Myocardial infarctionI21.9

In 1920, Harold Pardée was the first to describe the phenomenon of deep Q in fresh myocardial infarction. The broad Q was named after him as the so-called Pardée Q (anxiety worm 2014).

In 1996, Sgarbossa developed the Sgarbossa criteria, named after him, with the help of which a myocardial infarction can also be detected in a left bundle branch block. These criteria were modified by Smith in 2012 (Sgarbossa 1996 / Smith 2012).

Myocardial infarction (MI) was defined at the end of the 1950s by the WHO in terms of an epidemiological approach and was adapted several times in the following years. It was not until 2000 that it was defined under a clinical approach by the ESC (European Society of Cardiology) and the ACC (American College of Cardiology). A few years later the UDMI (Universal Definition of Myocardial Infarction) supplemented the clinically defined version (Thygesen 2018).

A myocardial infarction (MI) is a sudden event. Slowly developing coronary stenoses rarely precede an MI, since a slowly developing stenosis quickly develops a collateral circulation (Kasper 2015).

In MI, ischemic myocardial necrosis with:

• Increase in troponin cTN (so-called main criterion [Stierle 2017])
  • on admission or after 3 - 6 h > 99 percentile
  • relevant increase and/or decrease in troponin concentration within 3 - 6 h (Stierle 2017)

In addition, at least one of the following criteria (so-called secondary criteria - Stierle 2017) must be met:

• ischemically caused complaints
• newly occurred significant ST changes or a newly occurred left bundle branch block
• newly appeared Q-waves in the ECG
• imaging evidence of loss of vital myocardium or evidence of a new regional disturbance of wall movement
• Detection of an intracoronary thrombus (by angiography or autopsy - Herold 2020)

The MI belongs to the group of acute coronary syndrome, along with unstable angina pectoris. On the basis of the ECG changes a differentiation is made between:

• STEMI (ST- elevation myocardial infarction). In STEMI there is a persistent ST elevation > 20 min and an increase in troponin.

and a

• NSTEMI (Non- ST- elevation myocardial infarction). NSTEMI lacks persistent ST elevation. The increase of troponin is present (Herold 2020).

According to ESC the following 5 types of infarction are found:

• MI type 1: Spontaneously occurring MI in which myocardial necrosis occurs due to a consecutively reduced blood flow. The causes are:
  • Plaque rupture
  • Lacerations or dissection with formation of an intraluminal thrombus in one or more coronary arteries. In postmortem MI, an acute atherothrombosis is found in the artery supplying the myocardial infarction. Thus the criteria for MI type 1 are fulfilled (Thygesen 2018).
• MI type 2: Ischemia-induced MI due to, for example:
  • Coronary spasms
  • Embolisms in the coronaries
  • Arrhythmias
  • Anemia
  • Hypertension
  • Hypotension
• MI type 3: If death occurs in a patient with typical symptoms indicating myocardial ischemia and the ECG shows suspected new changes in the form of ischemia, but the cTN values are not yet present or are not yet abnormal, the patient is called MI type 3 (Thygesen 2018).

• MI type 4: In type 4 a distinction is made between:
  • Type 4 a: Occurrence of MI during or immediately after PCI (percutaneous transluminal coronary angioplasty)
  • Type 4 b: Occurrence of MI as a result of stent thrombosis
• Type 4 c: Occurrence of an MI as a result of residual stenosis after PCI (Stierle 2017).
• MI type 5: appearance of an MI during or immediately after CABG (coronary artery bypass grafting)

Special cases of an MI:

• Recurrent infarction: If a re-infarction occurs within 28 days after an MI, this is called a recurrent infarction (Thygesen 2018).
• MINOCA infarction: In a MINOCA infarction (without obstructive coronary atherosclerosis), an MI occurs without the presence of obstructive coronary heart disease (= stenosis > 50 %). The prevalence of MINOCA infarction is estimated at 6 % - 8 % (w>m). MINOCA infarction is more frequent in NSTEMI than in STEMI (Thygesis 2018):
  • Rupture of arteriosclerotic plaques
  • Coronary thrombosis
  • Coronary Spasm
  • spontaneous dissection of a coronary vessel

The incidence of myocardial infarction shows great geographical variation.

Currently, myocardial infarctions per 100,000 inhabitants / year are found in:

• France: 55
• Sweden, Belgium, Czech Republic, Japan: < 100
• the Mediterranean countries: 80 - 120
• Germany: 120 (Herold 2020)

The disease affects far more often the male sex.

Premenopausal women account for only 4% of patients with MI (Waldecker 2003). However, once atherogenic risk factors become more important after the onset of menopause, there is an increasing gender alignment (Kasper 2015).

Myocardial infarction occurs according to a circadian rhythm that is between 6:00 am to 12:00 pm. This is caused by an increase in clotting activity during this period (Herold 2020).

Associated non-cardiac diseases:

• Diabetes mellitus (Kasper 2015).
• Pheochromocytoma (the MI represents a rare complication [Mauser 2001]).
• Sepsis (MI is a frequently overlooked complication during the course of sepsis [Hoffmann 2002])
• Iron deficiency (serum ferritin and transferrin saturation).

Iron def iciency has significant prognostic significance. In one study, iron deficiency was shown to have a high prevalence to acute coronary syndrome (ACS). 29.1% of patients with ACS (of whom 42.8% were women) had low iron levels.

The risk of cardiovascular mortality and nonfatal myocardial infarction was increased by 73% in these patients during a 4-year follow-up period (Zeller 2018).

