Coronary heart diseaseI25.9
Synonym(s)
HistoryThis section has been translated automatically.
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. It is almost always terminated within an hour".
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).
DefinitionThis section has been translated automatically.
Coronary artery disease (CAD) is defined - from an angiographic point of view - as the presence of a significant stenosis of at least one epicardial coronary artery (Pinger 2019).
CHD can manifest clinically as:
1. asymptomatic CHD
- silent ischaemia
2. symptomatic CHD
- chronic coronary syndrome = CCS (formerly also referred to as "stable CHD" [Stiles 2019])
- stable angina pectoris (reversible myocardial ischemia causes thoracic pain)
- Acute coronary syndrome (ACS):
- ST- elevation myocardial infarction (STEMI = ST- segment- elevation myocardial infarction with persistent ST- elevation of > 20 min. and increase in troponin
- Non-ST elevation myocardial infarction (NSTEMI = Non-ST segment elevation myocardial infarction with increase in troponin, but without ST segment elevation)
- unstable angina pectoris (without increase in troponin)
4. signs of heart failure due to ischemic heart muscle damage
5. cardiac arrhythmia
6. sudden cardiac death
ClassificationThis section has been translated automatically.
According to the clinical course, a distinction is made between:
- Chronic CHD
- Acute coronary syndrome
- Special forms such as
- Syndrome X (angina pectoris symptoms, typical changes in the ECG, but the coronary arteries are completely unremarkable)
- Prinzmetal- Angina (coronary artery spasm) (Stierle 2017)
Occurrence/EpidemiologyThis section has been translated automatically.
In industrialized countries, CHD causes more secondary diseases, deaths and economic costs than any other disease (Kasper 2015). Coronary heart disease is one of the most important widespread diseases, with a lifetime prevalence of 9.3 % for the 40-79 year olds. In Germany alone, coronary heart disease causes 14 % of all deaths. This makes CHD the most common cause of death in industrialized countries.
There is a gender difference in favour of women with regard to angina pectoris, but this will level off in the course of life (Stierle 2017), as the 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)
Men are 50% likely to develop CHD during their lifetime, women 32% (Pinger 2019).
The initial manifestation of coronary heart disease is:
- 55% are diagnosed as angina pectoris.
- at 25% as acute coronary syndrome
- at 20% as sudden cardiac death
Associated non-cardiac diseases:
- migraine is present in about 25% of patients
- Raynaud's phenomenon in about 33 % (Stierle 2017)
EtiopathogenesisThis section has been translated automatically.
Pathophysiology
Coronary stenosis initially results from damage to the coronary endothelium. This is triggered by certain risk factors or certain noxae (see below "Causes").
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).
Pathogenesis; Pathogenetically, both increased coronary resistance and extracoronary factors play a role.
1. increased coronary resistance:
- this can result from vasal major factors such as:
- Macroangiopathy > 90%.
- Microangiopathy (small vessel disease)
- Coronary spasm (can be triggered by cocaine, among other things)
- Coronary anomalies
- arteriovenous coronary fistulas
- congenital myocardial bridges
- and by myocardial additional factors such as:
- cardiac 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 cardiac work, an angina pectoris attack occurs.
2. extracoronary factors:
- These may be cardiac such as:
- hypertrophic cardiomyopathy
- Aortic valve defects (e.g., due to severe left ventricular hypertrophy in aortic valve stenosis [Kasper 2015]).
- Arrhythmias
- and extracardiac such as by:
- Increased oxygen demand in e.g. fever, hyperthyroidism, physical exertion, etc.
- Reduced oxygen supply, e.g., in anemia, high altitude, lung diseases, sleep apnea syndrome, CO poisoning, etc.
- increased viscosity of blood in e.g. erythropoietin- doping, hyperfibrinogenemia, multiple myeloma, polycythemia vera etc (Herold 2019 / 2020).
Causes: The causes for the occurrence of premature atherosclerosis are very diverse. The main factors would be:
- LDL- cholesterol- elevation > 160 mg/dl.
- HDL- cholesterol- lowering < 40 mg/dl.
for men ≤ 40 mmol / l
for women ≤ 50 mmol / l
- arterial hypertension
- Diabetes mellitus with HbA1c values > 7%.
- use of tobacco
- familial disposition (in first-degree family members, the occurrence of infarctionbefore the age of 55 years [m] or before the age of 65 years [w])
- Age > 55 years (m) or > 65 years (w) (Herold 2019 / 2020).
However, other factors also play a role such as:
- Obesity with an abdominal circumference of > 94 (m) or > 80 (w)
- atherogenic diet
- low social status
- lack of physical exercise
- Lipid metabolic disorders e.g. hypertriglyceridemia ≥ 150 mg/dl.
- Impaired glucose tolerance with fasting BG values ≥ 100 mg/dl.
- Hyperfibrinogenemia ≥ 3.5 g/l
- Inflammatory conditions in CHD patients
- Following thoracic radiotherapy
- After heart transplantation
- obstructive sleep apnea
- prolonged stay under increased fine dust load
- genetic alterations (so far 20 gene regions are known to be associated with an increased risk of myocardial infarction )
- etc (Herold 2019 / 2020).
Presence of certain diseases such as:
Etc (Pinger 2019).
In case of an infarction event before the age of 30, the following causes should be excluded in particular:
- familial lipid metabolism disorders
- Thrombophilia (e.g. due to an antiphospholipid syndrome)
- hypothyroidism and associated hypercholesterolemia
- Vasculitides such as:
- panarteritis nodosa
- Kawasaki syndrome
- Takayasu arteritis
- Anomalies of the coronaries
- Diseases of the coronaries (e.g. after surgery of congenital vitias)
- Drug abuse of:
- Cocaine
- marijuana
- Hyperviscosity syndrome such as:
- multiple myeloma
- polycythaemia vera
- essential thrombocythemia (Herold 2019 / 2020)
Clinical featuresThis section has been translated automatically.
The main symptom of CHD is attacks of angina pectoris, also called stenocardia.
These attacks can be triggered by physical stress (isometric rather than dynamic [Stierle 2017]), psychological stress, cold outside temperatures and food intake (so-called postprandial angina pectoris).
They are predominantly retrosternal and can radiate into the neck, lower jaw, teeth, shoulder, left (and also right) arm up to the ulnar fingertips [Herold 2019 / 2020].
