Polymorphisms in the Genes for Coagulation Factors II, V, and VII in Patients With Ischemic Heart Disease

1999 ◽  
Vol 123 (12) ◽  
pp. 1230-1235
Author(s):  
Yue Jin Feng ◽  
Andrew Draghi ◽  
Douglas R. Linfert ◽  
Alan H. B. Wu ◽  
Gregory J. Tsongalis
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Coagulation Factors ◽  
The United States ◽  
Ischemic Heart ◽  
Factor Vii ◽  
Control Groups ◽  
Sequence Of Events ◽  
Increased Risk ◽  
And Control

Abstract Background.—Cardiovascular disease remains the leading cause of mortality in the United States, accounting for approximately 33% of all deaths in this country. Of these deaths, most are due to acute myocardial infarctions (AMIs), which are associated with thrombotic coronary artery obstruction and/or occlusion. These events could potentially be due to alterations in genes coding for coagulation factors. Several polymorphisms have been described in the factor II, V, and VII genes, which may predispose one to increased risk for ischemic heart disease (IHD). Objective.—To determine if mutations in 3 coagulation factor genes could predispose an individual to increased risk for arterial thrombosis as a mechanism for developing unstable angina (UA) or AMI. Methods.—We examined 125 hospitalized patients (mean age, 53 ± 6 years, 79 men and 46 women), including 32 with AMI, 68 with UA, and 25 noncardiac controls, for a genetic predisposition for increased risk of IHD. EDTA-anticoagulated whole blood was collected at the time of hospital admission. DNA was extracted, and the polymorphisms were detected by polymerase chain reaction amplification of these genes with subsequent restriction enzyme digestion and gel electrophoresis. Results.—Our results showed that 3 (9.4%), 3 (4.4%), and 1 (4%) individuals were heterozygous for prothrombin G20210A and 3 (9.4%), 5 (7.4%), and 1 (4%) individuals were heterozygous for factor V Leiden in the AMI, UA, and control groups, respectively. The following genotype frequencies for the factor VII R353Q polymorphism were identified: 25 (78.1%), 56 (82.4%), and 18 (72%) with RR and 7 (21.9%), 12 (17.6%), and 7 (28%) with RQ in the AMI, UA, and control groups, respectively. No QQ homozygotes were identified. For the HVR4 size polymorphism, the following genotypes were identified: 3 (9.4%), 4 (5.9%), and 5 (20%) individuals with H7H7; 11 (34.4%), 33 (48.5%), and 12 (48%) with H6H7; and 18 (56.2%), 31 (45.6%), and 8 (32%) with H6H6 genotypes in the AMI, UA, and control groups, respectively. There were no H7H5 and H6H5 genotypes found in this study. Conclusions.—Although the frequency differences of these polymorphisms in patients with AMI and UA were not statistically significant from those in controls, several trends are consistent with what has been reported in the literature. Although any of these or other undefined genetic abnormalities may result in IHD, it is possible that phenotypic predisposition to IHD initially presents as UA. A larger population study addressing the significance of these polymorphisms in the sequence of events that lead to IHD, including cases of UA, is warranted.

Factor VII Clotting Assay: Influence of Different Thromboplastins and Factor VII-Deficient Plasmas

1991 ◽  
Vol 65 (02) ◽  
pp. 160-164 ◽  
Author(s):  
Marina Poggio ◽  
Armando Tripodi ◽  
Guglielmo Mariani ◽  
Pier Mannuccio Mannucci ◽  
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Dose Response ◽  
Response Curve ◽  
Ischemic Heart ◽  
Factor Vii ◽  
Response Curves ◽  
Assay Sensitivity ◽  
Clinical Laboratories ◽  
Coagulant Activity

