, Volume 24, Issue 2, pp 132-139

Angina pectoris bei extrakoronaren Erkrankungen

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Zusammenfassung

Als Angina pectoris wird der durch eine myokardiale Ischämie ausgelöste Brustschmerz bezeichnet. Die Sauerstoffversorgung des Myokards hängt dabei sowohl vom Sauerstoffangebot als auch vom aktuellen Sauerstoffbedarf ab. Weil die Koronarreserve ca. 500% des Ruhebedarfs entspricht, spielt bei den Ursachen der Angina pectoris die Koronarstenose quantitativ die weitaus größte Rolle. Andererseits wird durch den Pathomechanismus der Angina pectoris deutlich, daß viele Faktoren, die das Gleichgewicht von Sauerstoffangebot und-bedarf verändern, Angina pectoris auslösen können. Dabei sind die Wandspannung, die Kontraktilität, die Herzfrequenz, der Katecholaminspiegel im Blut, die Koronarperfusion und die Sauerstoffkapazität des Blutes zu nennen. Die Aortenstenose, die hypertensive Herzkrankheit, Kardiomyopathien und die Anämie sind Erkrankungen, die diese Faktoren wesentlich beeinflussen und dadurch Angina pectoris in sensu strictu auslösen können. Als molekularbiologischer Mechanismus der Angina pectoris ist die Abgabe von Adenosin bei myokardialer Ischämie ins Interstitium bekannt. Es wird zum größeren Teil vom Endothel aufgenommen, aber es hat ebenfalls eine Funktion als Botenstoff: Wenn Adenosin Gesunden intravenös verabreicht wird, erzeugt es bei den Probanden Angina-pectorisähnliche Schmerzen.

Abzugrenzen von den genannten extrakoronaren Auslösern der Angina pectoris sind die nichtkardiogenen Brustschmerzen. Diese Abgrenzung ist in vielen Fällen bereits durch eine genaue Anamneseerhebung möglich. Zu nennen sind das dissezierende Aortenaneurysma, die Perikarditis, die Lungenembolie, der muskuloskelettale und der psychovegetative Thoraxschmerz.

Therapeutisch steht bei Angina pectoris aus extrakoronarer Ursache die therapie der Grundkrankheit im Vordergrund.

Abstract

Chest pain can arise from cardiovascular or noncardiovascular causes. Among the latter are the skin, the chest wall, intrathoracic structures, or subdiaphragmatic organs. The problem to attribute the chest discomfort to either the heart or extracardiac organs arises because the heart, pleura, aorta, and esophagus are all supplied by sensory fibers from the same spinal segments.

In contrast to the diseases mentioned above, angina pectoris in sensu strictu is defined as chest pain or discomfort of cardiac origin that arises because of temporary imbalance between myocardial oxygen supply and demand. The metabolic oxygen requirements of the myocardium are essentially dictated by myocardial contraction since only a fraction of the consumed oxygen is needed by the quiescent heart. Therefore, the factors that primarily influence myocardial oxygen consumption include heart rate, the force of cardiac contraction, and myocardial wall tension, as determined by pressure (afterload), volume (preload), and wall thickness. Extracoronary diseases, e. g. hypertensive heart disease, aortic stenosis or cardiomyopathies, can influence these factors and induce angina pectoris (Figure 1). On the other hand, different diseases influencing the oxygen supply, e. g. anemia, can cause angina pectoris, too. In addition, the modulation of the coronary tone by mediators and cytokines can cause angina, coronary spasm being one example.

The neurophysiological substrate of angina pectoris are ganglia which are present within the heart, particularly in epicardial fat. The sympathetic nervous system is the main conveyer of afferent pain fibers from the heart and pericardium, but many fibers may travel by the vagus and the phrenic nerves. Therefore, multiple thoracic structures may cause similar pain syndromes in the distressed patient. The blood supply of intrinsic cardiac ganglia arises primarily from branches of the proximal coronary arteries. Adenosine, among a number of substances, can modulate the activity generated by cardiac afferent nerve endings and intrinsic cardiac neurones. During myocardial ischemia adenosine is released in large quantities into the interstitial space. Given as an intravenous bolus to healthy volunteers or to patients with ischemic heart disease and angina pectoris, adenosine provokes angina pectoris-like pain, which is similar to habitual angina pectoris with regard to quality and location. But other mediators (e. g. bradykinin, histamine, prostaglandins, potassium, lactate) can be involved in the development of angina pectoris, too.

As most emphasis should be given to the most serious causes first, the cardiologist has to consider ischemic cardiac disease in the differential diagnosis of nearly every case of acute chest pain. The differential diagnosis contains several causes of nonischemic cardiac chest pain.

Dissecting aortic aneurysm may cause severe anterior chest pain that can be mistaken for myocardial infarction. Patients frequently will note the sudden onset of the pain rather than the relatively slower onset of ischemic pain. Furthermore, they feel as a tear and describe it as the most severe pain they have ever had.

Pericarditis can be characterized as a sharp precordial knife-like pain that is often increased by lying down, breathing, swallowing, or any other thoracic motion. Radiation of pericardial pain is often relieved by sitting up or leaning forward. It may involve the shoulders, upper back, and neck because of the irritation of the diaphragmatic pleura.

Acute pulmonary embolism is associated with severe chest pain. It may mimic acute myocardial infarction. Pulmonary embolism should be suspected when dyspnea or tachypnea seems to be disproportionate to the severity of the chest pain.

Diffuse esophageal spasm is the extracardiac condition that is confused most often with ischemic cardiac chest pain. This pain presents as a deep thoracic pain that may be present over most of the thorax. It may extend down the anteromedial side of the arms and forearms. It may be relieved by nitrates, making it even more confusing.

Emotional disorders are among the most common causes of chest pain. Usually the discomfort is described as tightness or aching. Because the pain is often midsternal in location and because it can be quite severe, it can be confused with ischemic chest pain. Many times, the history can be helpful in differentiating this pain.

Chest pain may come from various muscle and ligament injuries in the chest wall. Costochondritis is a fairly common cause of anterior chest pain. Other causes include cervical or thoracic osteoarthritis, ruptured cervical disks, or compression of the neurovascular bundle by a cervical rib or shortened anterior scalene muscle.

The treatment of angina pectoris induced by extracoronary diseases must be a therapy of the extracoronary disease first. But it is worth mentioning that often extracoronary induced angina pectoris is accompanied by non-significant coronary artery stenosis.