Heart Failure Master [Compatibility Mode]
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Transcript of Heart Failure Master [Compatibility Mode]
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M AM AKK
2014
Learning goals
Definition
Epidemiology
Determinants of cardiac performance
Types of HF
Etiology of HF
Pathophysiology
Prognosis
Diagnosis
Management
Heart failure is a clinicalsyndrome characterized byinadequate systemicperfusion to meet the body'smetabolic demands as aresult of impaired cardiacpump function.
DefinitionDefinition
The overall prevalence of heart failure was est imated as 1.0% to 1.6%, rising
from 0.1% in the 30-39 age range to 4.2% at 70- 79.
Hospital admissionsPatients with HF account for about 1,000,000 hospital admissions annually.
Hospital Re-admissionsOne-third of these patients are re-admitted within 90 days for recurrentdecompensation.
Mortality Although much progress has been made in the treatment of HF, there is a20% overall annual mortality, particularly in patients with NYHA IV symptoms.
Approximately 50% of patients with severeheart failure due to LV dysfunction
will die within 2 years. Many patients die suddenly from malignant ventricular arrhythmias or MI.
Epidemiology
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Determinants of cardiac performance
1. Pre loadIs the stress on the myocardial wall in an intact ventricle at the endof diastole - just prior to ventricular contraction - this is related tothe end diastolic pressure and volume - which ultimatelyaffect themuscle fiber length.
22.. Afterload Is the tension or "wall stress" acting after the onset of
shortening/contraction - and is primari ly mediated by arter ialpressure. As arterial pressure/resistance rises, stroke volume falls- which can cause acute exacerbations of CHF in patients withfailing hearts, especially those with diastolic dysfunction .
33.. ContractilityContractilityIs also referred to as the inotropic state. When preload and afterload are
constant, increasing contractility (with drugs for example) can augment
the cardiac output .
4. Others Strokevolume(SV) - the amount of blood ejectedwith each systole Cardiac output (CO) - which is [SV]x [Heart Rate] (beats per min) =
CO(normal is~5-6 L/M)
End diastolic volume (EDV).
Ejection fraction (i.e., the portion of blood ejected with each systole)which is the [SVdivided by EDV] x 100 (normal is 55-65%.
Determinants of cardiac performance
1. Systolic Dysfunction (SHF) vs. Diastolic Dysfunction (DHF):
Systolic failureis a disorder of impaired myocardial contractility - leading to areduced ejection fraction and a reduced stroke volume. This is associated withan elevated end diastolic left ventricular volume and pressure.
Diastolic failure is a disorder of impaired myocardial relaxation leading toreduced filling in diastole and an elevated diastolic pressure. The ejectionfraction may be normal or reduced.
Types of HF Syndrome 2. Forward HF vs. Backward HF:Backward failure is characterised by increased systemic venous pressure in the right
heart side and increased pulmonary venous pressure in the left heart side. For example,
development of fluid retention raises the workload and thereby worsens backward
failure.
Types of HF Syndrome
Forward failure shows a reduced blood flow volume (ejection) into the aorta ( left heartside) and pulmonary artery (right heart side). Forward heart failure worsens by increasedvasoconstriction which further reduces the ejection. In contrast, vasodilators improve it.
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3. Left sided HF vs. Right sided HF:
Left sided HF
There is a reduction in the left ventricular output and/or an increase in the leftatrial or pulmonary venous pressure.
Right sided HF
There is a reduction in RV output. Causes of isolated r ight heart fai lureinclude chronic lung disease (cor pulmonale), multiple pulmonary emboli and
pulmonary valvular stenosis.
Bivent.HF
Failure of the left and right heart may develop because the disease process
(e.g. dilated cardiomyopathy or ischaemic heart disease) affects both ventricles,
or because disease of the left heart leads to chronic elevation of the left atrial
pressure, pulmonary hypertension and right heart failure.
5. Acute Vs chronic HF:
Acute HF means acute onset or decompansation of CHF characterized by signs ofpulmonary and /or per ipheral congestion, including pulmonary edema and/orperipheral edema with /or without sign of peripheral hyoperfusion.
