With 120,000 new cases per year, heart failure (HF) has become a major public health problem, which is growing with the aging of the population. It is characterized by the presence of functional symptoms (shortness of breath, fatigue, etc.) related to a disorder of cardiac function objectified by ultrasound imaging, radiological or isotopic.
The IC is also a genuine general disease by its neuroendocrine impact and limiting certain peripheral circulation, especially kidney. It corresponds to a variety of etiologies and mechanisms dominated by coronary disease, and in subjects younger, with dilated cardiomyopathy.
Real progress has been achieved over the last 25 years thanks to the development of drug and technical innovations, and a double prevention of cardiac involvement effort and its progressive aggravation.
Nevertheless, the IC remains a serious disease and sudden death one still current problem.
TREATMENT OF CHRONIC HEART FAILURE:
The goals of treatment of chronic heart failure insuffi (ICC) are:
– Improve functional tolerance and quality of life;
– Reduce the frequency and duration of repeated hospitalizations (and therefore the cost of the disease);
– Slow the progression of ventricular failure (IV), failing to prevent it;
– Ultimately reducing mortality both overall (which was estimated at 50% in 5 years, before the introduction of angiotensin converting enzyme inhibitors and beta-blockers) and sudden.
General rules of life:
Traditional recommendations, particularly as a quiet life, a regular diet with little or no salt, restricted alcohol, are always appreciated.
The regular practice of a determined individually exercise increases, as long as it lasts, functional exercise tolerance, especially due to ‘repackaging’ peripheral muscle.
Where possible, “personalized therapeutic education” aims to make the patient an active actor of his disease and its treatment, and to ensure it also psychological support.
The information of the patient and his immediate concerns:
– The disease and monitoring criteria: weight, urine output, pulse, blood pressure lying and standing, degree of breathlessness on exertion or orthopnea, subcutaneous infiltration sloping, etc. ;
– Optimal daily management of the disease and its treatment, including self-medication if it is well understood. In addition to the objectives and the side effects of each drug, the patient should know the therapeutic remedies that are prohibited: negative inotropic agents (Class I antiarrhythmic drugs, inhibitors of calcium double cardiac and arterial tropism) untimely beta blockers (even by eye) arterial vasoconstrictors. He must also know the therapeutic remedies that require prior notice to any custom administration: Nonsteroidal anti-inflammatory drugs, corticosteroids, lithium and tricyclic antidepressants (which may increase the arrhythmogenic risk), sildenafil (Viagra®) in case of hypotension, etc.
It is shown that a well understood and followed therapeutic education is the guarantee of a good compliance to treatment and gets a functional improvement, reduction in the frequency and length of hospital stay, and probably also mortality.
Processing aids factors:
Adjuvants factors intervene frequently in the destabilization of the IC they can help to reveal. A systematic inventory is needed, as well as their timely correction and possible prevention.
These factors include:
– Increased metabolic needs of the body fever and intercurrent infections, hyperthyroidism, pregnancy, etc.
– Failure of the other partners of systemic oxygen transport anemia, hypoxemia, etc.
– Errors in the monitoring of the CI abusive physical effort sodium overload, untimely interruption of treatment of IC or its causes (hypertension, coronary ischemia, etc.);
– Abnormal heart rhythm (TRC) is a very common complication of IC.
Even in a healthy heart, a profound slowing or extreme tachycardia may result in a few hours a clinical IC. Atrial fibrillation (AF) is the most common, ventricular tachycardia hemodynamically most poorly supported. The one and the other may require an adjustment by external electric shock in an emergency. If FA, slower ventricular rate can also be obtained by amiodarone and / or digitalis, knowing that, especially in the elderly, these treatments can exceed their goal.
The possibility of a specific etiological treatment is to search systematically for might upset the prognosis of HF.
All ICC not ventricular shortcomings fall at one time or another in their evolution, a surgical or percutaneous interventional gesture: chronic constrictive pericarditis, tricuspid or mitral stenosis, atrial thrombosis or artificial valve thrombosis.