SummaryBeing a putative predictor of ischemic heart disease, the measurement of factor VII (FVTI) coagulant activity will be presumably requested to clinical laboratories with increasing frequency. To assess the influence on FVII assays of different thromboplastins and FVII-deficient plasmas we compared performances of all possible combinations of 5 thromboplastins and 6 deficient plasmas. The reproducibility of the clotting times of the dose-response curves for human and rabbit thromboplastins were acceptable (CV lower than 7%), whereas bovine thromboplastin had a higher CV. Reproducibility was very similar for all deficient plasmas when they were used in combination with a given thromboplastin. Responsiveness of the dose-response curve did not depend on the deficient plasma but rather on the thromboplastin: one rabbit thromboplastin was the least responsive, the bovine thromboplastin the most responsive, the human and the remaining two rabbit thromboplastins had intermediate responsiveness. Assay sensitivity to cold-activated FVII varied according to the thromboplastin: the bovine thromboplastin was the most sensitive, the human thromboplastin the least sensitive, of the three rabbit thromboplastins two were relatively sensitive, one was almost insensitive. In conclusion, our results indicate that thromboplastin rather than deficient plasma is the crucial factor in the standardization of FVII assay.

scholarly journals Increased Remnant Cholesterol Explains Part of Residual Risk of All-Cause Mortality in 5414 Patients with Ischemic Heart Disease

2016 ◽  
Vol 62 (4) ◽  
pp. 593-604 ◽  
Author(s):  
Anne-Marie K Jepsen ◽  
Anne Langsted ◽  
Anette Varbo ◽  
Lia E Bang ◽  
Pia R Kamstrup ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Ldl Cholesterol ◽  
Hdl Cholesterol ◽  
Hazard Ratio ◽  
Residual Risk ◽  
Ischemic Heart ◽  
Increased Risk ◽  
All Cause Mortality ◽  
Remnant Cholesterol

Abstract BACKGROUND Increased concentrations of remnant cholesterol are causally associated with increased risk of ischemic heart disease. We tested the hypothesis that increased remnant cholesterol is a risk factor for all-cause mortality in patients with ischemic heart disease. METHODS We included 5414 Danish patients diagnosed with ischemic heart disease. Patients on statins were not excluded. Calculated remnant cholesterol was nonfasting total cholesterol minus LDL and HDL cholesterol. During 35836 person-years of follow-up, 1319 patients died. RESULTS We examined both calculated and directly measured remnant cholesterol; importantly, however, measured remnant cholesterol made up only 9% of calculated remnant cholesterol at nonfasting triglyceride concentrations <1 mmol/L (89 mg/dL) and only 43% at triglycerides >5 mmol/L (443 mg/dL). Multivariable-adjusted hazard ratios for all-cause mortality compared with patients with calculated remnant cholesterol concentrations in the 0 to 60th percentiles were 1.2 (95% CI, 1.1–1.4) for patients in the 61st to 80th percentiles, 1.3 (1.1–1.5) for the 81st to 90th percentiles, 1.5 (1.1–1.8) for the 91st to 95th percentiles, and 1.6 (1.2–2.0) for patients in the 96th to 100th percentiles (trend, P < 0.001). Corresponding values for measured remnant cholesterol were 1.0 (0.8–1.1), 1.2 (1.0–1.4), 1.1 (0.9–1.5), and 1.3 (1.1–1.7) (trend, P = 0.006), and for measured LDL cholesterol 1.0 (0.9–1.1), 1.0 (0.8–1.2), 1.0 (0.8–1.3), and 1.1 (0.8–1.4) (trend, P = 0.88). Cumulative survival was reduced in patients with calculated remnant cholesterol ≥1 mmol/L (39 mg/dL) vs <1 mmol/L [log-rank, P = 9 × 10−6; hazard ratio 1.3 (1.2–1.5)], but not in patients with measured LDL cholesterol ≥3 mmol/L (116 mg/dL) vs <3 mmol/L [P = 0.76; hazard ratio 1.0 (0.9–1.1)]. CONCLUSIONS Increased concentrations of both calculated and measured remnant cholesterol were associated with increased all-cause mortality in patients with ischemic heart disease, which was not the case for increased concentrations of measured LDL cholesterol. This suggests that increased concentrations of remnant cholesterol explain part of the residual risk of all-cause mortality in patients with ischemic heart disease.