4. High-output failure
A rare cause of heart failure caused by thyrotoxicosis, arteriovenous fistulae,
Paget's disease, pregnancy, or severe chronic anemia. In such cases,
additional causes of heart failure are often present.
Coronary artery diseaseMyocardial infarctionIschaemia
Hypertension
CardiomyopathyDilated (congestive)Hypertrophic/obstructiveRestrictivefor example, amyloidosis, sarcoidosis,haemochromatosisObliterative
Valvular and congenital heart diseaseMitral valve diseaseAortic valve disease
Atrial septal defect,ventricular septal defect
Arrhythmias
TachycardiaBradycardia (complete heart block, the sick sinussyndrome)Loss of atrial transportfor example, atrial fibrillation
Alcohol and drugs
AlcoholCardiac depressant drugs ( blockers, calciumantagonists)
High output failure
Anaemia, thyrotoxicosis, arteriovenous fistulae,Pagets diseasePericardial diseaseConstrictive pericarditisPericardial effusion
Primary right heart failure
Pulmonary hypertensionfor example, pulmonaryembolism, cor pulmonale, Tricuspid incompetence
Etiology of HF ACC/AHA GH F C
NYHA I NYHA II NYHA III NYHA IV
Slight limitation in physicalactivity. More strenuousactivity causes shortness of
breathexample, walkingon steep inclines and severalflights of steps. Patients inthis group can continue tohave analmost normal lifestyleand employment
No limitation in physical activitydespite presence of heartdisease.
This can be suspected only ifthere is a history of heart disease
which is confirmed byinvestigationsexample,echocardiography
More marked limitation ofactivity which interferes with
work.Walking on the flatproduces symptoms
Unable to carry out anyphysical activity without
symptoms. Patientsare breathless at rest .
ASYPTOMATIC MILD MODERATE SEVERE
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ACC/AHA GH F C
Stage AStage AAt high risk forAt high risk forHF but withoutHF but without
structural heart diseasestructural heart diseaseor symptoms of HFor symptoms of HF
Stage BStage BStructural heartStructural heart
disease but withoutdisease but withoutsymptoms of HFsymptoms of HF
Stage CStage CStructural heart diseaseStructural heart disease
with prior or currentwith prior or currentsymptoms of HFsymptoms of HF
Stage DStage DRefractory HFRefractory HF
requiring specializedrequiring specializedinterventionsinterventions
e.g., Patients with: Hypertension
Diabetes melliusor
Patients
Using cardiotoxins
With FHx CM
StructuralStructuralHeartHeartDiseaseDisease
e.g., Patients with: Previous MI
LV systolicdysfunction
Asymptomaticvalvular disease
SymptomsSymptomsof HFof HFdevelopdevelop
e.g., Patients with: Known structural
heart disease Shortness of
breath and fatigue,reduced exercisetolerance
RefractoryRefractorysymptomssymptomsof HF atof HF atrestrest
e.g., Patients whohave symptoms at restdespite maximalmedical therapy (e.g.,those who arerecurrentlyhospitalizedor cannot be safelydischarged fromhospital withoutspecializedinterventions)
In le ft ventr icular sys to lic dys func tion,regardless of the etiology, cardiac output islow and pulmonary pressures are high,
leading to pulmonary congestion.
I nit ia lly, as a d irect result of decreas ecardiac output and systemic perfusion, thebody activates several neurohormonalpathways in order to increase circulatingblood volume. This response is adaptive
and designed to preserve normal blood flowto systemic organs.
over t ime, these responses can becomemaladaptive or counterproductive, leadingto progression of the disease andworsening of symptoms.
Pathophysiology of HF
Pathophysiology of HF
ReninRenin--angiotensin systemangiotensin system
VasopressinVasopressin
AldosteroneAldosterone
sympatheticsympatheticnervous systemnervous system
AdaptiveAdaptivemechanismmechanism
EndothelinEndothelin
CytokinesCytokines
MaladaptiveMaladaptivemechanismmechanism
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Pathophysiology of HF
The sympathetic nervous system
Increases heart rate and contractility, both of which increase cardiac output.Circulating catecholamines also cause arteriolar vasoconstriction in nonessential vascular beds and stimulate secretion of renin. Unfortunately,catecholamines aggravate ischemia, potentiate arrhythmias, promote cardiacremodeling, and are directly toxic to myocytes.
