Angina pectoris I20.9

Author: Dr. med. S. Leah Schröder-Bergmann

All authors of this article

Last updated on: 29.10.2020

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Synonym(s)

Acute thoracic pain; Breast tightness; Chest pain; Herzenge; Shorthand

History
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Approximately 2000 years ago, Seneca described an angina pectoris attack (AP) as follows: "Brevis autem valde et procellae similis est impetus, intra horam fere desinit" ("The attack is short but violent and resembles a storm. It is almost always over within an hour").

In 1768 two authors - Rougnon and Heberden - described the symptoms of an angina pectoris attack. Until today there is a dispute of priorities among them concerning the first describer (Wagner 1985).

The term "unstable angina pectoris" has been used since 1971.

In 1989 Eugene Braunwald introduced a classification (see "Classification" below) of unstable AP for the first time, which was widely accepted and recognized worldwide (Weber 2004).

A special form of AP, the so-called Prinzmetal angina (also known as variant angina or vasospastic angina (Stierle 2017), was named in 1959 after its first describer, the American cardiologist Myron Prinzmetal (1908 - 1987) (Geisler 2006).

Definition
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Angina pectoris is defined as episodically occurring chest pain as a consequence of temporary myocardial ischemia (Kasper 2015). This is a leading symptom of the manifestation of coronary heart disease (Herold 2020).

Classification
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The AP is divided into

Stable AP: A stable AP can be triggered by physical and psychological stress. It disappears at rest and after administration of nitrates. According to the classification of the Canadian Cardiovascular Society (CCS), stable AP is divided into the following 4 degrees of severity. However, the allocation to the individual degrees of severity is not possible (multiple triggers of AP) or does not make sense in many patients. The problem is known, but a reformation of the classification is not yet available (Pinger 2019). The CCS classification differentiates between:

  • CCS grade I: There are no symptoms under normal everyday stress. AP seizures only occur during very high and continuous exertion (e.g. when clearing snow, endurance running etc.).
  • CCS grade II: There are only minor restrictions during normal activities. An AP occurs, for example, when climbing stairs, climbing mountains, in cold weather, etc.
  • CCS grade III: Here there is a clear limitation of the daily performance. AP occurs when dressing, walking slowly, doing housework, etc.
  • CCS grade IV: AP occurs at rest. This degree of severity is already partly evaluated as unstable AP (Dißmann 2019).

Unstable AP: The unstable AP is - in addition to the ST elevation myocardial infarction (STEMI) and the non-ST elevation myocardial infarction(NSTEMI ) - part of the acute coronary syndrome. According to ACC / AHA 2007, unstable AP is defined as follows:

  • AP at rest, which lasts longer (> 20 min)
  • new AP with at least severity level CCS III
  • AP already known, but increasing in duration, frequency and intensity (at least CCS III)
  • AP already known to occur at a reduced load level (at least CCS III) (Pinger 2019).

The unstable AP is divided into a:

  • primarily unstable AP: this means any firstangina with at least severity CCS III (Pinger 2019)
  • Secondary unstable AP: These include AP showing increasing severity, duration and frequency of seizures, resting AP, post-infarction AP, etc. (Herold 2020)

Eugene Braunwald formulated the classic idea of unstable AP in 1989 according to severity, clinical circumstances and possible medication. C. W. Hamm modified it in 2000.

  • Severity I: newly occurring AP < 2 months with pronounced intensity, which occurs at least 3 x / d or known AP, which increases in frequency and already occurs at significantly lower exposure
  • Severity II: AP that occurred in the last month but not within the last 48 h at rest.
  • Severity III: AP which has occurred at rest within the last 48 hours.
  • ___________________________________________________________________
  • Severity A: Secondary AP that occurs as a result of fever, infections, tachyarrhythmia absoluta, hypotension, anemia or hyperthyroidism.
  • Severity B: Primary unstable AP
  • Severity level C: Unstable AP that occurs within 2 weeks of an infarction .
  • ___________________________________________________________________
  • Severity 1: AP with no or little medication
  • Severity 2: AP under standard medication
  • Severity 3: AP under maximum therapy including i. v. nitro administration (Pinger 2019 / Braunwald 1989 / Hamm 2000)