Patients complain of dull, oppressive pain with a feeling of thoracic tightness (heart stabbing speaks against angina pectoris). The pain usually swells (crescendo character) and is never dependent on breathing or movement (Stierle 2017).
The attacks usually subside by resting after 5 - 15 minutes and by the administration of nitroglycerine after 1 - 2 minutes (Herold 2019 / 2020).
Typical angina pectoris seizures can be absent in:
- - diabetes mellitus
- - Renal insufficiency
- - Women
- - older patients > 75 years
- - Currently undergoing heart surgery
- - For heart transplantation
Often these patients only complain about unspecific symptoms such as
- - nausea
- - Shortness of breath
- - Swindle
- - Pain in the epigastrium (Herold 2019 / 2020)
Sometimes, however, patients with a CHD also present with signs of heart failure or cardiomegaly for the first time. In these patients typical AP-attacks are missing. However, there are almost always anamnestically unspecific symptoms, such as general weakness, poor performance, depression (Kasper 2015).
ImagingThis section has been translated automatically.
Nuclear medicine diagnost ics: Nuclear medicine diagnostics in combination with stress testing include:
- Myocardial perfusion scintigraphy (MPS)
- Single photon emission computed tomography (SPECT)
- Positron emission tomography (PET) (Herold 2019 / 2020)
As part of the initial diagnosis, scintigraphy is recommended in the following patients with moderate and high suspicion of CHD:
- in the case of a previously unremarkable stress ECG
- in patients with a contraindication for a stress ECG.
However, it is not recommended as a screening procedure by the ESC 2011 (Pinger 2019).
MPS and SPECT are performed with 99m technical-labeled perfusion markers such as sestamibi or tetrofosmin. There is irreversible loss of activity in the scarred areas of the myocardium. In the areas that are ischemic under stress, the reduction in activity is reversible. If ischemia is detected in 10% of the total myocardium in the left ventricle (corresponding to ≥ 2 of the total 17 segments of the heart), there is a high risk of cardiac events.
PET: Positron emission tomography (PET) represents a noninvasive study of myocardial perfusion and viability. By using isotopes, it is possible to differentiate between a
- normal myocardium
- hibernating myocardium (myocardium in hibernation; in this case there is an increased uptake of FDG [labeled sugar fluorodeoxyglucose] in regions showing decreased blood flow)
- stunned myocardium (regional dysfunction is found with normal blood flow)
- necrotic myocardium (reduction in blood flow and metabolism).
These stress tests to detect ischemia have high prognostic significance. If they are completely unremarkable, the risk of infarction or cardiovascular death in the next 2 - 3 years is hardly increased (Herold 2019 / 2020).
Echocardiography: Routine annual follow-up echocardiography is not recommended by the ESC. The figures of diagnostic value vary widely in the literature and are given as follows:
- Stress echo with dynamic stress:
Sensitivity is reported to be 80%-85%, specificity ranges from 80%-88%.
- Stress MRI with dobutamine:
Sensitivity is reported as 79 % - 83 %, specificity ranges from 82 % - 86 %.
- Stress MRI with vasodilator:
Sensitivity is reported as 67% - 94%, specificity ranges from 61% - 85%.
- SPECT with dynamic stress:
Sensitivity is reported as 73% - 92%, specificity ranges from 63% - 87%.
- SPECT with vasodilator:
Sensitivity is reported as 90% - 91%, specificity ranges from 75% - 84% (Pinger 2019).
Stress echocardiography can be performed in patients
- with contraindication for the stress ECG
- for vital signs diagnosis before revascularization
- To assess the functional relevance of a stenosis before PCI or ACVB.
- for evaluation of a suspected residual stenosis after PCI
- for stratification of the risk (Pinger 2019)
Coronary CT angiography (CCTA): A CCTA allows noninvasive 3-D reconstruction of the coronary vessels. For the detection of a 50% stenosis, the sensitivity is 94% and the specificity is 87%. The positive predictive value is 88%, and the negative predictive value is 93% (Pinger 2019).
Cardio CT - Multislice computed tomography (MSCT) / dual-source computed tomography (DSCT): With the clinically introduced MSCT, up to 64 slices can be acquired simultaneously. Limitations exist so far especially in case 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 used since 2006 (Luhmann 2009). Both examination methods are suitable for patients with low to moderate pretest probability of CHD. The sensitivity is close to 100%, as is the negative predictive value. Stents and coronary bypasses as small as 3 mm can be assessed. In contrast to conventional invasive cardiac catheterization, it 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 cardiac catheter with 5 mSv - 12 mSv.
The limitation of these methods - compared to invasive cardiac catheterization - are found in:
- pronounced cardiac arrhythmias
- a calcium score of > 400 (Herold 2019 / 2020)
MR angiography: MR angiography plays practically no role in the visualization of coronary morphology because of its poor spatial resolution. However, to detect myocardial perfusion defects, stress MRI - similar to myocardial scintigraphy - is suitable.
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 at probable high risk of events, especially in case of inadequate response to medical treatment.
- Patients at high risk according to the non-invasive risk evaluation, if 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.
No indications are:
- lack of willingness of the patient to undergo revascularizing therapy
- in the absence of therapeutic consequences
- In patients with high comorbidity, if the risk of coronary angiography is greater than the benefit from confirming the diagnosis (Herold 2019 / 2020).
Absolute contraindication: An absolute contraindication exists in the case of
- general rejection of any revascularization that may be required
- Lack of prospect of improvement in quality of life or life expectancy (Pinger 2019).
Relative contraindication are:
- Presence of active bleeding
- severe coagulopathy
- acute and previously untreated infection
- existence of an unexplained fever
- decompensated heart failure
- pulmonary edema
- acute renal failure
- acute apoplexy
- severe anemia
- manifest hyperthyroidism
- uncontrolled hypertension
- digitalis intoxication
- severe symptomatic electrolyte imbalance
- an anaphylactic reaction to contrast media proven by documentation
- presence of a severe, life-limiting illness
- lack of patient cooperation due to mental or systemic illness (Pinger 2019).
Complications and risks of coronary angiography:
- INR should be < 2.0: However, it has been shown that no increased bleeding complications occurred when interruption of oral anticoagulation was omitted.
