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 Heart Failure Treatment & Management

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john



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PostSubject: Heart Failure Treatment & Management   Wed Jun 22, 2011 8:56 am

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Heart Failure Treatment & Management

Approach Considerations

Once
the diagnosis of heart failure is established, a number of
pharmacologic strategies are available to limit and reverse the
manifestations of HF. In particular, blocking the renin-angiotensin
system and the beta-adrenergic system improves mortality rates among
patients with heart failure. Use of angiotensin-converting enzyme
inhibitors (ACEIs), as well as angiotensin receptor blockers (ARBs),
increases survival and decreases repeat hospitalizations. These benefits are also observed with several beta blockers, including metoprolol and carvedilol.[20] Patients
often have difficulty tolerating either ACEIs or beta-blockers. A
number of additional drug regimens can be used in these cases. These
drugs include loop and thiazide diuretics, as well as aldosterone
antagonists. Diuretic therapy decreases ventricular diastolic pressure,
reducing ventricular wall stress and maximizing subendocardial
perfusion. Digoxin, a cardiac glycoside, is used to improve
symptoms associated with HF by enhancing cardiac contractility. Although
digoxin does not confer a survival benefit, it has reduced the number
of hospitalizations that occur due to worsening heart failure. Enthusiasm
has once again developed for the use of vasodilator therapy with a
combination of hydralazine and isosorbide dinitrate.[21] A
study by Dunlay et al examined medication use and adherence among
community-dwelling patients with HF. The study found that medication
adherence was suboptimal in many patients, often because of cost. Finally,
when their condition is refractory to standard therapy, patients often
require hospitalization to receive intravenous (IV) diuretics,
vasodilators, and inotropes. When progressive end-stage heart
failure occurs despite maximal medical therapy, the criterion standard
for therapy has been heart transplantation. Other surgical options
include CABG, valve replacement or repair, ventricular restoration,
ICDs, cardiac resynchronization therapy (CRT), and VADs. Mechanical
circulatory devices are available for bridging the patient to recovery
and transplantation. Clinical application of artificial-heart technology
is still immature, but total artificial hearts (TAHs) are approved for
use as a bridge to heart transplantation.

Heart Failure: A Companion to Braunwald's Heart Disease




GET IT HERE




New CABG Findings from STICH

The
role of coronary artery bypass grafting (CABG) in patients with
coronary artery disease (CAD) and heart failure has been unclear.
Clinical trials from the 1970s that established the benefit of CABG for
patients with CAD excluded patients with an ejection fraction (EF) of
less than 35%. In addition, major advances in medical therapy and
cardiac surgery have taken place since these trials.[23] The
Surgical Treatment of Congestive Heart Failure (STICH) study was
designed to address the question of whether CABG with intensive medical
therapy, as compared with medical therapy alone, confers an additional
survival benefit in patients with an EF of less than 35%. STICH included
1212 patients with an ejection fraction of 35% or less and CAD amenable
to CABG. Patients were randomized to either CABG or medical therapy
alone and followed up for a median of 56 months. The STICH study
found no significant difference between medical therapy alone and
medical therapy plus CABG with respect to death from any cause (the
primary study outcome). Except for 30-day mortality, however, secondary
study results favored CABG: Compared with study patients assigned to
medical therapy alone, patients assigned to CABG had lower rates of
death from cardiovascular causes and of death from any cause or
hospitalization for cardiovascular causes.[23]

Treatment of Acute Heart Failure

Acute
heart failure is a rapid or gradual onset of signs and symptoms of
heart failure that result in urgent, unplanned hospitalization or office
or ED visit. This is the result of a sudden increase in filling
pressures leading to systemic and pulmonary congestion, regardless of
the cardiac output. Most patients who present with acute heart failure
have exacerbation of chronic heart failure, with only 15-20% having
acute de novo heart failure. More than 50% of patients with acute heart
failure have preserved LVEF (>40%). Less than 10% of patients
presenting with acute heart failure are hypotensive and require
inotropic therapy. Pulmonary edema is a medical emergency and only one
of the presentations of acute heart failure. A systematic and
expeditious approach is required, starting in the emergency room,
continuing during hospitalization, and extending after discharge to the
outpatient setting. ED care consists of stabilizing the patients’
clinical condition; establishing the diagnosis, etiology, and
precipitating factors; and initiating therapies to rapidly provide
symptom relief. Use of oxygen if blood oxygen saturation is less
than 90% and noninvasive positive pressure ventilation (NIPPV) provides
patients with respiratory support to avoid intubation. NIPPV has
been shown to decrease the rate of intubation and mechanical ventilation
by 50% and to decrease hospital mortality by 40%. No difference has been noted between continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BIPAP).Use
of analgesics, such as morphine sulfate and benzodiazepines, helps with
patients’ anxiety, distress, and dyspnea. Morphine sulfate also
decreases preload. If arrhythmia is present and uncontrolled
ventricular response is thought to contribute to the clinical scenario
of acute heart failure, then either pharmacologic rate control or
emergent cardioversion with restoration of sinus rhythm is recommended. Relief
of congestion is achieved using IV diuretics and vasodilators. If the
patient is hypotensive, use of either inotropic therapies and/or
mechanical circulatory support (eg, intra-aortic balloon pump,
extracorporeal membrane oxygenator, left ventricular assist device
[LVAD]), in addition to continuous hemodynamic monitoring, is indicated.


Indications for Hospitalization

Most
patients requiring hospitalization should be admitted to a telemetry
bed or intensive care unit (ICU); a small percentage can be admitted to
the floor or observation unit. The goal is to continue the diagnostic
and therapeutic processes started in the ED. Treatment includes the
following:

  • Volume and hemodynamic
    status are optimized using careful clinical monitoring, and the heart
    failure medical regimen is optimized.
  • Heart failure education, behavior modification, and exercise and diet recommendation are made.
  • The patient must be on a stable oral regimen for at least 24 hours before discharge.
Stevenson
and colleagues postulated treatment for acute heart failure based on
volume and perfusion status of the patient (warm and wet, warm and dry,
cold and wet, cold and dry). To ensure compliance and
understanding of a complex medical regimen, a follow-up phone call is
made 3 days after discharge by a nurse with training in heart failure.
Ideally, the patient should be seen in clinic 7-10 days after discharge.
Heart Failure Society of America guidelines for hospitalization

The
2006 Heart Failure Society of America (HFSA) guidelines recommend
hospitalization for acute heart failure if the following are present[21] :

  • Severe decompensated heart failure (low blood pressure, renal dysfunction, altered mentation)
  • Dyspnea at rest
  • Hemodynamically significant arrhythmia
  • Acute coronary syndrome
Hospitalization should be considered if the following are present:

  • Worsening congestion (weight gain >5 kg)
  • Worsening signs and symptoms of systemic or pulmonary congestion, even in the absence of weight gain
  • Major electrolyte abnormalities
  • Associated comorbid conditions
  • Repeat ICD (implantable cardioverter-defibrillator) firings
  • New diagnosis of heart failure with signs of active congestion
Hospital discharge

Patients
are ready for discharge when exacerbating factors have been addressed,
volume status has been optimized, diuretic therapy has been successfully
transitioned to oral medication with discontinuation of IV vasodilator
and inotropic therapy for at least 24 hours, and oral chronic heart
failure therapy has been achieved with stable clinical status. Patient
and family education should be completed, and extensive postdischarge
instructions and follow-up in 3-7 days must be arranged. Patients with
difficult and complicated disease should be referred to a disease
management program.[24] Different
monitoring methods have been implemented by physicians in an attempt to
reduce hospitalization for heart failure, from telephone monitoring to
different device monitoring and intense clinical monitoring. The results
have been equivocal, regardless of the severity of heart failure. No
difference in death or hospitalization for heart failure between
standard outpatient monitoring and intense telemonitoring for heart
failure have been found.[25, 26]

