detailed discussion about heart failure with reduced ejection fraction and newer aha guidelines for approach and management.

1. DR.AFRIN NEEHA , DNB GENERAL MEDICINE.
HEART FAILURE
DEFINITION, PHENOTYPES & CAUSES,
PATHOPHYSIOLOGY,EVALUATION, MANAGEMENT IN HFrEF.

2. DEFINITION
• HF is de
fi
ned as complex clinical syndrome with symptoms and signs that
result from any functional or structural impairment of ventricular
fi
lling or
ejection of blood.
• Acute HF /ADHF refers to rapid onset or worsening of symptoms of HF.(ACS,
Acute valvular dysfunction, hypertensive urgency post craniotomy syndrome.

3. PHENOTYPES AND CAUSES

4. PHENOTYPES AND CAUSES
• HF with reduced vs preserved ejection fraction: EF<40%, and EF >50%
• HF with recovered EF:initially <40%, with GDMT improvement in EF.
• HF with mildly reduced EF (HFmrEF): EF ranges between 40%-50%
• (Acquired)CAD accounts for 2/3rd cases of HF,(HTN -75%, DM:10-40%
• Congenital causes of HF in adults:three pathophysiological groups:1)uncorrected defects 2)non intervention
3)repaired or palliated defects
• More common disorder: hypertrophic and arrhythmogenic CMP , others :heart muscle disease (genes encoding
laminin , Titin, muscular dystrophies and mitochondrial disease.
• Systemic disease: Amyloidosis and sarcoidosis, autoimmune :SLE and RA, infectious: chagas, HIV, high output
state: anemia, thyrotoxicosis.
• Other predisposing conditions: end stage renal disease, cirrhosis, AV
fi
stula, pages disease , nutritional
de
fi
ciency :beri-beri.

10. PATHOPHYSIOLOGY

11. Cont..
• Neuro hormonal activation: SNS and RAAS: plays a critical role in the development of HF.
• Unchecked compensatory mechanisms: excessive vasoconstriction , baroreceptor
dysfunction , direct myocardial toxicity, volume retention, electrolyte and renal abnormalities.
• Vasodilatory hormones: ANP, BNP , PGE1, prostacyclin(PGI2), adrenomedullin , NO,
bradykinin: systemic and pulmonary vasodilation, increased sodium and water excretion,
inhibition of renin and aldosterone and baroreceptor modulation.
• Neprilysin?
• Endothelia plays a important role in pulmonary HTN and Rt -VHF.
• SGLT2 activity and its deleterious e
ff
ects? Sodium and water retention , endothelial
dysfunction , impaired calcium handling , abnormal myocardial metabolism.

12. Cont..
• Dyssynchrony and electrical instability in HF ?
• Mechanical dyssynchrony describes the di
ff
erences in the timing of contraction or relaxation between the left
ventricular (LV) and right ventricular (RV) (interventricular dyssynchrony), or between di
ff
erent myocardial
segments of the LV (intraventricular dyssynchrony). It is commonly observed in patients with congestive
heart failure (CHF), which is caused by electromechanical delay in some regions of the failing heart and will
result in further reduction of cardiac function.
• The correction of cardiac electromechanical delay is suggested to be one of the major mechanisms for CRT
bene
fi
ts. Therefore, direct measurement of mechanical dyssynchrony by echocardiography has become
clinically relevant in estimating the likelihood of response when ECG as a surrogate marker may fail.
• FMR?
• The basic mechanism of FMR is believed to be the mismatch between increased mitral lea
fl
et tethering due
to the outward displacement of papillary muscles and reduced closing force caused by LV systolic
dysfunction.
• Data from multicenter CRT trials revealed 13-50% reduction in FMR during 6- to 12-month follow up after
the device therapy

13. Cont..
• Normal dictum: low /normal CO with increased SVRC , in high out HF, low
SVR and high CO.
• Most common causes of high output HF : obesity, liver disease, AV shunts,
lung disease, MPD.
• Gut congestion , microbiome, cardiorenal and abdominal interactions?
• Trimethylamine N oxide :poor outcomes in acute and chronic HF.
• Microbe generated uremic toxins such as indoxyl sulphate: important role in
development of HF.

15. EVALUATION

16. Cont..(HISTORY)
• SOB- Lt HF cardinal manifestation
• Left HF: pulmonary venous congestion , Right HF: systemic venous congestion- weight Gail , lower extremity
edema, abdominal symptoms?
• Misdiagnosis of biliary tract disease.
• Anasarca?
• Mechanism? J receptor activation, increased ventilatory drive and reduced blood
fl
ow to respiratory muscles
thereby lactic acidosis and dyspnea.
• Orthopnea?
• PND?
• Central sleep apnea and cheyne stokes respiration : due to sensitivity of respiratory centre to PCO2 and
prolonged circulatory time.
• Low output syndrome?
• Mental dullness, depressed efect, confusion, fatigue and weakness.

