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Progressive Heart Failure –Etiopathogenesis, Invasive and 59
Noninvasive Evaluation

a lot of therapeutic and prognostic implications. nephrine and angiotensin II play pivotal roles in pro-
moting progressive heart failure Tailored heart fail-
• HF with reduced EF [HFrEF] : HF patients with uretherapy requires the identification and treatment
LVEF < 40%
of the detrimental pathophysiological factors in each
• HF with preserved EF [HFpEF] : HF patients with individual patient.
LVEF ≥50%
Heart failure patients suffer from recurrent hospi-
• HF with midrange EF [HFmrEF]: HF patients talization. With each hospitalization, there is likely
withLVEF40–49% myocardial and renal damage which contributes to
progressive LV or renal dysfunction, leading to an in-
Stages of Heart failure is often looked at 4 stages.
They include evitable downward spiral. Comprehensive strategies
should focus on factors during hospitalization and
• Stage A : High risk of developing heart failure also during the early recovery period soon after dis-
• Stage B : Asymptomatic LV dysfunction charge to target stressors that probably contribute to
the vulnerability of patients.
• Stage C : Past or current symptoms of HF

• Stage D : Refractory of end stage heart failure PREDICTORS OF PROGRESSIVE HEART
FAILURE:
If chronic stable HF deteriorates, suddenly or slowly,
often leading to hospital admission, the condition is Heart rate variability and progressive heart failure:
described as ‘decompensated’ HF A reduced value of SDNN, is a very important and
independent predictor of progressive heart failure
The term progressive heart failure is used to de- and mortality. SDNN is the standard deviation of all
scribe patients with progressive increase in severity normal-to-normal RR intervals in the ECG. Patients
of symptoms, recurrent decompensation and severe with progressive heart failure have increased sym-
cardiac dysfunction pathetic nerve activation,increased cardiac norepi-
nephrine spillover, elevated plasma catecholamine &
AETIOPATHOGENESIS OF PROGRESSIVE renin levels, decreased vagally mediated heart rate
HEART FAILURE fluctuations. All these factors contribute or reduction

An intricate interplay of underlying pathophysiolog- of SDNN observed in progressive heart failure.
ical mechanisms determines the progression and SDNN is a potential marker for changes in myocardi-
clinicalpresentation of heart failure. The process ofre- al size and geometry, both of which may be involved
modelling and neurohumoral activation, through cen- with heart failure progression. This also could be a
tral and peripheral mechanisms, increases suscepti- reason for reduction of SDNN observed in progres-
bility toarrhythmias and exacerbates the progression sive heart failure. A recent study shows that chronic
of ischaemic disease and heart failure. Ischaemia in- sinoatrial node stretch reduces HRV, suggesting that
duces arrhythmias and myocardialinfarction, which in SDNN may be a marker for adverse changes of car-
turn may cause increased neurohumoral activation diac structure.
and cardiac remodelling.
Hyponatremia and progressive heart failure: Serum
Patients with progressive heart failure have increased sodium correlates closely with plasma renin activity.
sympathetic nerve activation(8), cardiac norepineph- Hyponatremia in patients with chronic heart failure
rine spillover (an index of sympathetic nerve traffic to has been shown tobe a predictor of progression and
the heart, and elevated plasma catecholamine, and mortality from pump failure. Lee and Packer reported
renin levels. that patients with severe chronic HF (with mean EF
The decrease in vagally mediated heart rate fluctu- ∼17%) and serum sodium levels <137 mmol/l) have a
ations in patients with heart failure is directly pro- life expectancy half that of patients with serum so-
portional to the level of muscle sympathetic nerve dium levels >137 mmol/l. In another study Lee and
activity and plasma norepinephrine levels. Packer, showed that patients whose serum sodium
levels increased in response to ACE inhibition had
The intimate relationship between the sympathetic a better prognosis. The mechanism by which hypo-
and renin-angiotensin-aldosterone systems, is that natremia predicts HF progression may involve neu-
stimulation of one increases activity of the other. rohumoral activity, including particularly that of the
Both norepinephrine and angiotensin II are strong renin-angiotensin-aldosterone system.
promoters of cardiac myocyte hypertrophy and ne-
crosis/ There is compelling evidence that norepi- Serum creatinine and progressive heart failure: Alter-

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