Diuretic Therapy

Diuretics
remain the mainstay of therapy and the current standard of care for
acute heart failure. IV administration of a loop diuretic (ie,
furosemide, bumetanide, torsemide) is preferred initially due to
potential poor absorption of the oral forms in the presence of bowel
edema. The dose and frequency of administration depend on the diuretic
response 2-4 hours after the first dose is given. If the response is
inadequate, then increasing the dose and/or increasing the frequency can
help to enhance diuresis. The patient is considered diuretic resistant
if either of the following is necessary:

  • More than 80 mg IV bolus or more than 2 mg/kg of furosemide for an appropriate response
  • More than double the diuretic dose or a second agent in the form of a thiazide diuretic
Volume
status, sodium, water intake, and hemodynamic status for signs of poor
perfusion need to be reevaluated in case of diuretic resistance. Although
diuretic resistance was thought to be a side effect of diuretics, a
meta-analysis demonstrated that this phenomenon is mostly a result of
advanced heart failure. Eventually, alternative strategies, such as
hemodialysis or ultrafiltration, may be used to overcome it. Other
agents, such as vasopressin antagonists and adenosine receptor blockers,
can be used to assist diuretics. Transition to oral diuretic
therapy is made upon reaching a near-euvolemic state. The oral diuretic
dose is usually equal to the IV dose. Usually, 40 mg/d of furosemide is
equivalent to 20 mg of torsemide and 1 mg of bumetanide. Weight, sign
and symptoms, fluid balance, electrolyte levels, and renal function have
to be monitored carefully on a daily basis. Patients with acute
decompensated heart failure who are receiving diuretic therapy by bolus,
continuous infusion, or at a high dose as compared with a low dose
appear to have no significant differences in their global assessment of
symptoms or in renal function changes.[27]

Vasodilator Therapy

Vasodilators
are recommended as first-line therapy for patients with acute heart
failure in the absence of hypotension in addition to diuretic therapy
for relief of symptoms. Vasodilators will decrease preload and/or
afterload. Nitrates are potent venodilators. They decrease
preload, therefore decreasing LV filling pressure and relieving
shortness of breath. They also selectively produce epicardial coronary
artery vasodilatation and help with myocardial ischemia. Although
nitrates can be used in different forms (sublingual, oral, transdermal,
IV), the most common route in acute heart failure is IV. Their use is
limited by tachyphylaxis and headache. Sodium nitroprusside is a
potent balanced arterial and venous vasodilator resulting in a very
efficient decrease of intracardiac filling pressures. It requires not
only careful hemodynamic monitoring using indwelling catheters but also
monitoring for cyanide toxicity, especially in the presence of renal
dysfunction. It is particularly helpful for patients who present with
severe pulmonary congestion in the presence of hypertension and severe
mitral regurgitation. The drug should be titrated to off rather than
abruptly stopped due to the rebound potential. Nesiritide (human
BNP analog) is a vasodilator that subjectively has been demonstrated to
alleviate dyspnea faster when compared with diuretics alone or in
combination with low-dose nitroglycerin (Vasodilation in the Management
of Acute Congestive Heart Failure [VMAC] trial). The drug can be
initiated if systolic blood pressure is greater than 100 mm Hg at a
continuous drip of 0.005 mcg/kg/min with or without an IV bolus of 2
mcg/kg. Continuous infusion can be titrated to a maximum of 0.03
mcg/kg/min, although this dose has been associated with more renal
dysfunction and hypotension, and the additional decongestive benefit at a
higher dose is questionable. Long-term effects on mortality and renal
function are under investigation. Inotropes improve short-term
symptoms and hemodynamics in patients with evidence of cardiogenic shock
and end-organ dysfunction. Their use long term (Randomized Evaluation
of Mechanical Assistance for the Treatment of Congestive Heart Failure
[REMATCH] trial) or in patients not in cardiogenic shock (normotensive
and without evidence of end organ perfusion; Outcomes of a Prospective
Trial of Intravenous Milrinone for Exacerbations of Chronic Heart
Failure [OPTIME HF]) is not indicated and increases mortality. An
adrenergic agonist (dopamine, dobutamine, epinephrine, norepinephrine), a
phosphodiesterase inhibitor (milrinone, enoximone), or a calcium
sensitizer (levosimendan) can be used.

Adrenergic Agents

Adrenergic agonists are used in case of significant hypotension to improve cardiac output and organ perfusion.Dobutamine,
a beta-receptor agonist, increases inotropy and chronotropy and
decreases afterload, thereby improving end-organ perfusion. Doses of
5-10 mcg/kg/min are used, although in the presence of a beta-blocker,
higher doses may be necessary. Careful hemodynamic and patient
monitoring is required. Dopamine has beta-receptor agonist
properties in doses of 3-7.5 mcg/kg/min and can be used as a positive
inotrope. Initiation of it can precipitate arrhythmia due to inhibition
of norepinephrine uptake. Doses of more than 7.5 mcg/kg/min will produce
more peripheral vasoconstriction via alpha stimulation and can
precipitate heart failure. Doses of more than 10 mcg/kg/min are used
mostly for refractory hypotension in the presence of cardiogenic shock.
In doses of less than 3 mcg/kg/min, it produces splanchnic vasodilation
due to the stimulation of dopaminergic receptors. Milrinone is a
phosphodiesterase inhibitor (PDEi) that increases inotropy, chronotropy,
and lusitropy, acting via cyclic guanosine monophosphate (cGMP) to
increase the intramyocardial adenosine triphosphate (ATP). It is a
potent vasodilator agent, being a venous and arterial vasodilator, and
it is used in patients with pulmonary hypertension. Milrinone can be
used in the presence of a beta-blocker. Milrinone is thought to create
less tachycardia, since it does not directly stimulate beta-receptors.
Milrinone is usually initiated at 0.25 mcg/kg/min and can be titrated up
to 0.75 mcg/kg/min. The half-life is 2.4-6 hours, and the drug needs to
be adjusted for renal function. Milrinone is usually avoided in
patients with severe hypotension. Milrinone should not be used routinely
in patients with heart failure exacerbation in the absence of
cardiogenic shock, since it has been shown to increase mortality
(OPTIME-CHF). Oral therapy with ACEI /ARB is usually continued.
Adjustment of dose or temporary withholding may be necessary if
hypotension persists and hinders diuresis or if renal function worsens. Beta-blockers
are usually continued in the same dose or at a slightly reduced dose,
with the exception of situations requiring IV inotropic therapy where
they are temporarily stopped. Usually, beta-blockers are resumed prior
to discharge if patient condition allows. Ultrafiltration was
shown to be an effective alternative to intravenous diuretics in the
Ultrafiltration Versus Intravenous (IV) Diuretics for Patients
Hospitalized for Acute Decompensated Heart Failure (UNLOAD) trial.[28] Use
of ultrafiltration for fluid reduction is now a class IIa
recommendation for patients with refractory heart failure that is not
responsive to medical therapy.

