Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationships between aortic stenosis, coronary artery disease, angina pectoris, and myocardial infarction were examined in 173 patients with isolated calcific aortic stenosis who had coronary arteriography as well as cardiac catheterization. All were over age 40 and had definite cardiac symptoms; 156 later had aortic valve replacement. Coronary lesions narrowing the lumen by 50% or more were present in 37% of patients aged 40 to 59 and 68% of those aged 60 to 82. Coronary disease was present in 64% of patients with angina pectoris and 33% of those without angina. Angina which occurred only in association with dyspnea on exertion was associated with coronary disease in 45% of instances, whereas angina which also occurred on exertion without any dyspnea or which occurred with emotional stress, after meals, during sleep, or at rest unprovoked was associated with coronary disease in 80% of instances. Patients with coronary disease without any chest pain or with atypical pain considered nonanginal were men, usually over age 60, with congestive heart failure as the predominant symptom. Electrocardiograms showing transmural inferior or anterolateral infarction nearly always indicated coronary disease, while QS patterns in Leads V1-2 occurred frequently with normal coronary arteries. Serum cholesterol was elevated in 23% of those with coronary disease and 8% of those without. A group of patients with moderate aortic stenosis could be identified, with aortic valve areas of 0.55 to 0.80 cm. per square meter, in whom coronary disease was the sole or chief cause of symptoms. The operative mortality rate with aortic valve replacement was 9.6% in those with coronary disease and 1.4% in those without significant coronary disease. Coronary disease is frequently present in patients with calcific aortic stenosis, particularly in those over 60, those with angina, and those with symptoms despite only moderate aortic stenosis. The type of anginal syndrome, the ECG evidence of transmural infarction, and the coronary risk factors provide additional clues for clinical diagnosis.
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PMID:Aortic stenosis, angina pectoris, and coronary artery disease. 30 Feb 16

The diagnostic accuracy of 14-lead exercise electrocardiography was evaluated in 112 women who had no history of myocardial infarction and underwent coronary angiography. The sensitivity of ST-segment displacement of 0.1 mV or more in any of 14 ECG leads was 0.79 for coronary artery stenosis of at least 70%; the specificity was 0.66. Results were similar using bipolar ECG leads CC5 and CM5 or 11 standard ECG leads. The ST-segment shifts that occurred only during exercise were associated with a 77% false-positive rate (10 of 13). Downsloping ST-segment depression did not provide more diagnostic information than horizontal ST-segment depression in the three clinical subsets of women. In women with typical angina pectoris, ST-segment depression of at least 0.15 mV for 0.08 second after the J point or a final treadmill time less than 360 seconds was predictive of proximal left or multivessel coronary artery disease. In the women with probable angina or nonspecific chest pain, this finding was not of diagnostic value. ST-segment elevation of 0.1 mV or more in leads V1-2 or a VL predicted proximal stenosis of at lest 80% in the left anterior descending coronary artery in all six women with typical angina pectoris. Maximal exercise testing in women with typical angina provides important diagnostic information when 11 standard ECG leads are recorded. In women with probable angina or nonspecific chest pain, diagnostic exercise testing is less useful and bipolar leads CC5 and CM5 are sufficient for most clinical purposes.
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PMID:Diagnostic accuracy of exercise ECG lead systems in clinical subsets of women. 707 2

Certain angina and coronary artery disease forms do not respond to Ca2+ channel blockers, and a role for vasoactive eicosanoids such as PGF2alpha in Ca2+ antagonist-insensitive coronary vasospasm is suggested; however, the signaling mechanisms are unclear. We investigated whether PGF2alpha-induced coronary smooth muscle contraction is Ca2+ antagonist insensitive and involves activation of a PKC-dependent pathway. We measured contraction in single porcine coronary artery smooth muscle cells and intracellular free Ca2+ concentration ([Ca2+]i) in fura 2-loaded cells and examined cytosolic and particulate fractions for PKC activity and reactivity with isoform-specific PKC antibodies. In Hanks' solution (1 mM Ca2+), PGF2alpha (10-5 M) caused transient [Ca2+]i increase followed by maintained [Ca2+]i increase and 34% cell contraction. Ca2+ channel blockers verapamil and diltiazem (10-6 M) abolished maintained PGF2alpha-induced [Ca2+]i increase but only partially inhibited PGF2alpha-induced cell contraction to 17%. Verapamil-insensitive PGF2alpha contraction was inhibited by PKC inhibitors GF-109203X, calphostin C, and epsilon-PKC V1-2. PGF2alpha caused Ca2+-dependent alpha-PKC and Ca2+-independent epsilon-PKC translocation from cytosolic to particulate fractions that was inhibited by calphostin C. Verapamil abolished PGF2alpha-induced alpha-but not epsilon-PKC translocation. PMA (10-6 M), a direct activator of PKC, caused 21% contraction with no significant [Ca2+]i increase and epsilon-PKC translocation that were inhibited by calphostin C but not verapamil. Membrane depolarization by 51 mM KCl, which stimulates Ca2+ influx, caused 36% cell contraction and [Ca2+]i increase that were inhibited by verapamil but not GF-109203X or calphostin C and did not cause alpha- or epsilon-PKC translocation. Thus a significant component of PGF2alpha-induced contraction of coronary smooth muscle is Ca2+ antagonist insensitive, involves Ca2+-independent epsilon-PKC activation and translocation, and may represent a signaling mechanism of Ca2+ antagonist-resistant coronary vasospasm.
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PMID:Ca2+ antagonist-insensitive coronary smooth muscle contraction involves activation of epsilon-protein kinase C-dependent pathway. 1460 78