Associated noncardiac disease in coronary artery disease:

• migraine is present in approximately 25% of patients
• Raynaud 's syndrome in about 33% (Stierle 2017).

Pathophysiology: Initially there is damage to the coronary endothelium. This is caused by certain risk factors or certain noxious agents (see "Causes" below). Due to the damage of the endothelium, the surface of the inner vessel wall becomes irregular and fibromuscular plaques are deposited, which lead to a stenosis of the coronaries (Greten 2010). This stenosis causes an imbalance between oxygen demand and oxygen supply in the area of the respective myocardium, which is supplied by the stenosed vessel (Lapp 2014). In addition, damage to the endothelium causes a regulatory disturbance of coronary vasodilation or vasoconstriction. As a result, the endothelium is no longer able to react to physical stress by dilating the coronary arteries. The transition to MI is usually initiated by a tear in an atheromatous plaque, which is followed by a thrombosis of the coronary arteries (Herold 2020).

The MI is primarily caused by arteriosclerosis, which leads to coronary heart disease via coronary stenosis. Only rarely is an embolism in the coronaries the cause (Herold 2020).

The causes for the occurrence of arteriosclerosis are very different. The main factors are:

• LDL- cholesterol increase > 160 mg/dl
• HDL- Cholesterol reduction < 40 mg/dl
• arterial hypertension
• Diabetes mellitus with HbA1c values > 7
• tobacco use
• family disposition (first-degree family members have an infarction before the age of 55 [m] or before the age of 65 [w])
• Age > 55 years (m) or > 65 years (w) (Herold 2020)

But other factors also play a role, such as:

• Obesity with an abdominal girth of > 94 (m) or > 80 (w)
• atherogenic diet
• low social status
• lack of physical exercise
• Lipid metabolic disorders e.g. hypertriglyceridemia ≥ 150 mg/dl
• Disturbance of glucose tolerance with fasting FC values ≥ 100 mg/dl
• Hyperfibrinogenemia ≥ 3.5 g/l
• Inflammatory conditions in CHD patients
• Z. n. thoracic radio
• For heart transplantation
• obstructive sleep apnea
• longer stay under increased fine dust load
• genetic changes (so far 20 gene regions are known to be associated with an increased risk of myocardial infarction) (Herold 2020)

Presence of certain diseases such as:

• lupus erythematosus, rheumatoid arthritis, antiphospholipid syndrome and others (Pinger 2019)

In the case of an infarction before the age of 30, the following causes in particular should be excluded:

• familial lipid metabolism disorders
• Thrombophilia (e.g. due to an antiphospholipid syndrome)
• hypothyroidism and hypercholesterolemia associated with it
• Vasculitides such as:
  • polyarteritis nodosa
  • Kawasaki's syndrome
  • Takayasu arteritis
• Anomalies of the coronaries
• Diseases of the coronary arteries (e.g. after surgery of congenital vitiligo)
• drug abuse of:
  • Cocaine
  • Marijuana
• Hyperviscosity syndrome, such as:
  • multiple myeloma
  • polycythaemia vera
  • Essential thrombocythemia

Pathogenesis: Pathogenetically, both increased coronary resistance and extracoronary factors play a role.

1. increased coronary resistance:

• ...which can be caused by a number of key vascular factors..:
  • 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 secondary 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 (Herold 2020)

2. extracoronary factors:

• which can 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:
  • Increased oxygen demand 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 e.g. erythropoietin doping, hyperfibrinogenemia, multiple myeloma, polycythemia vera, etc.

Triggering factors for MI may include:

• sudden exertion
• stronger blood pressure fluctuations in stress situations

According to the MONICA study (Keil 2005), the typical infarct symptoms are only present in about 40% of all infarcts. These typical symptoms are:

intense and persistent angina pectoris pain, which can hardly be influenced by rest or nitro administration (in contrast to stable angina pectoris)

• the retrosternal pain can radiate into
  • the neck / throat
  • lower jaw
  • teeth
  • shoulder area
  • both (!) arms (with focus on the ulnar sides of the forearms), which can radiate into the ulnar fingertips
• pain below the xyphoid 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)
• Cardiac arrhythmias in the form of ventricular tachycardia, ventricular fibrillation, AV blockages occur in about 95%.
• Frequent drop in blood pressure with cerebral dysfunction
• symptoms of left heart failure with shortness of breath occur in approx. 33 % of cases
• in right ventricular infarction:
  • absence of pulmonary congestion
  • Neck vein congestion
  • often bradycardia (Herold 2020)
• sweating
• cold extremities
• Increase in body temperature up to 38 degrees C (Kasper 2015).

In approximately 5%, there is reproducible chest pain triggered by local pressure (Pinger 2019)

In about 15 % of patients with MI, the typical symptoms are absent. This particularly frequently affects the following group of patients:

• Diabetes mellitus
• Renal insufficiency
• Women
• elderly patients > 75 years
• post cardiac surgery
• After heart transplantation (Herold 2020)

They are more likely to experience non-specific symptoms, such as:

• Nausea
• Shortness of breath
• Dizziness
• pain in the epigastrium
• subfebrile temperature
• anxiety

So-called "silent infarctions" occur in approx. 20 % of patients. Diabetics are particularly affected (as a result of autonomic diabetic neuropathy).

In about 40% of patients, MI is the first manifestation of angina pectoris. These patients have no history of angina pectoris attacks.

In NSTEMI, thoracic pain lasts > 10 - 15 min, but occasionally longer (Stierle 20017).

In STEMI, pain symptoms persist for > 20 min (Kasper 2015).