ReninRenin--angiotensinangiotensin systemsystem:StimulationStimulation ofof thethe reninrenin--angiotensinangiotensin systems ystem asas aa resu ltresult o fof increasedincreasedsympatheticsympathetic stimulationstimulation andand decreaseddecreased renalrenal perfusionperfusion resultsresul ts inin fur therfurtherarteriolararteriolar vasoconstriction,vasoconstriction, sodiumsodium andand waterwater retention,retention, andand releaserelease ofof
aldosteronealdosterone..
AldosteroneAldosterone::IncreasedIncreased aldosteronealdosterone,, inin turn,turn, leadsleads toto sodiumsodium andand waterwater retention,retention, endothelialendothelialdysfunctiondysfunction andand organorgan fibrosisfibrosis..
Pathophysiology of HF
VasopressinVasopressin: In heart failure,In heart failure, baroreceptorbaroreceptor and osmotic stimuli lead toand osmotic stimuli lead to
vasopressin release from the hypothalamus causingvasopressin release from the hypothalamus causing reabsorptionreabsorption of waterof waterin the renal collecting duct.in the renal collecting duct.
EndothelinEndothelin:: endolthellinendolthellin levels are elevated in heart failure and correlatelevels are elevated in heart failure and correlatewith severity of disease and prognosis.with severity of disease and prognosis. EndothelinEndothelin is an endogenousis an endogenous
vasoconstrictor and growth factor.vasoconstrictor and growth factor.
Cytokines:Cytokines: Levels of the proLevels of the pro--inflammatory cytokines also are elevated ininflammatory cytokines also are elevated inheart failure, and contribute to cardiacheart failure, and contribute to cardiac cachexiacachexia and apoptosis.and apoptosis.
Pathophysiology of HF
Although these neurohormonal pathways initially are compensatory andbeneficial, eventually, they are deleterious, and neurohormonal modulation isthe basis for modern treatment for heart failure.
Enhanced neurohormonal stimulation of the myocardium also causes apoptosisor programmed cell death, worsening of ventricular contractility and death.
With continuous neurohormonal stimulation, the left ventr ic le undergoesremodeling consisting of left ventricular dilatation and hypertrophy.
Left ventricular chamber dilatation causes increased wall tension, worsens
subendocardial myocardial perfusion, and may provoke ischemia in patientswith coronary atherosclerosis.
Furthermore, left ventricular chamber dilatation may cause separation of the
mitral leaflets and mitral regurgitation leading to pulmonary congestion.
Pathophysiology of HF
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Pathophysiology of HF Pathophysiology of HF
In contrast, natriuretic peptides are hormonesreleased by secretory granules incardiac myocytes. They have a beneficial influence in heart failure, includingsystemic and pulmonary vasodilation, enhanced sodium and water excretion,and suppression of other neurohormones.
Pathophysiology of HF
500 pg/mL, then HF is highly likely (PPV = 90%)
100500 pg/mL, consider the baseline BNP is elevated due to stableunderlying dysfunction, right ventricular failure from cor pulmonale, acutepulmonary embolism, or renal failure
In diastolic dysfunction, the primary abnormality is impaired left ventricularrelaxation causing high diastolic pressures and poor filling of the ventricles. Inorder to increase diastolic fil ling, left atrial pressure increases until it exceedsthe hydros tatic and oncot ic pressures in the pulmonary capil laries and
pulmonary edema ensues. As a resul t, patients are often symptomatic withexert ion when increased heart rate reduces left ventr icular f il ling time andcirculating catecholamines worsen diastolic dysfunction.