Hemodynamic Monitoring

Invasive
hemodynamic monitoring is indicated for patients who have respiratory
distress, patients who have signs of impaired perfusion, when
intracardiac pressures cannot be determined based on clinical
examination, or if there is no improvement in clinical status despite
maximal heart failure therapy.[29] Invasive
hemodynamic monitoring, although not indicated for stable patients with
heart failure responding appropriately to medical therapy (the
Evaluation Study of Congestive Heart Failure and Pulmonary Artery
Catheterization Effectiveness [ESCAPE] trial showed no mortality or
hospitalization benefit[30] ), is recommended in the following situations for patients with acute decompensated heart failure (class IIa recommendation):

  • Patients with uncertain fluid status, perfusion, or systemic or pulmonary vascular resistance
  • Patients with persistent symptomatic hypotension despite initial therapy
  • Patients with worsening renal function despite initial therapy
  • Patients who require parenteral vasoactive agents
  • Patients who may be considered for advanced device therapy or transplantation


Anticoagulation Administration

Patients
with heart failure and depressed LVEF are thought to have an increased
risk of thrombus formation due to low cardiac output. Anticoagulation
with an international normalized ratio (INR) goal of 2-3 is indicated in
the presence of LV thrombus, thromboembolic event with or without
evidence of an LV thrombus, and paroxysmal or chronic atrial
arrhythmias. Routine anticoagulation with warfarin in patients with
normal sinus rhythm, heart failure, and LV dysfunction has proven not to
be superior to aspirin alone in decreasing death, MI, and stroke and
can be associated with an increased risk of bleeding in the Coumadin arm
(WATCH trial).[31]

Use of Intravenous Iron

A
significant benefit from using IV iron in patients with heart failure
and iron deficiency was demonstrated in a study by Anker et al. The
investigators examined how treatment with ferric carboxymaltose (IV
iron) would decrease symptoms in patients with heart failure, reduced
LVEF, and iron deficiency (with or without anemia). In this study, 459
patients with NYHA functional class II or III were randomly given (in a
2:1 ratio) 200 mg IV ferric carboxymaltose or placebo (saline). At 24
weeks, 50% of subjects receiving ferric carboxymaltose reported much or
moderate improvement on the self-reported Patient Global Assessment,
compared with 28% of subjects receiving placebo. Subjects with an NYHA
functional class I or II at 24 weeks included 47% in the ferric
carboxymaltose group compared with 30% in the placebo group.[32]

Preventive Therapy for Patients at High Risk for Developing Heart Failure (Stage A Patients)

Stage
A patients have risk factors for developing heart failure (eg,
hypertension, diabetes mellitus, obesity, metabolic syndrome, sleep
apnea, patients with a family history of dilated cardiomyopathy or using
cardiotoxins). They should be treated with aggressive risk factor
modification, education, and angiotensin-converting enzyme inhibitor
(ACEI)/angiotensin receptor blocker (ARB) if diabetes mellitus or
vascular disease is present (HOPE, SOLVD-prevention).

Treatment of Heart Failure with LV Systolic Dysfunction (Stages B, C, D)

Medical therapy for heart failure focuses on the following 3 main goals:

  • Preload reduction
  • Reduction of systemic vascular resistance (afterload reduction)
  • Inhibition
    of the RAAS systems and vasoconstrictor neurohumoral factors produced
    by the sympathetic nervous system in patients with heart failure
The
first 2 goals provide symptomatic relief. While reducing symptoms,
inhibition of the RAAS and neurohumoral factors also results in
significant reductions in morbidity and mortality rates. Preload
reduction results in decreased pulmonary capillary hydrostatic pressure
and reduction of fluid transudation into the pulmonary interstitium and
alveoli. Afterload reduction results in increased cardiac output and
improved renal perfusion, facilitating diuresis in the patient with
fluid overload. Inhibition of the RAAS and SNS produces vasodilation,
thereby increasing cardiac output and decreasing myocardial oxygen
demand. Stage B treatment

Stage B includes asymptomatic
patients with LV dysfunction from previous myocardial infarction, LV
remodeling from left ventricular hypertrophy, and asymptomatic valvular
dysfunction. In addition to heart failure education and aggressive risk
factor modification, treatment with ACEI/ARB (SOLVD-prevention, SAVE,
VALIANT) and/or beta blockade (SOLVD prevention, SAVE, Capricorn) is
indicated. Evaluation for coronary revascularization either
percutaneously or surgically, as well as correction of valvular
abnormalities, may be indicated. Treatment with an implantable cardioverter-defibrillator
(ICD) for primary prevention of sudden death in patients with an LVEF
of less than 30% more than 40 days post-MI is reasonable if expected
survival is more than 1 year (MADIT II). There is less evidence for
implantation of an ICD in patients with nonischemic cardiomyopathy, an
LVEF less than 30%, and no heart failure symptoms. There is no evidence
for use of digoxin in these populations (DIG trial).[33] Aldosterone-receptor blockade with eplerenone is indicated for post–MI LV dysfunction (EPHESUS). Stage C treatment

Stage
C includes patients with NYHA class II and III heart failure, and stage
D includes patients with refractory end-stage heart failure (class IV).
Therapeutic measures that improve symptoms and mortality and
morbidity include use of ACEI/ARBs, beta-blockers, aldosterone-receptor
blockers, hydralazine and nitrates in combination, and cardiac
resynchronization with or without an implantable
cardioverter-defibrillator.

Management of Heart Failure With Normal LV Ejection Fraction

Treatment
of HFNEF is directed toward alleviating symptoms and addressing the
underlying condition triggering HFNEF. There is a paucity of randomized,
controlled studies addressing HFNEF. Control of blood pressure, volume,
or other risk factors is the mainstay of therapy. Lifestyle
modification, including a low sodium diet, restricted fluid intake,
daily weights, exercise, and weight loss, is important. Evaluation of
cardiac ischemia or sleep apnea as potential precipitating factors
should also be considered. Careful diuretic therapy is
recommended to avoid hypotension. ACEI/ARBs are used as indicated for
patients with evidence of atherosclerotic disease, post-myocardial
infarction, diabetes mellitus, and hypertension. Use of candesartan in
CHARM-Preserved,[34] irbesartan
in I-PRESERVED, or perindopril in PEP-HF revealed no change in
mortality; however, the trend was toward improved morbidity and
hospitalizations. Some evidence shows LV reverse remodeling using
losartan and valsartan, with improvement in diastolic function and
regression of LVH. Beta-blockers are indicated for patients with
prior myocardial infarction, hypertension, and atrial fibrillation for
control of ventricular rate. In the ADHERE registry, the subset of
patients with HFNEF not treated with beta blocker had a higher
mortality, potentially due to the higher incidence of CAD in this
population.[35] Aldosterone-receptor
blockers are indicated in hypertension and to reduce myocardial
fibrosis, although no randomized, controlled studies have been performed
to evaluate their role in HFNEF. Calcium-channel blockers may
improve exercise tolerance via their vasodilatory properties, and
nondihydropyridine calcium-channel blockers are also used for
ventricular rate control in patients with atrial fibrillation.
Amlodipine has antianginal properties and is also indicated in
hypertension. Restoration of sinus rhythm should be considered if
the patient remains symptomatic despite the above efforts. Use of
digitalis or inotropes in patients with HFNEF is not indicated.