Special forms of angina pectoris

  • Angina-equivalents: In this case, a diastolic dysfunction in myocardial ischemia is associated with dyspnea or reduced exercise tolerance. Thoracic pain, however, is absent in this clinical picture (Stierle 2017).
  • Atypical angina: Atypical angina pectoris is pain that is either not load-dependent and does not respond to nitro administration or pain that shows an atypical localisation, such as forearm pulling, abdominal pressure, etc. The risk of developing CHD is between 43% and 70% for men and 15% to 54% for women (the risk increases with the patient's age) (Stierle 2017)
  • Angina nocturna (also known as angina decubitus): This form of AP causes nocturnal, sleep-induced AP attacks and/or sudden dyspnoea (Herold 2020). The symptoms occur mainly in the first half of the night. Presumably, a fluid backflow while lying down causes an increased ventricular wall tension due to the increased preload. The symptoms subside quickly when the patient sits up, as does the administration of nitro. Prophylactically, the preload can be reduced by diuretics (Stierle 2017).
  • Broken Heart Syndrome (see below "Tako- Tsubo- Cardiomyopathy")
  • Fixed vs. variant threshold angina: "Fixed- AP" is a stable threshold below which no AP occurs. Only when this threshold is exceeded does AP occur. In "Variant threshold AP" there are other triggering factors besides the stress threshold, such as temperature, wind from the front, meals, etc., which have a dynamic vasoconstrictory effect (Stierle 2017).
  • Cocaine-induced chest pain: This pain occurs in a temporal relationship with cocaine use. Cocaine has the property of triggering a generalised activation of the sympathetic nervous system, which in turn leads to coronary vasospasms. Regular cocaine abuse also causes accelerated arteriosclerosis. It is not uncommon for myocardial infarctionto occur in the further course of the disease - despite the younger age of the patients (Stierle 2017).
  • Microvascular angina (formerly called syndrome X): This clinical picture is not uniformly defined. Typically, the occurrence of stress-induced angina pectoris symptoms, corresponding changes in the ECG and other positive evidence of ischemia are considered to be typical. However, the coronary arteries are completely inconspicuous (Stierle 2017).
  • Prinzmetal angina: This leads to attacks of angina pectoris with a reversible ST elevation. A troponin increase is missing. Coronary angiography often reveals stenoses. Passive coronary spasms may occur in the stenosed area. For these patients there is an increased risk of acute coronary syndrome (Herold 2020).
  • REM sleep induced AP: This occurs preferentially in the 2nd half of the night. It is caused by strongly fluctuating RR and pulse values during a REM phase. The ventricle shows no myopathic damage. Beta-blockers can be given as prophylaxis for this form of AP. (Stierle 2017).
  • Silent myocardial ischaemia: In about 1/3 of all patients with stable AP and in almost all patients with unstable AP, so-called "silent myocardial ischaemia" occurs in addition and is painless. Exclusively painless ischemias are found in about 5% of patients with coronary stenosis. These are particularly frequent diabetics and smokers. These silent ischemias represent a considerable risk factor for the occurrence of a myocardial infarctionin the following years. Whether these infarctions can be prevented or reduced by drug treatment of silent ischemias is unknown (Stierle 2017).
  • Syndrome X: see above. "Microvascular angina
  • Tako- Tsubo- Cardiomyopathy (so called "Broken Heart Syndrome"): This is a special form of regional cardiomyopathy caused by a functional disorder of the autonomic nervous system. The clinical picture almost exclusively affects women. Typical is the endsystolic form of the left ventricle with a balloon-like distension of the apex. The treatment corresponds to that of a STEMI or N-STEMI with the exception of the - in this case not necessary - re-perfusion therapy (Stierle 2017).
  • Walk(-ing) through- Angina: In this case an AP is performed at the beginning of a stressful activity. However, this disappears in the further course of the stress by release of vasodilatory metabolites (Herold 2020).

