Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

78 patients with hypercholesterolemia were treated with beta-pyridylcarbinol from 1964 to 1966. In 1972 42 patients could be contacted again, 37 of them were reexamined. 14 of these 42 patients were still taking beta-pyridylcarbinol in 1972. Those who had taken more than 0.9 gm per day had a lower serum cholesterol level than in the beginning of the treatment in 1964. Clinical signs of atherosclerosis (angina pectoris and peripheral arterial disease) were significantly less in this group of patients. Besides a few flush reactions or heartburn no side effects to treatment were noted. The two groups of patients, with whom the 14 were compared, included 9 who had been taking clofibrate since 1966 and 19 patients without drug treatment for hypercholesterolemia. Both groups had higher serum cholesterol levels than the group of 14 with beta-pyridylcarbinol treatment over 8 years.
 ...
PMID:[Treatment of hypercholesterolemia with beta-pyridylcarbinol. Experiences after long term treatment over 8 years (author's transl)]. 81 96

The effects of estrogen on cardiovascular risk factors have been less well defined in men than in women. We measured lipid and lipoprotein concentrations, lipoprotein particle size distributions, lipoprotein (a), homocysteine, and markers of thrombosis and fibrinolysis in 18 [corrected] healthy elderly men (age 74 +/- 3 years, mean +/- S.D.) before and after 9 weeks of treatment with 0.5, 1 or 2 mg/day of oral micronized 17beta-estradiol. LDL-C (-6%), apo B (-9%), triglyceride (-5%), and homocysteine (-11%) concentrations decreased with estradiol, whereas HDL-C (+14%) increased. Intermediate-size VLDL subclass concentrations were lowered and LDL and HDL subclass levels altered in such a way as to cause average LDL and HDL particle size to increase. Lipoprotein (a) did not change. Fibrinogen (-13%) and plasminogen activator inhibitor-1 (PAI-1) concentrations (-26%) decreased, but there were no changes in thrombotic markers including thrombin-antithrombin III complex, prothrombin fragment 1.2, D-dimer, antithrombin activity, protein-C and S and von Willebrand factor antigen. Breast tenderness occurred in four men and heartburn in five but did not require discontinuation of treatment. We conclude that oral estrogen in men reduces homocysteine, fibrinogen, and PAI-1 concentrations and favorably influences VLDL, LDL and HDL subclass levels without increasing markers of thrombotic risk.
Atherosclerosis 1998 Apr
PMID:Oral estrogen improves serum lipids, homocysteine and fibrinolysis in elderly men. 962 79

Atherosclerosis is the most important cause of acute coronary syndromes. The mediators that trigger vasospasm, including endothelin and serotonin, are synthesized and secreted into circulation from atherosclerotic plaques and surrounding tissues. A 68-year-old man was hospitalized due to acute coronary syndrome four times in a one-year period. The patient presented to emergency service again with heartburn and a pressure-like pain in his upper abdomen in February 2012. He was admitted to the coronary care unit with the detection of a more than three-fold increase in troponin values and ischemic changes on electrocardiography. By decision of the cardiology council, the endothelin receptor antagonist, bosentan was added to the treatment. There were no contraindications to this medication according to his blood and hepatic indicators. After confirmation of the Social Security Institution, bosentan was started as 62.5 mg twice a day. After the first month, the dose was increased to 125 mg b.i.d. As of completion of the eighth month of treatment with bosentan, the patient had not been hospitalized due to angina attack or acute coronary syndrome.
...
PMID:A new hope in the treatment of coronary vasospasm: bosentan. 2416 96