Management of Right Ventricular Failure

Management
of RV failure includes treatment of the underlying cause; optimization
of preload, afterload, and RV contractility; maintenance of sinus
rhythm; and AV synchrony. Hypotension should be avoided, since it can
potentially lead to further RV ischemia. General measures should be
applied, such as sodium and fluid restriction; moderate physical
activity avoiding isometric exercises; avoiding pregnancy; compliance
with medications; and avoiding, or rapid treatment of, precipitating
factors such as sleep apnea, PE, sepsis, arrhythmia, ischemia, high
altitude, anemia, and hypoxemia. In patients with severe
hemodynamically compromising RV failure, inotropic therapy is used with
dobutamine 2-5 mcg/kg/min, dobutamine and nitric oxide, or dopamine
alone. Milrinone is preferred if the patient is tachycardic or on
beta-blockers. Use of ACEI/ARB is beneficial if RV failure is
secondary to LV failure; their efficacy is not known in isolated RV
failure. The same recommendation applies for use of beta-blockers. The
role of nesiritide in RV failure is not well defined. Use of digoxin in
RV failure associated with chronic obstructive pulmonary disease (COPD),
not associated with LV dysfunction, appears not to improve exercise
tolerance or RVEF. Anticoagulation indications are standard for
evidence of intracardiac thrombus, thromboembolic event, pulmonary
arterial hypertension, paroxysmal or persistent atrial
fibrillation/flutter, and mechanical right-sided valves. Hypoxemia should be corrected and positive pressure should be avoided when mechanical ventilation is needed.Atrial septostomy can be considered as a palliative measure in very symptomatic patients who failed standard therapy.RV mechanical assist device is indicated only for RV failure secondary to LV failure or post–cardiac transplantation.Prognosis
of RV failure is dependent on the etiology (better for volume overload,
pulmonary stenosis, and Eisenmenger syndrome). Decreased exercise
tolerance predicts poor survival.

Management of Cardiorenal Syndrome

Cardiorenal
syndrome reflects advanced cardiorenal dysregulation manifested by
acute heart failure, worsening renal function, and diuretic resistance.
It is equally prevalent in patients with HFNEF and those with LV
systolic dysfunction. Worsening renal function is one of the 3
predictors of increased mortality in hospitalized patients with heart
failure regardless of the LVEF (ADHERE registry). Cardiorenal syndrome can be classified into 5 types:

  • CR1
    - Rapid worsening of cardiac function leading to acute kidney injury
    (HFNEF, acute heart failure, cardiogenic shock, and RV failure)
  • CR2 - Worsening renal function due to progression of chronic heart failure
  • CR3 - Abrupt and primary worsening of kidney function leading to acute cardiac dysfunction (heart failure, arrhythmia, ischemia)
  • CR4 - Chronic kidney disease leading to progressive cardiac dysfunction, LVH, and diastolic dysfunction
  • CR5 - Combination of cardiac and renal dysfunction due to acute and chronic systemic conditions.
Pathophysiology
for CR1 and CR2 is complex and multifactorial, involving neurohormonal
activation (RAAS, SNS, AVP, natriuretic peptides, adenosine-receptor
activation), low arterial pressure, and high central venous pressure,
leading to lower transglomerular perfusion pressure and decreased
availability of diuretics to the proximal nephron. This results in an
increased reabsorption of sodium and water and poor diuretic
response—hence, diuretic resistance despite escalating doses of oral or
intravenous diuretics and need for combination diuretic therapy or
ultrafiltration. A sudden increase in creatinine can be seen
after initiation of diuretic therapy and is often mistaken on clinical
examination as overdiuresis or intravascular depletion (even in the
presence of fluid overload), prompting most physicians to decrease
and/or stop ACEI/ARB and/or diuretics. When diuresis or ultrafiltration
is continued, an improvement in renal function, decrease in total body
fluid, and increase in response to diuretics, as CVP is lowered, is
noted. Use of low-dose dopamine to increase kidney perfusion has contradictory data with no randomized controlled studies.Use
of nesiritide, a synthetic natriuretic peptide, to increase diuresis
has not been studied, and this agent should not be used unless the
patient is in pulmonary edema and needs heart failure symptom relief. A
meta-analysis of several trials using nesiritide suggests the potential
of worsening renal function, although this has not been demonstrated in
prospective trials. The Efficacy of Vasopressin Antagonism in
Heart Failure Outcome Study with Tolvaptan (EVEREST) trial showed that
the vasopressin antagonist tolvaptan in acute heart failure in addition
to diuretic therapy facilitates diuresis; however, it has no impact on
mortality or hospitalizations.[36] Adenosine receptor antagonists are in trial to evaluate their role in acute heart failure.


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PostSubject: Re: Heart Failure Treatment & Management   Wed Jun 22, 2011 8:57 am

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Heart Transplantation

When progressive end-stage heart failure occurs despite maximal medical
therapy, the criterion standard for therapy has been heart
transplantation. Since Christian Barnard performed the first orthotopic
heart transplantation in 1967, the world has seen tremendous advancement
in the field of cardiac transplantation. Compared with patients
who receive only medical therapy, transplant recipients have fewer
rehospitalizations, marked functional improvements, enhanced quality of
life, more gainful employment, and longer lives, with 50% surviving 10
years postoperatively.[37] Heart
transplantation is associated with a 1-year survival rate of 83%, which
decreases in a linear manner by approximately 3.4% per year. Careful
selection of donors and recipients, as well as efforts to minimize
potential perioperative dangers (ischemic times, pulmonary hypertension,
mechanical support, cardiogenic shock), is critical for ensuring good
outcomes. The single greatest advancement for ensuring long-term
function of the allograft is the development of immunologic modulators,
pioneered by Dr. Norman Shumway at Stanford University. Steroids and
antipurine metabolites, including azathioprine and mycophenolate mofetil
(MMF), have been widely used. Central to current
immunosuppression regimens are the calcineurin inhibitors cyclosporine
and tacrolimus. These drugs inhibit cellular pathways responsible for
the production of interleukin (IL)-2 and subsequent T-cell activation.
They inhibit the nuclear translocation of cytoplasmic factors needed to
bind to the IL-2 gene promoter. Immunosuppressive regimens have evolved
from cyclosporine to the predominant use of tacrolimus. Triple-drug
therapy consisting of steroids, calcineurin inhibitors, and MMF has
become standard initial immunotherapy after heart transplantation.Additional
agents, such as antithymocyte globulin, rapamycin, and IL-2-receptor
antagonists, also have important roles in modern immunosuppression
protocols. The Achilles heel of the long-term success of heart
transplantation is the development of coronary graft atherosclerosis,
the cardiac version of chronic rejection. Coronary graft atherosclerosis
is uniquely different from typical coronary artery disease in that it
is diffuse and usually not amenable to revascularization. Furthermore,
although heart transplantation is a feasible solution for patients with
end-stage heart disease, its use is limited by an inadequate donor
supply. In the United States, fewer than 2500 heart transplantation procedures are performed annually.[38] Each
year, an estimated 10-20% of patients die while awaiting a heart
transplant. Of the 5 million people with heart failure, approximately
30,000-100,000 have such advanced disease that they would benefit from
transplantation or mechanical circulatory support This
disparity between the number of patients needing transplants and the
availability of heart donors has refocused efforts to find other ways to
support severely failing hearts.

