Toronto General Hospital, University of Toronto, 200
Elizabeth Street, 4N 504, Toronto, ON M5G 2C4,
Canada.
E-mail address: anna.woo@uhn.on.ca (A Woo).
1551-7136/07/$ - see front matter Ó 2007 Elsevier Inc All rights reserved.