Pathophysiology of diastolic HF
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1. Arrhythmias, especially atrial fibrillation2. Infections(especially pneumonia)3. Acute myocardial infarction4. Angina pectoris or recurrent myocardial ischaemia5. Anaemia6. Alcohol excess
7. Iatrogenic causefor example, postoperative fluid replacement oradministration of steroids or non steroidal anti inflammatory drugs
8. Poor drug compliance, especially in antihypertensive treatment9. Thyroid disordersfor example, thyrotoxicosis10. Pulmonary embolism11. Pregnancy
12. Administration of a drug with negative inotropic properties (e.g. -blocker) or f luid-retaining propert ies (e.g. non-steroidal anti-inflammatory drugs, corticosteroids)
13. Intravenous fluid overload, e.g. post-operative i.v. infusion
Precipitating causes of heart failure
11. ArrhythmiasAtrial fibrillation; ventricular arrhythmias (ventricular
tachycardia, VF); bradyarrhythmias
2. ThromboembolismStroke; peripheral embolism; deep venous
thrombosis; pulmonary embolism
3. GastrointestinalHepatic congestion and hepatic dysfunction; malabsorption
4. MusculoskeletalMuscle wasting
5. RespiratoryPulmonary congestion; respiratory muscle weakness;pulmonary hypertension (rare)
6. Renal failure due to : Low cardiac output- Diuretics (as side effect)7. Hypokalemia due to : High aldestrone levels- Potasium losing diuretics8. Hyperkalemia due to: Drugs such as Sprinolactone +ACEI- R. dysfunction9. Sudden death in 50% of Pt.s because of V.F
Complications of heart failure
Morbidi ty and mortal ity for all grades ofsymptomatic chronic heart failure are high,with a 20-30% one year mortality in mild tomoderate heart failure and a greater than50% one year mortal ity in sever e hear tfailure.
Prognosis of HF
D
C A
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I
Initial investigations
x Chest radiographyx Electrocardiographyx Echocardiography, including Doppler studiesx Haematology testsx Serum biochemistry, including renal function and glucose concentrations,
liver function tests, and thyroid function testsx Cardiac enzymes (if recent infarction is suspected), BNP.
Other investigations
X Radionuclide imagingx Cardiopulmonary exercise testingx Cardiac catheterisationx Myocardial biopsyfor example, in suspected myocarditis
Investigations if heart failure is suspected
M H.F.
:
M S T P () . S
B ( )
P
R
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M: P
T :
P
N
P
A HF
H
C
M, ,
M: P
T :
P
N
Treatment objectives
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I , 19 RCT
4 .
D .
F .
2 .
C ,
.
, .
?
S (NHA III)
T
O
P (HFPEF)
HFREF: D 2012
EuropeanHeart Journal (2012) 33, 17871847
doi:10.1093/eurheartj/ehs104
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:
( )
20% .
29%
(
)
40% 6 .
31% 1
27%
SOLVD Investigators. N Engl J Med 1992;327:685-91SOLVD Investigators. N Engl J Med 1991;325:293-302CONSENSUS Study Trial Group. N Engl J Med 1987;316:1429-35
(Chronic Heart Failure)
SOLVD Treatment
16% mortality
1. Angiotensin Converting EnzymeInhibitors (ACE-inhibitors)
Block the renin-aldosterone-angiotensin system by inhibiting the conversionof angiotensin I to angiotensin II vasodilation and Na+ retention
bradykinin degradation its levelPG secretion & NO
Decrease cardiac preload & afterload
Major anti-remodeling effectson myocardium and vessels
Mainstay in HF: they improve cardiac function, symptoms, and survival
Angiotensin Converting EnzymeInhibitors (ACE-inhibitors) M
C ( )
H ?? , , , ?
T
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P ACEI
L
A NSAID
F /
A
C N/H
Study Drug
HFSeverity
TargetDose (mg) Outcome
US Carvedilol1 carvedilol mild/moderate
6.25-25 BID
48% disease progression(p= .007)
CIBIS-II2 bisoprolol moderate/severe
10 QD 34% mortality (p
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I B
: A , O O ACEI ( )
S I ( 24 )
: NHA I I ( )
: M D I , N
M
H F
( )
S H BB.
E B
F; ;
G D
Use of best beta-blocker invarious settings
Aldosterone antagonists
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What about patients with mild HF?
EPHESUS
MRAs?
Severity of heart failurePost MI
P
HF 37%
Reductions were also seen in rates o f death from any cause (24%),
cardiovascular death (24%), hospitalization for any reason (23%),and HF hospitalization (42%).
Reductions were also seen in rates o f death from any cause (24%),
cardiovascular death (24%), hospitalization for any reason (23%),and HF hospitalization (42%).