17. Physical examination
• General appearance:cardiac cachexia?
• Unintentional weight loss of >5% over 12 months, with bitemporal and upper body
muscle wasting.
• Vital signs: pulses alterans, low grade fever?
• JVP: normal<=8, hepatojugular re
fl
ux? Abdomino jugular test?kussmauls sign?rise in
JVP on inspiration due to severe biventricular failure.
• LUNG EXAMINATION
• CARDIAC EXAMINATION?s3 vs s4 gallop(volume overload -negative prognostic
signi
fi
cance vs HFpEF), loud P2 in PAH, holosystolic murmur in MR and TR.
• ABDOMEN and EXTREMITIES: cardiac cirrhosis, congestive splenomegaly, ascites.

18. DIAGNOSIS
• Routine labs
• CXR
• ECG:Q waves- ischemic disease, Q waves with reduced QRS voltage(pseudo
infarct )-restrictive /in
fi
ltrative CMP.
• AF+CHF= need for anticoagulation
• Non invasive imaging
• Biomarkers
• Invasive studies

21. USE OF BIOMARKER-HF
• BNP- more sensitivity than speci
fi
city , hence to exclude HF , than to rule in .
• Higher levels of BNP /PRO BNP associated with higher risk for adverse short and long-term outcomes
in patients with heart failure.
• As a pre discharge investigation to follow the TRAJECTORY of HF.
• In patients who are at risk for HR, screening with BNP , helps in PREVENTING the development of new
onset of heart failure or LVD.
• In CHF , for RISK STRATIFICATION.
• To PROGNOSTICATE in patients hospitalized for HF.
• In patients who present with dyspnea ,to support a DIAGNOSIS or exclusion of HF.
• Obsesity is associated with lower levels of BNP, reduced diagnostic sensitivity.

23. Non invasive
• CMR, SPECT or radionuclide ventriculography, PET /Cardiac CT provides complimentary and additional information to Cardiac USG.
• TTE provides information regarding cardiac structure and function and identi
fi
es abnormalities of myocardium, heart valves, and
pericardium. Echocardiography reveals structural and functional information that predicts subsequent risk.
• Quanti
fi
cation of cardiac structure and function, including LVEF measurements, ventricular dimensions and volumes, evaluation of
chamber geometry, and regional wall motion ,diastolic function and estimates of LV
fi
lling and left atrial pressure.42
The tricus- pid valve
regurgitant gradient, coupled with inferior vena cava diameter and its response during respi-ration, provides estimates of systolic PA
pressure and central venous pressure. Indices of myocardial deformation, such as global longitudinal strain, may identify subclinical
LV systolic dysfunction, which has been associated with greater risk of developing HF or recurrent HF hospitalizations.
• Reevaluation of EF (>40 days after MI, >90 days after revascularization, >90 days after GDMT) is useful to determine candidacy for
implantable cardioverter-de
fi
brillator (ICD) or cardiac resynchronization therapy (CRT). Finally, repeat surveillance of LV function is
appropriate in patients exposed to treatments that potentially damage the myocardium, such as chemotherapy ,
• CMR: provides noninvasive characterization of the myocardium that may provide insights into HF cause.62
Late-gadolinium
enhancement, re
fl
ect- ing
fi
brosis and damaged myocardium, can iden- tify acute and chronic MI.63,64
and identify HF caused by CAD65,66
Patterns of late-gadolinium enhancement or speci
fi
c T-1 and T-2 techniques can suggest speci
fi
c in
fi
ltrative and in
fl
ammatory
cardiomyopathies, such as myocarditis, sarcoid- osis, Fabry disease, Chagas disease, noncom- paction, iron overload, and
amyloidosis.1
•

24. Cont..
1.HF is often caused by coronary atherosclerosis, and evaluation for ischemic
heart disease can help in determining the presence of signi
fi
cant coronary
artery disease (CAD).

26. TREATMENT

27. Cont..
• Class 2-4 NYHA: acei , arbs , b blockers + MRA
• Soluble guanylcyclase stimulators
• Myosin activators:omecamtiv mecarbil
• Digoxin:mild inotropic, attenuate carotid baroreceptor activity and sympatho inhibitory.
• Oral diuretics
• 2nd gen CCB
• Statins
• Anti in
fl
ammatory therapy
• Anti coagulation and anti platelet.
• Drugs that modify the ventricular remodeling:
• Arb
• Acei
• MRA
• B blockers

37. THANK YOU