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1

heart failure 

•Heart failure is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood.

A CLINICAL DIAGNOSIS All HF patients, regardless of ejection fraction status (EF value), have the clinical syndrome of heart failure (HF).

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heart failure epidemiology

•In the US 6.5x 10⁶ have it

•Over age 65 years incidence: 10 per 1000

• > 68,000 die per year with HF as 1⁰ Dx

•2.4-3.6 X 10⁶ hospitalized per year

•40—50% annual mortality rate

•Women: More have it and more die of it than men

•blacks have the highest risk for HF

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two most common underlying causes of HF

•coronary artery disease

•hypertension

 

•CORONARY ARTERY DISEASE 60-75%

•HYPERTENSION IN 75% INCLUDING THOSE WITH CAD

•CAD, HTN AND DIABETES INTERACT TO AUGMENT RISK

•20-30% of cases of HFrEF cause is unknown = nonischemic or dilated or idiopathic cardiomyopathy

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the two presentations of HF in terms of LVEF

LV EJECTION FRACTION = SV/EDV

HFrEF EF ≤ 50%

HFpEF EF ≥ 50% I

t is only in HFrEF that evidence - based pharmacotherapy has been demonstrated to confer morbidity and mortality benefits (M&M).

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HFrEF

•EF≤ 40%

•Also referred to as systolic HF.

•Trials of pharmacotherapy have mainly enrolled subjects with HFrEF, and it is only in these patients that therapies with morbidity/ mortality benefits have been shown

•coronary artery disease

•HTN --> LVH --> increased O2 demand

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HFpEF

•EF ≥ 50% Most common EF normal, SV low - not filling up enough, reduced preload

•Also referred to as diastolic HF.

•Various criteria have been used to further define HFpEF.

•The diagnosis is one of exclusion of other potential noncardiac causes of symptoms suggestive of HF.

•To date efficacious therapies have not been identified

•hypertension --> LVH --> less room

•aortic stenosis

•hypertrophic cardiomyopathy

•restrictive cardiomyopathy

 

• ABOUT 50% OF PERSONS WITH HF

• RELATIVELY NORMAL LV FUNCTION

• DIASTOLIC HF

• CARDIAC OUTPUT LIMITED BY:

-ABNORMAL LV FILLING

-DISORDERED VENTRICULAR RELAXATION DURING EXERCISE

• VENTRICULAR PRESSURES ELEVATED FOR A GIVEN VOLUME WITH: PULMONARY CONGESTION DYSPNEA PERIPHERAL EDEMA

• OLDER WOMEN WITH

a-FIBRILLATION

- HTN

–DM

-OBESITY CKD

• HYPERTENSION THE CAUSE IN ~ 60% TO 89%

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other causes of HF

*Genetic defects Most are autosomal dominant

-Genes that encode cytoskeletal proteins

•Alcohol

•Cancer chemotherapeutic agents

-Trastuzumab (Herceptin®)

–Anthracyclines - Adriamycin 

•Cocaine

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associated disorders

DISEASES OF:

 PERICARDIUM

 MYOCARDIUM

 HEART VALVES

 GREAT VESSELS

 PERIPHERAL VESSELS

 METABOLIC ABNORMALITIES

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clinical syndrome

 DYSPNEA

 FATIGUE EXERCISE INTOLERANCE

FLUID RETENTION

Sx 2 0 to impaired LV function

ECHO evidence of systolic and / or diastolic dysfunction

Pulmonary/splanchnic congestion & Peripheral edema

Exercise intolerance little fluid retention

Others c/o edema, dyspnea or fatigue

 No single diagnostic test

 A clinical Dx based on Hx & PE

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All HF Patients, Regardless of EF value, Have the Clinical Syndrome HF

•Abnormal left ventricular (LV) filling dynamics

• Elevated LV diastolic pressure

• LV systolic and diastolic dysfunction

• Neurohormonal activation

• Impaired exercise tolerance, frequent hospitalization, and reduced survival.