Coronary Artery Bypass Grafting

Studies of medical versus surgical therapy for CAD have historically focused on
patients with normal LV function. However, a significantly increased survival rate in a subset of patients with LVEFs of less than 50% after coronary bypass surgery, in comparison with the survival rate in patients who were randomly selected to receive medical therapy, was
demonstrated in the Veterans Affairs Cooperative Study of Surgery. This survival benefit was particularly evident at the 11-year follow-up point
(50% vs 38%). Surgical revascularization prolonged survival to agreater degree than did medical therapy in most clinical and angiographic subgroups in the Coronary Artery Surgery Study (CASS) of
patients with left main equivalent disease.[40] Of
importance, this study demonstrated that surgical therapy markedly improved the 5-year cumulative survival rate in patients with an EF of
less than 50% (80% vs 47%). These
early randomized trials were limited by their inclusion of patients whohad what is currently considered a good EF. That is, many patients referred for coronary revascularization live with EFs of less than 35%. Investigators from Yale and the University of Virginia, among many others, have
published their results of CABG in patients with extremely poor LV function who were on the transplant waiting list. In patients with EFs of less than 30% who had CABG, the survival rate was 80% at 4.5years, according to a study by Elefteriades et al. This figure approaches that of cardiac transplantation. Kron et al reported a similar 3-year survival rate of 83% in patients who underwent coronary bypass with an EF of less than 20%.[43] Surgical
revascularization can reduce mortality rates, improve NYHA classification, favorably alter LV geometry, and increase LVEFs in patients with ischemic heart failure and substantial areas of viable myocardium, according to a number of studies. For instance, surgical
revascularization confers a dramatic survival benefit in patients with a substantial amount of hibernating myocardium (this term is used to describe regions of the heart that are dysfunctional under ischemic conditions but that can regain normal function after blood flow is restored). Forpatients with at least 5 of 12 segments showing myocardial viability, revascularization has been found to result in a cardiac mortality rate
of 3%, versus 31% for medically treated patients with viable myocardium.
The Surgical Treatment of Congestive Heart Failure (STICH) study
is a prospective, randomized trial intended to determine the role of CABG in patients with heart failure. The
first hypothesis tests whether CABG with intensive medical therapy, as compared with medical therapy alone, confers an additional survival
benefit in patients with an EF of less than 35%. End points of interest are morbidity and mortality rates, quality of life, and economic effects
of the treatment strategies. The STICH study did not demonstrate an improvement in survival in patients with an ejection fraction of 35%
or less and coronary artery disease amenable to CABG. In this study, 1212 patients were randomized to either CABG or medical therapy alone. Although a reduction in cardiovascular mortality and
hospitalization was found, no improvement in overall survival due to
CABG was noted. Surprisingly, the presence of viable, hibernating myocardium was not predictive of improved outcomes from CABG. Taken
together, these findings suggest that in the absence of severe angina or left main disease, medical therapy alone remains a reasonable option
for patients with an ejection fraction of 35% or less and coronary artery disease. Furthermore, current methods of assessing myocardial
viability/hibernating myocardium may not accurately predict benefit from revascularization. MRI has become particularly useful for evaluating both abnormalities in wall motion and viable myocardium, and
MRI results aid in predicting the success of revascularization in patients with low EFs.[18] Many
surgeons have evolved their practices to meet the demands of high-risk
patients and to adopt measures to improve graft patency. The adoption of
techniques on and off cardiopulmonary bypass, as well as beating-heart
techniques for revascularization, highlight the aim of treating
high-risk patients.[49] Regarding this goal, preventive strategies include the increased use of bilateral mammary and arterial grafting.[50] Although
many standards for the treatment of CAD were established via
randomized, controlled medical versus surgical trials in the 1970s, no
large studies have addressed similar issues as they relate to current
medical practice, especially those issues that are important to patients
with ischemic cardiomyopathies. The Surgical Treatment of
Congestive Heart Failure (STICH) study is a prospective, randomized
trial intended to determine the role of CABG in patients with heart
failure.[46] [47] The
first hypothesis tests whether CABG with intensive medical therapy, as
compared with medical therapy alone, confers an additional survival
benefit in patients with an EF of less than 35%. End points of interest
are morbidity and mortality rates, quality of life, and economic effects
of the treatment strategies. The estimated completion date for STICH is
December 2012.


Heart Failure: A Companion to Braunwald's Heart Disease




GET IT HERE




Aortic Valve Replacement

Diseases
of the aortic valve can frequently lead to the onset and progression of
HF. Although the natural histories of aortic stenosis and aortic
regurgitation are well known, patients are often followed up
conservatively after they present with clinically significant heart
failure. HF is a common indication for aortic valve replacement (AVR),
but one must be cautious in patients with low EFs and possible aortic
stenosis. If no inducible gradient is present (a finding that suggests
some ventricular reserve), the outcome with standard AVR is poor. In
this situation, transplantation might be the only option, although the
use of percutaneous valves, an apical aortic conduit, or an LVAD might
offer an intermediate solution. Of the 3 classic symptoms of
aortic stenosis—syncope, angina, and dyspnea—the last is the most robust
risk factor for death. Only 50% of patients with dyspnea in this
setting are still alive within 2 years.[51] Angina is associated with a mortality risk of 50% within 5 years, whereas syncope confers a 50% mortality risk in 3 years. In
the converse, the age-corrected survival rate for patients undergoing
AVR for aortic stenosis is similar to that for the normal population.[52] Once patients develop severe LV dysfunction, the results of AVR are somewhat guarded.[53] Because
of poor LV function, these patients are unable to develop significant
transvalvular gradients (ie, low-output, low-gradient aortic stenosis).
Critical in the preoperative decision process is determining if the
ventricular dysfunction is truly valvular (which improves with
replacement) or if it reflects other forms of cardiomyopathy, such as
ischemia or restrictive processes (which do not improve with
replacement). Precise measurement of the area of the aortic valve
is difficult, because the calculated area is directly proportional to
cardiac output. Also, the Gorlin constant varies at lower outputs.
Therefore, in this situation, valvular areas might be considered
critically small when at surgery the valve is found to be only
moderately diseased. Preoperative evaluation with dobutamine testing to
increase contractile reserve or with vasodilator-induced stress
echocardiography by using the continuity equation rather than the Gorlin
formula can be helpful in making this distinction. The results can
guide the physician or surgeon in determining if the patient is a
candidate for the relatively high-risk procedure.[54] Nevertheless,
because of the possibility of ventricular recovery and lengthened
patient survival, most patients with heart failure and aortic stenosis
are offered valve replacement.[55] Timing
of surgical intervention for aortic insufficiency is more challenging
in patients just described than in patients with aortic stenosis.
However, as before, once symptoms occur and once evidence of LV
structural changes become apparent, morbidity and mortality due to
aortic insufficiency increase.[56] As
with aortic stenosis, early intervention before the onset of severe LV
dysfunction is crucial to improving the survival of patients with aortic
insufficiency, as shown in a retrospective review from the Mayo Clinic.
In this study, 450 patients receiving AVR for aortic insufficiency were
compared according to ranges of EF (< 35%, 35-50%, >50%).
Although the group with severe dysfunction had an operative mortality
rate of 14%, the EF improved, and the group's 10-year survival rate was
41%.[57] [58]

