Mechanical complications after acute myocardial infarction

The typical five mechanical complications after myocardial infarctionSee heart attack. include:

1. Acute mitral valveHeart valve between the left atrium and left ventricle. It got its name because of its shape, which has a strong resemblance to a bishop’s mitre. insufficiencyinsufficient fulfilment of a function (pumping weakness of the heart, leakage of the heart valves). due to papillary muscleThere are elongated, cone-shaped muscle projections on the inner wall of the heart chambers. They arise directly from the heart muscle tissue and are connected to the edges of the leaflet valves at the other end by tendon threads. During contraction of the ventricles, they also contract, preventing the valves from recoiling (bulging) into the atria. rupture (partial or complete rupture)
2. VentricularArising from the ventricle. septal defect
3. Rupture of the free myocardial wall with consecutive pericardial tamponadeFilling of the pericardial sac with fluid, e.g. with blood as a result of a ruptured heart wall or with fluid as a result of a pericardial effusion. This increases the pressure on the heart and thus hinders the pumping action. It represents a life-threatening situation and requires urgent treatment.
4. Pseudoaneurysm of the left ventricleLower chamber of the heart. A healthy heart has two ventricles (right and left).
5. Ventricular aneurysmAbnormal dilatation of a blood vessel or a chamber of the heart. of the left ventricle

The first four complications mentioned are especially associated with high morbidity and lethality. Successful management of these complications is highly complex and requires excellent multidisciplinary collaboration between cardiac surgeons, cardiologists and intensive care physicians, as well as the relevant nursing staff. The typical patient presenting with mechanical complications after myocardial infarctionIf the blood supply to an organ or part of an organ is interrupted (arterial occlusion due to thrombosis, embolism), the affected cells die and this area is gradually replaced with connective tissue. An infarction leads to a weakening of organ function, e.g. after a heart attack the pumping action of the heart is restricted. is the elderly woman with heart failure and chronic renal failure who developed her first myocardial infarction in the process. On admission to hospital, these patients are often already in cardiogenic shockLife-threatening condition due to the severely reduced pumping capacity of the heart. The heart is not pumping enough blood into the circulation. The following causes, for example, can lead to cardiogenic shock: heart attack, acute leakage of the aortic or mitral valve, pericardial tamponade, inflammation of the heart muscle (myocarditis) or the inner lining of the heart (endocarditis), etc. with a high catecholamine or vasopressor requirement and not infrequently already intubated and mechanically ventilated. The five typical mechanical complications with their incidence, pathophysiology, clinical presentation, course and therapy are discussed in detail below.

Acute mitral valve regurgitation with papillary muscle rupture (partial or complete)

The incidence of acute mitral regurgitation due to partial or complete papillary muscle rupture after myocardial infarction is 0.05 to 0.26 per cent and is associated with a lethality of 10 to 40 per cent. If, in the course of a myocardial infarction, there is a reduction in blood flow or a complete interruption of blood flow to the papillary muscles, rupture may occur. The posteromedial papillary muscle is more frequently affected because, unlike the anterolateral papillary muscle, it is supplied by only one coronary vessel, either the circumflex branch or the right coronary artery. The severity of the patient’s clinical symptoms is determined by whether the papillary muscle is partially or completely torn off. Patients with acute mitral regurgitation typically present with acute pulmonary oedema 3 to 5 days after acute transmural ST elevation myocardial infarction. After appropriate diagnostics, primarily by means of echocardiography, and intensive medical stabilisation, there is an indication for emergency mitral valve replacement, either biological or mechanical. The affected coronary arteries are often supplied with bypasses. The perioperative lethality in this case is about 20 per cent. The survival rate after surgical intervention is over 70 per cent, whereas the survival rate after conservative, medicinal and intensive medical therapy alone is only 30 per cent. Alternatively, for patients who cannot undergo cardiac surgery, an interventional therapy strategy using MitraClip as a so-called “edge-to-edge repair” can be considered.