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Aldosterone antagonists
Block aldosterone receptors
Can be used in advanced HF, to further inhibit the R-A-A system after
complete uptitration of ACE-inhibitors
Check often for risk of hyperkalemia
Available agents: spironolactone, eplerenone
C A I
S/E HF!!
O (25/)
:
S (> 5%)
N
10% ( 6.0 C I
E 25/
S
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Angiotensin II antagonists
1.1. Are ARBs more effective than ACEAre ARBs more effective than ACE--inhibitors?inhibitors?
2.2. Are ARBs as effective as ACE inhibitors?Are ARBs as effective as ACE inhibitors?
3.3. Is the combination of an ARB & an ACEIs the combination of an ARB & an ACE--inhibitors more effective than ACEinhibitors more effective than ACE--
inhibitor monotherapy?inhibitor monotherapy?
4.4. Are ARBs effective in patients who cannot tolerate ACEAre ARBs effective in patients who cannot tolerate ACE--inhibitors?inhibitors?
5.5. Are ARBs effective in patients with heart failure and preserved leftAre ARBs effective in patients with heart failure and preserved leftventricular function?ventricular function?
NO
PRO
YESYES
NOT SURE??
O EF
Diuretics
The most effective symptomatic reliefThe most effective symptomatic relief
Usually shortUsually short--term IV therapy followed by longterm IV therapy followed by long--term PO therapyterm PO therapy
ThiazidesThiazides::
HCTZ, chlorthalidone
Loop diuretics:Loop diuretics:
Furosemide, torasemide,, bumetanidebumetanide,, etacrynicetacrynic acidacid
Mixed agents:Mixed agents:
Metolazone, nesiritide
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D ( )
E & , .
I & .
G .
T &
F
S /
Diuretics
C D
H
H & M
H &
D I >
G
L
Aspirin/oral anticoagulants
Aspirin is recommended in all pat ients w ith coronary heart d isease,diabetes or any other established form of atherosclerotic disease, unlesscontraindicated by bleeding diathesis.
Oral anticoagulants are recommended in patients withparoxysmal/permanent atrial fibrillation, or those with previous embolicevents (eg in poor LVcontractilty) and hugely dilated LV.
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Antiarrhythmics
Most common cause of sudden cardiac death in HF is ventriculartachyarrhythmia
Antiarrhythmic drugs may suppress PVC but may induce VT or VF!!!
Only amiodarone has a reasonably safe profile in HF, but no impact ofamiodarone on prognosis.
Remember the many toxic effects of amiodarone:
lung, thyroid, eye, liver
Digitalis glycosides (digoxin, digitoxin)
Their role has declined in recent years (DIG Study)
Digitals does not affect mortality in CHF patients but causes significant:
Reduction in hospitalization
Reduction in symptoms of HF
Actions:
Positive inotropic effect
Arrhythmogenic effect
Vagotonic effect
Digoxin in high risk HF patients subgroup:HF hospitalization or HF mortality
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Digitalis glycosides (digoxin, digitoxin)
Digoxin levels should be 1.0 2.0 ng/dL, but narrow & variable therapeutic
window (check serum!)
Toxicity - non cardiac manifestations:
Anorexia, nausea, vomiting, headache, xanthopsia sotoma, disorientation
Toxicity - cardiac manifestations:
Sinus bradycardia and arrest, A/V block (usually 2nd degree), atrialtachycardia with A/V block, development of junctional rhythm in patients with
AF, PVC, VT/ VF (bi-directional VT)
S D
D .
M (NHA II/III)
C NHA III
L
D , ,
0.125/
(Vaso) Dilators: nitrates & hydralazine
Reduction of afterload by arteriolar vasodilatation (hydralazin) LVEDP, O2consumption, myocardial perfusion, stroke volume and CO
Reduction of preload by venous dilation
(nitrates) venous return load on both ventricles
Usually maximum benefit achieved by using both agents, but currentlyapproved (in US).
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N/H
C ACEI
R
C
S
D ISDN 4060 TID
H 25100 TID QID
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2
S
I?