Mitral Valve Repair

Mitral
valve regurgitation can either cause or result from chronic heart
failure. Its presence is an independent risk factor for cardiovascular
morbidity and mortality.[59] In
addition to frank rupture of the papillary muscle in association with
acute MI, chronic ischemic cardiomyopathies result in migration of the
papillary muscle as the ventricle dilates. This dilation causes tenting
of the mitral leaflets, restricting their coaptation. Dilated
cardiomyopathies can have similar issues, as well as annular dilatation.
In addition to mitral regurgitation, the alteration in LV geometry
contributes to volume overload, increases LV wall tension, and leaves
patients susceptible to exacerbations of heart failure.[60] Mitral
valve surgery in patients with heart failure has gained favor because
it abolishes the regurgitant lesion and decreases symptoms. The
pathophysiologic rationales for repair or replacement are to reverse the
cycle of excessive ventricular volume, to allow for ventricular
unloading, and to promote myocardial remodeling. Among other
researchers, a group from Michigan has advocated mitral repair in the
population with heart failure. Bolling and colleagues demonstrated that
mitral valve repair increased the EF, improved heart failure classes
from 3.9 to 2.0, and decreased the number of hospitalizations.[61] Additional
effects with repair in these patients are the increase in coronary
blood-flow reserve afforded by the reduction in LV volume.[62] Despite
the potential benefits of mitral reconstruction surgery, a
retrospective review showed no decrease in long-term mortality among
patients with severe mitral regurgitation and significant LV dysfunction
who underwent mitral valve repair.[63] Mitral
valve annuloplasty was not predictive of clinical outcomes and did not
improve mortality. Factors that did improve mortality were ACEI
inhibitor use, beta blockade, mean arterial pressures, and serum sodium
concentrations. The results of this analysis were not overly surprising.
For example, in most patients in this situation, heart failure is not
due to flail leaflets but is secondary to ventricular dysfunction. Cardiomyopathy-associated
mitral regurgitation most commonly involves the insertion of either a
complete or a partial band attached to the annulus of the mitral valve.
Thus, mitral repair deals with only 1 aspect of the patient's overall
pathophysiologic condition. That is, annuloplasty rings may assist with
tenting of the leaflet, but they do not address displacement of the
papillary muscle with ventricular scarring.[64] In many patients, the underlying problem (ie, primary myopathy) continues unabated. In
evaluating studies of heart failure with mitral regurgitation, it is
important to separate the etiology (eg, ischemic vs dilated) as well as
the surgical approaches. Future trials must be designed to distinguish
differences among various surgical strategies, such as annuloplasty,
resuspension of the papillary muscle, secondary chordal transection,
ventricular reconstruction, passive restraints, and chordal-sparing
valve replacement. Paramount in these procedures is to have little or no
residual mitral regurgitation.[65] If
repair is deemed improbable, mitral replacement should be performed.
Traditional mitral valve replacement includes complete resection of the
leaflets and the chordal attachments. This destruction of the
subvalvular apparatus results in ventricular dysfunction. In patients
with mitral regurgitation and heart failure, preservation of the chordal
attachments to the ventricle with valve replacement might provide
similar results to, or even better results than, those of annuloplasty.[66] [67] Although
the benefits in terms of quality of life (decreased heart failure)
might not portend increased survival in these high-risk patients,[68] [69] they likely keep low–EF mitral valve interventions in the armamentarium of surgeons who manage heart failure. In
general, ischemic mitral regurgitation is a ventricular problem. Many
operations allow for coaptation and no mitral regurgitation when the
patient leaves the operating room. However, as the left ventricle
continues to dilate, mitral regurgitation often recurs. Therefore, it is
overambitious to say that annuloplasty cures this condition. As a
result, many other approaches have been attempted (eg, chordal cutting,
use of restraint devices, papillary relocation). However, results have
been mixed.

Ventricular Restoration

After
a transmural myocardial infarction occurs, the ventricle pathologically
remodels from its normal elliptical shape to a spherical shape. This
change in geometry is in part responsible for the constellation of
symptoms associated with HF and decreased survival.[70] [71] Several
ventricular restoration techniques exist. All aim to correct the
above-described pathologic alteration in geometry. Most approaches
involve incising and excluding nonviable myocardium with either patch or
primary reconstruction to decrease ventricular volume. Although the
initial enthusiasm for ventricular resection to treat nonischemic
dilated cardiomyopathies (the Batista procedure) has faded, a
long-established finding is that resection of dyskinetic segments
associated with LV aneurysms can increase patients' functional status
and prolong life.[72] [73] The
success of early lytic and percutaneous therapy for acute MI has
decreased the incidence of true LV aneurysms. As such, ventricular
restoration now focuses on excluding relatively subtle regions of
akinetic myocardium. Benefits from ventricular restoration using
the technique Dor described were reported in 2004 by the International
Reconstructive Endoventricular Surgery Returning Torsion Original Radius
Elliptical Shape to the Left Ventricle (RESTORE) group.[74] The
investigators reported that among the patients studied, EFs increased
from 29.6% to 39.5%, the end-systolic volume index decreased, and NYHA
functional classes improved from 67% class III/IV before surgery to 85%
class I/II after surgery. Similarly, a significantly improved
5-year survival rate in patients with ischemic cardiomyopathy who
underwent ventricular restoration and CABG, versus patients who
underwent CABG, was demonstrated by Yamaguchi et al.[71] Survival rates were 90% versus 53.5%, respectively. The
current level of enthusiasm for performing ventricular remodeling
surgery in patients with heart failure is high. Apart from the RESTORE
trial, most studies have been single-institution, retrospective
analyses. Although many believe that ventricular remodeling is warranted
for dyskinetic and large akinetic segments of the myocardium, some are
beginning to perform this procedure even on hypokinetic regions. The
major study of ventricular reconstruction has been the aforementioned
STICH trial, funded by the National Institutes of Health. A goal of the
study, aside from that previously mentioned, is to shed light on the
importance of revascularization and ventricular geometry in patients
with akinetic, low-EF ventricles. The STICH investigators are
prospectively and randomly selecting patients with this condition to
receive CABG versus CABG and ventricular reconstruction, with a
prolonged follow-up included in the research.[46]

Implantable Cardioverter-Defibrillators

The
role of the ICD has rapidly expanded. Patients with heart failure are
5-10 times more likely to die of sudden death than are members of the
general population. Sudden death from ischemic and nonischemic sustained
ventricular tachyarrhythmias has been remarkably reduced such that
current AHA guidelines recommend an ICD in virtually all patients with
an EF of less than 35%. ICDs are a class I, level of evidence A,
recommendation for secondary prevention of sudden cardiac death in
patients with current or prior heart failure symptoms and LV dysfunction
who survived cardiac arrest, have evidence of ventricular fibrillation,
or have hemodynamically unstable ventricular tachycardia (MADIT I). ICD
therapy is a class I, level of evidence A, recommendation for primary
prevention of sudden death in patients with nonischemic dilated
cardiomyopathy or ischemic heart disease at least 40 days post-MI who
have an LVEF of 35% or less, have NYHA class II or III heart failure,
are on optimal heart failure therapy, and have a life expectancy of more
than 1 year (SCD-Heft, MADIT II). Patients with NYHA class III heart
failure who are managed with ICD therapy have a significant and large
reduction in hospitalization.[75] Of
interest, prophylactic use of an ICD at the time of low-EF CABG failed
to improve survival compared with revascularization alone.[76] This
observation speaks to the importance of the independent influence of
CABG on reducing mortality in ischemic cardiomyopathies. One approach is
to prophylactically place LV epicardial leads on patients with
conduction delays at the time of high-risk heart failure surgery. These
leads are tunneled for future connection to a traditional transvenous
atrial and RV biventricular pacer-defibrillator. The benefit of this
strategy remains to be proven prospectively. In moderately
symptomatic heart failure patients with an LVEF of 35% or less, primary
prevention with an ICD provides no benefit in some cases but substantial
benefit in others, and the ICD benefit can be predicted, according to a
study by Levy et al. Analysis of data from the placebo arm of the
Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) showed that
patients could be classified into 5 groups on the basis of predicted
4-year mortality. In the treatment arm, ICD implantation decreased
relative risk of sudden cardiac death by 88% in patients with the lowest
baseline mortality risk versus 24% in the highest-risk group. ICD
treatment decreased relative risk of total mortality by 54% in the
lowest-risk group but provided no benefit (2%) in the highest-risk
group.[77]

