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)

In order to ascertain the most effective index for predicting coronary sclerosis, the concentration of lipids, lipoproteins, and apoproteins in serum were determined in 45 males aged over 44 with angiographically diagnosed effort angina and in 153 male controls aged over 44 without ischemic heart disease (IHD) on physical examination. The results of our study are summarized as follows. 1) Alcohol intake of 25 g/day or more and smoking of 20 cigarettes/day or more showed significant odds ratios of 0.47 and 2.33, respectively. 2) By decrease of 10 mg/dl in HDLC level or of 10 mg/dl in Apo-AI level, the possibility of coronary sclerosis increases twofold after adjusting the effects of confounders. 3) LDLC/HDLC and Apo-B/Apo-AI are effective indices for predicting coronary sclerosis and, in particular, the probability of coronary sclerosis increases 3.8 times by increase of 0.5 in Apo-B/Apo-AI.
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PMID:Coronary sclerosis risk factors in males with special reference to lipoproteins and apoproteins: establishing an index. 228 5

The levels of plasminogen activator inhibitor (PAI), protein C (pC), total cholesterol (TC), high and low density lipoprotein cholesterols (HDLC and LDLC), apolipoproteins A1 (apoA1) and B (apoB) were measured in 45 patients with coronary heart disease angiographically documented and 10 healthy subjects without coronary heart disease and coronary atherosclerosis as evidenced by coronary angiography and provocative tests. Twenty three patients had primary angina (PA) with a duration of less than 3 months, twenty two patients presented with chronic coronary heart disease (CCHD) with a duration of more than 4 months. In general, a negative correlation between PAI and HDLC levels in the patients under study (r = -0.413; p = 0.02), it was higher in PA (r = -0.687; p = 0.02), but disappeared in CCHD (r = 0.027). The content of PAI correlated with the cholesterol index (r = 0.654; p less than 0.001 in the whole group), more greatly in PA (r = 0.865; p = 0.001) than in CCHD (r = 0.506, NS). There was a good correlation between the levels of pC and apoB in the whole group (r = 0.606; p less than 0.001) and in PA (r = 0.662; p = 0.001), but not in CCHD (r = 0.288, NS). The content of pC also correlated with a apoB/apoA1 ratio (r = 0.445; p = 0.002 in the whole group of patients). This correlation was significantly positive in PA (r = 0.455; p = 0.044), but not in CCHD (r = 0.022). Thus, higher levels of PAI coincided with atherogenic changes in those of HDLC, and an increase in the content of pC was in agreement with that of apoB. The interrelationships are particularly typical of early stages of CHD.
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PMID:[Plasminogen activator inhibitor and protein C: their relation to plasma lipids and lipo- and apoproteins in ischemic heart disease of different duration]. 239 63

Our specific aim was to assess within-family clustering of high-density lipoprotein cholesterol (HDLC) levels in kindreds identified through probands with primary hypoalphalipoproteinemia, and to determine whether, and to what degree, familial aggregation of HDLC less than or equal to the tenth percentile represents a heritable trait, familial hypoalphalipoproteinemia. Our probands were selected arbitrarily by virtue of HDLC less than or equal to the age-sex-race-specific tenth percentile as the sole dyslipoproteinemia, with an additional requirement that they be normotriglyceridemic (triglyceride levels less than the 90th percentile). The probands were also required to have primary hypoalphalipoproteinemia, not secondary to diseases and/or drugs. Fifteen of the 16 probands were men; 12 were referred because of premature myocardial infarction, angina, or stroke, 2 because of family history of premature myocardial infarction or stroke, and 2 because of low HDLC observed on routine health examinations. Two of the 16 kindreds exhibited three-generation vertical transmission of bottom decile HDLC. In three kindreds, there was also three-generation vertical transmission of bottom decile HDLC, but top decile triglycerides accompanied bottom decile HDLC in one or more generations. Eight kindreds displayed two-generation vertical transmission of bottom decile HDLC. After excluding probands, there were 11 critical matings (bottom decile HDLC by normal), with 30 living offspring, all of whom were sampled. Of these 30 offspring, 13 had bottom decile HDLC, 17 had HDLC greater than tenth percentile. The ratio of offspring with bottom decile HDLC to those of HDLC greater than tenth percentile was 13:17 (0.76/1), not significantly different from the ratio of 1/1, the ratio predictive of a dominant trait, X2(1) = 0.53, P greater than 0.4. The nearly 1:1 segregation ratio for the group of offspring was not due to the aggregation of sibships with, in general, most of the sibs, or none of the sibs affected; within-family expression of low HDLC was also not sex-linked. The 13 hypoalphalipoproteinemic offspring of 11 critical matings included only two subjects whose bottom decile HDLC was accompanied by top decile triglyceride. Our data suggests that not only (by selection) was low HDLC in the probands the sole dyslipoproteinemia, but that the segregation of low HDLC in offspring of critical matings was primarily accounted for by isolated low HDLC, not by hypoalphalipoproteinemia secondary to hypertriglyceridemia. Familial hypoalphalipoproteinemia is a heritable disorder with a pattern of transmission not significantly different from that expected by a hypothesis of mendel
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PMID:Primary and familial hypoalphalipoproteinemia. 669 57