Ventricular septal defect after myocardial infarction

The incidence of ventricular septal defect (VSD)Defect in the ventricular septum. after acute myocardial infarction is 0.3 per cent. Risk factorsCollective term for factors that can pose a health risk. These include alcohol and nicotine consumption, obesity, high blood pressure, sugar and fat metabolism disorders, high cholesterol levels, stress, lack of exercise, etc. are increased age, female gender and delayed therapy of myocardial infarction. In 70 per cent of cases, so-called apical or anterior ventricular septal defects occur, in which the left anterior descending arteryA blood vessel leading away from the heart that transports oxygenated blood to the organs. Arteries pulsate and can be palpated on the wrist, for example (pulse). The aorta is the main artery of the body. is affected as the supplying vessel. PosteriorSomething at the back / behind. VSDs with the right coronaryConcerning the coronary vessels that supply blood to the heart muscle. artery as the supplying vessel are present in 30 per cent. The lethality of untreated VSD is 80 per cent in the first 30 days after myocardial infarction. Patients typically present 3 to 5 days after myocardial infarction with dyspnoeaAll forms of breathing disorders that lead to shortness of breath., orthopnoea, hypotensionLow blood pressure. A systolic pressure of below 100 mmHg is known as hypotension. Due to family history, this can occur, for example, perfectly normally in young slim women., oliguria and cold periphery due to the more or less pronounced left-to-right shuntA natural or surgically created short-circuit connection between normally unconnected areas (e.g. between two vessels).. After appropriate diagnostics by means of echocardiography, the patient is stabilised in intensive care. The treatment of choice is surgical closure of the VSD using a patchA patch is used to “patch” holes, the patches are usually made of plastic or the patient’s own pericardial tissue.. In this case, the procedure is delayed by 7 days in haemodynamically stable patients under intensive medical supervision until  the adjacent tissue has stabilised by means of connective and scar tissue. The surgical techniques used are either a Daggett patch repair or a David infarct exclusion, possibly with concomitant bypassA vascular bridge. A bypass is used to circumvent narrowed sections of blood vessels. This allows organs to be supplied with sufficient blood again, for example.. Emergency surgery is only considered in haemodynamically unstable patients in refractory cardiogenic shockIn medicine, shock refers to a life-threatening condition in which the oxygen supply to the body’s cells is reduced. E.g. as a result of circulatory collapse due to a severely reduced pumping capacity of the heart (myocardial infarction), extreme loss of fluid due to bleeding or in septic clinical pictures and allergic reactions. and is associated with a high concomitant lethality. Alternatively, interventional treatment with an Amplatzer® Septal OccluderCollapsible double umbrella that closes an open site after deployment, e.g. an open ductus Botalli. The occluder is guided into the heart with a special catheter. Device can be considered.  Although the initial success rate is very high at 80 to 100 per cent, complications such as embolisation of the occluder device, device failure in the sense of insufficient closure of the VSD or ventricular arrhythmias and haemolysis frequently occur during the course of the procedure.

Pseudoaneurysm of the left ventricle after myocardial infarction

Pseudoaneurysms of the left ventricle are very rare and are a special form of the previously mentioned rupture of the free ventricular wall. This is a covered perforationProcess at the end of which a breakthrough has taken place. If deliberate, the artificial creation of a breakthrough. of the ventricular wall. If, after transmural myocardial infarction, adhesions and malformations of the epicardium with the adjacent pericardiumThe pericardium is the third and outermost skin of the heart. It has the function of a protective shell that prevents overstretching of the heart muscle. Since it consists of two layers, it also serves as a sliding surface for the movements of the heart. occur in the context of the accompanying inflammatory reactions, the pericardium adhered as a result prevents blood from escaping from the left ventricle in the area of the rupture of the ventricular wall.  Pseudoaneurysms are most common in the lateral and posterior wall of the left ventricle. This can be explained by the recumbent position of patients hospitalised for myocardial infarction.  The clinical symptoms are often non-specific, so that a pseudoaneurysm can often remain undetected for a long time. Symptoms include dyspnoea, signs of heart failure and chest pain. This complication affects men more often than women. The diagnostic tools are echocardiography, computed tomography and magnetic resonance imagingMagnetic resonance imaging, MRI. Diagnostic procedure without the use of X-rays. Magnetic fields are used to produce images of organs and body structures.. Treatment is urgent surgical closure of the perforation site using PTFE reinforced direct suture or Gore-Tex, Dacron or pericardial patch closure. Alternatively, arterial retrograde interventional closure with an Amplatzer® Septal Occluder Device is possible in inoperable patients . Placement is carried out under transoesophageal echocardiography and fluoroscopy control.

Aneurysm of the left ventricle after myocardial infarction

True aneurysms of the left ventricle after myocardial infarction can remain undetected for a long time. Surgical therapy is considered for refractory heart failure, ventricular arrhythmias that persist with maximal pharmacological therapy and after interventional ablationDestruction of congenital, additional conduction pathways that cause cardiac rhythm disturbances. This is performed with the help of heat generation through cardiac catheters. attempts, and recurrent thromboembolism from the aneurysm despite effective anticoagulationInhibition of blood clotting by means of medication (e.g. Marcumar, Heparin). Colloquially also incorrectly referred to as “blood thinning”. therapy. Here, there is a IIa recommendation according to the American College of Cardiologists (ACC) and the American Heart Association (AHA) of 2004, with an evidence level B. Surgical treatment consists of plication or excision of the aneurysm with concomitant reconstruction of the left ventricle using endoventricular patches.