HEART FAILURE

Definition

A clinical picture resulting from decreased cardiac performance with cardiac output lower in comparison with peripheral necessities.

Etiology

Cardiomyopathies (primary myocardial disease ) Ischemic heart disease Haemodynamic overload Arrhythmias In fact any severe heart disease is possible to evolute towards heart failure syndrome

Pathology

myocardial cells performance of existing myocites

Pathophysiology

systolic performance (LV, RV or both) diastolic performance (LV, RV or both) forward heart failure ( cardiac output) backward heart failure (congestive syndrome) left side heart failure right side heart failure chronic heart failure acute heart failure

Pathogenesis
Adaptation mechanisms I Hypertrophy Dilatation heart rate (tachycardia) contractility (notfunctionning)

Adaptation mechanisms II

peripheral A +V O2 extraction Redistribution of cardiac output peripheral vasoconstriction blood volume and of venous return ( Na and H2O retention)

Realised through:

Cathecolamines RAA system

Signs and symptoms

1.

Heart:

- sinus tachycardia - ventricular gallop (S3) - regurgitation systolic murmur: - mitral regurgitation - tricuspid regurgitation 2. exercise capacity

Congestive syndrom

Lungs: - dyspnea, - rales, - dullness, - pleural effusion Liver: - hepathomegaly - tenderness Peripheral edema Ascites, pleural effusion, pericardial effusion (rare) Venous distention : jugular hepatojugular reflux Cyanosis: - peripheral - central

Low output syndrom

Weakness, fatigue Pallor weight Oliguria SBP DBP Cerebral symptoms

Investigations

Echocardiography - LV, RV or both - contractility - LA, RA or both - LVEF, RVEF or both - PAPs - MR, TR - diastolic LV dysfunction: - abnormal relaxation - pseudonormalisation - restriction

Rx (chest x ray)

cardiac chambers Cardiothoracic ratio >0,55 Pulmonary congestion Pulmonary arterial hypertension Pleural effusion

ECG
- always abnormal Morphologycal abnormalities - of the underlying disease - necrosis - hypertrophy - arrhythmias: - atrial fibrillation - ventricular: PVB, VT, - sinus tachycardia

Exercise stress testing

To establish the exercise capacity (METS) and NYHA class (also possible an a clinical basis)

Rare investigations

Cardiac angiography Coronarography Myocardial biopsy MRI CT multislice

Biochemical date

BNP, ANP Lipids Liver function tets Glycemia Ions: Na, K Creatinine Haematocrit

The proposed explanation for the Starling effect, whereby a greater end-diastolic fiber length develops a greater force.

Compensated hypertrophy functions poorly compared with transgenic models and athlete's heart. Left panel, Left ventricular hypertrophy (LVH) in which wall stress, the relationship between the radius of the LV chamber and the thickness of the LV wall (h), is normalized (N) in response to sustained pressure load acting via angiotensin II (A-II). Contrary to the wall stress correction hypothesis, LV mechanical function is reduced and not maintained. The impaired mechanical function is the direct result of increased fibrosis and apoptosis intermixed with growth signaling. Middle panel, Lesser hypertrophic response to pressure load in transgenic mice with inhibited Gq signaling, so that angiotensin II that leads to maladaptive signaling cannot operate. Although the transgenic wall stress has increased, as shown by the lower ratio of wall thickness, h, to the radius, R, mechanical function is less reduced than in the compensated heart of the wild type. Right panel, Adaptive growth patterns if ERK kinase is transgenically overexpressed or in the athlete's heart through Akt activation, when the truly compensated well-adapted state is reached. N = normal;

MAPK = mitogen-activated protein kinase; ERK = extracellular signal regulated kinase; Akt = protein kinase B

Pressure-volume loop of left ventricle. Note the effects of alpha-adrenergic catecholamines with both positive inotropic (increased slope of line Es) and increased lusitropic (relaxant) effects. The total pressure-volume area (for control area, see abcd) is closely related to the myocardial oxygen uptake. The area cde is that component of work spent in generating potential energy (PE). Es = slope of pressure-volume relationship.

Wall stress increases as the afterload increases. The formula shown is derived from the Laplace law. The increased left ventricular (LV) pressure in aortic stenosis is compensated for by LV wall hypertrophy, which decreases the denominator on the right side of the equation. R = radius.

