scholarly journals Gallstone Disease and Increased Risk of Ischemic Heart Disease

2015 ◽  
Vol 35 (10) ◽  
pp. 2073-2075 ◽  
Author(s):  
Giovanni Targher ◽  
Christopher D. Byrne
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Gallstone Disease ◽  
Ischemic Heart ◽  
Increased Risk

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.

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.

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.

393Ischemic burden by vasodilator stress CMR predicts long-term all-cause death and the effect of revascularization in patients with known or suspected stable ischemic heart disease

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
V Marcos Garces ◽  
J Gavara ◽  
C Rios-Navarro ◽  
P Racugno ◽  
A Bellver Navarro ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Ischemic Heart ◽  
Vasodilator Stress ◽  
Clinical Event ◽  
Stable Ischemic Heart Disease ◽  
Late Enhancement Imaging ◽  
Increased Risk ◽  
Stress Cmr

Abstract Background In patients with stable ischemic heart disease (SIHD) the effect of revascularization on all-cause death (the most verifiable clinical event) is unknown. Objectives We explored the potential of the ischemic burden as derived from vasodilator stress cardiovascular magnetic resonance (CMR) to guide decision-making in this scenario. Methods In a large prospective multicenter registry, we recruited 6389 patients (mean age 65±11 years, 38% female) submitted to undergo vasodilator stress CMR for known or suspected SIHD. Baseline and CMR characteristics were prospectively recorded. The ischemic burden (at vasodilator stress first-pass perfusion imaging) and necrosis extent (at late enhancement imaging) were computed (17-segment model). The effect of CMR-related revascularization (within the following three months) on all-cause death (revised using the unified regional electronic health system registry) was explored. Results During a 5.75-year median follow-up, 717 (11.2%) all-cause deaths were documented. In multivariable analyses, more extensive ischemic burden (per 1-segment increase) independently related to all-cause death (1.05 [1.03–1.07], p<0.001). In 1034 patients (517 revascularized, 517 non-revascularized) strictly 1:1 matched for the independent predictors of outcome and of undergoing CMR-related revascularization (age, diabetes mellitus, male sex, LVEF, ischemic burden and necrosis extent), CMR-related revascularization did not significantly alter all-cause death rate (13.3% vs. 13.3%, p=0.54). Nevertheless, a potent interaction existed with the ischemic burden (p<0.001). CMR-related revascularization independently reduced the risk of all-cause death in 430 patients with ischemic burden >5 segments (9.3% vs. 16.3%, HR 0.56 [0.32–0.98], p=0.02) but it independently increased risk in 604 patients with ischemic burden ≤5 segments (16.2% vs. 11.3%, HR 1.59 [1.03–2.45], p=0.037). Figure 1. CMR-related revascularization Conclusions In patients with known or suspected stable ischemic heart disease the ischemic burden as derived from vasodilator stress CMR can be helpful to predict the effect of revascularization on long-term all-cause death. Acknowledgement/Funding Funded by “Instituto de Salud Carlos III”/FEDER (PIE15/00013, PI17/01836, and CIBERCV16/11/00486 grants) and Generalitat Valenciana (GV/2018/116).

Serum bilirubin and risk of ischemic heart disease in middle-aged British men

1995 ◽  
Vol 41 (10) ◽  
pp. 1504-1508 ◽  
Author(s):  
L H Breimer ◽  
G Wannamethee ◽  
S Ebrahim ◽  
A G Shaper
Keyword(s):  
Risk Factors ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Confidence Intervals ◽  
Serum Bilirubin ◽  
Forced Expiratory Volume ◽  
Ischemic Heart ◽  
Middle Aged ◽  
Low Concentrations ◽  
Increased Risk

Abstract The possibility that low concentrations of serum bilirubin may be associated with increased risk of ischemic heart disease has been examined in a prospective study of 7685 middle-aged British men. During 11.5 years there were 737 major ischemic heart disease (IHD) events. A U-shaped relationship was observed between serum bilirubin and risk of IHD. Low bilirubin was associated with several cardiovascular risk factors, in particular smoking, low concentrations of high-density lipoprotein cholesterol, low forced expiratory volume in 1 s, and low serum albumin. The U-shaped relationship persisted even after adjusting for several risk factors. Compared with men in the lowest fifth of the distribution (bilirubin &lt; 7 mumol/L), those in the middle range (8-9 mumol/L) showed a 30% reduction in relative risk [RR = 0.68 (95% confidence intervals 0.51-0.89)] in IHD, whereas men in the top fifth (&gt; 12 mumol/L) showed similar risk to the lowest fifth [RR = 0.99 (95% confidence intervals 0.73-1.34)], which persisted after exclusion of men with bilirubin &gt; 17 mumol/L. The significance of this U-shaped relationship is unclear, but it could be interpreted as support for the role of endogenous antioxidants in the etiology of IHD.

Sign in / Sign up

Export Citation Format

Share Document