- Metformin: Metformin administration should be interrupted no later than the day of the study. Continue therapy only after creatinine levels are stable (this is usually the case after 48 h).
- Anaphylaxis: The risk of recurrence of anaphylaxis can be reduced by H1 and H2 blockers and by cortisone.
- Eriprocedural apoplexy: To date, there is no established therapy for eriprocedural apoplexy. In the vast majority of cases, this is likely to be an embolism due to arteriosclerotic plaques. CCT to exclude bleeding should be performed in all cases (Pinger 2019).
- The mortality of the procedure is on average 0.15%: mortality for an emergency indication is higher than that for an elective procedure (Herold 2019 / 2020). In the vast majority of cases, the causes of mortality are a consequence of acute myocardial infarctionor arise from pump failure of the left ventricle (Lapp 2014).
- The occurrence of myocardial infarction is 0.8%: the cause may be dissection of the ostium or coronary emboli (due to air, atheroma, thrombi) (Lapp 2014).
- Triggering ventricular fibrillation 0.4%: Ventricular fibrillation can be triggered by a forceful injection of contrast into a small right coronary artery or proximal side branch (Lapp 2014) (Stierle 2017).
- Short-term asystole or bradycardia 0.06%: These can be triggered during contrast injection into the right coronary artery. Since in most cases they last only a few seconds, no further therapeutic measures are required in this case (Lapp 2014).
- Cerebrovascular ischemia / emboli 0.4%: These are caused by wall arterial thrombi, thrombi on the catheter or guidewire, or air emboli (Lapp 2014).
- Vascular complications in 0.3% (Stierle 2017).
- Occurrence of aneurysm spurium or AV fistulae at the puncture site.
- Vascular spasm: Spasm may occur during probing of both vessels, but preferably in the area of the right coronary artery. Because the spasm may be catheter-induced, correction of the catheter should follow sublingual or intracoronary application of 0.4 - 1.0 mg nitroglycerin.
- Acute renal failure
- Hematoma (Herold 2019 / 2020).
Vascular access routes: Different access routes are available for coronary angiography. The two most common routes are radial artery access and femoral artery access.
- Access via the radial artery (so-called modified Sones technique [Herold 2019 / 2020]).
The advantages of the radialis approach are:
- local complications such as inflammation, compression of the nerves, AV fistulas and bleeding are much less frequent
- compression time is shorter due to the small vessel diameter and anatomical location
- vagal reactions are less frequent
- the patient can be mobilized immediately
- there are advantages in the selective visualization of bypasses of the internal mammary artery. However, if bilateral mammary bypasses are to be visualized, the femoral approach is usually used.
The disadvantages are that:
- in older and/or obese patients, it is not uncommon to find highly tortuous vascular courses
- calcifications of the upper extremity occur more frequently
- spasms of the artery can occur
In addition, the radial artery is often difficult to puncture for the less experienced examiner (Gotthardt 2017).
Relative contraindications to radial access include:
- single-arm patients
- dialysis patients with a shunt in place
- Vasculitides
- M. Raynaud's disease
- pathological Allen test for the detection of circulatory disorders (however, this test has lost its importance in the meantime)
- multiple bypasses with simultaneous need to probe a contralateral internal mammary bypass
- Existing need to use large drill heads for rotablation (Gotthardt 2017).
- Access via the femoral artery (so-called Judkins technique [Herold 2019 / 2020]).
Here, the right femoral artery is predominantly punctured.
The advantages are
- technically simple and quickly accessible puncture.
The disadvantages of femoral puncture are
- subsequent prolonged immobilization of the patient
- often - despite the use of current occlusion systems - additional manual compression required
- occurrence of extensive hematomas
- risk of infection of the puncture site with subsequent abscessing
- Formation of an AV fistula,
- pressure damage of the femoral nerve (due to the anatomical proximity)
- Formation of pseudo-aneurysms, etc. (Gotthardt 2017).
In all patients - according to the current ESC- guideline - the radial access route is indicated as the primary route, since in both the RIVAL- study (RadIal Vs femorAL Access for Coronary Interventions [Jolly 2011]) and the RIFLE STEACS- study (Radial Versus Femoral Randomized Investigation in ST-Elevation Acute Coronary Syndrome [Romagnoli 2011]) a significant difference with regard to mortality (5.2% vs. 9.2%, p = 0.020) and bleeding complications (7.8% vs. 12.2%, p = 0.026) in favor of radial access was demonstrated.
The following diagnostic procedures can be additionally performed during coronary angiography:
- Coronary angioscopy (to assess vessel morphology and any plaques present).
- intravascular ultrasound (also used to assess vessel morphology and the presence of plaques)
- optical coherence tomography (OCT provides high resolution of luminal and intramural vascular structures)
- intracoronary Doppler flow measurement to determine the fractional flow reserve = FFR (a hemodynamically effective coronary stenosis exists from an FFR < 0.80 with a specificity of 100%)(Herold 2019 / 2020)
DiagnosisThis section has been translated automatically.
First, the typical symptoms of angina pectoris should be recorded anamnestically. Although these make the diagnosis probable, absence of symptoms does not rule out CHD.
A "pretest probability" is possible at www.escardio.org.
According to ESC guidelines, values:
- < 15 % probability no further diagnosis is required
- between 15 % and 85 % a stress ECG(meanwhile losing importance in favor of imaging) and imaging should be performed
- > 85 % the presence of CHD is considered confirmed and a cardiac catheterization should be performed.
The 10-year cardiovascular risk can be calculated with the help of calculators, e.g. by:
- 1. PROCAM- Risk calculator (PRospektiven CArdiovaskulären Münsterstudie) (www.cmd-taskforce.org/risk-assessment/). This is used to make statements about the probability of fatal and non-fatal cardiovascular events. Evaluation of the test:
- A high risk exists with multiple risk factors. In this case, the 10-year risk for lethal and non-lethal events is > 20%.
- A medium risk is present with 2 risk factors. The 10-year risk for lethal and non-lethal events is 10% - 20%.
- A low to moderate risk is present with 1 risk factor. The 10-year risk for lethal and non-lethal events is < 10 %.
- 2 ESC risk calculator score (www.scores.bnk.de/esc.html). With this score, statements can be made about the probability of fatal cardiovascular events.