Major determinants of the oxygen (O2) demand of the normal heartheart rate, wall stress, and contractile function. For use of pressure-volume area as index of oxygen uptake,

Mechanisms for generalized sympathetic activation and parasympathetic withdrawal in HF. A, Under normal conditions, inhibitory (-) inputs from arterial and cardiopulmonary baroreceptor afferent nerves are the principal influence on sympathetic outflow. Parasympathetic control of heart rate is also under potent arterial baroreflex control. Efferent sympathetic traffic and arterial catecholamines are low, and heart rate variability is high. B, As HF progresses, inhibitory input from arterial and cardiopulmonary receptors decreases and excitatory (+) input increases. The net response to this altered balance includes a generalized increase in sympathetic nerve traffic, blunted parasympathetic and sympathetic control of heart rate, and impairment of the reflex sympathetic regulation of vascular resistance. Anterior wall ischemia has additional excitatory effects on efferent

sympathetic nerve traffic. See text for details. Ach=acetylcholine; CNS=central nervous system; E=epinephrine; Na+=sodium; NE=norepinephrine.

Effects of reactive oxygen species (ROS) on cardiac myocyte phenotype. Through activation of kinase cascades such as mitogen-activated protein kinase (MAPK), ROS can induce myocyte hypertrophy. ROS can also alter the activity and expression of Ca2+-handling proteins including SERCA2A and the Na+/Ca2+ exchanger to alter myocardial contractility. Mitochondrial ROS may be particularly prone to induce apoptosis by stimulating the mitochondrial release of cytochrome c, which is necessary for the activation of caspase cascades. NADPH=reduced nicotinamide

adenine dinucleotide phosphate; TNF=tumor necrosis factor.

Unloading of high-pressure baroceptors (circles) in the left ventricle, carotid sinus, and aortic arch generates afferent signals that stimulate cardioregulatory centers in the brain, resulting in the activation of efferent pathways in the sympathetic nervous system. The sympathetic nervous system appears to be the primary integrator of the neurohumoral vasoconstrictor response to arterial underfilling. Activation of renal sympathetic nerves stimulates the release of arginine vasopressin (AVP). Sympathetic activation also causes peripheral and renal vasoconstriction, as does angiotensin II. Angiotensin II constricts blood vessels and stimulates the release of aldosterone from the adrenal gland, and it also increases tubular sodium reabsorption and causes remodeling of cardiac myocytes. Aldosterone may also have direct cardiac effects, in addition to increasing the

reabsorption of sodium and the secretion of potassium and hydrogen ions in the collecting duct. The lines designate circulating hormones.

TREATMENT

Recommended Therapies to Reduce Risk Include:

Treating known risk factors (hypertension, diabetes, etc.) with therapy consistent with contemporary guidelines Avoiding behaviors increasing risk (i.e., smoking excessive consumption of alcohol, illicit drug use) Periodic evaluation for signs and symptoms of HF Ventricular rate control or sinus rhythm restoration Noninvasive evaluation of LV function Drug therapy Angiotensin Converting Enzyme Inhibitors (ACEI) Angiotensin Receptor Blockers (ARBs)

DIURETICS

ARB and CHF Update 2005

In patients with systolic dysfunction

ARBs are good alternative to ACE-inhibition in symptomatic patients intolerant to ACE-inhibitors to improve morbidity and mortality (level of evidence B, class I) ARBs and ACE-inhibitors have similar efficacy in CHF (level of evidence B, class I) After acute myocardial infarction with signs of heart failure or left ventricular dysfunction, ARBs have similar efficacy to ACEinhibitors (level of evidence B, class I)

ESC Guidelines for the Diagnosis and Treatment of CHF - 2005

ARB and CHF Update 2005

ARBs can be considered in combination with ACEinhibitors in patients who remains symptomatic, to reduce mortality (level of evidence B, class IIa) and hospital admission for heart failure HF (level of evidence A, class I)

ESC Guidelines for the Diagnosis and Treatment of CHF - 2005

ARBs

Usual dose (mg)

Losartan

50-100

Irbesartan

150-300

Candesartan

8-16

Valsartan

80-120

Telmisaratan

20-160

Eprosartan

200

Tasosartan

100-200

Stage C Therapy
(Reduced LVEF with Symptoms)

Digitalis
I IIa IIb III

Digitalis can be beneficial in patients with current or prior symptoms of HF and reduced LVEF to decrease hospitalizations for HF.

Stage C Therapy
(Reduced LVEF with Symptoms)

Hydralazine and Isosorbide Dinitrate

I IIa IIb III

The addition of a combination of hydralazine and a nitrate is reasonable for patients with reduced LVEF who are already taking an ACEI and betablocker for symptomatic HF and who have persistent symptoms.

I IIa IIb III

A combination of hydralazine and a nitrate might be reasonable in patients with current or prior symptoms of HF and reduced LVEF who cannot be given an ACEI or ARB because of drug intolerance, hypotension, or renal insufficiency.