Synonym: congestive heart failure, congestive cardiac failure
According to the WHO, heart failure is defined as reduced physical resilience due to a functional ventricular disorder.
It's a clinical syndrome of different etiology.
In some cases, the cause of heart failure remains unknown.
According to its clinical degree of severity, heart failure is divided into 4 NYHA stages:
Furthermore, heart failure can be divided into 4 stages according to the AHA American Heart Association:
A slightly rougher classification can be made:
Depending on the affected part of the heart, you can differentiate between:
Heart failure develops when the pumping performance is not sufficient anymore to adequatly provide the heart itself and other extracardial organ areas with blood, oxygen and substrates. As compensation, several different adaptation mechanisms are turned on. With them, the maintenance of the required cardiac output temporarily succeeds. In cases of chronic activation, these mechanisms, however, contribute to the progression of heart failure, where a vicious cycle develops.
In most cases, chronic heart failure is caused by a reduction of the contractile heart muscle tissue. In histology, you can see pathological growth of individual heart muscle cells (myocytic hypertrophy) on the one hand, on the other hand, you can see an increased loss of cells (myocytic apoptosis).
At the beginning, the activation of the sympathetic nervous system and the release of catecholamines lead to an increase in heart rate and contraction force. With increasing heart failure, the level of noradrenaline rises. At the same time, the number of cardiac beta receptors is reduced (downregulation. Therefore, noradrenaline has a less and less inotropic effect, but it increases the peripheral resistance (afterload).
The activation of the renin-angiotensin-aldosterone system leads to vasoconstriction via an increased production of angiotensin, and thereby, it increases the preload. This effect is enhanced by aldosterone, which causes the retention of sodium and water.
The activation of ADH (vasopressin) also leads to retention of water, and thereby to an increase of the preload.
In later stages of the disease, these helpful neuroendocrine compensation mechanisms, however, lead to a deterioration of the hemodynamic situation of the heart failure, and thereby, to a "vicious cycle", which needs therapeutic interruption.
The natriuretic peptides (NP) are the most important antagonists of the renin-angiotensin-aldosterone system (RAAS). With their main function, the reduction of the plasma volume and of the blood pressure, they protect the healthy heart from an excessive volume and pressure load. NPs are released eg. due to high pressure or over-expansion of the atria. Therefore, BNP is a good parameter in heart failure to ensure the diagnosis and estimate prognosis. This value, however, can be increased (obesity with BMI > 30), or decreased (renal failure, COPD, myocarditis) by other factors. Therefore, medical history, clinical symptoms and echocardiographical findings are always to take into consideration for evaluation.
Remodelling is defined as a number of molecular, biochemical and cellular meachanisms that change structure and function of the heart after its damage.
The symptoms of heart failure are versatile. These include, among others:
Diagnostics of an eventual
Since the beginning of the 21st century, with the determination of the plasma concentration of the brain natriuretic peptide BNP, or NT-proBNP, a test that can also be useful in daily routine diagnostics of heart failure is available. As per degree of heart failure, the levels are moderately to highly inreased, while normal BNP and NT-proBNP levels in an untreated patient mostly exclude presence of heart failure. The normal range depends on age and gender. The measurement of BNP for differential diagnosis and follow-up of heart failure, meanwhile, has been integrated into the guidelines of the German Cardiac Society and German Pediatric Cardiology Society.
|blood cell count||
|urea and creatinine|
|y-GT (possibly GOT, GPT)||
|total protein, albumin|
|blood tests which can be used for rarer and particular questions:|
|CK, LDH, troponin||
|cholesterol, HDL, LDL||
No-medicinal therapy of heart failure consists of a number of general measures which reduce the work load of the heart, or, respectively, should prevent further damage of the myocardium:
Medicinal therapy depends on the degree or stage of heart failure. Moreover, the symptoms (eg. edemas) as well as presence of concomitant diseases (eg. hypertension) are important factors for the determination of the exact medication. The most commonly used drug classes are:
The medicinal intervention in the fluid and electrolyte balance requires daily weight controls of the patient.
Surgical ventricular reduction, mechanical support systems
This is the last resort when other therapy options fail.
Therapy of heart failure primarily depends on the trigger cause. The following table gives an overview of the potential therapeutic approach.
|Causes||Possible therapeutic approaches|
|1. Chronic ischemic heart disease||Possibly revascularization|
|2. LV-remodelling after myocardial infarction||Conservative-medicinal|
|3. Hibernating myocardium (vital myocardium with chronic ischemia)||Early revascularization|
|Hypertension, hypertensive heart disease with hypertrophic LV||Medicinal control of hypertension|
|1. Dilatative Cardiomyopathy (DCM, idiopathisc form)||Physical rest, medication, alternative therapies, and consider HTX|
|2. DCM subsequent to toxic damage due to alcohol, drugs, or medication||Strict abstinence from alcohol; strict abstinence from drugs (especially cocaine); revision and possibly change of medication (eg. NSAR, cytostatics, etc.)|
|3. Hypertrophic CMP with obstruction (HOCM)||High-dose medication verapamil; discussion: DDD pacemaker; catheter ablation of the septum hypertrophy or surgical myectomy|
|4. Hypertrophic CMP without obstruction||High-dose verapamil|
|5. Restrictive CMP, idiopathic form||Discussion of HTX|
|6. CMP in storage diseases (amyloidosis, hemochromatosis)||Symptomatic therapy and treatment of the underlying disease, eg. chemotherapy in plasmocytoma, venesection in hemochromatosis|
|Chronic or acute atrial fibrillation||Medicinal normalization of the heart rate; possibly rhythmization (electrical/medicinal)|
|Typical atrial flutter||Catheter-guided HF ablation|
|Supraventricular tachycardia with reentry mechanism (eg. WPW-syndrome)|
|Persistent ventricular tachykarda||ICD (Implantable Cardioverter Defibrillator), antiarrhythmics, possibly HF ablation|
|Arrhythmogenic right-sided ventricular cardiomyopathy (ARVCM)||Antiarrhythmics; ICD (only rarely leads to heart failure)|
|Sinus or AV node diseases||Possibly DDD(R)-pacemaker|
|Absolute bradyarrhythmia in chronic atrial fibrillation||Revision of the medication; possibly VVI(R) pacemaker implant|
|Heart valve diseases||Surgical valve replacement or valvuloplasty|
|Inflammatory heart diseases|
|1. Acute myocarditis||Symptomatic|
|2. Acute endocarditis with hemodynamically relevant valvular dysfunction||Surgical sanitation (valve replacement)|
|3. Acute rheumatic fever||Antibiotics|
|4. Constriktive pericarditis||Surgical sanitation pericardectomy|
|Cardiac involvement in vasculitis and other autoimmune diseases||Immunosuppressive therapy of the underlying disease; symptom oriented therapy|
|Cardiac involvement in endocrine and metabolic diseases||Compensation of the hormonal and metabolic factors|
|Diabetic autonomous neuropathy|
|Anemia||Transfusion and determination of the cause|
|Renal failure||Possibly dialysis|
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