Cardiac Resynchronization Therapy

Patients
with heart failure and interventricular conduction abnormalities
(roughly defined as those with a QRS interval >120-130 ms) are
potential candidates for CRT by means of an inserted biventricular
pacemaker. CRT aims to improve cardiac performance by restoring the
heart's interventricular septal electrical and mechanical synchrony.
Thus, it reduces presystolic mitral regurgitation and optimizes
diastolic function by reducing the mismatch between cardiac
contractility and energy expenditure.[78] Data
support significant improvement in mortality and morbidity when
patients with Class II HF and an LVEF of 30% or less and QRS duration of
more than 150 msec treated with optimal medical therapy receive CRT-ICD
device versus ICD alone (MADIT CRT and RAFT investigators).[79] CRT
is indicated for patients with an LVEF of 35% or less, sinus rhythm,
and NYHA class III and IV symptoms who are on optimal medical therapy
and have evidence of cardiac desynchrony as evidenced by QRS duration
more than 120 msec (class I, level of evidence A) (COMPANION, CARE-HF).[80] CRT,
with or without an ICD, may be reasonable for patients with chronic
atrial fibrillation, an LVEF of 35% or less, an NYHA class III and IV,
and QRS duration more than 120 msec on optimal medical therapy (class
IIa, level of evidence B). CRT with or without an ICD is reasonable for
patients who have frequent RV pacing, LVEF of 35% or less, and NYHA
class III and IV and are on optimal heart failure therapy (class IIa,
level of evidence C; DAVID trial). Regarding technique, 3 cardiac
leads are placed transvenously: an atrial lead, an RV lead, and an LV
lead, which is threaded through the coronary sinus and out one of its
lateral-wall tributaries. Surgeons have assisted difficult transvenous
LV placements by epicardially inserting LV leads using a number of
techniques. Examples include mini-thoracotomy, thoracoscopy, and
robotically assisted methods. Several prospective, randomized
trials have been performed to evaluate the effectiveness of CRT. The
Multicenter InSync Randomized Clinical Evaluation (MIRACLE) study group
demonstrated an improvement in NYHA functional class, quality of life,
and EF.[81] A
reduction in the risk of heart failure events in patients treated with
CRT plus an ICD over that of individuals treated with ICD alone was
demonstrated in patients with mild cardiac symptoms, a reduced EF, and a
wide QRS complex. In this investigation, the Multicenter Automatic
Defibrillator Implantation Trial with Cardiac Resynchronization Therapy
(MADIT-CRT), 1820 patients with an ejection fraction of 30% or less, a
QRS duration of 130 msec or more, and NYHA class I or II symptoms were
randomly assigned to receive CRT plus an ICD or an ICD alone. During
an average follow-up of 2.4 years, death from any cause or a nonfatal
heart-failure event occurred in 17.2% of patients in the CRT-ICD group
versus 25.3% of patients in the ICD-only group. In particular, a 41%
reduction in the risk of heart-failure events occurred in patients in
the CRT group, which was evident primarily in patients with a QRS
duration of 150 msec or more. CRT was associated with a significant
reduction in LV volumes and improvement in the EF. No significant
difference occurred between the 2 groups in the overall risk of death.[82] In
a follow-up to the MADIT-CRT trial, women seemed to achieve a better
response result from resynchronization therapy than men, with a
significant 69% reduction in death or heart failure and 70% reduction in
heart failure alone.[83] In
addition to augmenting functional capacity, CRT also appears to
favorably affect mortality. The Comparison of Medical Therapy, Pacing,
and Defibrillation in Heart Failure (COMPANION) trial demonstrated an
increase in survival only when biventricular pacing (seen on the
electrocardiogram [ECG] below) was used with a defibrillator.[84] However,
the Cardiac Resynchronization-Heart Failure (CARE-HF) trial showed a
36% reduction in death with biventricular pacing alone.[85] In both studies, mortality was largely due to sudden death.


ECG shows biventricular pacing (double ventricular pacing spikes).

Ventricular Assist Devices

In
1963, Dr Michael DeBakey reported the first clinical use of a VAD in a
patient who had cardiac arrest after aortic valve replacement (AVR).
Unfortunately, the patient died. Three years later, Dr DeBakey
successfully implanted a newer device in a patient who could not be
weaned from cardiopulmonary bypass.[86] This
patient received mechanical support for 10 days, which allowed the
myocardium to recover, and was successfully discharged from the
hospital. Since this early era, the development of VADs has progressed
rapidly, and these devices are now invaluable tools in the treatment of
heart failure. A number of devices are available to support the
acutely or chronically decompensated heart. In some cases of extreme
cardiopulmonary failure, the only recourse is complete support with
extracorporeal membrane oxygenation (ECMO). Despite encouraging results
with ECMO for the management of cardiogenic shock, most patients
requiring circulatory assistance can be helped with ventricular support
alone. Depending on the particular device used, the RV and LV can be
assisted with an LVAD, a right VAD (RVAD), or a biventricular assist
device (biVAD). In concept, LVADs, RVADs, and biVADs are all
similar. Blood is removed from the failing ventricle and diverted into a
pump that delivers blood to either the aorta (in the case of an LVAD)
or pulmonary artery (in the case of an RVAD). These devices can often be
placed temporarily to allow the myocardium to recover, as in patients
with acute viral myocarditis or those who have undergone cardiotomy. VADs
are most commonly used to bridge the acutely failing heart to eventual
heart transplantation. This method allows patients to recover from
end-organ damage, to obtain rehabilitation, and possibly to go home
before definitive heart transplantation. Patients with severe HF
who are not transplant candidates and who otherwise would die without
treatment are candidates for lifetime use of VADs. In this situation,
the devices can be placed and are intended for indefinite therapy. For
example, patients with end-stage heart failure who are receiving
inotrope therapy and who are not candidates for transplantation should
be given an LVAD for lifetime use. Destination therapy with LVADs is
superior to medical therapy in terms of quantity and quality of life,
according to the Randomized Evaluation of Mechanical Assistance for the
Treatment of Congestive Heart Failure (REMATCH) trial and several later
studies. How frequently this strategy is used may ultimately depend on
healthcare economics.