A very high risk of fatal cardiovascular events of ≥ 10% exists with:
- documented cardiovascular disease such as: such as post-myocardial infarction, cerebral insult, acute coronary syndrome (ACS), coronary arterial bypass grafting (CABG); peripheral arterial disease (PAVD)
- Existing diabetes mellitus with ≥ 1 risk factor and / or end-organ damage.
- Severe chronic renal dysfunction with an eGFR: < 30 ml/min/1.73m3.
A high risk of fatal cardiovascular events of 5%-10% is associated with:
- diabetes mellitus without risk factors and without end-organ damage
- moderate chronic renal dysfunction with an eGFR between 30 - 59 ml/min/1.73m3
- a moderate risk of fatal cardiovascular events is 1% - 5%.
- a low risk of fatal cardiovascular events is < 1% (Herold 2019 / 2020).
- 3. CARRISMA- Risk Calculator (CARdiovascular RIsiko-MAnagement in Primary Prevention) (www.carrisma-pocket-ll.de). This software, developed by Prof. Helmut Gohlke, Bad Krozingen, takes into account BMI, number of cigarettes smoked, and physical activity.
- 4. Framingham risk calculator for the USA (www.nhlbi.nih.gov) (Herold 2019 / 2020).
The timing of the effects of CHD are shown in the so-called "ischemic cascade".
1. perfusion reduction
This can be detected by myocardial scintigraphy or adenosine stress MRI.
2. metabolic disturbance (detectable in a PET)
3. relaxation disorders (assessable by echocardiography)
4. contractile dysfunction (detectable in stress echo or dobutamine stress echo)
5. increase of filling pressure (can be detected in the right heart catheter)
6. ECG changes (these can be seen in the stress ECG)
7. angina pectoris (to be ascertained by history) (Pinger 2019)
Inspection and palpation
- Levine sign: patient clenches fist in front of chest when describing pain (Stierle 2017).
Resting ECG: The resting ECG shows no changes - even in severe CHD - in up to 50% of cases. These occur in these cases only at or after an infarction (Herold 2019 / 2020). In angina pectoris attack is also found in about 50% (Pinger 2019) no changes. If so, there is ST-segment elevation, which may be followed by ST-segment depression (Stierle 2014). However, all types of disturbances in depolarization or repolarization may occur, as the specificity of the resting ECG is low (Pinger 2019). Under treatment with a calcium antagonist, the ST- pathway normalizes (Stierle 2014). Typical ECG- changes, such as new ST- T- distance change, development of pathological Q- jags, new left bundle branch block [Stierle 2017]) are found in STEMI. However, these changes should - if possible - always be compared with a pre-ECG (Herold 2019 / 2020).
Long-term ECG: In the long-term ECG, silent ischemia can be diagnosed by horizontal or descending ST depression ( > 1 mm for > 1 min duration) under everyday conditions (Pinger 2019). It is also possible to record nocturnal angina pectoris attacks or nocturnal silent ischemias (Herold 2019 / 2020). However, it is not possible to make prognostic statements on endpoints, such as the occurrence of unstable angina, myocardial infarction or cardiac death, by the frequency and duration of ischemic episodes according to the TIBET - study (Total Ischaemic Burden European Trial). (Dargie 1996). According to ESC 2013, the indication for a long-term ECG is exclusively in the case of V. a. a Prinzmetal ang ina (Pinger 2019).
Exercise ECG: In cases of suspected CHD, an exercise ECG (ergometry) is still part of the initial diagnosis. However, it is becoming less and less important due to the ever-evolving imaging. According to the ESC of 2013, sensitivity is reported to be 45%-50%, while specificity is between 85%-90% (Pinger 2019). It can only be performed under a resuscitation standby (defibrillator), as ergometry carries the following risks:
- 1 to 2 serious adverse events per 10,000 examinations.
- the risk of ventricular fibrillation is 1: 15,000
- the risk of death is 1: 42.000 (Herold 2019 / 2020)
The stress ECG can be performed differently:
- Symptom-limited: In this case, the load is increased as long as it is tolerated by the patient.
- Heart rate limited: The suboptimal load is performed until a certain heart rate limit is reached (220 - life years - 10% to 15% or under therapy with beta-blockers: 167 - 0.7 x life years and also - 10% to 15% ) (Pinger 2019).
The test is considered pathological if an ST- stretch depression of at least 0.1 mV is measured between 60 ms - 80 ms after the J- point (transition from the QRS- complex to the ST- stretch) (Pinger 2019). If an ST-segment depression of ≥ 0.1 mV already exists at rest, a stress ECG should not be performed. Medication with digitalis, quinidine, and antidepressants may cause a drug-induced decrease in ST segment. If justifiable, these medications should be discontinued before the stress ECG (Herold 2019 / 2020), otherwise the stress ECG is not used for the diagnosis of CHD due to insufficient specificity (Pinger 2019).
Absolute contraindications for a stress ECG are:
- acute myocardial infarction ( ≤ 2 days)
- high-grade main stem stenosis of the left coronary artery (Herold 2019 / 2020).
- persistent unstable angina pectoris
- Hemodynamically effective arrhythmias that are as yet uncontrolled
- severe symptomatic aortic valve stenosis
- severe heart failure in stage NYHA III and IV (Herold 2019 / 2020)
- decompensated heart failure
- deep vein thrombosis
- severe pulmonary hypertension (Herold 2019 / 2020)
- pulmonary infarction
- pulmonary embolism
- acute myocarditis
- acute pericarditis
- active endocarditis
- acute aortic dissection
- significant aneurysm of the aorta or heart (Herold 2019 / 2020)
- existing physical inability to adequately and safely perform the test (Pinger 2019).
Relative contraindications are:
- non-severe main stem stenosis (Herold 2019 / 2020) or its equivalent
- moderate to severe valvular stenosis with unclear relationship to symptoms
- prolongation of QT time (increased risk of ventricular fibrillation [Herold 2019 / 2020])
- uncorrected diseases such as
- Anemia
- Electrolyte disturbances
- hyperthyroidism
- severe arterial hypertension with values at rest of systolic > 200 mmHg and diastolic > 110 mmHg
- Tachyarrhythmia with uncontrolled ventricular rate
- Atrial fibrillation with uncontrolled ventricular rate
- Bradyarrhythmia (Herold 2019 / 2020)
- acquired high-grade or complete AV block
- HOCM with a pronounced resting gradient
- Inability of the patient to cooperate (e.g., due to mental retardation, etc.) (Pinger 2019).