Echocardiography: In echocardiography,:

• almost always regional disturbances of wall motion (rWbSt). However, old scars cannot be distinguished from fresh ischemia in this case (Kasper 2015).

These regional wall motions occur very early in MI, even before enzyme or ECG changes. Absence of wall motion is 95% predictive of MI (Herold 2020).

• Absent or reduced thickness increase in the infarct zone (Herold 2020).
• Assessment of left ventricular ejection fraction (is prognostically significant see "Internal Therapy" below).
• Assessment of a possible right ventricular infarction
• exclusion of a
  • ventricular aneurysm
  • pericardial effusion
  • intraventricular thrombus

Possible evidence of severe complications of MI:

• Ventricular septal defect
• Mitral valve regurgitation (Kasper 2015)

Cardiac MRI: Cardiac MRI plays a minor role in the diagnosis of myocardial infarction. At the earliest, necrosis can be detected after 1 h by a late enhancement in the T1-weighted image after administration of gadolinium. In the T2-weighted image, edema can be detected to differentiate between an acute and a chronic lesion. The specificity is 96% (Pinger 2019).

Coronary angiography: Coronary angiography represents one of the most important measures with regard to diagnosis and therapy in acute MI. For detailed information on indications, contraindications, performance, etc., see Coronary Angiography.

At this point, only factors important for MI are mentioned.

Coronary angiography performed <4 h after infarct onset reveals complete vessel occlusion in approximately 90% (Pinger 2019). The following diagnostic or therapeutic measures are additionally performed during coronary angiography:

• Coronary angioscopy (to assess vessel morphology and any plaques present).
• intravascular ultrasound (also 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 %)
• percutaneous catheter intervention (PTCA or PCI) with stent insertion

The highly sensitive troponin (hs- Tn) is the decisive biomarker for the detection of an MI. The sensitivity is 80 % after 3 h and 100 % after 10 h to max. 5 days. Specificity is 98 % - 99 % (Pinger 2019).

Earliest detection approx. 1 - 2 h after onset of pain, as troponins indicate damage to the myocardium, not ischemia (Stierle 2017). The maximum is usually reached after 12 h. A normalization of the value is found after about 1 - 2 weeks.

The troponin value correlates with the size of the infarct.

Troponin T:

• in STEMI ≥ 1.0
• in NSTEMI ≥ 0.01 to ≤ 1.0 (Stierle 2017).

Other causes of troponin elevation may include:

• Myocardial damage without evidence of acute ischemia.
• Pulmonary embolism
• cardiac decompensation
• Myocarditis
• stress cardiomyopathy
• cardiac surgery
• percutaneous coronary intervention (PCI)
• hypertensive crisis
• aortic dissection
• aortic valve stenosis
• Tachyarrhythmias
• Bradyarrhythmias
• Apoplexy
• acute or chronic renal failure
• sepsis
• heavy physical exertion, e.g. marathon running

Creatine kinase (total CK): In infarction, total CK rises within 4 - 8 h and returns to reference range after 48 - 72 h. However, the specificity is low(Kasper 2015). The ratio between CKMB / CK in the presence of an MI is usually 10 % - 20 % (Herold 2020).

Other causes of an increase in total CK can be:

• Myocarditis
• i. m. injections
• Trauma
• operations
• physical exertion
• childbirth
• arterial embolisms / occlusions
• epileptic seizures
• resuscitation
• Muscle diseases such as:
  • polymyositis
  • muscular dystrophy
  • Injury of the muscle
  • Rhabdomyolysis
• Intoxications
• Delirium tremens
• Alcoholism
• Heroin use
• necrotizing pancreatitis
• Malignancies
• acute hepatocellular necrosis
• endocrine myopathies such as:
  • M. Addison's disease
  • Hypoparathyroidism
  • Hypothyroidism
  • Hyperthyroidism
• Coxsackie B infection
• Trichinosis
• Medications such as:
  • Lipid-lowering drugs
  • CSE inhibitors
  • tricyclic antidepressants
  • Vincristine
  • Psychotropic drugs
  • cyclosporine

Laboratory chemistry should also be used to 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.)
• Urinalysis for
  • glucosuria
  • Indications of kidney disease (including microalbuminuria) (Kasper 2015).

Furthermore (for more details see above under "Associated non-cardiac diseases):

• Serum iron (often decreased)
• Transferrin saturation (often decreased) (Zeller 2018)

Inspection and palpation: Typically, patients hold the clenched fist in the middle of the sternum when describing pain (Levine sign), the hand is placed flat on the sternum or both hands, fingertips facing each other are placed on the sternum from the lateral side to indicate girdling tightness. Sensitivity for cardiac pain is approximately 80% and specificity is approximately 49% (Edmondstone 1995).

Auscultation: Although MI itself does not cause typical murmur phenomena, the patient should be auscultated daily, as complications may cause the following auscultation findings:

• pericardial rubbing (in pericarditis epistenocardica)
• Systolic at:
  • necrotic septal perforation of the ventricle
  • mitral regurgitation secondary to papillary muscle dysfunction
  • dilatation of the heart with relative AV-valve insufficiency
• moist rales in the presence of pulmonary congestion or pulmonary edema

• 3rd heart sound due to paradoxical splitting of the 2nd heart sound as a result of left ventricle dysfunction (Kasper 2015 / Pinger 2019).

ECG: ECG recording is the initial diagnostic test in MI. With the help of the ECG, statements can be made:

• the localization of the affected area
• the extent of the infarct
• the age of the infarct

A distinction is made between direct and indirect signs of infarction:

• direct infarct signs are caused by a tap directly above the infarct area
• indirect infarct signs are mirror-inverted changes in the opposite leads (Herold 2020).

