Monovascular disease I25.11

Last updated on: 05.06.2022

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History
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Synonyms

Coronary single-vessel disease; coronary artery disease; CAD; stenosing coronary sclerosis; ischemic heart disease; degenerative heart disease; coronary artery disease; degenerative heart disease; ischemic heart disease (IHD); coronary artery disease (CAD); coronary heart disease (CHD);

Initial describer

The effects of coronary heart disease in the form of an angina pectoris attack (AP attack) were described by Seneca about 2000 years ago as follows: "Brevis autem valde et procellae similis est impetus, intra horam fere desinit" ("Short but violent and like a storm is the attack. Almost always it is finished within an hour").

(Wagner 1985)

In 1768, two authors, Rougnon and Heberden, independently described the symptoms of an angina pectoris attack. To this day, there is a dispute of priorities regarding the first describer (Wagner 1985).

The first surgical-therapeutic measures in the form of revascularization by balloon dilatation were developed by the German cardiologist Andreas Gruntzig and first performed in 1977 ibid (Lapp 2014).

The first successful bypass surgery was performed by DeBakey and Denis Garrett in Houston in 1964. However, it was not published until 1973 (Mueller 2001). From there, some writings mention Rene Favaloro, who performed the first bypass surgery in Cleveland in 1967 (Gerabeb 2007).

In 1974, the first balloon dilatation - initially called PTCA, later PCI - was performed in Zurich by Andreas Grüntzig (Aumiller 2018).

Definition
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Single-vessel disease is defined as at least 50% stenosis of a single one of the three vascular systems: R. interventricularis anterior, R. circumflexus and A. coronaria dextra. If the stenosis is at least 90%, collaterals are formed (Roskamm 2013).

Occurrence/Epidemiology
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Single-vessel disease is found in

  • < 50 years to 8%
  • 50 - 60 year olds 51
  • > 60 years to 41 % (Sieberer 2021)

There is a gender difference in favor of women with regard to coronary artery disease. No separate data are available regarding single-vessel disease.

However, the gender difference equalizes over the course of life (Stierle 2017), as atherogenic risk factors become more important in women after the onset of menopause (Kasper 2015):

  • 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).

For more details see coronary heart disease

Etiopathogenesis
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The single-vessel disease is caused by arteriosclerosis. The causes for the occurrence of arteriosclerosis are very different. The main factors would be:

- LDL- cholesterol- increase > 160 mg/dl

- HDL- cholesterol- decrease < 40 mg/dl:

- for men ≤ 40 mmol / l

- for women ≤ 50 mmol / l

- arterial hypertension with values > 140 / 90 mmHg

- Diabetes mellitus with HbA1c values > 7%.

- use of tobacco

- familial disposition (in first-degree family members, the occurrence of an infarction occurs before the age of 55 years in men or before the age of 65 years in women)

- Age ≥ 55 years in men or ≥ 65 years in women (Herold 2022).

- Obesity with an abdominal circumference of > 94 (m) or > 80 (w)

- atherogenic diet

- low social status

- lack of physical activity

- Lipid metabolic disorders, e.g., hypertriglyceridemia ≥ 150 mg/dl, Lp (A) elevation

- Glucose tolerance disorder with fasting BG values ≥ 100 mg/dl.

- Hyperfibrinogenemia ≥ 3.5 g/l

- inflammatory conditions in CHD patients

- early onset of menopause

- hyperfibrinogenemia with values > 3.5 g / l

- prolonged stay under increased exposure to particulate matter

- genetic changes (Herold 2022)

The presence of certain diseases also plays a role such as:

- lupus erythematosus

- rheumatoid arthritis

- antiphospholipid syndrome (Pinger 2019)

Pathophysiology
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Coronary stenosis initially results from damage to the coronary endothelium.

Due to the damage of the endothelium, the surface of the inner vessel wall becomes irregular and fibromuscular plaques are deposited, leading to stenosis of the coronaries (Greten 2010). This stenosis causes a mismatch between oxygen demand and oxygen supply in the area of the respective myocardium supplied by the stenosed vessel (Lapp 2014).

In addition, the damage to the endothelium causes a regulatory disturbance of coronary vasodilation or vasoconstriction. As a result, the endothelium is no longer able to respond to physical stress by dilating the coronaries. Instead, it causes a constriction of the vessels (Greten 2010).

Clinical features
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The initial manifestation of coronary artery disease is:

  • in 55 % as angina pectoris
  • in 25% as acute coronary syndrome with its 3 entities:
    • unstable angina pectoris without troponin elevation
    • NSTEMI = non- ST-segment elevation with troponin elevation
    • STEMI = ST-segment elevation myocardial infarction with troponin elevation and persistent ST-segment elevation after 20 min.
  • in 20 % as sudden cardiac death (Herold 2022)

In single-vessel disease, angina pectoris attacks occur in approximately 14.7% of cases and in Z. n.non-transmural myocardial infarction in 46.7% (Roskamm 2013).

These attacks can be triggered by physical stress (isometric rather than dynamic [Stierle 2017]), psychological stress, by cold external temperatures and food intake (so-called postprandial angina).

They are predominantly retrosternal in location and may radiate to the neck, mandible, teeth, shoulder, left (and also in right) arm to the ulnar fingertips (Herold 2020).

Patients complain of dull, pressing pain with thoracic tightness (cardiac stabbing argues against angina). The pain usually swells (crescendo character) and is never respiratory or motion related (Stierle 2017).

The attacks usually subside by rest after about 5-15 min or by administration of nitroglycerin after 1-2 min (Herold 2022).