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The Clinical Manifestations of HF are Similar Regardless of the EF

• Reduced exercise tolerance

• Dyspnea on exertion

• Orthopnea

• Paroxysmal nocturnal dyspnea

• Peripheral edema

• Pulmonary congestion apparent on chest radiographs or computed tomography (CT) scans

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HF Classification

•NYHA A functional classification-Sx Classes I-IV

•ACC/AHA Stages using risk factors and structural abnormalities Stages A-D

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precipitating causes of HF

PRECIPITATING CAUSES

•Arrhythmias

•Thyrotoxicosis

•Pregnancy

•Myocarditis

•Myocardial infarction

•PE

•Infective endocarditis

•Infection

•Hypertension

•Anemia

•Physical, dietary, fluid, environmental or emotional excesses

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HF Neurohumoral activation

• RENIN ANGIOTENSIN ALDOSTERONE ANGIOTENSIN II (Ang II) ALDOSTERONE

• SYMAPATHETIC NERVOUS SYSTEM NOREPINEPHRINE (NE)

• VASOPRESSIN(ADH)

• ENDOTHELIN

• CYTOKINES

• NATRIURETIC PEPTIDES (BNP, NT-pro- BNP)

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Indicators of Cardiac Stress, Malfunction & Injury

 Inflammation – TNF, Interleukins & CRP

 Oxidative stress – Oxidized low density lipoproteins

 Neurohormonal pathway activation – NE, Ang II, Aldosterone, ADH & Endothelin

 Extracellular matrix remodeling – Matrix metalloproteinases

 Myocyte injury – cardiac specific troponins ***diagnosis

 Myocyte stress – Brain natriuretic peptide (BNP) & N-terminal pro-BNP (NT pro-BNP)

***diagnosis and monitoring

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LV REMODELING IN HFrEF

• LV remodeling develops in response to a series of complex events that occur at the cellular and molecular levels. These changes include:

• (1) Myocyte hypertrophy

• (2) Alterations in the contractile properties of the myocyte

• (3) Progressive loss of myocytes through necrosis, apoptosis, and autophagic cell death

• (4) β-adrenergic desensitization

• (5) Abnormal myocardial energetics and metabolism

• (6) Reorganization of the extracellular matrix

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Determinants of Myocardial Function

Preload - determines volume and therefore sarcomere length 

Contractility – determined by Ca²⁺ availability 

Afterload - determines how much work the heart must do to successfully eject blood

Heart rate - contributes to Ca²⁺-loading of SR and therefore contractility

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source of natriuretic peptides

SOURCE

•BRAIN

•HEART

•VASCULATURE

•KIDNEY

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action of natriurectic peptides

•VASODILATION

•NATRIURESIS

•RAAS INHIBITION

•SNS INHIBITION

•ANTIPROLIFERATIVE

•ANTIHYPERTROPHIC

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BNP

 Dx of HF

 Association between concentration and severity

 Correlates with neurohormonal activation: SNS, RAAS & Endothelin

 Assessment of response to therapy

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BIOMARKERS OF RESPONSE TO CARDIAC INJURY/ STRESS

NEUROHORMONAL ACTIVATION – NE – ANG II – ADH – ALDOSTERONE – ENDOTHELIN

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Activation of the SNS

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HF PATHOPHYSIOLOGY NOREPINEPHRINE

• ↑CONTRACTILITY & HEART RATE

• ↑VENTRICULAR PRELOAD & AFTERLOAD

• CONSTRICTION AFFERENT GLOMERULAR ARTERIOLE

• ↑RENIN

• ↑PROXIMAL TUBULAR Na⁺ REABSORPTION

• ↓REGULATION OF β-1 RECEPTORS

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activation of the RAS

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HF PATHOPHYSIOLOGY ANGIOTENSIN II

Angiotensin II actions are similar to those of norepinephrine and also include:

• Increase in CNS sympathetic outflow

• Enhancement of peripheral noradrenergic (norepinephrine) neurotransmission

• Release of aldosterone

• Actions on myocytes and other cells to alter cardiovascular structure and function = remodeling

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HF PATHOPHYSIOLOGY ALDOSTERONE

Aldosterone, released from the adrenal cortex and produced locally, has actions that include:

• Increase in renal reabsorption of Na+ and H2O and increased renal excretion of K+ /H⁺

• Stimulation of collagen synthesis causing fibrosis (remodeling)

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HF PATHOPHYSIOLOGY ANTIDIURETIC HORMONE (VASOPRESSIN)

Antidiuretic hormone: release occurs as a consequence of baroreceptor activation by low cardiac output. The actions which serve to increase blood pressure and cardiac preload include:

• Vasoconstriction with increase in systemic vascular resistance

• Stimulation of thirst

• Increase in water reabsorption in the renal collecting ducts