With the help of the so-called Sgarbossa criteria, it is possible to recognize a STEMI even in the presence of a pre-existing left bundle branch block.

• Sgarbossa A: There is concordant ST elevation > 1 mm in at least 1 lead (5 points).
• Sgarbossa B: There is a concordant ST- depression of at least 1 mm in leads V1, V2 or V3 (3 points)
• Sgarbossa C: An elevation of the ST- distance of ≥ 5 mm in a lead with concomitant discordant deflection in the region of the QRS- complex (2 points).

A reasonably reliable conclusion can be made from a value of ≥ 3 points.

The specificity is 98%, the sensitivity 20% (Jahn 2019).

Somewhat more exact statements can be made with the modified Sgarbossa criteria according to Smith.

• Sgarbossa C modified

  :At least one elevation of the discordant ST- distance of ≥ 1 mm is found, provided it measures ≥ 25 % of the preceding S- wave

  .

  (Gotthardt 2018)

STEMI: In a STEMI, one differentiates between 3 different stages:

1st stage / acute stage (fresh infarct): As the earliest ECG- change occurs a short-term T- elevation, the so-called asphyxiation T or also called T- en- dôme. Subsequently, an injury potential is formed between the healthy and the damaged myocardium with an ST elevation lasting up to 20 minutes, the so-called monophasic deformation of the ventricular complex. In this process, the ST segment descends immediately from the descending R and merges into a plateau or dome shape with the T wave.

Typical changes are ST segment elevation at the J point (transition from QRS complex to ST segment). These are

• in men < 40 years: V2 and V3 ≥ 0.25 mV

• in men > 40 years: V2 and V3 ≥ 0.20 mV

• in women: V2 and V3 ≥ 0.15 mV

• In all other leads (each in at least 2 contiguous leads) ≥ 0.1 mV.

Atypical changes are:

• Left bundle branch block

• an isolated ST elevation in aVR

• ventricular stimulated rhythms

2nd stage (intermediate stage):

• ST elevation decreases (DD: e.g. cardiac wall aneurysm, pericarditis, Prinzmetal angina).
• R- reduction or R- loss occurs.
• A QS complex is formed or a deep Q-spike, so-called pathological Q, also referred to as Pardée Q with a width of ≥ 0.04 sec and a depth of > ¼ R (DD: e.g., hypertrophic cardiomyopathy, pulmonary embolism [S1 Q3 III type], WPW syndrome [sternal positive type])
• Appearance of a terminal negative T- wave with an acute negative isosceles T- wave. DD: e.g. NSTEMI, secondary stage of pericarditis, myocarditis, hypertrophic obstructive cardiomyopathy).

3rd stage / chronic stage (old infarct):

• Persistence of terminal negative T or normalization of T.
• possibly reconstruction of a small R- junction
• deep Q (usually persists throughout life)

As a guideline regarding the localization of the infarct, the following classification is valid:

• RIVA proximal:
  • large infarct in the area of the anterior wall
  • V1 to V6, aVL, I as direct infarct signs
  • (II), III, aVF as indirect infarct signs
• RIVA after departure of diagonal branches:
  • anteroseptal infarct
  • V1 to V4, aVL, I as direct infarct sign
  • (II), III, aVF as indirect infarct signs
• Diagonal branch:
  • Lateral infarct
  • V5 to V7, aVL, I as direct infarct signs
  • no indirect infarct signs
• Posterolateral branch:
  • Posterolateral infarct
  • V5 to V6, aVF, II, III as direct infarct signs
  • V1 to V3, aVL, I as indirect infarct signs
• RCX:
  • strictly posterior posterior wall infarct
  • V7 to V9, aVF, III as direct infarct signs
  • V 1 to V2 as indirect infarct signs
• RCA:
  • inferior posterior myocardial infarction / right ventricular infarction
  • V1 , V 3r to V6r, aVF, II, III as direct infarct signs
  • V1 to V3 as indirect infarct signs

Within the first 24 h, the ECG may still be unremarkable. It is therefore recommended to repeat the recording at intervals of 24 hours. If no infarct-typical changes occur and troponin I/T and CK-MB remain negative, an infarct is excluded (Herold 2020).

NSTEMI: In NSTEMI, the ST-segment elevation typical of STEMI is absent. It may be present:

• ST-segment elevations in 20%-25%, which may persist for several days (Kasper 2015).
• transient ST elevations
• T- waves can be normal or negative (Stierle 2017).

NSTEMI predominantly affects the left ventricular region. From the ECG with leads typical of an infarct, the exact area of occlusion is virtually impossible to localize because the coronaries are variable and the type of supply is unknown (Stierle 2017).

The so-called "big five" of thoracic pain include - besides MI:

• pulmonary embolism
• Aortic dissection
• Boerhaave syndrome (spontaneous rupture of the esophagus after strong vomiting)
• Tension pneumothorax
• unstable angina pectoris (no increase in troponin)
• acute pericarditis
• Pulmonary embolism (D- dimer increase)
• acute dissection of the aorta (Kasper 2015)
• Acute abdomen (in particular a posterior wall infarction can be projected infradiaphragmatically)
• Stress cardiomyopathy (also known as Tako- Tsubo- cardiomyopathy)

Further differential diagnoses see coronary heart disease.

A distinction is made between early and late complications.

• Early complications: The most dangerous period in MI is the first 48 hours. This is when the so-called early complications occur. Approximately 40% of patients with MI die during this period. The most frequent complications are cardiac arrhythmias and heart failure.