The causes of left ventricular failure (VIP) or straight (IVD) are very diverse: mechanical overload (mainly blood pressure [hypertension] and valve disease), coronary artery disease, cardiomyopathy. In almost all etiologies, ventricular hypertrophy (HV) represents a compensatory phenomenon more or less well adapted to the causal mechanism (“remodeling”). Eventually the level of ejection and ventricular filling pressure, stimulation of noradrenergic and angiotensin-renin systems play a prominent role in the genesis and also in the imperfections of this “remodeling” (HV “pathological”).
Valvular almost always relate to a specific treatment. If the correction of the condition requires surgical remedies, must be indicated before the remote prognosis is affected by left ventricular hypertrophy (LVH) irreversible.
Coronary artery disease:
Coronary disease involves many different mechanisms, affecting both the contraction and filling of the left ventricle (LV).
Mechanically possible posti-nfarctus effects are increased by ischemia either permanently or more often intermittent (effort, spasm, etc.), which aggravates the “pathological” nature of LVH.
Prevention of abortion – a major therapeutic target in coronary disease – is best ensured by revascularization when a muscle extended territory is threatened and as early as possible in the acute stage of myocardial infarction.
At a minimum, the correction of risk factors (hypertension, hypercholesterolemia, diabetes, etc.), prevention of access ischemia, antiplatelet therapy and statins are a preventive treatment of IC.
Cardiomyopathy (CM) are a heterogeneous group according to anatomical intimate causal mechanism: CM dilated, restrictive CM (fibrosis, various myocardial infiltration, etc.), hypertrophic CM.
The etiology of these CM is usually little or no known.
Only some special treatment justified ent non cardiology: general disease, inflammatory or not, diabetes, hemochromatosis, weaning a toxic (including alcohol), etc.
Some CM hypertrophic obstructive say, are improved by embolization or failing resection of the septum.
Drug treatment of chronic heart failure:
Apart diuretics and digitalis, the main drugs of IC did not exist or were not used in this indication there 25 years. Their efficacy has been objectively evaluated and how to use them well codified in chronic abortion “systolic” traditional form of abortion, which corresponds to the impairment of systolic ejection performance of the pump VG, with expansion and reduction in the ejection fraction (EF <40%).
Treatment of chronic dilated abortion:
Table I shows the current European consensus on the indications of different therapeutic classes according to clinical classes of New York Heart Association (NYHA). Very schematically:
– I: no functional disorder;
– II: moderate limitation of physical fitness;
– III inconvenience to daily efforts of moderate intensity lower than the “ordinary” efforts;
– IV discomfort (almost) even permanently at rest.
For the same patient classification can change with the spontaneous evolution or processed.
These therapeutic recommendations (I, II) were developed by experts consideration essentially studies “controlled” but whose interpretation is yet sometimes difficult.
Certainly the results are generally oriented in the same statistical sense, but the numerical results and comments are far from unambiguous: the difference between studies in drug dosages, duration of treatment and follow-up, the mean age of the patients The etiology of IC.
Furthermore, the number of patients may be insufficient to achieve statistical significance, and there is inclusion bias (over-representation of ischemic heart disease and post-myocardial, underrepresentation of women and the elderly, etc.). Finally, the different therapeutic classes unevenly reach all therapeutic goals, but they complement usually leads to an additional combination therapy. The interference of most drugs with neuroendocrine systems stimulated in the IC is not certainly by coincidence.
Drugs that interfere with the renin-angiotensin system:
Angiotensin converting enzyme:
Angiotensin-converting enzyme (ACE) inhibitors, angiotensin I to angiotensin II (AII), but also the degradation of bradykinin, became the basic treatment of chronic abortion. Their dual arterial and venous vasodilator effect, they reduce intra-LV pressure and slow the “remodeling” VG.
They also intervene on the quality of LVH, especially by inhibiting the development of fibrosis. ACE inhibitors are the only drugs to be shown in four clinical stages of the disease, including in the asymptomatic patient.
They reach all the goals of treatment of IC, including a sustained reduction (at least 4 years) the absolute overall mortality (4-9%), although a modest or no effect on the occurrence of sudden death. As with hypertension, they appeared less effective in black subject.