Absolute discontinuation criteria are:
- ST- elevation of ≥ 1 mm with the exception of leads with Q- jag (as a sign of a previous old infarct), AVL, V1 and AVR (Pinger 2019).
- ST- decrease of ≥ 0.3 mV (Herold 2019 / 2020).
- Blood pressure drop > 10 mmHg under increasing stress accompanied by signs of ischemia (Pinger 2019)
- Hypertensive dysregulation with RR- values of systolic > 230 mmHg or diastolic ≥ 115 mmHg.
- Absence of systolic blood pressure rise
- occurrence of polymorphic extrasystoles
- Occurrence of volleys
- Occurrence of a higher-grade AV block
- Occurrence of bundle branch block
- Signs of reduced perfusion such as pallor, cyanosis, etc.
- Occurrence of moderate to severe angina pectoris
- Central venous symptoms such as dizziness, ataxia, presyncope, etc.
- Arrhythmias and / or ventricular tachycardias that are not compatible with the required cardiac output, such as sustained ventricular tachycardias > 30 sec (Herold 2019 / 2020)
- ECG or blood pressure monitoring are no longer warranted
- The patient's wish (Pinger 2019).
Relative discontinuation criteria are:
- horizontal or descending ST- decrease of > 2 mm measured 60 ms - 80 ms after the J- point in a patient with ischemia
- Blood pressure drop of > 10 mmHg under increasing stress, even without signs of ischemia (Pinger 2019)
- Occurrence of couplets (Herold 2022).
- increasing angina pectoris
- Fatigue
- shortness of breath
- Sweating
- muscle cramps
- muscle pain
- Arrhythmias that may compromise hemodynamic stability with increasing complexity (does not apply to ventricular tachycardias)
- Occurrence of bundle branch block indistinguishable from ventricular tachycardia
- Increase in blood pressure > 250 / > 115 mmHg (Pinger 2019).
Differential diagnosisThis section has been translated automatically.
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 severe vomiting)
5. tension pneumothorax
CHD is most likely NOT present if any of the following questions are answered yes:
- Change in pain on deep inhalation or exhalation?
- Change in pain on thoracic flexion or rotation?
- 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)
Otherwise, differential diagnosis of the following diseases are possible:
1. cardiac chest pain such as.
- angina pectoris
- Acute coronary syndrome
- Dressler syndrome (so-called postmyocardial infarction syndrome)
- hemodynamically effective tachycardia
- hypertensive crisis
- aortic vitium(aortic valve insufficiency or stenosis)
- mitral valve prolapse
- hypertrophic cardiomyopathy
- Perimyocarditis
- Stress taco-tsubo cardiomyopathy
- Anomalies of the coronaries
- Vasculitides such as:
- Panarteritis nodosa
- Takayasu arteritis
- Kawasaki syndrome (Herold 2019 / 2020)
- Spontaneous coronary artery dissection (affects between 66%-80% women; in one-third, dissection occurs postpartum)
- Bland- White- Garland syndrome (the left coronary artery originates in the main trunk of the pulmonary artery [Apitz 1998]) (Pinger 2019)
2. non-cardiac chest pain caused by:
- pleural or pulmonary causes such as:
- Pulmonary embolism
- chronic cor pulmonale
- Pleurisy (respiratory pain)
- Lung carcinoma
- Pancoast tumor
- pleurodynia due to e.g. Coxsackie B virus infection, Bornholm disease
- (Tension) pneumothorax
- Diseases of the mediastinum or aorta such as:
- Mediastinal tumor
- Mediastinitis
- aortic dissection
- intramural hematoma of the aorta
- Diseases of the esophagus and stomach such as:
- reflux disease
- esophageal motility disorders such as diffuse esophageal spasm (Barsony-Teschendorf syndrome), nutcracker esophagus (hypertensive peristalsis [Siewert 2006]), achalasia
- Mallory- Weiss- syndrome (tearing of the mucosa and / or submucosa of the esophagus occurring after severe vomiting )
- Boerhaave's syndrome (spontaneous rupture of the esophagus after severe vomiting)
- Ventricular ulcer (Pinger 2019)
- Diseases in the region of the ribs such as:
- Tietze syndrome (pressure-dolent swelling of the ribs in the area of the bone-cartilage boundary)
- Rib fracture
- Thoracic trauma
- Diseases in the area of the spine such as:
- Bechterew's disease
- Cervical spine osteochondrosis
- BWS osteochondrosis
- Diseases in the area of the nerves such as:
- herpes zoster
- abdominal diseases that may radiate to the thorax such as:
- Acute pancreatitis
- Biliary colic
- cholecystitis
- Roemheld syndrome (postprandial thoracic pain independent of CHD)
- functional thoracic pain such as:
- Da Costa syndrome (functional pain in the heart area without organic cause)
- genetic diseases such as:
- most severe pain in the thorax or upper abdomen in sickle cell disease (v. Schweinitz 2009) (Herold 2019 / 2020).
General therapyThis section has been translated automatically.
There are different therapeutic approaches for coronary stenosis. The treatment or progression of the stenosis can be carried out by:
1. elimination of the risk factors
2. conservative therapy
3. surgical therapy
Elimination of risk factors. The main risk factors are:
- Hypercholesterolemia: The target value for total cholesterol should be < 175 mg/dl and for LDL cholesterol < 100 mg/dl. (For more details see "Conservative therapy" p. 5 below)
- arterial hypertension: The target blood pressure should be 140 mmHg at systolic values ≤ and / or diastolic values of ≤ 90 mmHg and < 135 / 85 mmHg at self-measurement (Herold 2019 / 2020)
- Diabestes mellitus: According to the recommendations of the ESC 2013, an HbA1c target value of < 7.0 % (= 53 ml/l) should be aimed for (Pinger 2019 / Wehling 2005)
Other risk factors are:
- Nicotine abuse: Stopping smoking reduces the cardiovascular 10-year risk by up to 50% (Herold 2019 / 2020). The reduction of mortality during nicotine withdrawal has been proven in studies. The NNT value (number needed to treat) is 22.
