Histamine, the main amine released during allergic reactions, can provoke coronary arterial spasm manifested as angina pectoris This has been shown during clinical and laboratory studies The effects of histamine on cardiac function are mediated via H1- and H2- receptors situated on the four cardiac chambers and coronary arteries Coronary arteries of cardiac patients are hyperactive and contain stores of histamine which can initiate coronary artery spasm Clinical observations indicate that angina pectoris or acute myocardial infarction can be provoked by acute allergic reaction The coincidental occurrence of chest pain and allergic reaction accompanied by clinical and laboratory findings of classical angina pectoris seems to constitute the syndrome of allergic angina The clinical symptoms of allergic angina include chest discomfort, dyspnoea, faintness, nausea, pruritus and urticaria They are accompanied by signs such as hypotension, diaphoresis, pallor and bradycardia There are also electrocardiographic findings indicating myocardial ischaemia, arrhythmias and conduction defects Thus, in patients undergoing acute allergic reaction, the development of chest pain could be explained by the mechanism of coronary arterial spasm provoked by the release of histamine, which constitutes the syndrome of allergic angina

Histamine-induced coronary artery spasm: the concept of allergic angina.

Mitral Valvular Disease: A Clinicopathologic Survey of the Conditions Causing the Mitral Valve To Function Abnormally

Anatomic and functional features of the normal and abnormal mitral valve are reviewed. Of 1,010 personally studied necropsy patients with severe (functional class III or IV, New York Heart Association) cardiac dysfunction from primary valvular heart disease, 434 (43%) had mitral stenosis (MS) with or without mitral regurgitation (MR): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 189 (44%) patients, and associated with aortic stenosis in 152 (35%), with pure (no element of stenosis) aortic regurgitation in 65 (15%) patients, and with tricuspid valve stenosis with or without aortic valve stenosis in 28 (6%) patients. The origin of MS was rheumatic in all 434 patients. Of the 1,010 necropsy patients, 165 (16%) had pure MR (papillary muscle dysfunction excluded): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 97 (59%) patients, and associated with pure aortic regurgitation in 45 (27%) and with aortic valve stenosis in 23 (14%) patients. When associated with dysfunction of the aortic valve, pure MR was usually rheumatic in origin, but when unassociated with aortic valve dysfunction it was usually nonrheumatic in origin. Review of operatively excised mitral valves in patients with pure MR unassociated with aortic valve dysfunction disclosed mitral valve prolapse (most likely an inherent congenital defect) as the most common cause of MR. Excluding the patients with MR from coronary heart disease (papillary muscle dysfunction), mitral prolapse was the cause of MR in 60 (88%) of the other 68 patients, and a rheumatic origin was responsible in only 3 of the 68 patients, all 68 of whom were greater than 30 years of age. Mitral anular calcification in persons aged greater than 65 years is usually associated with calcific deposits in the aortic valve cusps and in the coronary arteries. Because calcium in each of these 3 sites is common in older individuals residing in the Western World, it is most reasonable to view mitral anular calcification in older individuals as a manifestation of atherosclerosis. Mitral anular calcium appears to be extremely uncommon in persons with total serum cholesterol levels less than 150 mg/dl. Mitral anular calcium may produce mild MR and, if the deposits are heavy enough, MS.

Morphologic features of the normal and abnormal mitral valve.

The left ventricular papillary muscles appear to be the last portions of the heart to be perfused by coronary arterial blood. As a consequence they are sensitive anatomic markers of myocardial ischemia. Foci of necrosis or fibrosis therefore are commonly seen in these structures, particularly the posteromedial papillary muscle, which has a poorer blood supply than does the anterolateral muscle. Coronary arterial luminal narrowing is the most common cause of necrosis or fibrosis of the left ventricular papillary muscles. Other conditions, all associated with inadequate cardiac output, which may produce these lesions include left ventricular outflow tract obstruction, especially that resulting from congenitally malformed aortic valves, acute valvular regurgitation (infective endocarditis), various cardiomyopathies, and primary endocardial fibroelastosis with or without anomalous origin of one or both coronary arteries from the pulmonary trunk. Various infiltrative diseases, including inflammation (Aschoff b...

Left ventricular papillary muscles. Description of the normal and a survey of conditions causing them to be abnormal.

Relation between eosinophilia and endomyocardial disease

Löffler's fibroplastic parietal endocarditis, eosinophilic leukemia, and Davies' endomyocardial fibrosis: the same disease at different stages?

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Löffler's fibroplastic parietal endocarditis, eosinophilic leukemia, and Davies' endomyocardial fibrosis: the same disease at different stages?