Should be considered to reduce the risk of HFhospitalization in patients in sinus rhythm with an EF 35%,a HR remaining 70 b.p.m., and persisting symptoms(NYHA class IIIV) despite treatment with an evidence-based dose of beta-blocker (or maximum tolerated dosebelow that), ACE inhibitor (or ARB), and an MRA (or ARB)
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Inotropes
Improve myocardial contractility (adrenergic agonists, dopaminergic
agents, phosphodiesterase inhibitors, calcium-channel sensitizers):dopamine, dobutamine, milrinone, amrinone, levosimendan
Most studies showed long-term mortality with inotropic agents.
Yet beneficial at short-term use for peripheral hypoperfusion +/- pulmonary
edema refractory to diuretics and vasodilators
Only use them in acute conditions such as cardiogenic shock, as bridge toanother lasting intervention (eg transplant).
Invasive Non-surgical treatment in HF
ImplantableImplantable cardiovertercardioverter debribillatorsdebribillators (ICD)(ICD)
Cardiac resynchronization therapy (CRT)Cardiac resynchronization therapy (CRT)
I (ICD)
P EF35% CHF ICD ()
P T SCD ICD ( )
P T EF 3040% ICD ( )
Angina, reversible ischaemia,Coronaryrevascularisation
(PTCA, CABG)
Significant valve disease (AS, MR)Valve replacement (or repair)
End stage heart failureCardiac transplantation
Short term ventricular supportegawaiting for transplantation
Ventricular assist devices
Stem cells- cardiac reconstructionNovel surgical techniques
Type of surgery Reason
Surgical management of HF
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C
I
S
1 80% 90%
5 70%
10 50%
L .
Non-pharmacological measures
Compliance: give careful advice about disease, treatment, and self helpstrategies
Diet: ensure adequate general nutrition and, in obese patients, weightreduction
Salt: advise patients to avoid high salt content foods and not to add salt
(particularly in severe cases of CHF)
Fluid: Advice overloaded patients and those with severe CHF to res tricttheir fluid intake
Alcohol: advise moderate alcohol consumption.
Smoking: avoid smoking.
Exercise: regular exercise should be encouraged
Vaccination: patients should consider influenza and pneumococcal
vaccinations
TAILORED T
: 1. S, , (); 2.
M
(O, 2 2005)
M
I II III IV
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Control Volume Improve Clinical Outcomes
Diuretics
Digoxin
-BlockerACEIor ARB
AldosteroneAntagonist
or ARB
Treat Residual Symptoms
CRT an ICD*
HDZN/ISDN*
*In selected patients
N , ,
HFPEF.
D
HFREF.
A
,
AF.
T HFREF
HFPEF, CCB.
()
()
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2
Spironolactone (25mg/d) improved diastolic function.
Did not improve exercise capacity, NYHA class, or quality of life
No significant differences in death or hospitalization rates.
Was safe and not associated with severe adverse events
Can be considered in patients with diastolic heart failure for
improving cardiac function and blood pressure control
Spironolactone (25mg/d) improved diastolic function.
Did not improve exercise capacity, NYHA class, or quality of life
No significant differences in death or hospitalization rates.
Was safe and not associated with severe adverse events
Can be considered in patients with diastolic heart failure for
improving cardiac function and blood pressure control
TOPCAT is a multi-center, international, randomized, double blindplacebo-controlled trial of the aldosterone antagonist,
spironolactone, in 3,445 adult subjects with heart failure and leftventricular ejection fraction of at least 45%, recruitedinternationally from over 200 clinical centers in the US, Canada,
Russia,Republic of Georgia, Argentina, and Brazil.
Enrollment started in August 2006 and recently ended on January31, 2012.
Potassium Spiro Placebo P (chi-sq)
Hyperkalemia(5.5 mmol/L)
322(18.7%)
157(9.1%)
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Spironolactone(N = 1722)
Placebo(N = 1723)
HR (95% CI)
Primary Outcome320 (18.6%)5.9/100pt-yr
351 (20.4%)6.6/100pt-yr
0.89 (0.77-1.04)P=0.138
Hospitalization for HeartFailure
206 (12.0%)3.8/100pt-yr
245 (14.2%)4.6/100pt-yr
0.83 ( 0.69-0.99)P=0.042
Multiple HF HospP
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T
T .
P .
I .
P HF .
R
.
E ?