- Lack of aerobic physical activity: The reduction of mortality due to lack of aerobic activity has been confirmed in studies. In addition, physical activity can increase HDL cholesterol by 4.6%. According to ESC 2013 ≥ the training should be done 3 times/week for 30 minutes. Even light physical activity increases life expectancy by 3 years (Herold 2019 / 2020).
- Weight control: Being overweight not only increases the risk of coronary disease, but also that of hypertension, diabetes mellitus and hyperlipidemia. The abdominal girth in men should ideally be < 94 cm and in women < 80 cm (Suter 2005). The ideal BMI value is between 20 - 25 kg/m2 (Herold 2019 / 2020) (Pinger 2019).
Internal therapyThis section has been translated automatically.
Drug treatment involves the use of drugs
- to reduce the myocardial oxygen demand by:
- Reduction of contractility, heart rate and afterload
- improving the myocardial oxygen supply by:
- Reduction of the vascular tone in the coronary arteries
- Extension of the diastol duration (frequency reduction)
- Reduction of left ventricular end-diastolic pressure (preload)
- reduce the risk of thrombotic coronary occlusion
- to lower the LDL- cholesterol (Renz- Polster 2008)
1st beta-blockers: Beta-blockers are among the first choice therapy. They reduce the oxygen demand of the heart by lowering the heart rate by 20 % - 25 % (Wehling 2005), as well as contractility and blood pressure under stress (Herold 2019 / 2020). However, caution is advised in patients with chronic obstructive pulmonary disease, diabetes mellitus and PAD. There is a relative contraindication for these diseases, as they can increase bronchial obstruction, reduce the warning signs of hypoglycaemia (e.g. sweating, tachycardia) and aggravate the symptoms of claudication (Renz- Polster 2008).
Therapy suggestion:
1. e.g. Metoprolol 200 mg/d
or Atenolol 100 mg/d (Wehling 2005)
2. calcium channel blockers (calcium antagonists)
Long-acting calcium channel blockers such as verapamil, amlodipine etc. are second choice drugs. They lead to cardiac relief by blocking the L (long- lasting) calcium channels and thus reduce the afterload (Herold 2019 / 2020). This has also been proven to reduce morbidity (Renz- Polster 2008). Short-acting preparations such as unretarded nifedipine only lead to a strong blood pressure reduction in the short term 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)
3rd ACE inhibitors: ACE inhibitors reduce the pre- and post-load and have an additional antiproliferative effect (Christ 2019). They should preferably be used in patients with the following concomitant diseases:
- Heart Failure
- diabetes mellitus
- arterial hypertension (Herold 2019 / 2020)
The KHK lethality is demonstrably reduced (Renz- Polster 2008).
Therapy suggestion: e.g. Ramipril Initial dose: 1 x 1.25 - 2.5 mg/d, then dose increase. However, the maximum dose of 10 mg/d should not be exceeded (Stierle 2017).
4. antiplatelet therapy: Antiplatelets are an important - if not the most important - preventive drug. Therapy suggestion: ASS 100 mg/d or in case of intolerance (the far more expensive) clopidogrel 75 mg/d (Stierle 2017) (Wehling 2005).
5) Cholesterol synthesis inhibitors (statins): Statins should be used in principle in all patients up to the tolerated maximum dose (Herold 2019 / 2020). The target value for total cholesterol is < 175 mg/dl and for LDL cholesterol < 100 mg/dl. These values cannot usually be achieved by a diet alone and an appropriate lifestyle (Renz- Polster 2008)
Therapy suggestion: Simvastatin 20 mg - 40 mg/d (Lundgren 2018)
6th 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 orally.
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).
Operative therapieThis section has been translated automatically.
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 world) and coronary bypass surgery (ACVB or CABG [coronary artery bypass graft]) (Stierle 2017).
Indications: The indications for the individual procedures are partly dependent on the SYNTAX score.
The syntax score is an angiographic score based on 9 anatomical criteria and can be used to make statements on perioperative risk assessment.
In Europe, the European System for Cardiatic Operative Risk Evaluation (Euro- Score) is the most commonly used. The individual risk can be calculated using a web-based calculator (www.euroscore.org./calc.html). However, the Euro- SCORE overestimates the mortality risk in individual patient groups (Stierle 2017).
The recommendations according to the German Society for Cardiology, Heart and Circulation Research 2012 (ESC Pocket Guidelines) for generally stable patients and lesions for which both procedures are suitable and which have a low expected surgical mortality are as follows: (see also below the update of the syntax study of 2019)
- 1- GE or 2- GE without proximal LAD stenosis:
- ACVB: IIb- C
- PCI: I-C
- 1- GE or existing proximal LAD stenosis:
- ACVB: I- A
- PCI: I- A
- 2-GE with proximal LAD stenosis:
- ACVB: I- B
- PCI: I- C
- Main stem stenosis left and syntax score ≤ 22:
- ACVB: I- B
- PCI: I- B
- Main stem stenosis on the left and syntax score 23 - 32:
- ACVB: I- B
- PCI: II a- B
- Main left main stenosis and syntax score ≥ 32:
- ACVB: I- B
- PCI: III- B
- 3- GE and syntax score ≤ 22:
- ACVB: I- A
- PCI: I- B
- 3- GE and syntax score 23 - 32:
- ACVB: I- A
- PCI: III- B
- 3- GE and syntax score ≥ 32:
- ACVB: I- A
- PCI: III- B (Stierle 2017)
Addendum: The COURAGE study published in 2007 already showed that PCI does not lead to a life-prolonged benefit in stable CHD. PCI is only indicated in stable CHD if there is a lack of self-control or if complications occur.
The following patients represent a classic indication for PCI:
- the symptomatic patient
- the patient with acute coronary syndrome (ACS) (Pachinger 2007)
However, the COURAGE study was criticized by advocates of the invasive strategy because of methodological weaknesses (Overbeck 2012). Initial results of the ISCHEMIA study (International Study of Comparative Health Effectiveness with Medical and Invasive Approaches), which was launched in 2012 and involves 8,518 patients (5,179 randomised), were presented at the congress of the American Heart Association (AHA) in Philadelphia in 11/2019. One composite (consisting of cardiovascular death, myocardial infarction, resuscitation after cardiac arrest, heart failure or hospitalization for unstable angina) occurred in the first year:
- Patients with invasive treatment in 5.3
- Patients with drug treatment in 3.4
After 4 years a composite joined:
- Patients with invasive treatment in 13,3
- Patients with drug treatment in 15.5
The number of deaths was 6.5 % versus 6.4 %. The study is to be continued for another 5 years, so that a final evaluation is still pending (Hochman 2019).