Abstract TP197: Countries With an Inverse Ratio of Ischemic Stroke and Ischemic Heart Disease- Analysis of Global Burden of Disease Data

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Talha Jilani ◽  
Iryna Lobanova ◽  
Brandi R French ◽  
Farhan Siddiq ◽  
Camilo R Gomez ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ischemic Stroke ◽  
Ischemic Heart Disease ◽  
Burden Of Disease ◽  
The United States ◽  
American Samoa ◽  
Marshall Islands ◽  
Ischemic Heart ◽  
Global Burden Of Disease ◽  
Global Burden

Background: Ischemic heart disease is more prevalent than ischemic stroke in most countries, including the United States; however, recent data suggests that ischemic stroke may be more prevalent in some countries. We performed this study to identify the countries with an inverse ratio of ischemic stroke and ischemic heart disease and associated attributes. Methods: We analyzed the data using the Global Burden of Disease (GBD) website; GBD Compare tool published by the Institute for Health Metrics and Evaluation (IHME), Seattle, Washington for the year 2017. We categorized individual 195 countries based on the ratio of ischemic stroke/ischemic heart disease and divided them into ≥1.0, 0,5-99, and <0.5. Gross domestic product (GDP) per capita for each country was calculated using data from Worldometers. Results: There were 51, 125, and 19 countries with the ratio of ischemic stroke/ischemic heart disease and divided them into ≤0.5, 0.5-0.99, and ≥1.0 respectively (see Table). The range of ratio was between 0.24 and 1.86. Countries with inverse ratio included China (1.86), North Korea (1.31), Guam (1.28), Taiwan (1.20), Marshall Islands (1.15), Timor-Leste (1.16), South Korea (1.13), Seychelles (1.11), Northern Mariana Islands (1.10), Cambodia (1.09), Federated States of Micronesia (1.08), American Samoa (1.07), Samoa (1.06), Kiribati (1.04), Solomon Islands (1.03), Fiji (1.02), Indonesia (1.02), Mauritius (1.01), and Vanuatu (1.00). Conclusions: Approximately 1 out of 10 countries have an inverse ratio of ischemic stroke / ischemic heart disease incidences. The inverse ratio is predominantly driven by a lower incidence of ischemic heart disease.

scholarly journals Modern statin therapy in clinical practice: The lower the better

2013 ◽  
Vol 141 (1-2) ◽  
pp. 104-106 ◽  
Author(s):  
Edita Stokic
Keyword(s):  
Heart Disease ◽  
Cardiovascular Risk ◽  
Ischemic Heart Disease ◽  
Statin Therapy ◽  
Meta Analysis ◽  
Ischemic Heart ◽  
Mortality And Morbidity ◽  
Increased Risk ◽  
Coronary Events ◽  
Risk Treatment

Lipid and lipoprotein disorders are well known risk factors for atherosclerosis and its complications. The level of atherogenic LDL-cholesterol (LDL-C) is directly related to an increased risk of occurrence and progression of ischemic heart disease. Epidemiological and clinical studies have shown that the use of statin therapy to decrease LDL-C can significantly reduce the incidence of mortality, major coronary events and the need for revascularization procedures in the different groups of patients. The findings of a large meta-analysis conducted by the Cholesterol Treatment Trialists? (CTT) collaborators showed that every 1.0 mmol/l reduction of atherogenic LDL-C is associated with a 22% reduction in cardiovascular diseases mortality and morbidity. However, despite the impressive results of the benefits of statin therapy, the EUROASPIRE study showed that about 50% of patients with ischemic heart disease did not achieve target LDL-C levels. According to the new ESC/EAS Guidelines for the Management of Dyslipidaemias in patients with a very high cardiovascular risk, treatment goal should be to decrease LDL-C below 1.8 mmol/l or ?50% of initial values. In the majority of patients that can be achieved by statin therapy. For this reason an adequate choice of statins is of crucial importance, whereby the needed reduction in atherogenic LDL-C, after the identification of its target level based on the assessment of total cardiovascular risk, can be achieved.

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