1. cardiac arrhythmias

They occur in about 95 % - 100 % of patients. They are differentiated between:

• ventricular extrasystoles: They are the most common, also 95% - 100%. They are polymorphic VES, couplets, R on T phenomenon. These are considered so-called warning arrhythmias, as they are associated with an increased risk of ventricular fibrillation. However, ventricular fibrillation can also occur acutely without previous warning arrhythmias.
• Ventricular tachycardia and ventricular fibrillation: Ventricular fibrillation occurs most frequently within the first 4 h after the infarction event and in 80% within the first 24 h. Ventricular fibrillation also causes death in 80% of patients who die suddenly from infarction.
• Atrial fibrillation with absolute tachyarrhythmia: This is a prognostically unfavorable sign.
• bradycardic arrhythmia: This may be sinus bradycardia or AV block. The latter occurs preferentially in inferior infarction (Herold 2020).
• Limb block: When a new bifascicular limb block (RSB plus LAH = left anterior hemiblock or LPH = left posterior hemiblock) occurs, there is a high risk of complete AV- block. Therefore, implantation of a pacemaker should be performed early in these cases (Stierle 2017).

2. heart failure

• Left heart failure and cardiogenic shock: Both left heart failure and cardiogenic shock can be caused by:
  • A functional failure of the myocardium. If the MI involves approximately 20% of the left ventricle, signs of left heart failure are always detectable. Infarction of about 40% results in cardiogenic shock in the majority of cases, with a lethality rate of more than 90%.
  • Cardiac arrhythmias: due to treatment with neg. ionotropic agents such as antiarrhythmics, beta-blockers
  • a volume deficiency
  • Rare causes are:
    • Ventricular septal perforation (leading to acute left-right shunt and pulmonary flooding; auscultatory findings include a new onset systolic; diagnosis by color Doppler)
    • Papillary muscle rupture (signs of acute mitral regurgitation; new onset of systolic on auscultation)
    • Rupture of the ventricular wall with cardiac tamponade (this is often a covered perforation)
    • Pericardial effusion (anticoagulants are relatively contraindicated).

Cardiogenic shock is defined as:

• arterial hypotension (RR systolic < 90 mmHg).
• Cardiac index < 2.2 l/min/m2 (normal value: > 2.5 l/min/m2)
• PCW- pressure > 15 mmHg (norm value: 8 - 12 mmHg)

Cardiogenic shock occurs due to:

• pump failure of the left ventricle (in about 80 %)
• Mechanical complications such as papillary muscle dysfunction (6.9%), infarct-related ventricular septal defect ( 3.9%), rupture of the ventricular wall (1.4%) (Stierle 2017).

Diagnosis of left heart failure:

• RGs auscultable over the basal lung fields.
• appearance of a 3rd heart sound
• Radiologically detectable signs of pulmonary congestion
• In color Doppler / echocardiography:
  • evidence of hypo- or akinetic infarct areas
  • Ventricular septal perforation
  • dysfunction or rupture of a papillary muscle
  • Pericardial effusion
  • Ejection fraction should be estimated on echo

Right heart failure: Right heart failure may occur in the setting of a right ventricular infarction. Clinically, hypotension, increased central venous pressure, no evidence of pulmonary congestion are found. Heart failure after MI is determined by the Killip classification:

• Killip I (lethality approximately 6%): No evidence of pulmonary congestion
• Killip II (lethality approximately 18%): Auscultatory RGs < 50 % of the lungs, appearance of a 3rd heart sound. Neck vein congestion or increased CVD.
• Killip III (lethality approx. 36 %): Occurrence of pulmonary edema with auscultatory RGs > 50% of the lung.
• Killip IV (lethality approx. 70 % - 80 %): Cardiogenic shock (Stierle 2017).

3. reinfarction after lysis

Within hours to a few days, reocclusion of the vessel occurs in approximately 4% of patients after successful fibrinolysis. In this case, direct PTCA / PCI is recommended. In contrast, a vessel primarily treated with a stent is still open after 2 years with a > 98 % probability (Stierle 2017).

Latecomplications: We speak of late complications if they occur > 48 h after the infarction.

These include:

• Cardiac wall aneurysm: Cardiac wall aneurysm occurs in up to 20% of all infarct patients. ECG may show persistent ST elevations. Diagnosis is made by echocardiography.

• Arterial emboli: The risk of developing arterial emboli is present in patients with murine left ventricular thrombus and occurs in approximately 5% of patients.
• Early pericarditis: Pericarditis epistenocardica occurs a few days after the event and is now rarely found in patients surviving infarction (<5%).

• Postmyocardial infarction syndrome: Postmyocardial infarction syndrome, also known as "late pericarditis" or "Dressler's syndrome", occurs in approximately 3% of patients within 1-6 weeks after MI.
• Arrhythmias
• Heart failure
• Persistent or recurrent angina pectoris: Up to 20% of patients experience a recurrence of angina pectoris or ST elevations. This particularly affects patients after NSTEMI or known multivessel disease or after thrombolysis (Stierle 2017).