They should be used to maximum possible dose according to blood pressure and renal tolerance.
Initiation is traditionally at low doses with gradual increase every 4 to 7 days under repeated monitoring of creatinine and potassium levels. The interference IEC / acetyl salicylic acid is negligible in clinical practice.
In addition to their classic cons-indications, side effects are possibly three bothersome:
– T oux forcing most often to stop;
– Orthostatic hypotension leads as to minimize diuretics before reducing doses of ACE inhibitors;
– An increase in serum creatinine less than 30% that do not require stopping the IEC, but limits the dose (and those of diuretics) under enhanced monitoring of renal function and electrolytes.
Antagonists of angiotensin II (ARB):
They block more completely than the IEC IIA training, but lack of action on bradykinin. Due to their good tolerance, they are unanimously recommended as a valid alternative to ACE inhibitors when coughing or hypotension or renal failure. Candesartan has shown, at least in one study, an additional cost of benefits in combination with ACE inhibitors in terms of cardiovascular mortality and rehospitalization.
– In discontinuous administration, they may occasionally be used to increase the daytime functional tolerance, or prevent nocturnal pulmonary stasis. In the long term, their place is very small, as well as that of the nitro-combination hydralazine (HDZ).
Calcium arterial vasodilator inhibitors:
– Calcium channel blockers almost exclusive arterial vasodilators (dihydropyridine) have no deleterious effect on the evolution of an abortion and can be used to enhance the treatment of hypertension or myocardial ischemia: nicardipine (Loxen®), amlodipine ( Amlor®), felodipine (Flodil®), etc.
Against long-stated formally in the IC, they remain in the presence of congestive signs.
Three are currently marketing authorization (MA) in HF: carvedilol (Krédex®), bisoprolol (Cardensiel®), metoprolol (Seloken®). They would act by reducing BP and sympathetic hypertonia that depletes heart A1 receptors and promotes arrhythmias. They inhibit the LV dilation and have a cumulative effect with ACE inhibitors on total mortality (relative risk reduction of around 35% over 15 months), and especially sudden (down to 45%). They are also active on the black subject. They are recommended if the patient remains symptomatic despite the IEC (stages II, III) and keep in an indication of inadequate coronary principle stage IV where their introduction should nevertheless be very cautious in specialized areas. It is the same in the elderly or receiving digoxin and / or amiodarone, due to the risk of bradycardia.
Apart from the usual cons-indications, starting treatment is done by remote rule (minimum 15 days) of a flare, and always very gradually. As an indication, for a target dose of 10 mg bisoprolol (Cardensiel®), the initial dose is 1.25 mg under strict supervision for several hours. Depending on the tolerability, the dose is increased by separate levels of several days or weeks. Daily control pulse, BP, weight and diuresis is required.
Clinical tolerance (dyspnea, fatigue) is often suitable until the second or third month. The occurrence of a flare requires dose reduction, if not immediately stop beta blockers. If potentiation of side effects with other therapeutic classes, you must first reduce the doses of these and try to keep the beta-blocker treatment, even in moderate doses, keeps a positive preventive effect on sudden death.
They are the preventive and curative treatment of fluid retention.
They are the most used (furosemide [Lasilix®] and bumetanide [Burinex®]) due to renal tolerance and their dose / effect relationship almost linear. The usual daily dose of oral furosemide is 20 to 60 mg in stage III, doubled or tripled in stage IV to reach 1000 mg / day intravenously continues in extreme cases. Stages II and certainly I, the use of furosemide may be occasional: the patient must learn to master the best of its daily necessities and fatigue the diuretic-salt-free diet complementarity.
A dosage of brain natriuretic peptide (BNP) provides additional information for the diagnosis of HF and the existence of an upstream slow. With proximal diuretics, the risk of mortality rhythm is real. Potassium supplements and magnesium is necessary in case of prolonged treatment or in large doses. The association of small doses of furosemide thiazide diuretic can overcome an addiction phenomenon possible in the long term. The administration of diuretics does not eliminate the direct discharge serous effusions poorly tolerated. If pushed too dehydration, serum and salt intake should be monitored closely.