Mechanical Circulatory Devices

Nearly
30 different mechanical circulatory devices are in use or are in the
preclinical phase. These devices, which include pneumatic, electric,
pulsatile, and rotary pumps, differ conceptually in their mode of
function. In the United States, several FDA-approved options are
available for bridging the patient to recovery and transplantation.
These options include the following:

  • Abiomed BVS 5000 circulatory support system (Abiomed, Inc, Danvers, Mass), which is typically used for short-term support
  • Abiomed AB5000 circulatory support system (Abiomed, Inc)
  • Centrimag or Levitronix system (Thoratec, Pleasanton, Calif)
  • Thoratec paracorporeal and intracorporeal LVAD and RVAD (Thoratec)
  • Novacor LVAD (World Heart Inc, Oakland, Calif)
  • HeartMate I LVAD (Thoratec)
In
addition, several small, axial-flow devices, including the Heartmate II
(Thoratec) and Jarvik 2000 Flowmaker (Jarvik Heart, Inc, New York, NY),
are actively involved in clinical trials. Although the HeartMate LVAD
(Thoratec) is the only device that is FDA approved for destination
therapy, several other devices are actively being studied in the United
States for use as destination therapy. These include the HeartMate II
LVAD (Thoratec) and the DeBakey-Noon LVAD (MicroMed Cardiovascular, Inc,
Houston, Tex). Each device used as a bridge to transplantation
has its good and bad points. For example, the HeartMate device
(Thoratec) does not require warfarin anticoagulation, unlike the other
well-known pulsatile pump (Novacor; World Heart). However, it is not as
durable as the other pump. The newer axial-flow pumps are relatively
small and easy to insert, and they reduce morbidity. However, the effect
of long-term continuous flow has yet to be determined. Despite
the presumed weaknesses of the therapies just described, the survival
rate through heart transplantation for patients receiving VADs is
roughly 70%. This rate is impressive given this desperately sick cohort
of patients. Furthermore, the evolving technology raises a host of
clinical and physiologic questions that, when studied and answered,
continue to advance the field. Results of the REMATCH study have been widely discussed.[87] The
study offers the only prospective, randomized data from a comparison of
very sick, non–transplant-eligible patients with heart failure
receiving optimal medical therapy with patients receiving an
early-generation HeartMate LVAD. In brief, respective survival rates of
medically treated and LVAD-treated patients were 25% and 52% at 1 year,
and 8% and 23% at 2 years. In addition to their survival advantage, LVAD
patients had improvements in several measures of quality of life. Modifications
in technique and perioperative care have decreased the high rates of
LVAD-related morbidity and mortality observed in the REMATCH trial.[88] Although
REMATCH was a single study in very-high-risk patients, the data serve
as proof of concept for the future development of VAD technologies. Despite
the need for an external energy source, most patients can use
mechanical circulatory devices in the outpatient setting. Many patients
have lived productive lives for longer than 4-6 years with their
original device (depending on the device).

Total Artificial Heart

The
creation of a suitable total artificial heart (TAH) for orthotopic
implantation has been the subject of intense investigation for decades.[89] In
1969, Dr. Denton Cooley implanted the Liotta TAH (no longer made) into a
high-risk patient after failing to wean the patient off cardiopulmonary
bypass after LV aneurysm repair. The patient was sustained until, after
3 days, a donor heart became available, but the patients subsequently
died from pneumonia and multiple organ failure.[90] The
historical development of the TAH is rich with technological genius,
device failure, and personal intrigue. Compared with LVADs, the TAH has
several potential advantages, including the ability to assist patients
with severe biventricular failure, a lack of device pocket and thus a
lessened risk of infection, and the opportunity to treat patients with
systemic diseases (eg, amyloidosis, malignancy) who are not otherwise
candidates for transplantation. At present, 2 TAHs are receiving the most attention:

  • CardioWest TAH (SynCardia Systems, Inc, Tucson, Ariz)
  • AbioCor TAH (Abiomed, Inc)
The
CardioWest TAH is a structural cousin of the original Jarvik-7 TAH
(Jarvik Heart, Inc) that was implanted into patient Barney Clark with
great publicity in 1982. In 2004, investigators reported data that
allowed this device to become the only FDA-approved TAH for use as a
bridge to transplantation. Nearly 80% of patients survived to
transplantation, versus only 46% in a control medical arm. Respective
survival rates at 1 and 5 years with the device were 86% and 64%,
compared with 69% and 34% in the control group. The main limitation of
this TAH is its external power source and large control console.[91] The
AbioCor TAH involves a novel method of transcutaneous transmission of
energy, freeing the patient from external drivelines. The patient
exchanges the external battery packs, which can last as long as 4 hours.
This TAH is unique in that it is the first TAH to use coils to transmit
power across the skin; therefore, no transcutaneous conduits are
needed. This feature allows for the advantages of a closed system, which
potentially reduces sources of infection, a known complication of
earlier devices. The first clinical implantation of this TAH was
performed in July 2001. Before the end of 2004, 14 patients had received
this device as part of a trial of patients whose expected survival was
less than 30 days. Although all subsequently died, 4 patients were
ambulatory after surgery, and 2 were discharged from the hospital to a
transitional-care setting. One of the discharged patients was discharged
on postoperative day 209. A limitation of the AbioCor TAH is its large
size, which permits its implantation in only 50% of men and 20% of
women. The CardioWest and AbioCor TAHs require recipient
cardiectomy before implantation. The devices are similar in that they
are sewn to atrial cuffs and to the great vessels after the native heart
is explanted. The next TAH to emerge clinically will be a
second-generation TAH from Abiomed, Inc. The AbioCor II replacement
heart is designed to be 35% smaller than older models and to function as
a durable pump for longer than 5 years. Despite more than 40
years of effort, the clinical application of artificial-heart technology
is still immature. However, with the approval of the CardioWest device
and with new efforts to create small pumps, TAHs will ultimately be
routine components of heart failure surgery for very sick patients with
heart failure and biventricular failure.

Treatment of Comorbidities

Comorbidities
should be treated aggressively. Sleep apnea has an increased prevalence
in heart failure and is associated with increased mortality due to
further neurohormonal activation, although randomized, controlled data
are lacking. A long-term study involving 283 patients investigated
whether obstructive sleep apnea (OSA) and/or central sleep apnea (CSA)
was associated with an increased risk of malignant cardiac arrhythmias
in patients with congestive heart failure.[92] The
study concluded that OSA and CSA are independently associated with an
increased risk for ventricular arrhythmias and appropriate
cardioverter-defibrillator therapies. Anemia is also common in
chronic heart failure. Whether anemia is a reflection of the severity of
heart failure or contributes to worsening heart failure is not clear.
Potential etiologies of anemia in heart failure involve poor nutrition,
ACEIs, the RAAS, inflammatory cytokines, hemodilution, and renal
dysfunction. Anemia in heart failure is associated with increased
mortality.

Diet

Dietary
sodium restriction to 2-3 g/d is recommended. Fluid restriction to 2
L/d is recommended for patients with evidence of hyponatremia (Na <
130 mEq/dL) or in patients whose fluid status is difficult to control,
despite sodium restriction and the use of high-dose diuretics. Caloric
supplementation is recommended for patients with evidence of cardiac
cachexia.

Consultations

Consultation
with subspecialists depends on the underlying cause of HF. Heart
failure is now an area of subspecialization within cardiology. If
the acute episode is attributed to an acute MI, acute cardiac ischemia,
or acute dysrhythmia, consultation with a cardiologist is warranted. Consultation
with a nephrologist is indicated for emergent/urgent hemodialysis in
patients with renal failure whose episode is attributed to fluid
overload. If heart failure results from acute valvular
dysfunction, consultation with a cardiothoracic surgeon and a
cardiologist for urgent valve replacement may be indicated, depending on
the integrity of the valve involved. In patients who develop
cardiogenic shock, consultation with a cardiologist is generally
indicated in order to provide rapid diagnosis and aggressive treatment
with various modalities (pharmacologic and/or mechanical), to maximize
cardiac performance and improve hemodynamics, and, in some cases, to
place an intra-aortic balloon pump to serve as a temporizing measure
prior to surgery (ie, for valve replacement or coronary
revascularization). Patients with refractory end-stage heart
failure (stage D, NYHA class IV) are often difficult to manage as
outpatients. Therefore, referral to a heart failure program with
expertise in management of refractory heart failure is useful.



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PostSubject: Re: Heart Failure Treatment & Management   Sat Dec 03, 2011 9:25 am

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