• Recurrent infarction

The acute treatment of a patient with MI should consist of:

• Raising the upper part of the body (for breathing difficulties)
• O2 Administration of 4 - 8 l / min via a nasal probe, provided that the oxygen saturation is < 90
• Administration of nitroglycerine: ambulant sublingual 1 - 3 strokes, after reaching the clinic via perfusor (1mg - 5 mg / h i. v.); contraindications: systolic RR- values < 90 mmHg, intake of PDE- 5 inhibitors such as Viagra
• Morphine for severe pain (3 mg - 5 mg i. v., then 2 mg every 5 - 15 min. until the pain is relieved; side effects: nausea, respiratory depression, hypotension)
• for nausea: administration of an antiemetic e.g. metoclopramide
• in case of a vagal reaction administration of atropine 0.5 mg i. v.
• initial anticoagulation:
  • heparin (e.g. enoxaparin 2 x 1 mg / kg bw / d s. c. [Stierle 2017])
  • ASA (initial 160 mg - 325 mg parenterally or see left, then 75 mg - 100 mg/d p. o.) According to the ISIS-2 study, the immediate administration of ASA leads to a reduction in mortality of over 20 % (Herold 2020 / Stierle 2017).
• Beta-blocker in symptomatic patients with systolic blood pressure values > 100 mmHg at a heart rate of > 55 / min.; Dosage: 5 mg - 15 mg i. v. (Stierle 2017)

The assignment of the patient with MI should already be made from the emergency ambulance in centers with PCI- possibility (Herold 2020).

Patients with a NSTEMI should be immediately admitted to a coronary angiography to decide on the further procedure. Patients with a STEMI have an urgent indication for revascularization (see "Surgical Therapy" below).

If an acute PCI is not possible within 120 min after initial contact, a conservative therapy with fibrinolysis activators (see "Surgical Therapy" below) should be performed (Herold 2020).

Dual antiplatelet therapy (DAPT):

• Acetylsalicylic acid: ASA should be administered parenterally or s. l. orally for life after the initial dose of 160 mg - 325 mg (dose: 75 mg - 100 mg /d)
• plus ticagrelor: initial 180 mg, then 2 x 90 mg / d
• Contraindications:
  • anamnestic intracranial bleeding
  • current hemorrhages

alternative:

• Prasugrel: initially 60 mg, subsequently 10 mg / d
• Contraindications:
  • anamnestic intracranial bleeding
  • ischemic insult
  • transient ischemic attack
  • current bleeding

Note: however, prasugrel is not used in patients ≥ 75 years of age or with a body weight ≤ 60 kg

alternative:

• Clopidogrel: initially 300 - 600 mg, then 75 mg / day.

Beta-blocker: i. v. administration of a beta-blocker should be performed in all patients without contraindication, regardless of fibrinolysis or PCI. If contraindications exist (such as systolic RR < 120 mmHg, heart rate < 60 / min, acute heart failure), reevaluation should be performed after the first 24 h . Early beta-blockers do not reduce lethality, but they lead to a decrease in recurrent ischemia and re-infarction (Kasper 2015). Dosage recommendation:

• Atenolol 5 mg - 10 mg initial i. v., then 100 mg / day.

or

• Metoprolol 5 mg - 10 mg initial i. v., then 4 x 50 mg / d orally and after another 2 days 2 x 100 mg / day (Pinger 2019).

ACE- inhibitors: Treatment with ACE inhibitors should be performed in the absence of contraindications in the first 24 h in all patients - but especially in the following:

• Anterior wall infarction
• Pulmonary congestion
• LVEF < 40
• diabetes mellitus
• Heart failure (Stierle 2017).
• Note: If intolerance to ACE- inhibitors exists, administration of angiotensin receptor blockers (AT1- blockers) is recommended. ACE inhibitors reduce mortality in STEMI. Maximum benefit is seen in high-risk patients in particular.(Kasper 2015).
• Dosage recommendation:
  • Captopril: 6.25 mg initial, 2 h later 12.5 mg, 12 h later 25 mg, then 2 x 50 mg / day.

Or

• Ramipril 2 x 2.5 mg, then 2 x 5 mg / day (Pinger 2019).

Renin- angiotensin- aldosterone inhibitor (RAAS): There is an indication for the administration of a renin- angiotensin- aldosterone inhibitor indefinitely in patients with:

• impaired left ventricular function
• Heart failure
• Intolerance to an ACE inhibitor (Kasper 2015).
• Dosage recommendation:
  • Valsartan: 20 mg in 4 increments to 2 x 160 mg as a maintenance dose.

Cholesterol synthesis enzyme inhibitors (CSE- inhibitors) / statins: Patients with MI should receive high-dose statins early after MI and this should be independent of the initial cholesterol level.

Dosage recommendation:

• Pravastatin: 40 - 80 mg / day (Pinger 2019).

• Note: The target value of LDL- cholesterol should be < 70 mg / dl (Herold 2020).

Iron carboxymaltose i. v. in case of existing iron deficiency (see above "Occurrence": Associated non-cardiac diseases) (Zeller 2018).

STEMI: Patients with STEMI should receive prompt revascularization. This can be done by:

• primary PCI
• fibrinolysis

Primary PCI: Immediate primary PCI is the modality of choice for all patients with persistent ST- stretch elevation and symptoms of ischemia of ≥ 12 h. However, there are strict time limits for performing PCI in this setting. It should be performed no later than 120 min after initial contact. If direct PCI is not possible within 120 min after initial contact, it is recommended to initiate immediate lysis in patients with STEMI, taking into account the contraindications. After lysis has been performed, cardiac catheterization should be performed within 24 h but not before 3 h (Stierle 2017).

(For detailed information on revascularization, see coronary artery disease).

Thrombolysis is not performed in patients with an NSTEMI (Stierle 2017).

