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Toronto Notes 2019 Heart Failure 7. Anticoagulants: warfarin for prevention of thromboembolic events
■ prior thromboembolic event or AFib, presence of LV thrombus on echo
8. Ivabradine: selective inhibition of the If current
■ recommended for CV death and hospitalization prevention in patients with HFrEF and symptomatic despite treatment with appropriate doses of GDMT, with a resting HR >70 bpm, in sinus rhythm and a prior HF hospitalization within 12 mo
Cardiology and Cardiac Surgery C37
Chronic Treatment of CHF
• ACEI*
• β-blockers*
• ± Mineralocorticoid receptor antagonists* • Diuretic
• ±Inotrope
• ±Antiarrythmic
• ±Anticoagulant
*Mortality benefit
Ivabradine and Outcomes in Chronic Heart Failure (SHIFT): A Randomized Placebo-Controlled Study Lancet 2010;376:11-17
Study: randomised, double-blind, placebo-controlled, parallel-group trial.
Population: patients with symptomatic heart failure and LVEF of 35% or lower, in sinus rhythm with HR greater than or equal to 70bpm, had been admitted to hospital for heart failure within previous year, on stable background treatment included beta blocker if tolerated. Intervention: ivabradine titrated to a maximum of 7.5 mg twice daily vs. placebo.
Outcome: primary endpoint was composite of cardiovascular death or hospital admission for worsening heart failure.
Results: 793 (24%) patients in the ivabradine group and 937 (29%) of those taking placebo had a primary endpoint event (HR 0.82, 95% CI 0.75–0.90, p<0.0001). Fewer serious adverse events occurred in the ivabradine group (3388 events) than in the placebo group (3847; p=0.025). 150 (5%) of ivabradine patients had symptomatic bradycardia vs. 32 (1%) of the placebo group (p<0.0001). Median follow-up was 22.9 (IQR 18–28) months. Conclusions: Results support the importance of heart-rate reduction with ivabradine for improvement of clinical outcomes in heart failure and confirm the important role of heart rate in the pathophysiology of this disorder. Note: Limitation of this study was that only 26% of patients were on target β-blocker doses. Ivabradine currently recommended in these patients when HR is not controlled on maximum tolerated β-blocker dose or there is a contraindication to β-blocker use.
Higher New York Heart Association Classes and Increased Mortality and Hospitalization in Patients with Heart Failure and Preserved Left Ventricular Function
Am Heart J 2006;151:444-450
Purpose: To establish the association between NYHA class and outcomes with heart failure and preserved systolic function.
Methods: Retrospective follow-up study (median 38.5 mo) of 988 patients with heart failure with ejection fracture >45%. Estimated risks of various outcomes using Cox proportional hazard models. Results: Adjusted hazard ratio for all-cause mortality for NYHA class II, III, IV patients was 1.54, 2.56, and 8.46, respectively. Adjusted hazard ratio for all-cause hospitalization for NYHA class II, III, IV patients was 1.23, 1.71, and 3.4, respectively. Conclusions: Higher NYHA classes were associated with poorer outcomes in patients with heart failure and preserved systolic function. Proportions of NYHA I, II, III, and IV patients who died of all causes during the study were 14.3%.
Cell membrane current
Ivabradine administration
0mV
AB
If -channel at Sinoatrial Node
+++ ++++ +++++
++++
++
+
+ +
+
B
A
Ivabradine
Figure 40. Ivabradine mechanism of action
Procedural Interventions
• resynchronizationtherapy:symptomaticimprovementwithbiventricularpacemaker
• considerifQRS>130msec,LVEF<35%,andpersistentsymptomsdespiteoptimaltherapy • greatest benefit likely with marked LV enlargement, mitral regurgitation, QRS >150 msec • ICD: mortality benefit in 1° prevention of sudden cardiac death
■ prior MI, optimal medical therapy, LVEF <30%, clinically stable
■ prior MI, non-sustained VT, LVEF 30-40%, EPS inducible VT
• LVAD/RVAD(seeVentricularAssistDevices,C38)
• cardiactransplantation(seeCardiacTransplantation,C38)
• valverepairifpatientissurgicalcandidateandhassignificantvalvediseasecontributingtoCHF(see
Valvular Heart Disease, C42)
RATIONALE FOR HEART FAILURE TREATMENT:
Reduce afterload + augment contractility=improve cardiac output + relieve pulmonary congestion
NORMAL
HEART FAILURE
Failing heart
Pulmonary congestion
LEFT VENTRICULAR END-DIASTOLIC PRESSURE (preload)
Figure 41. Effect of heart failure treatment on the Frank-Starling curve
Sleep-Disordered Breathing
B A
I D
Slowed rate of diastolic depolarization = reduced heart rate
A = diuretic or venodilator (nitrates)
A’ = aggressive diuresis or venodilation
I = inotopes (contractility) D = ACEI (vasodilation)
B = inotrope +ACEI
A’
HEART FAILURE + TREATMENT
© Young M. Kim 2012
• 45-55%ofpatientswithCHFhavesleepdisturbances,includingCheyne-Stokesbreathingandsleep apnea (central or obstructive)
• associatedwithaworseprognosisandgreaterLVdysfunction
• nasalcontinuouspositiveairwaypressure(CPAP)iseffectiveintreatingsymptomsofsleepapneawith
secondary beneficial effects in cardiac function and symptoms
NYHA Proportion of All-Cause
Hospitalization
I 60.7% II 65.2% III 77.7% IV 75.0%
Proportion of All- Cause Mortality
14.3% 21.3% 35.9% 58.3%
Hypotension
STROKE VOLUME (cardiac output)
©ShirleyLong 2019