Occurrence/Epidemiology
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Overall, an AP affects the male sex in about 70% of cases. This figure is even higher at the age of under 50 years. However, it should also be borne in mind that in women, AP is often atypical (Kasper 2015). The gender difference in favour of women will level out in the course of life (Stierle 2017), as the atherogenic risk factors become more important in women after the onset of menopause (Kasper 2015).

The percentage of AP-attacks depending on age and sex is:

  • Men 45 - 54 years: 2 % - 5 %
  • Women 45 - 54 years: 0,1 % - 1,0
  • Men 65 - 74 years: 10 % - 20
  • Women 65 - 74 years: 10 % - 15 % (Pinger 2019)

Etiopathogenesis
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Pathophysiology

In an AP attack, the perfusion pressure decreases in the poststenotic area of the coronary artery. The end-diastolic ventricular pressure, on the other hand, increases. This initially leads to a disturbance of the blood flow in the inner layer of the myocardium and, in the case of transmural hypoperfusion, to a deterioration of the pump function of the affected ventricle (Herold 2020).

The cause of AP is almost always (Neurath 2015) fixed coronary stenosis, which leads to a myocardial oxygen deficiency and is associated with a reproducible circulatory load (Stierle 2017). AP can typically be triggered by:

  • physical stress (isometric rather than dynamic stress)
  • stressful meals
  • physical refrigeration
  • emotional stress (Stierle 2017)

The following changes are the cause of AP:

First, increased coronary resistance. This can be caused by major vascular factors such as:

  • Macroangiopathy > 90%.
  • Microangiopathy (small vessel disease)
  • Coronary spasms (can be triggered by cocaine, among other things)
  • Coronary anomalies
  • arteriovenous coronary fistulas
  • congenital myocardial bridges
  • Additional myocardial factors such as:
    • Heart Hypertrophy
    • Increased end-diastolic pressure in the ventricles
    • Tachycardia / Tachyarrhythmia in atrial fibrillation
    • arterial hypertension

As soon as tachycardia and hypertension exceed a critical limit due to the increase in heart work, an angina pectoris attack occurs.

Extra coronary factors. These can be cardiac factors such as:

  • hypertrophic cardiomyopathy
  • Aortic valve defects (e.g. due to severe left ventricular hypertrophy in aortic valve stenosis [Kasper 2015])
  • Rhythm disturbances
  • and extracardiac such as:
    • Increased oxygen demand (Neurath 2015) in case of e.g. fever, hyperthyreosis, physical exertion etc.
    • Decreased oxygen supply, e.g. in anaemia, high altitude, lung diseases, sleep apnoea syndrome, CO poisoning, etc.
    • Increased blood viscosity in cases of erythropoietin doping, hyperfibrinogenemia, multiple myoma, polycythemia vera, etc. (Herold 2019 / 2020).

Clinical features
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In AP, the following pain symptoms are predominant:

  • Retrosternal pain with radiation in
    • the neck / the back of the neck
    • Lower jaw
    • Teeth
    • Shoulder area
    • both (!) arms (with focus on the ulnar sides of the forearms), which can radiate into the ulnar fingertips
  • Pain in the epigastrium (rarely also below the navel)
  • typically the region of the trapezius muscle remains painless (pain in this area is typical of pericarditis - Kasper 2015)

The pain symptom can be triggered by:

  • physical stress (isometric rather than dynamic)
  • emotional burdens
  • Cold
  • postprandial etc. (Herald 2020)

This pain is described as dull, oppressive with a feeling of thoracic constriction (a stabbing thoracic pain speaks against angina pectoris). It usually swells (crescendo character) and is never dependent on breathing or movement (Stierle 2017).

However, these typical symptoms may be absent in:

  • diabetes mellitus
  • Renal insufficiency
  • Women
  • older patients > 75 years
  • Currently undergoing heart surgery
  • At present according to heart transplantation (Herold 2020)

In these constellations there are rather unspecific symptoms, such as

  • Nausea
  • Shortness of breath
  • Swindle
  • epigastric pain

Unstable angina pectoris (associated with a significantly worse prognosis) is characterized by the occurrence of AP:

  • progressive under stress
  • calmly occurring
  • occurring during sleep (Kasper 2015)

Depending on the symptoms, one speaks of a typical or atypical or non-thoracic pain symptomatology. The following 3 characteristics are characterized:

  • characteristic expression of the retrosternal pain (pain lasting up to 10 minutes; stitches never lasting only seconds [Pinger 2019])
  • Triggering of the symptoms by physical or psychological stress
  • a reduction in symptoms through physical rest or administration of a short-acting nitrate

If all 3 symptoms are present, one speaks of a "typical angina pectoris". If only 2 criteria are fulfilled, it is called "atypical angina pectoris". If a single symptom or none of the criteria is present, there is a "non-cardiac pain". If an AP does not respond to complete rest or to the administration of a nitrate, the diagnosis of AP should be questioned in principle (Kasper 2015).

Imaging
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Cardio CT - Multi-layer computed tomography (MSCT) / Dual-source computed tomography (DSCT)

With the MSCT, which was clinically introduced in 1998, up to 64 layers can be recorded simultaneously. Up to now, restrictions have mainly existed in cases of increased heart rate, stents and severe coronary calcifications (Mahnken 2007). A further development is the DSCT with two tube detector systems, which has been in use since 2006 (Luhmann 2009).

Both examination methods are suitable for patients with low to medium pre-test probability of CHD. The sensitivity is almost 100 %, as is the negative predictive value. Stents and coronary bypasses from a size of 3 mm can be evaluated.

In contrast to conventional invasive cardiac catheters, this method can also be used to visualize the vessel walls and thus non-calcified (so-called soft plaques), mixed and calcified plaques. The radiation exposure of 1 mSv is significantly lower than that of the invasive heart catheter with 5 mSv - 12 mSv.

The limitations of these methods - compared to an invasive heart catheter - are found in:

- pronounced cardiac dysrhythmia

- a calcium score of > 400 (Herold 2019 / 2020)

Coronary angiography

Indications for coronary angiography after ESC 2013 are:

  • Degree of recommendation / evidence level I / C:

This degree of recommendation includes

  • Patients with angina pectoris CCS III or with a probably high event risk, especially if the response to drug treatment is insufficient

For further details see also Coronary heart disease

Diagnosis
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The diagnosis of the disease underlying angina pectoris - coronary heart disease - is described in detail there. Only individual criteria that are important for AP are highlighted here.

Medical history: The threshold for the occurrence of AP varies from person to person. Patients often know the threshold above which AP occurs in them. In these patients, the stenosis of the coronary arteries and the myocardial oxygen supply are fixed. Ischemia is only triggered by an increase in myocardial oxygen demand.

However, there are also patients in whom the threshold fluctuates considerably during the course of the day. In these patients, changes in the oxygen supply, e.g. changes in coronary vessel tone, most probably play a role (Kasper 2015).

Inspection and palpation: In describing the pain during an AP attack, the patient typically clenches his fist over the sternum - also known as the Levine sign (Stierle 2017)

Resting ECG: In about 50 % of the patients no changes in the ECG are visible. Otherwise, there may be a ST elevation, which may be followed by an ST lowering (Stierle 2014). Also all kinds of disorders of depolarisation or repolarisation are possible. The specificity of the resting ECG with regard to AP is generally considered to be very low (Pinger 2019).

Exercise ECG: The most common method to diagnose AP is the exercise ECG.

For example, in a male person > 50 years of age with a history of typical angina pectoris, which also occurs during exercise ECG, the sensitivity is 98%. False positive or false negative results are to be expected in about 1/3 of the patients (Kasper 2015).

Persistent unstable angina pectoris is an absolute contraindication for the exercise ECG. The occurrence of moderate to severe angina pectoris is one of the absolute termination criteria, whereas the occurrence of increasing angina pectoris is only a relative termination criterion. (Pinger 2019). The absence of a rise or a drop in blood pressure under stress is a sign of ischemia and should be evaluated as such (Kasper 2015).

Long-term ECG: According to ESC 2013, the indication for a long-term ECG exists only for Prinzmetal angina (Pinger 2019). Otherwise, the examination can possibly give indications of nocturnal AP-attacks (Herold 2020).