Conservative therapy with activators of fibrinolysis: Fibrinolysis is performed in patients with STEMI who cannot undergo prompt PCI and in whom there are no contraindications. Absolute contraindications to fibrinolysis:

• intracranial hemorrhage
• hemorrhagic apoplexy
• apoplexy of unclear etiology
• ischemic apoplexy < 6 mon.
• CNS injuries
• intracranial neoplasms
• atrioventricular malformations
• Aortic dissection
• Surgery/trauma/head injury < 3 weeks
• gastrointestinal bleeding < 1 mon.
• history of known hemorrhagic diathesis (with the exception of menses)
• Noncompressible puncture (such as liver biopsy, lumbar puncture) performed in the last 24 h (Stierle 2017).

Relative contraindications:

• oral anticoagulation
• Gravidity
• Delivery ≤ 1 week
• TIA within the last 6 months
• infective endocarditis
• active gastric ulcer
• advanced liver disease
• protracted or traumatic resuscitation
• refractory hypertension (RR systolic > 180 mmHg and / or diastolic > 110 mmHg) (Stierle 2017).

The following substances are used for fibrinolysis:

• Streptokinase: Streptokinase is the only one of the mentioned agents that has an indirect fibrinolytic effect. It should be pre-injected with corticosteroids because of antigenicity.
• Dosage recommendation: Streptase: 1.5 million U i. v. over a period of 30 - 60 min.
• Enoxaparin: As adjunctive therapy: initially in patients < 75 years a bolus of 30 mg i. v. , after 15 min and then every 12 h until discharge or revascularization 1 mg / kg s. c. In patients > 75 years every 12 h 0.75 mg / kg. Bolus administration should not be given (Herold 2020).
• Alteplase: Alteplase has a direct fibrinolytic effect. As a bolus, 15 mg i. v., followed by 0.75 mg / kg over a period of 30 min, followed by 0.5 mg / kg over 60 min i. v.. The total dose should be ≤ 100 mg.

• Reteplase: Also has a direct fibrinolytic effect. 10 U as a bolus and again 10 U at 30 min intervals i. v.

Note: Concomitant antithrombotic drugs such as heparin or fondaparinux should be used.

• Heparin. Dosage recommendation: As a bolus, 60 U / kg i. v. (maximum dose 4,000 U). Subsequently as i. v. infusion maximum over 48 h 12 U / kg, maximum 1,000 U / h. Target value aPTT: 50 s - 70 s. Control respectively after 3, 6, 12, 24 h.
• Fondaparinux: Fondaparinux should only be used in combination with streptokinase. Contraindication: creatinine > 3.0 mg / day. Dosage recommendation: As a bolus administration 2.5 mg i. v., then 2.5 mg s. c. / d until discharge ref. to a maximum of 8 days.

After i. v. application of the thrombolytic, a TIMI- 3- flow occurs within 90 min in 50% of patients (Stierle 2017).

Indirect signs of successful reperfusion are:

• Regression of ST-segment elevation in the ECG by 50%-75%.
• Disappearance of the infarct pain

Direct signs of successful reperfusion: these are detectable exclusively by coronary angiography.

Complications: Arrhythmias sometimes occur during reperfusion (Herold 2020). There is also a risk of intracranial hemorrhage. It is 0.9% (Stierle 2017).

Success rate: Recanalization occurs in approximately 70%-80% of cases. Early lysis can reduce the lethality of MI by about 50 %.

Prognosis: Reocclusion occurs in about 20 % - 25 % of cases after successful lysis. Therefore, it is recommended to perform coronary angiography in all patients at short notice for further therapeutic decision (e.g. performance of PCI or bypass surgery). Without reperfusion therapy, approximately 50% of infarct vessels are reopened after 2 weeks (Pinger 2019).

NSTEMI: Patients with a definite NSTEMI should undergo coronary angiography according to ACC / AHA (2016). However, coronary angiography is rarely appropriate in cases of low to moderate probability of NSTEMI. The further procedure is done depending on the findings of coronary angiography (Pinger 2019).

Patients should be monitored for 24-48 hours after a simple MI. Bed rest is recommended for 12 - 24 h or until the CK value drops significantly.

With a large transmural MI, there is an increased risk of a cardiac wall rupture in the 1st week. For this reason, mobilisation should be delayed to avoid wall tension due to physical exertion. In a very small MI, discharge from inpatient treatment is possible after 72 h at the earliest, provided that early rehabilitation is organised (Stierle 2017).

The integration into everyday or professional life can be carried out gradually. The patient should be encouraged to participate in an outpatient heart group (Herold 2020).

The hospital lethality lies with patients:

• with primary PCI of about 5 %.
• with systemic thrombolysis at about 10
• Patients without revascularization therapy in 15

The most common causes of death from MI are:

• occurrence of ventricular fibrillation (most frequent)
• Pump failure (second most common cause)

40% of patients do not survive the first day after the Ml. Most of them die within the first hours after the onset of symptoms. According to the MONICA project (monitoring trends and determinants in cardiovascular disease) 50% of all patients with MI die within the first 4 weeks. In the 2 following years after discharge from hospital, another 5 % - 10 % of all MI patients die of sudden cardiac death.

With the help of the Killip classification, statements can be made about the further prognosis with regard to the disturbance of the pump function.

• Stage I: Auscultatory no RGs, no 3rd heartbeat, no signs of decompensation; lethality < 5 %
• Stage II: A 3rd heart sound is auscultable, over a maximum of 50% of the lung tissue RGs are auscultable due to heart failure, there is a pulmonary venous pressure increase; lethality up to 20%.
• Stage III: Due to severe heart failure, more than 50% of the lung tissue RGs can be auscultated or there is pulmonary oedema; lethality up to 40%

• Stage IV: Cardiogenic shock with hypotension (systolic blood pressure ≤ 90 mmHg), peripheral vasoconstriction, oliguria, cyanosis, cold sweat; lethality up to 90% (Herold 2020 / Pinger 2019 / Siegenthaler 2006)

Forrester classification:The Forrester classification was also developed for further prognosis of patients after myocardial infarction. It mainly considers clinical signs of peripheral perfusion disturbance and pulmonary capillary pressure values (Siegenthaler 2006).

