Abstract #994705: The High Prevalence of Coronary Calcification and Increased Risk for Coronary Heart Disease in Patients with Sheehan’s Syndrome

2021 ◽  
Vol 27 (6) ◽  
pp. S109-S110
Author(s):  
JAVAID AHMAD BHAT ◽  
Mehak Afroze ◽  
Hardeep Singh ◽  
Shahnaz A. Mir
2021 ◽  
pp. jech-2020-214358
Author(s):  
Pekka Martikainen ◽  
Kaarina Korhonen ◽  
Aline Jelenkovic ◽  
Hannu Lahtinen ◽  
Aki Havulinna ◽  
...  

BackgroundGenetic vulnerability to coronary heart disease (CHD) is well established, but little is known whether these effects are mediated or modified by equally well-established social determinants of CHD. We estimate the joint associations of the polygenetic risk score (PRS) for CHD and education on CHD events.MethodsThe data are from the 1992, 1997, 2002, 2007 and 2012 surveys of the population-based FINRISK Study including measures of social, behavioural and metabolic factors and genome-wide genotypes (N=26 203). Follow-up of fatal and non-fatal incident CHD events (N=2063) was based on nationwide registers.ResultsAllowing for age, sex, study year, region of residence, study batch and principal components, those in the highest quartile of PRS for CHD had strongly increased risk of CHD events compared with the lowest quartile (HR=2.26; 95% CI: 1.97 to 2.59); associations were also observed for low education (HR=1.58; 95% CI: 1.32 to 1.89). These effects were largely independent of each other. Adjustment for baseline smoking, alcohol use, body mass index, igh-density lipoprotein (HDL) and total cholesterol, blood pressure and diabetes attenuated the PRS associations by 10% and the education associations by 50%. We do not find strong evidence of interactions between PRS and education.ConclusionsPRS and education predict CHD events, and these associations are independent of each other. Both can improve CHD prediction beyond behavioural risks. The results imply that observational studies that do not have information on genetic risk factors for CHD do not provide confounded estimates for the association between education and CHD.


2017 ◽  
Vol 3 ◽  
pp. 233372141769667 ◽  
Author(s):  
Minjee Lee ◽  
M. Mahmud Khan ◽  
Brad Wright

Objective: We investigated the association between childhood socioeconomic status (SES) and coronary heart disease (CHD) in older Americans. Method: We used Health and Retirement Study data from 1992 to 2012 to examine a nationally representative sample of Americans aged ≥50 years ( N = 30,623). We modeled CHD as a function of childhood and adult SES using maternal and paternal educational level as a proxy for childhood SES. Results: Respondents reporting low childhood SES were significantly more likely to have CHD than respondents reporting high childhood SES. Respondents reporting both low childhood and adult SES were 2.34 times more likely to have CHD than respondents reporting both high childhood and adult SES. People with low childhood SES and high adult SES were 1.60 times more likely than people with high childhood SES and high adult SES to report CHD in the fully adjusted model. High childhood SES and low adult SES increased the likelihood of CHD by 13%, compared with high SES both as a child and adult. Conclusion: Childhood SES is significantly associated with increased risk of CHD in later life among older adult Americans.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Elena M. Yubero-Serrano ◽  
Juan F. Alcalá-Diaz ◽  
Francisco M. Gutierrez-Mariscal ◽  
Antonio P. Arenas-de Larriva ◽  
Patricia J. Peña-Orihuela ◽  
...  

