Stable angina pectoris I20.9

Angina pectoris which can be regularly triggered by certain stress situations (e.g. physical exertion).

The stable AP is divided into 4 degrees of severity according to the classification of the Canadian Cardiovascular Society (CCS). However, the assignment to the individual degrees of severity is not possible (multiple triggers of an 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).

Special manifestations of stable AP are:

• Walking-through angina:

Here, AP occurs at the beginning of a stressful activity. However, this disappears in the further course of the stress by release of vasodilatory metabolites (Herold 2020).

• Angina nocturna: (also called angina decubitus)

With this form of AP, nightly AP seizures occurring from sleep and/or sudden dyspnoea occur (Herold 2020).

The symptoms occur preferably 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).

• Angina-equivalent:

Here, as a consequence of a diastolic dysfunction in myocardial ischemia, a dyspnea on exertion or a reduced ability to work under stress is observed. Thoracic pain, however, is absent in this clinical picture (Stierle 2017, Angstwurm 2014).

• 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 ischaemias" occur in addition and are 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. It is not known whether these infarctions can be prevented or reduced by drug treatment of silent ischemias (Stierle 2017).

In middle age, women are more often affected by stable AP than men. The high prevalence of functional heart diseases such as microvascular angina is suspected to be the cause (Montalescot 2013).

However, angina pectoris in general affects the male sex far more frequently (approx. 70%). [Kasper 2015]). However, the gender difference in favour of women levels off over the course of life (Stierle 2017), as atherogenic risk factors become more important in women after the onset of menopause (Kasper 2015).

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 pumping function of the affected ventricle (Herold 2020).

The following changes are the cause of AP:

1) Increased coronary resistance:

• this can be caused by main 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
• and by 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.

2. extracoronary factors:

These may be cardiac in nature 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 through:

• 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 2020)

A stable AP can typically be triggered by:

• physical stress (more by isometric than by dynamic)
• emotional strain
• stressful meals
• physical cold (Stierle 2017)

Stable angina pectoris does not worsen under prolonged stress, as it is caused by a stable (fixed) stenosis of the coronary arteries (Stierle 2017).

With an AP, the following occur predominantly

• retrosternal localized pain with radiation in
  • the neck / nape 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)

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)

Here there are rather unspecific symptoms, such as

• Nausea
• Shortness of breath
• Swindle
• Pain in the epigastrium (Herold 2020)

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 a low to medium pre-test probability (see coronary heart disease under "Diagnosis") of coronary heart disease. 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 the conventional invasive heart catheter, the vessel walls and thus non-calcified (so-called soft plaques), mixed and calcified plaques can also be detected. 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 2020)

Laboratory chemistry should determine parameters that accelerate atherogenesis, such as:

• Lipids
• BZ
• Creatinine
• hematocrit
• if necessary also thyroid values T3, T4 and TSH (in case of corresponding anamnestic data, examination findings etc.)
• Urine examination for
  • glucosuria
  • Indications of kidney disease (including microalbuminuria) (Kasper 2015)
• Troponin and CK- MB: Troponin does not increase in stable angina pectoris (Herold 2020). However, patients with a negative CK- MB still show an increase in troponin in about 15%-20%. Such cases are referred to as troponin-positive unstable angina, also known as "minor myocardial damage". Since the ESC / ACC consensus in 2000, this situation has been assessed as a myocardial infarction in the sense of an NSTEMI (Pinger 2019).

Diagnostics

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

Inspection and palpation: When describing the pain during an AP attack, the patient typically clenches his fist in the middle of the sternum - also known as the Levine sign. The hand is placed flat on the sternum or both hands, the fingertips facing each other, are placed laterally on the sternum to indicate the belt-shaped tightness. The sensitivity for cardiac pain is about 80%, the specificity about 49% (Edmondstone 1995)

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 a stable 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 abort criteria, whereas the occurrence of increasing angina pectoris is only a relative abort 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).

For more detailed information see exercise ECG below.