• Class I: PCWP < 18 mmHg (pulmonary capillary occlusion pressure). CI > 2.2 l / min / m² (heart index). There is no pulmonary congestion and no peripheral reduced blood flow. The heart activity is within the physiological range.
• Class II: PCWP > 18 mmHg. CI > 2.2 l / min / m2. There is an isolated congestion of the lungs, the periphery of the body is still sufficiently supplied with blood. Also known as "backward failure of the left heart".

• Class III: PCWP < 18 mmHg. CI < 2.2 l / min / m2. There is a peripheral reduced blood circulation. Also called "forward failure of the left heart".
• Class IV: PCWP > 18 mmHg. CI < 2.2 l / min / m2. Both congestion of the lungs and a peripheral reduced blood flow are detectable. The patient is in cardiogenic shock (Böhm 2000).

Improvement of prognosis: The prognosis can be improved by the following general measures:

• observance of nicotine withdrawal
• mediterranean diet
• aerobic physical exercise ≥ 3x a week for 30 - 45 min
• optimal adjustment of any arterial hypertension that may be present
• optimal adjustment of any diabetes mellitus that may be present
• regular flu vaccination 1 x yearly

Improvement of prognosis through the following medicinal or therapeutic measures:

• Beta-blockers without intrinsic activity: These lead to a decrease in cardiac output. Prolonged use leads to a reduction in heart rate, cardiac output and plasma renin activity. This reduces the risk of reinfarction and heart failure. There is also a decrease in rhythmically induced deaths. Dosage recommendation: Initially only 1/10 of the target dose should be administered. Increase the target dose very slowly and under constant clinical control of symptoms, weight and auscultation findings. Increase the dose every 14 days. Usually the adjustment takes several months.
• Bisoprolol 1 x 23, 75 mg / d, target dose 2 x 100 mg / day
• Carvedilol 3 x 3.125 mg / d, target dose 2 x 25 mg / day (Braun 2018 / Rietbrock 1991 / )
• Antiplatelet therapy After an MI, dual antiplatelet therapy (DAPT) should be given for 1 year. Recommended dosage:
  • Acetylsalicylic acid: ASS 75 mg - 100 mg /d lifelong (Herold 2020)
• plus
  • Clopidogrel: initially 300 - 600 mg, then 75 mg / day for 1 year
• or
  • Ticagrelor: initially 180 mg, then 2 x 90 mg / day. Contraindications (anamnestic intracranial bleeding, recent bleeding)
• or
  • Prasugrel: initially 60 mg, then 10 mg / day. Contraindications: anamnestic intracranial hemorrhage, ischemic insult, transient ischemic attack, recent hemorrhage. Note: Prasugrel is not used in patients ≥ 75 years or with a body weight ≤ 60 kg

• Oral anticoagulation in addition to DAPT: In the event of atrial fibrillation, a left ventricular thrombus or the necessity of inserting a heart valve, oral anticoagulation should also be administered (see also thrombosis prophylaxis).
• Cholesterol-lowering drugs / statins. Recommended dosage: Pravastatin: 40 - 80 mg / day (Pinger 2019). The target value of LDL cholesterol should be < 70 mg / dl. If this cannot be achieved, additional ezetimib or PCSK9 inhibitors should be given. Recommended dosage:
  • Ezetimib 10 mg / day
  • PCSK9 inhibitor e.g. Evolocumab 10 mg / day (Schwabe 2016))

• ACE inhibitors: After an MI, the heart undergoes a structural remodelling and adaptation process, the so-called "remodeling". These changes can lead to hypertrophy, expansion of the myocardial scar and dilatation of the left ventricle, which considerably worsen the further prognosis. With ACE inhibitors it is possible to stop this process and thus reduce overall mortality, as several studies (such as SAVE, TRACE, AIRE, etc.) have shown. Recommended dosage:
  • Captopril: 6.25 mg initial, 2 h later 12.5 mg, 12 h later 25 mg, then 2 x 50 mg/d
• or
  • Ramipril 2 x 2.5 mg, then 2 x 5 mg / d orally (Pinger 2019).
• or
  • If the patient experiences intolerances such as coughing or if there are contraindications, he/she can switch to Sartane (AT1 blocker). Dosage recommendation: Valsartan: 20 mg in 4 steps to 2 x 160 mg as maintenance dose
• Aldosterone receptor antagonist: If, despite treatment with beta-blockers and ACE inhibitors (or AT1 blockers), the patient's heart failure persists or the left ventricular ejection fraction (LV- EF) is reduced by < 35%, the administration of an aldosterone receptor antagonist is recommended.
• Aldosterone receptor antagonist. Recommended dosage:
  • Spironolactone: Starting dose: 1 x 25 mg, target dose 2 x 25 mg - 50 mg (Aktories 2017)

Cardiac Re-chronization Therapy: Cardiac re-chronization therapy should be performed in:

• a left femoral block QRS complex > 120 ms - 150 ms
• LV- EF ≤ 35 % of progressive heart failure (NYHA > II) despite optimal drug therapy
• Implantable defibrillator (ICD): If after optimal drug treatment > 40 days symptomatic heart failure NYHA II - III or a reduced left ventricular ejection fraction ≤ 35%, there is an indication for an ICD.

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