Diagnostics
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First, the typical symptoms of angina pectoris should be recorded anamnestically. Although these make the diagnosis probable, the absence of symptoms does not exclude single-vessel disease, since, for example, >50% of ischemic attacks are indolent in diabetics and women often have atypical symptoms (Herold 2022).

From there, a "pretest probability" regarding stenosing CHD available at www.escardio.org is recommended (Herold 2022).

Inspection and palpation

- Levine sign: patient clenches fist in front of chest when describing pain (Stierle 2017).

Resting ECG

The resting ECG shows - even in severe CHD - in up to 50% of cases no changes. In these cases, changes only occur during or after an infarction (Herold 2020).

Patients with coronary angiographic evidence of single-vessel disease showed clear ischemic signs on the ECG in only 53% of cases of NSTEMI (Sanaani 2017).

Long-term ECG

According to ESC 2013, the indication for a long-term ECG is exclusively in the presence of Prinzmetal's angina (Pinger 2019).

Stress ECG

Sensitivity is only 36-50% in single-vessel disease, in contrast to multivessel disease (Schunkert 2013).

Stress echocardiography

In this examination, the sensitivity of single-vessel disease is significantly higher at 75-80% (Schunkert 2013).

Imaging
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Nuclear medicine diagnostics

Nuclear medicine diagnostics in combination with stress tests include:

- Myocardial perfusion scintigraphy (MPS)

- Single photon emission computed tomography (SPECT)

- Positron emission tomography (PET)

(Herold 2020) For more details see Coronary artery disease.

Coronary angiography

Indications for coronary angiography according to ESC 2013 are:

- Recommendation grade / Evidence grade I / C:

This recommendation grade includes

- Patients with angina pectoris CCS III or likely to be at high risk of events, especially if there is an inadequate response to medical treatment

- Patients at high risk according to the non-invasive risk evaluation, provided that revascularization is likely to improve prognosis. In this patient group, coronary angiography is indicated even if there is little or no symptomatology of symptoms.

- Grade of Recommendation / Level of Evidence IIa / C:

This group includes patients with incongruent or conflicting findings in whom risk evaluation should be performed. (Stieles 2019)

For more details, see Coronary angiography.

Differential diagnosis
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The differential diagnosis of single-vessel disease is very extensive and corresponds to that of CHD (see d.).

A single-vessel disease is most likely NOT present if one of the following questions is answered with yes:

- Change in pain on deep inhalation or exhalation?

- Change in pain with thoracic flexion or torsion?

- Does the pain increase when pressing on specific areas of the thorax and/or abdomen?

- Has the pain been present for days or weeks and does it remain unchanged during usual activities of daily living?

- Does the pain decrease with physical activities? (Stierle 2017)

General therapy
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In the case of single-vessel disease, different therapeutic approaches can be found. Treatment or progression of stenosis can be done by:

1. elimination of risk factors such as hypercholesterolemia, arterial hypertension, diabetes mellitus, nicotine abuse, lack of physical activity, obesity (Pinger 2019).

2. conservative therapy (see below).

3. Surgical therapy (see below).

Surgical therapy involves revascularization for symptomatic reasons, in contrast to multivessel disease, in which revascularization is indicated for prognostic reasons (Siegenthaler 2005).

For detailed information, see Coronary artery disease.

Internal therapy
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Drug treatment involves attempting to use medications to

  • Reduce myocardial oxygen demand by influencing:
    • decrease contractility, heart rate and afterload
  • improving myocardial oxygen supply by.
    • Reduction of vascular tone in the coronary arteries
    • prolongation of diastolic duration (reduction of frequency)
    • lowering left ventricular end-diastolic pressure (preload)
  • reduce the risk of thrombotic coronary occlusion
  • lower LDL cholesterol

(Renz- Polster 2008)

The following drugs are used for this purpose:

1. beta blockers

2. calcium channel blockers (calcium antagonists)

3. ACE inhibitors

4. platelet aggregation inhibitors

5. cholesterol synthesis inhibitors (statins)

6. nitrates (Herold 2022)

For detailed information on drug treatment, including dosage recommendations, see Coronary artery disease.

Operative therapie
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In coronary single-vessel disease, the minimally invasive surgical technique (MIS) was shown to be equivalent to more invasive surgical techniques such as median sternotomy in a 2000 study byGulielmos et al.

Kasper (2017) recommends percutaneous coronary intervention (PCI, formerly also called "PTCA" = "percutaneous transluminal coronary angioplasty") for symptomatic single-vessel disease with normal left ventricular function.

Depending on the morphology, ostium stenoses of RIVA and RCX, occlusions or poorly accessible stenoses, and bifurcation stenoses are suitable to a limited extent (Bonzel 2009).

For detailed information on PCI, see "Coronary artery disease."

The remaining degree of stenosis after PCI is <50%, and the immediate success rate is 95%. Complications in the form of MACCE (major adverse cardiac and cerebrovascular events [Ziemer 2010]) such as myocardial infarction, insult, death occur in < 0.5% in stable angina and in 1% in unstable angina (Herold 2022).

Progression/forecast
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The prognosis of single-vessel disease is usually not unfavorable. The only exception is proximal RIVA stenosis due to its strategic importance (Eichstädt 2013).

Complication rates for PTCA are < 1% and success rates > 90% (Eichstädt 2013).

After PTCA, 79% of patients no longer have any cardiac symptoms after 10 years of observation (Dörfler 2015).

Without revascularization, the annual mortality rate for single-vessel disease is 3%-4% (Herold 2022).

Literature
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Last updated on: 05.06.2022