Correcting hyperaldosteronism proximal diuretics, spironolactone has the double advantage of a distal tubular diuretic effect (likely without direct input to control the potassium deficit proximal diuretics) and an antagonist of aldosterone (possibly by a myocardial antifibrosante action). In fact, his administration associated with drug references abortion allowed a further reduction in mortality, including sudden.
His prescription stages III and IV is usually desirable to moderate doses (12.5 to 25 mg). Regular monitoring of serum creatinine and electrolytes whole is imperative. Eplerenone, after a favorable review in the post-infarction, is being more comprehensive assessment.
Digitalis lost ground in the treatment of IC may be due to excess mortality ventricular TRC. They do not lead to reduction in overall mortality, but only the number of flare-ups and hospitalizations. Digoxin still recommended in patients with stages III, IV sinus rhythm, subject to not exclude beta-blockers. It is mainly used as a retarder of ventricular rate in case of AC.
Digitalis positive inotropic not:
The positive inotropic non digitalis (dobutamine, sympathomimetics, phosphodiesterase inhibitors) have a favorable immediate action on heart but pejorative condition on the long and even medium-term prognosis. They are still used intravenously in the most severe forms to allow for a few days or weeks, a “bridge” to transplantation.
Class I antiarrhythmic drugs:
Class I antiarrhythmic drugs are cons-indicated despite their ventricular arrhythmogenic action because of their negative inotropic action, such as calcium channel blockers, cardiac and arterial dual tropism.
Amiodarone is used, at least in France, to prevent and reduce all TRC.
Its effectiveness is recognized and decreases probably also sudden death. Nevertheless, it is little or no influence on total mortality.
Prevention of sudden death:
Complicating the evolution of an IC, prevention of sudden death is an important objective.
Most often attributed to ventricular fibrillation, sudden death globally accounts for nearly 50% of all deaths. The absolute risk increases with the severity of clinical abortions and LV dysfunction (Fe <40%), and the presence of spontaneous or triggered ventricular tachycardias. However, there is no individual predictor both really sensitive and specific. Moreover, the percentage of sudden deaths in relation to total mortality is higher in the less severe forms clinically improved or above (“illegitimate rhythmic dead” IC). Current drugs, only beta-blockers and spironolactone significantly reduce this risk.
The implantation of an implantable cardioverter defibrillator (ICD) is currently the most effective supplement for optimal pharmacological treatment.
They are now less used in abortion.
FMD (let alone a dilated left atrium) is their elective indication with akinetic scars extended or dyskinetic or thrombosis localized LV.
Treatment of so-called abortion “diastolic”:
Entities not well defi ned and again discussed, diastolic abortions are characterized by a normal LV ejection capacity or slightly altered, so by the dimensions of the LV cavity and a normal or near normal Fe.
They are related to a primary disorder of LV filling, usually by wall thickening. Favored by aging, current prevalence is increasing. Lack of studies to demonstrate the influence of the usual treatments for IC on mortality, unless the latter corrects a causal factor (hypertension, myocardial ischemia) or prevent CRT.
Treatment of chronic SCI:
In addition to some cases of congenital or acquired mechanical overload of the right ventricle, chronic IVD is generally the result of chronic pulmonary hypertension, or by independent pulmonary disease (chronic postembolic pulmonary heart, chronic respiratory failure), or more often from heart failure overall (ICG) Chronic whose evolution determines that of IVD.
Characterized clinically by the quantitative importance of fluid retention, chronic IVD require wider use of diuretics that the only abortion.
Prescription of anticoagulants is also higher because of the increased risk of venous thrombosis and pulmonary embolism.
The possibility of a relative overdose in case of congestive liver thrust must be known to the patient.
Treatment no alternative or complementary drug:
They are an undeniable therapeutic progress in recent years.
Implantable cardioverter defibrillators:
In patients with an EF <35%, implantable cardioverter defibrillators (ICDs) reduce, on a follow-up 2 years, the overall mortality (relative decrease of 25%) by reducing sudden death (almost double ). But their potential disadvantages are not negligible price, infections, probe displacement, faulty settings, inappropriate shocks, etc. Their current indications are probably too small in relation to their potential effectiveness. They are likely to expand with the technical and economic progress, in addition to optimal medical treatment of HF in the absence of antiarrhythmic “miracle.”