1.percutaneous catheter intervention: PTCA (percutaneous transluminal coronary angioplasty) is a technique that dilates narrowed coronary vessels, such as balloon dilatation and stent placement. The term PCI (percutaneous coronary intervention), which is commonly used in the Anglo-Saxon world, is used synonymously (Bonzel 2008).
Apart from PTCA there are other catheter methods which are only used for special indications and therefore have only a limited significance:
- Rotational angioplasty, also called rotablation. This is used for severely calcified stenoses or in case of outgoing stenoses.
- Directional coronary atherectomy (DCA), which is used for ostial stenoses
- Ultrasonic angioplasty or ultrasonic thrombolysis
- Cutting balloon for the treatment of complex stenoses
- Laser- PCI is used, for example, for calcified stenoses (Herold 2019 / 2020)
The standard method consists of dilating the coronary vessels with the aid of a balloon catheter. Drug-coated balloon catheters, so-called DCB, whose surface is coated with an antiproliferative drug are a further development (Stierle 2017). Initially, stents were only inserted if the balloon dilatation did not lead to the expected result. In the meantime - depending on the centre - approx. 80 % to 95 % of all PTCA are performed with stent implantation. As a result, the rate of re-stenosis and re-PTCA has been reduced (Stierle 2017).
A distinction is made for the stents between the
- uncoated stents (bare metal stents = BMS)
- the stents coated with an antiproliferative drug, so-called drug-eluting stents or DES
- resorbable coronary vascular scaffolds so-called scaffolds, which are remodeled by the body after months and thus allow the restoration of vascular mobility and vascular function. (Herold 2019 / 2020).
The highest success rate of > 95% is found in type A stenosis (classification of the degree of stenosis, see coronary stenosis ). For type B stenosis, the success rate is 90 % to 95 % and for type C stenosis between 80 % and 85 % (Stierle 2017). The remaining degree of stenosis is <50 %. Severe cardiac or cerebral complications can occur in the case of previously existing:
- stable angina pectoris in < 0.5%.
- unstable angina pectoris up to 1 % (Herold 2019 / 2020)
The rate of re-stenosis could be reduced to below 10 %. However, the delayed re- endothelialization of the stent has a disadvantageous effect, since it causes the risk of subacute stent thromboses to persist for a period of time that cannot be precisely quantified at present. For this reason, it is currently recommended to administer ASS 100 mg/d for life and, according to the ESC guidelines, to additionally administer an antiplatelet aggregation inhibitor (P2Y12 antagonist) e.g. clopidogrel for 6 months postoperatively (dosage recommendation: initially 300 mg p. o., then 75 mg - 150 mg/d [Stierle 2017]). (Kasper 2015).
Include an increased PTCA risk:
- advanced age.
- female sex
- Decrease of the systolic left ventricular function
- several vessels with a stenosis of > 70
- unstable angina pectoris
- Acute myocardial infarction < 24 h
- Performing the procedure under emergency conditions
- cardiogenic shock
- Heart Failure
- Accompanying diseases such as:
- Mitral valve insufficiency > grade II
- diseases of the aortic valve(aortic valve stenosis, aortic valve insufficiency)
- diabetes mellitus
- peripheral AVC
- Apoplexy
- Creatine increase of > 2 mg %
- dialysis patient
- Hypercholesterolemia
- intraluminal thrombus(Stierle 2017)
Periinterventional complications:
- vascular complications requiring surgery occur in 3% to 4% (Stierle 2017)
- Occurrence of a dissection of the coronary artery with acute coronary occlusion (occurs in approx. 7%): There are 3 possibilities of therapy:
- The method of the 1st choice is the insertion of a stent. The success rate is 85 %.
- emergency bypass surgery
- conservative infarct therapy (intensive care)
- occurrence of subacute stent thrombosis (this occurs within the first month in 0.5% - 5% of cases)
CAVE: NSAIDs should not be administered in combination with ASS / ADP receptor antagonists (clopidogel).
- Restenosis can be found after a
- Balloon dilatation in up to 40
- Stent implantation < 30
- after implantation of a coated stent (DES) < 10
- Over 95% of re-stenoses occur within 6 months.
- intravascular embolization
Protection systems should be used in bypasses (Herold 2019 / 2020).
- The mortality of the intervention is < 0.1 % (Stierle 2017)
2nd coronary bypass surgery (ACVB): In the meantime, coronary bypass surgery can be performed classically or minimally invasively (Herold 2019 / 2020).
a) Classic ACVB: It is performed via a sternotomy access and using a heart-lung machine.
- Arterial bypass, for example:
- LIMA (ITA) bypass. The coronary stenosis is bridged by the left internal thoracic artery (also known as internal mammary artery).
- RIMA bypass. The coronary stenosis is bridged by means of the right internal thoracic artery.
- A. radialis- Bypass
- A. gastroepiploica bypass (rare)
- Venous bypass (ACVB or CABG in the English-speaking world) e.g.:
- aortocoronary venous bypass (Herold 2020)
- V. saphena magna (cannot be used if varicosis exists)
- V. cephalica (mostly used in emergencies) (Stierle 2017)
b) Minimally invasive bypass surgery
There are different procedures for minimally invasive surgery:
- MIDCAB (minimally invasive direct coronary artery bypass):
After a left anterolateral, minimal thoracotomy, the ramus interventricularis anterior (RIVA) is revascularized by a left internal mammary artery bypass (LIMA bypass).
- TECAP (totally endoscopic coronary bypass):
As the name suggests, this procedure is performed completely endoscopically.
- OPCAB (off- pump coronary artery bypass):
In this procedure, the operative revascularization of a multi-vascular disease is carried out via a partial or complete sternotomy without a heart-lung machine on the beating heart.
- Hybrid procedure
The hybrid process is a combination of MIDCAP and PCI with no bypass material. (Herold 2019 / 2020). After a bypass operation, the patient should postoperatively take thrombocyte aggregation inhibitors such as ASS 100 mg/d. In case of intolerance, it is recommended to switch to antiplatelet inhibitors such as ADP receptor antagonists, e.g. clopidogel Adults/adolescents > 18 years: once/day 75 mg p.o. (Herold 2019 / 2020).
