The Total Number of Americans Living With Heart Failure is Projected to Increase 46% From ~5.8 Million in 2012 to ~8.5 Million In 2030

TAKE A
CLOSER LOOK

PATIENTS WHO HAVE HAD A

WORSENING HF EVENT

ARE AT INCREASED RISK FOR FUTURE EVENTS1

Worsening Heart Failure Burden Section

Globally, the total number of people living with HF is over 60 million and is projected to increase drastically within the next decade.1-3

 

HF = heart failure

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WHAT DO WORSENING  HF EVENTS LOOK LIKE?

A worsening HF event is characterized by progressively escalating signs and symptoms, requiring treatment with IV diuretics and/or hospitalization.1,4

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1 in 6 patients with HFrEF will experience a worsening HF event on average 18 months after initial diagnosis.1

 

HFrEF = heart failure with reduced ejection fraction

Risks of Worsening Heart Failure

Heart
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PATIENTS’ HEARTS ARE NEVER THE SAME AGAIN AFTER EACH WORSENING HF EVENT5

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IN A REAL WORLD SETTING

56% ARE

REHOSPITA­LIZED WITHIN 30 DAYS

OF THE WORSENING HF EVENT DESPITE RECEIVING AVAILABLE GUIDELINE RECOMMENDED THERAPIES1

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>1IN5

DIE WITHIN

2 YEARS OF THE

WORSENING HF EVENT1*

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Pathophysiology of Worsening Heart Failure

THERE ARE MANY PATHWAYS INVOLVED IN WORSENING HF

heart
path

Current therapies primarily address harmful effects of compensatory neurohormonal mechanisms
(e.g., SNS and RAAS).6-8

SNS4-6

Activation of the SNS results in:

  • Increased cardiac contractility
  • Activation of the RAAS
  • Increased heart rate
  • Myocardial ischemia & cardiomyocyte apoptosis over time

SNS = sympathetic nervous system; RAAS = renin-angiotensin-aldosterone system

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RAAS +/- NPS6,9

Overactivation of the RAAS results in:

  • Increased production of renin, angiotensin II & aldosterone
  • Decreased renal blood flow
  • Increased sodium resorption and water retention

Increased peripheral resistance to the NPS contributes to further vasoconstriction and water retention The NPS would normally counteract the activity of the SNS and the RAAS

 

NPS = natriuretic peptide system

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Recent evidence indicates the potential of targeting the

NO-sGC-cGMP pathway in heart failure.4

NO-sGC-cGMP5

In heart failure with reduced ejection fraction, patients have a shortage of a critical substance, sGC, leading to reduced cGMP, causing myocardial and vascular dysfunction. Currently there is no heart failure treatment that addresses that pathway.5

 

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In contrast to available therapeutic approaches of antagonizing counterregulatory neurohormonal pathways, restoring the balance of the NO-sGC-cGMP pathway enables improved outcomes for heart failure patients.4

 

NO-sGC-cGMP = nitric oxide-soluble guanylate cyclase-cyclic guanosine monophosphate

 

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Video on Worsening Heart Failure

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YYMMDD Author/Uploaded by

* In the same Real World study

References