Multisite pacing ventricular resynchronization:
Simultaneous stimulation VD and VG (via the coronary sinus) resynchronizes the two ventricular contractions. Their indication is carried in patients with stage III and IV with an EF <35% and especially having a ventricular asynchrony detected by a QRS duration> 120 ms and confirmed by echocardiography. Reduction already demonstrated functional signs and repeated hospitalizations appears to be linked to the extension of ventricular filling. The long-term effects, particularly on mortality, under evaluation, appear favorable.
Combining DAI and resynchronisateur, it emerges as the treatment of the most severe forms.
Ventricular audience of a few hours or days waiting allow a possible myocardial recovery: acute myocarditis, pre- or post-surgical failures, drug intoxication, etc. Technological advances also allow the implanted audience, prolonged (up to several months or even years) and constitute progress towards the old dream, often waiting for a possible heart transplant, artificial heart.
Surgical remedies, apart from the correction of mechanical overload of coronary surgery and certain anévrysmectomies, mainly centered around the transplant.
Transplantation is the last resort for refractory IC. Age over 70, active systemic disease, inadequate psychological terrain are the main cons-indications to a gesture whose indication must be seriously weighed in light of the shortage of donors and increasing wait times.
Attempts to “ventricular reduction,” the correction of functional mitral regurgitation
– Whose border with organic mitral insuffi ledge is not always obvious
– Not in a few years, found an undisputed place as “dynamic cardiomyopathy” and “external VG contention.”
TREATMENT OF ACUTE CARDIAC WEAKNESSES:
Symptomatic destabilization of CHF saw a flare usually justified only enhanced pharmacological treatment, especially diuretic IV, co-administration of nitroglycerin, reduction or discontinuation of beta-blocker therapy, correction of a factor triggering.
The delay of clinical, biological and radiological signs of hemodynamic improvement exposed to overtreatment and a “low speed”. Conversely, pulmonary edema “bronchoplégique” in a patient exhausted and desaturated O2, claims a temporary ventilatory support.
Severe heart failure sudden onset, let alone on a heart previously deemed normal and suddenly exceeded most often requires an etiological treatment:
– Pericardial decompression without any delay;
– Surgical correction (whose time depends on the clinical severity) of an intracardiac mutilation (bacterial endocarditis, ruptured mitral rope, mechanical complications of myocardial infarction);
– Revascularization of myocardial infarction in the process of constitution;
– Massive pulmonary embolism;
– Acute myocarditis;
– Poisoning: in those cases where circulatory insufficiency often predominates congestive signs, transient use of dobutamine or sympathomimetic amines IV, an ultra-conservative filling, a ventricular assist may save a few hours or Days to etiological treatment or transplantation.
Behind a rather unique symptomatic façade, the IC is a very diverse disease, always requiring etiological investigation and correction of triggers. Prevention – if possible – is the best treatment.
The treatment of CHF is heavy, and combination therapy requires regular clinical and biological monitoring in a dual concern for safety and therapeutic adaptation. A certain shyness about medical doses and associations, weariness of patients interrupting more or less completely and transiently their drugs are understandable. Enlightened cooperation of the patient is necessary.
The future of the ICC of treatment is diffi cult to identify:
– The best documented application of the current combination therapy for all forms of IV;
– The possible discovery of more effective drugs than current drugs, the logical mechanism of action do not result necessarily in a stable clinical efficacy.
Like the non-digitalis positive inotropic and vasodilatory non-physiological, the list goes medication left on the wayside: antagonists of endothelin, vasopressin receptor, TNF-alpha. There is uncertainty about the future of natriuretic peptides and inhibitors of endopeptidase, not sold.
Remain within reasonable time prior two real hopes:
– Widespread DAI reliable and less expensive to reduce mortality, including sudden death;
– The development of regenerative techniques or preservation of contractile cells of the heart and myocardial vasculature by gene therapy and / or cellular. After a long promising experimental phase, clinical trials are underway.