The following complications can occur with ACVB:
-
acute myocardial infarction
- with a new Q-prong occurs in 3.7
- perioperative Q-wave infarction is found at 4.6
- CK- MB- increase occurs in 90 % of patients (in 6 % the increase is up to 10 times the normal value)
- apoplectic insult occurs in 1 % to 1.7 % of patients
- Apoplexy rate in > 75 year olds is 2.7 % within the first 30 days p.o.
- Atrial fibrillation (if this lasts longer than 24 h, anticoagulation should be carried out for 4 weeks due to the increased risk of an apoplexy; dosage recommendation: 1 x 20 mg / d (dose adjustment for liver and kidney dysfunction [Encke 2015])
- Mediastinitis with a mortality rate of 25% occurs at 1% - 4% (prophylaxis: preoperative administration of a cephalosporin e.g. cefuroxime 1.5 g/d or clindamycin 600 mg/d for 1 to 2 days {Rossaint 2019} and strict avoidance of hyperglycaemia [max. blood sugar value: 150 - 180 mg/dl])
- Renal insufficiency occurs at about 8%. Newly required dialysis occurs in about 1 % of patients and in > 75 years of age in > 3.1 % and 3.5 % respectively. In patients > 70 years of age with a preoperative creatinine value > 2.5 mg/dl, alternatives to ACVB surgery should therefore be considered (Pinger 2019).
Angiographic long-term success. Openness of the bypass vessels is found:
- after 1 year in 78 % of veins
- after 1 year at IMA in 93 %
- after 5 years for veins in 65
- after 5 years at IMA in 88 %
- after 10 years for veins in 57 %
- after 10 years for veins in 90
- after 10 years with IMA bypass on the LED 99 % (pinger 2019)
success rate:
- Survival rate after 5 years is 83 % - 92 %
- Survival rate after 10 years at approx. 81 %
- after 5 years 67 % - 83 % are symptom-free (under sole drug therapy the figure is 38 %)
- after 10 years, 47% - 63% are still free of symptoms (42% with drug therapy alone) (Pinger 2019)
- bypass occlusion rate of the venous graft is:
- after 1 month at 12
- after 1 year 15 % - 31 % (Stierle 2017)
- after 10 years between 29 % - 68 % (Herold 2019 / 2020)
- after IMA (A. mammaria interna) - Bypass:
- after 10 years at only 5 % - 10
- A. radialis bypass:
- after 10 years between 17 % and 37 % (Herold 2019 / 2020)
Mortality:
- Hospital mortality is 1.1% for elective procedures and 2.6% after urgent surgery
- without or with main stem stenosis at 1.5 % and 2.5
- without or with diabetes mellitus at 1.6% and 2.6% respectively
- after 3 months the mortality rate is 1 % to 2 % (Stierle 2017)
- Compared to a venous bypass, 27% of patients die less within 15 years after using an A. mammaria bypass (Herold 2019 / 2020).
Progression/forecastThis section has been translated automatically.
The course of coronary heart disease depends on the following factors:
- the location of the stenosis. The annual lethality rate for a main stem stenosis of LCA without revascularization is > 30%.
- the number of coronary arteries affected (without revascularization). The annual lethality rate for a
- 1- Vascular disease is 3 % - 4
- 2- Vascular disease is 6 % - 8
- 3- Vascular disease is 10 % - 13 %
- the extent of myocardial ischemia. The risk of myocardial infarction increases with the frequency and severity of angina pectoris attacks.
- from the functional state of the left ventricle The prognosis is worsened by
- Increasing left heart failure (with a resting ejection fraction = EF < 35 % the annual mortality rate rises to > 3 %)
- Occurrence of high-grade ventricular dysrhythmia
- from the progression of coronary heart disease (Herold 2019 / 2020)
Note(s)This section has been translated automatically.
Comparison of PTCA and Bypass OP
The risk is higher with bypass surgery in the early postoperative stage than with PTCA. In the further course of the disease, however, the bypass surgery in patients with complex or multiple stenoses (e.g. disease of the left main stem, triple-vessel disease) shows an advantage with regard to the
- Occurrence of a myocardial infarction
- Need for new cardiological interventions
- Improving the quality of life
- lower overall mortality (according to syntax study) (Kasper 2015)
Syntax Study: At the congress in Paris in August 2019, the results of the 10-year study Syntax (Synergy between PTCA with TAXUS Drug-Eluting-Stent and Cardiac Surgery) with 1,800 patients were presented. In this study 93 % of the patients received PTCA and 95 % a bypass surgery. The following results were found:
- There were no differences between PTCA and ACVB when using 1st generation stents
- There were no significant differences in mortality. After 10 years, mortality was 27% in the PTCA group and 23.5% in the ACVB group. (HR 1.17 and p=0.092).
- Patients with coronary artery disease showed worse results with PTCA. Here a bypass surgery should be preferred (151 vs. 113 patients, 27.7% vs. 20.6%, HR: 1.41, p=0.006)
- in diabetics treated with medication there was no significant difference between the two groups
- in patients with a left main stem stenosis there was no difference in the 10-year survival rate in both groups
- in patients with complex coronary disease (corresponding to a SYNTAX score of > 33) bypass surgery should be preferred (33.8% vs. 26.3%, HR: 1.41)
Conclusion: In patients with a SYNTAX score > 33 (www.euroscore.org/calc.html) and / or coronary artery disease the bypass surgery should be preferred (Vetrovec 2019 / Einecke 2019).
Addendum: The results of the EXCEL study, which was published in November 2019 in the New England Journal of Medicine and started in 2010, show stent and bypass as equivalent therapies in case of main stem disease. This result triggered a discussion among cardiologists and heart surgeons. As a result, a BBC Newsnight survey in December 2019 published mortality results 5 years after the completion of the EXCEL study. The mortality was:
- 13 % after stent implantation
- 10 % after bypass surgery
In addition, unpublished data from the study showed an 80 % higher infarction rate in the PCI group.
The European Association of Cardio- Thoracic Surgery (EACTS) is currently reviewing the clinical guidelines. These were revised only last year on the basis of the 3-year results of the EXCELL study (Stone 2019; Holm 2019; Cohen 2019).
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