A 60-year-old homozygous patient with familial high density lipoprotein deficiency (Tangier disease) was examined by coronary angiography and intravascular ultrasound because of typical angina pectoris. We found a normal left ventricular function, moderately diffuse coronary sclerosis without stenosis, and no critical stenosis of peripheral arteries. Intravascular ultrasound revealed normal thickness and the three-layer appearance of the arterial intima, media, and adventitia within the peripheral arteries, and showed a single, discrete arteriosclerotic lesion in one iliac artery segment. The lack of severe atherosclerosis was remarkable insofar as massive foam cell formation in reticuloendothelial tissues and the virtually complete absence of circulating HDL is characteristic of Tangier disease and had been previously demonstrated in this patient.
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PMID:[Coronary angiography and intravascular ultrasound examination of a 60-year-old patient with familial HDL deficiency (Tangier disease)]. 805 48

Decreased adiponectin level, the adipose tissues hormone, is related to high body mass and insulin resistance, which are risk factors for atherosclerosis. It was shown, that cigarette smoking and high homocysteine (Hcy) level are associated with low level of adiponectin. In the presented study we search for the associations between 5 polymorphisms in genes involved in Hcy metabolism - methylenetetrahydrofolate reductase (MTHFR) and paraoxonase 1 (PON1), smoking, adiponectin levels and insulin resistance in subjects with coronary artery disease (CAD). The studied group consisted of 152 patients subjected to coronary arteriography. In 116 patients significant atherosclerotic changes in vascular vessels were confirmed (CAD group), remaining patients were considered as the control group. In studied group, the levels of glucose, insulin, adiponectin and blood lipids profile were measured. Adiponectin and insulin levels were determined by radioimmunological assays. The insulin resistance was calculated using mathematical HOMA model. MTHFR 677C>T, 1298A>C, PON1 -108C>T, L55M, Q192R polymorphisms were ascertained by PCR-RFLP methods. In the studied group (N = 152), significantly decreased adiponectin levels and higher degree of insulin resistance were present in subjects with angina pectoris (N = 129) and peripheral atherosclerosis (N = 32), whereas in the cases of CAD, confirmed in coronary arteriography (N = 116), only the higher degree of insulin resistance was noted. Arterial hypertension (p = 0.004), diabetes mellitus (p = 0.03) and smoking (p = 0.04) were the most significant vascular risk factors associated with the low adiponectin levels. In CAD group, negative correlations between the level of adiponectin and the dose of MTHFR 677T (r = - 0.238; p < 0.05) and PON1 55M (r = -0.251; p < 0.05 alleles were found. The MTHFR 677T allele was also correlated with degree of insulin resistance (r = 0.391; p < 0.05). In smokers, these genetic associations were stronger (r = -0.394; = -0.353; r = 0.440; respectively), which demonstrates, that the negative effects of MTHFR 677T and PON1 55M alleles are enhanced by smoking. Moreover, only in smokers the correlations between adiponectin levels and: the degree of insulin resistance (r = -0.465; p < 0.01) and the levels of HDLC (r = 0.479; p < 0.01) were seen. In summary, in CAD patients, particularly in smokers, occurrence of MTHFR and PON1 risk alleles is associated with the decreased adiponectin levels and/or increased degree of insulin resistance.
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PMID:[Smoking enhances the decrease of adiponectin level in patients with coronary artery disease, carriers of MTHFR 677T and PON1 55M alleles]. 2136 Sep 15