Laboratory: Laboratory chemical parameters that accelerate atherogenesis should be determined, such as:

  • lipids
  • BZ
  • Creatinine
  • Hematocrit
  • if necessary, also the thyroid gland values, e.g. TSH (with corresponding anamnestic data, examination results etc.)
  • Urine examination for
    • a glucosuria
    • Indications of kidney disease (including microalbuminuria)(Kasper 2015)
    • Troponin and CK- MB: Troponin does not rise in unstable angina pectoris (Herold 2020). However, patients with negative CK- MB show an increase in troponin in about 15 % - 20 %. In such cases one speaks of troponin positive unstable angina, also called "minor myocardial damage". Since the ESC / ACC consensus in 2000, this situation is considered a myocardial infarction in the sense of a NSTEMI (Pinger 2019).

Differential diagnosis
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The so-called "big five" of chest pain are:

1. acute coronary syndrome

2. pulmonary embolism

3. aortic dissection

4. boerhaave syndrome (spontaneous rupture of the esophagus after strong vomiting)

5. tension pneumothorax (Herold 2019 / 2020)

Furthermore, the following diseases are possible by differential diagnosis:

1. cardiac chest pain such as

2. non-cardiac chest pain caused by:

  • Pleural or pulmonary causes such as:
    • pulmonary embolism
    • chronic cor pulmonale
    • Pleuritis (respiratory pain)
    • Lung Carcinoma
    • pancoast tumor
    • Pleurodynia due to e.g. Coxsackie B virus infection, Bornholm disease
    • (tension) pneumothorax
  • Diseases of the mediastinum or the aorta such as:
    • Mediastinal tumor
    • Mediastinitis
    • Aortic dissection
    • intramural haematomas of the aorta
  • Diseases of the esophagus and stomach such as:
    • reflux disease
    • Motility disorders of the esophagus such as diffuse esophageal spasm (so-called Barsony Teschendorf syndrome), nutcracker esophagus (hypertensive peristalsis [Siewert 2006]), achalasia
    • Mallory- White- Syndrome (after strong vomiting, tears in the mucosa and/or submucosa of the esophagus)
    • Boerhaave syndrome (spontaneous rupture of the esophagus after strong vomiting)
    • Ventriculous ulcer (Pinger 2019)
  • Diseases of the ribs such as:
    • Tietze Syndrome (pressure dolent swelling of the ribs in the area of the bone-cartilage border)
    • Rib fracture
    • Torso Trauma
  • Diseases in the area of the spinal column such as:
    • ankylosing spondylitis
    • Cervical osteochondrosis
    • BWS- Osteochondrosis
  • Diseases of the nervous system such as:
    • shingles
  • abdominal disorders which may radiate to the thorax such as:
    • Acute pancreatitis
    • Biliary Colic
    • Cholecystitis
    • Roemheld syndrome (postprandial thoracic pain that is independent of CHD)
  • functional chest pain such as:
    • Da- Costa- Syndrome (functional pain in the heart area without organic cause)
    • Genetic diseases such as:
      • Sickle cell anemia: most severe pain in the thorax or upper abdomen in sickle cell anemia (v. Schweinitz 2009)
      • Cardiac neurosis: psychiatric diseases such as heart neurosis (Pinger 2019)

General therapy
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Therapeutic measures with regard to the disease underlying angina pectoris - coronary heart disease - are described in detail at this point. Only a few criteria that are of particular importance for the AP will be highlighted here.

The patient should first be informed in a detailed conversation about the possibilities of personal initiative and personal responsibility.

These include measures to increase the myocardial oxygen supply and to reduce the myocardial oxygen demand. This is possible, for example, by:

  • weight loss
  • atherogenic diet
  • Nicotine Stop
  • Avoid cold air
  • physical fitness training (80 % of the ischemia-inducing heart rate should not be exceeded) etc. (Kasper 2015)

Internal therapy
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The treatment of a stable AP is initially carried out with medication. The most common preparations are

Nitrates: Nitrates have been used clinically for over 125 years. They reduce left ventricular end-diastolic volume and pressure, decrease myocardial wall tension and oxygen demand, also lead to dilatation of epicardial coronary vessels and increase blood flow in collateral vessels (Kasper 2015). Nitrates are used for the therapy of acute angina pectoris attacks and for its prophylaxis.