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

Further more detailed information on the differential diagnosis see Angina pectoris

The treatment of a stable AP is usually 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 (Herold 2020)

Nitrates only have a purely symptomatic effect. Prognosis and lethality are not affected. In order to counteract the development of tolerance, a nitrate-free interval of 8 to 10 hours should take place (Herold 2020).

• Beta blockers: Beta blockers are the first choice in interval treatment of AP (Luippold 2010). By inhibiting the sympatho-adrenergic increase in heart rate, blood pressure and myocardial contractility, the reduction of myocardial oxygen demand is achieved. 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
• depressive syndrome in the medical history (Kasper 2015)

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 /day (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 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/day, unretarded in 3 - 4 single doses, retarded in 2 single doses (Stierle 2017)

Surgical therapy of stable angina pectoris is only indicated if drug treatment is no longer sufficient (Kasper 2015).

For detailed information on surgical treatment see coronary heart disease.

The natural course of stable angina pectoris consists of alternating symptomatic and asymptomatic phases, which can, however, be interrupted at any time by an acute coronary syndrome (Montalescot 2013). The prognosis of stable AP is favourable. The estimated annual mortality rate is approx. 0.6 % to 1.4 %, which is below the mortality rate of a mixed population of 1.2 % to 2.4 %.

A worse prognosis is shown by patients with:

• reduced function of the left ventricle and heart failure
• a large number of affected vessels
• proximal coronary stenoses
• a high degree of stenosis
• pronounced ischemia
• more limited functional capacity
• older age
• anamnestically significant depression
• pronounced AP (Montalescot 2013)

1. Angstwurm M et al. (2014) Mediscript StaR The state examination revision booklet for the Hammer Examination: 21 scripts plus registration booklet and 100-day learning plan. Urban and Fischer publishing house 25
2. Dißmann R et al. (2019) German Medical Association (BÄK), Federal Association of Statutory Health Insurance Physicians (KBV), Association of the Scientific Medical Societies (AWMF). National Health Care Guideline Chronic CHD - Long Version, 5th Edition. Version 1. 2019
3. Edmondstone WM (1995) Cardiac chest pain: does body language help the diagnosis? Brit Med J 311: 1660 - 1661
4. Herold G et al (2020) Internal medicine. Herold Publishing House 239
5. Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 96 - 100, 1580 - 1592
6. Kasper D L et al (2015) Harrison's Internal Medicine. Georg Thieme Publisher S 1923 - 1937
7. Lapp H et al (2014) The Cardiac Catheter Book: Diagnostic and interventional catheter techniques. Georg Thieme Publisher S 62
8. Luhmann N (2009) Functional diagnostics of the heart using dual-source computed tomography compared to magnetic resonance imaging: An animal study in pigs. Inaugural dissertation of the Medical Faculty of the Rheinisch-Westfälische Technische Hochschule Aachen
9. Luitppold G et al (2010) Oral examination pharmacology. Thieme Verlag Chapter 1.1.
10. Mahnken A H et al. (2007) Current status of MSCT angiography of coronary arteries. Dtsch Arztebl 104 (31 - 32) A- 2201 / B- 1948 / C- 1882
11. Montalescot G et al (2013) ESC Pocket Guidelines Management of Stable Coronary Artery Disease (CHD) German Society of Cardiology, Heart and Circulation Research (DGK) and the European Society of Cardiology
12. Neurath M F et al (2015) Checklist Anamnesis and clinical examination Thieme Verlag S 503
13. Renz- Polster H et al. (2008) Basic Textbook Internal Medicine: compact - tangible - understandable. Elsevier Urban and Fischer publishing house S 63
14. Pinger S (2019) Repetitorium Kardiologie: For clinic, practice, specialist examination. German medical publisher. S 27 - 77
15. Stierle U et al (2014) Clinical Guide to Cardiology. Elsevier Urban and Fischer 83 - 84, 92, 98 - 100
16. Unger F Et al (1995) Interventions on the heart. Springer Publishing House 14, 38
17. Wehling M et al (2005) Clinical Pharmacology. Thieme Publishing House 77