Chest Pain, Exercise Electrocardiography and Coronary Arteriography

Over the last 6 or 7 years Dr. Richard Ross and I in the department of medicine at Johns Hopkins Medical School have had a continuing interest in objective methods which might be used in assessing the individual who comes to the physician complaining of chest pain. Angina pectoris is many things; it is a metabolic defect with lactate excess, it is a certain pathological picture, it is a group of individuals who are disposed to have certain things happen to them, but most of all angina pectoris is pain in the chest. It is pain in the chest as far as the patient is concerned, and this is the symptom on which the physician has to base important decisions concerning diagnosis, prognosis and treatment. The problem with chest pain is that it is a very subjective complaint, and a discussion with the patient is certainly the most satisfactory way to establish its cause

Res Medica, April 1967, Special Issue – Lauder Brunton Centenary Symposium on Angina Pectoris

WelcomeHistorical SessionOpening AddressLauder BruntonHistory of Angina Pathophysiological SessionThe Pathology of AnginaExperimental Studies on the Myocardial Collateral CirculationFirst DiscussionCoronary Blood Flow and Myocardial Metabolism in Angina PectorisCardiac Function in Patients with AnginaSecond Discussion Therapeutic SessionThe Modern EpidemicIs Angina Preventable?Third DiscussionChest Pain, Exercise Electrocardiography and Coronary Arteriography(Correlative Studies in Angina PectorisPrognosis of Angina PectorisPanel DiscussionSumming U

Genome-Wide Association Study Identifies Two Novel Regions at 11p15.5-p13 and 1p31 with Major Impact on Acute-Phase Serum Amyloid A

Elevated levels of acute-phase serum amyloid A (A-SAA) cause amyloidosis and are a risk factor for atherosclerosis and its clinical complications, type 2 diabetes, as well as various malignancies. To investigate the genetic basis of A-SAA levels, we conducted the first genome-wide association study on baseline A-SAA concentrations in three population-based studies (KORA, TwinsUK, Sorbs) and one prospective case cohort study (LURIC), including a total of 4,212 participants of European descent, and identified two novel genetic susceptibility regions at 11p15.5-p13 and 1p31. The region at 11p15.5-p13 (rs4150642; p = 3.20×10−111) contains serum amyloid A1 (SAA1) and the adjacent general transcription factor 2 H1 (GTF2H1), Hermansky-Pudlak Syndrome 5 (HPS5), lactate dehydrogenase A (LDHA), and lactate dehydrogenase C (LDHC). This region explains 10.84% of the total variation of A-SAA levels in our data, which makes up 18.37% of the total estimated heritability. The second region encloses the leptin receptor (LEPR) gene at 1p31 (rs12753193; p = 1.22×10−11) and has been found to be associated with CRP and fibrinogen in previous studies. Our findings demonstrate a key role of the 11p15.5-p13 region in the regulation of baseline A-SAA levels and provide confirmative evidence of the importance of the 1p31 region for inflammatory processes and the close interplay between A-SAA, leptin, and other acute-phase proteins