Short-acting preparations, such as nitroglycerine, are rapidly absorbed through the mucous membranes.

  • Recommended dosage: 1-2 sublingual strokes (1 spray corresponds to 0.4 mg) up to 3 times daily with a minimum interval of 5 minutes between each dose (Kasper 2015).

Long-acting preparations include, for example, isosorbide dinitrate (ISDN).

  • Dosage recommendation: 1 x / d 1 retard preparation with 20 mg - 120 mg oral

Nitrates only have a purely symptomatic effect. Prognosis and lethality are not affected. To counteract the development of tolerance, an 8 to 10 hour nitrate-free interval should be carried out (Herold 2019 / 2020).

Betareceptor blockers: Betareceptor blockers are the first choice for interval treatment of AP (Luippold 2010). The reduction of myocardial oxygen demand is achieved by inhibiting the sympatho-adrenergic increase in heart rate, blood pressure and myocardial contractility. This blockage is most evident during physical exertion, whereas only slight changes are found under resting conditions. Patients with myocardial infarction have been shown to reduce both re-infarction rates and mortality (Kasper 2015). Relative contraindications are:

  • bronchial asthma
  • chronic obstructive pulmonary disease (COPD)
  • severe bradycardias
  • AV- transmission disturbances
  • Raynaud's syndrome
  • history of depressive syndrome

Therapy suggestion: For the treatment of AP, beta1-selective drugs such as Atenolol, Bisoprolol, Metoprolol etc. should be used: Atenolol 1 x 25 mg - 100 mg / d (Stierle 2017)

Calcium channel blockers (former name: calcium antagonists): Long-acting calcium channel blockers such as verapamil, amlodipine etc. are drugs of the 2nd choice, as they only influence the symptoms of AP, but do not improve the prognosis (Luippold 2010). They can be used as initial therapy for:

  • insufficient response to combination treatment with nitrates and beta-blockers
  • intolerable side effects of treatment with beta blockers (such as depression, fatigue, sexual dysfunction, etc.)
  • anamnestically known:
    • bronchial asthma
    • COPD
    • Sinus node disease
    • significant disturbance of the AV node transition
  • prinzmetal angina
  • symptomatic peripheral AVK (Kasper 2015)

Calcium channel blockers lead to cardiac relief by blocking the L (long-lasting) calcium channels and thus reduce the afterload (Herold 2019 / 2020). Short-acting preparations such as unretarded nifedipine only lead to a strong short-term reduction in blood pressure and should be avoided in long-term therapy (Stierle 2017), as they are associated with increased mortality.

In the case of an acute attack of angina pectoris, the oxygen demand is achieved by reducing the preload and postload, thus reducing the symptoms of an attack of angina pectoris (Renz- Polster 2008).

However, the reduction in frequency is only in the range of approx. 5 % (Wehling 2005).

  • Therapy suggestion: e.g. Verapamil 240 mg - 480 mg/d, unretarded in 3 - 4 single doses, retarded in 2 single doses (Stierle 2017)

Operative therapie
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Surgical therapy of angina pectoris is indicated:

Further indications see coronary heart disease

The surgical treatment consists of revascularization of the stenosed vessels. The two standard procedures are percutaneous catheter intervention (PTCA or PCI [percutaneous coronary intervention] in the Anglo-Saxon-speaking world) and coronary bypass surgery (ACVB or CABG [coronary artery bypass graft]) (Stierle 2017).

For detailed information on both procedures see Coronary artery disease

Progression/forecast
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Prognostic influence on the course of an AP:

  • Age
  • Function of the left ventricle
  • Severity and localization of the stenosis (Kasper 2015)

Indicate an increased risk of life-threatening cardiac events:

  • progressive AP
  • unstable AP
  • anamnesis post infarction- AP
  • refractory AP
  • Signs of heart failure
  • survived pulmonary oedema
  • Occurrence of a transient 3rd heartbeat
  • Mitral valve insufficiency
  • reduced ejection fraction
  • Heart enlargement (Kasper 2015)

Literature
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Last updated on: 29.10.2020