Abstract Background Peripheral artery disease (PAD) is recognized as a significant predictor of mortality and adverse cardiovascular outcomes in patients with coronary heart disease (CHD). In fact, coexisting PAD and CHD is strongly associated with a greater coronary event recurrence compared with either one of them alone. High-density lipoprotein (HDL)-mediated cholesterol efflux capacity (CEC) is found to be inversely associated with an increased risk of incident CHD. However, this association is not established in patients with PAD in the context of secondary prevention. In this sense, our main aim was to evaluate the association between CEC and PAD in patients with CHD and whether the concurrent presence of PAD and T2DM influences this association. Methods CHD patients (n = 1002) from the CORDIOPREV study were classified according to the presence or absence of PAD (ankle-brachial index, ABI ≤ 0.9 and ABI > 0.9 and < 1.4, respectively) and T2DM status. CEC was quantified by incubation of cholesterol-loaded THP-1 cells with the participants' apoB-depleted plasma was performed. Results The presence of PAD determined low CEC in non-T2DM and newly-diagnosed T2DM patients. Coexisting PAD and newly-diagnosed T2DM provided and additive effect providing an impaired CEC compared to non-T2DM patients with PAD. In established T2DM patients, the presence of PAD did not determine differences in CEC, compared to those without PAD, which may be restored by glucose-lowering treatment. Conclusions Our findings suggest an inverse relationship between CEC and PAD in CHD patients. These results support the importance of identifying underlying mechanisms of PAD, in the context of secondary prevention, that provide potential therapeutic targets, that is the case of CEC, and establishing strategies to prevent or reduce the high risk of cardiovascular events of these patients. Trial registrationhttps://clinicaltrials.gov/ct2/show/NCT00924937. Unique Identifier: NCT00924937


Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Elizabeth J Bell ◽  
Jennifer L St. Sauver ◽  
Veronique L Roger ◽  
Nicholas B Larson ◽  
Hongfang Liu ◽  
...  

Introduction: Proton pump inhibitors (PPIs) are used by an estimated 29 million Americans. PPIs increase the levels of asymmetrical dimethylarginine, a known risk factor for cardiovascular disease (CVD). Data from a select population of patients with CVD suggest that PPI use is associated with an increased risk of stroke, heart failure, and coronary heart disease. The impact of PPI use on incident CVD is largely unknown in the general population. Hypothesis: We hypothesized that PPI users have a higher risk of incident total CVD, coronary heart disease, stroke, and heart failure compared to nonusers. To demonstrate specificity of association, we additionally hypothesized that there is not an association between use of H 2 -blockers - another commonly used class of medications with similar indications as PPIs - and CVD. Methods: We used the Rochester Epidemiology Project’s medical records-linkage system to identify all residents of Olmsted County, MN on our baseline date of January 1, 2004 (N=140217). We excluded persons who did not grant permission for their records to be used for research, were <18 years old, had a history of CVD, had missing data for any variable included in our model, or had evidence of PPI use within the previous year.We followed our final cohort (N=58175) for up to 12 years. The administrative censoring date for CVD was 1/20/2014, for coronary heart disease was 8/3/2016, for stroke was 9/9/2016, and for heart failure was 1/20/2014. Time-varying PPI ever-use was ascertained using 1) natural language processing to capture unstructured text from the electronic health record, and 2) outpatient prescriptions. An incident CVD event was defined as the first occurrence of 1) validated heart failure, 2) validated coronary heart disease, or 3) stroke, defined using diagnostic codes only. As a secondary analysis, we calculated the association between time-varying H 2 -blocker ever-use and CVD among persons not using H 2 -blockers at baseline. Results: After adjustment for age, sex, race, education, hypertension, hyperlipidemia, diabetes, and body-mass-index, PPI use was associated with an approximately 50% higher risk of CVD (hazard ratio [95% CI]: 1.51 [1.37-1.67]; 2187 CVD events), stroke (hazard ratio [95% CI]: 1.49 [1.35-1.65]; 1928 stroke events), and heart failure (hazard ratio [95% CI]: 1.56 [1.23-1.97]; 353 heart failure events) compared to nonusers. Users of PPIs had a 35% greater risk of coronary heart disease than nonusers (95% CI: 1.13-1.61; 626 coronary heart disease events). Use of H 2 -blockers was also associated with a higher risk of CVD (adjusted hazard ratio [95% CI]: 1.23 [1.08-1.41]; 2331 CVD events). Conclusions: PPI use is associated with a higher risk of CVD, coronary heart disease, stroke and heart failure. Use of a drug with no known cardiac toxicity - H 2 -blockers - was also associated with a greater risk of CVD, warranting further study.


Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Donald Edmondson ◽  
Ian M Kronish ◽  
Jonathan A Shaffer ◽  
Louise Falzon ◽  
Matthew M Burg

Context: Recent evidence suggests that posttraumatic stress disorder (PTSD) may be associated with increased risk for coronary heart disease (CHD). Objective: To determine the association of PTSD to incident CHD using systematic review and meta-analysis. Data Sources: Articles were identified by searching Ovid MEDLINE, PsycINFO, Scopus, Cochrane Library, PILOTS database, and through manual search of reference lists. Study Selection: Prospective cohort studies that assessed PTSD in participants free of CHD and assessed subsequent CHD or cardiac-specific mortality. Data Extraction: We extracted estimates of the association of PTSD to incident CHD, as well as study characteristics. Odds ratios were converted to hazard ratios (HR), and a random-effects model was used to pool results. Data Synthesis: Five studies met our inclusion criteria (N= 401,712); 4 of these included depression as a covariate. The pooled HR for the magnitude of the relationship between PTSD and CHD was 1.53 (95% CI, 1.27-1.84) before adjustment for depression. The pooled HR estimate for the 4 depression-adjusted estimates (N= 362,388) was 1.22 (95% CI, 1.05-1.42). Conclusion: PTSD is independently associated with increased risk for incident CHD, even after adjusting for depression and other covariates. Figure 1. Forest plot of association of PTSD to incident MI or cardiac mortality Note: The area of each square is proportional to the study’s weight in the meta-analysis, and each line represents the confidence interval around the estimate. The diamond represents the aggregate estimate, and its lateral points indicate confidence intervals for this estimate.


Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
John W McEvoy ◽  
Faisal Rahman ◽  
Mahmoud Al Rifai ◽  
Michael Blaha ◽  
Khurram Nasir ◽  
...  

Diastolic blood pressure (BP) has a J-curve relationship with coronary heart disease and death. Because this association is thought to reflect reduced coronary perfusion at low diastolic BP, our objective was to test whether the J-curve is most pronounced among persons with coronary artery calcium. Among 6,811 participants from the Multi-Ethnic Study of Atherosclerosis, we used Cox models to examine if diastolic BP category is associated with coronary heart disease events, stroke, and mortality. Analyses were conducted in the sample overall and after stratification by coronary artery calcium score. In multivariable-adjusted analyses, compared with diastolic BP of 80 to 89 mmHg (reference), persons with diastolic BP <60 mmHg had increased risk of coronary heart disease events (HR 1.69 [95% confidence interval 1.02-2.79]) and all-cause mortality (HR 1.48 [95% confidence interval 1.10-2.00]), but not stroke. After stratification, associations of diastolic BP <60 mmHg with events were present only among participants with coronary artery calcium >0. Diastolic BP <60 mmHg was not associated with events when coronary artery calcium was zero. We also found no interaction in the association between low diastolic BP and events based on race. In conclusion, diastolic blood pressure <60 mmHg was associated with increased risk of coronary heart disease events and all-cause mortality in the sample overall, but this association appeared strongest among individuals with elevated CAC; suggesting that added caution may be needed when pursuing intensive BP treatment targets among persons with subclinical atherosclerosis.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Sanne A Peters ◽  
Rachel R Huxley ◽  
Mark Woodward

Introduction: A previous pooled analysis suggested that women with diabetes are at substantially increased risk of fatal coronary heart disease (CHD) compared with affected men. Additional findings from larger and more contemporary studies have since published on the sex-specific associations between diabetes and incident CHD. We performed a systematic review with meta-analysis so as to provide the most reliable evidence of any sex difference in the effect of diabetes on subsequent risk of CHD. Methods: PubMed MEDLINE was systematically searched for prospective population-based cohort studies published between on January 1, 1966 and February 13, 2013. Eligible studies had to have reported sex-specific estimates of the relative risk (RR) for incident CHD associated with diabetes, and its associated variability. Random effects meta-analyses with inverse variance weighting were used to obtain sex-specific RRs and their ratio (RRR). Results: Data from 64 cohorts including 858,507 individuals and 28,203 incident CHD events were included. The RR for incident CHD associated with diabetes compared with no diabetes was 2.83 (95% confidence interval [CI]: 2.37, 3.38) in women and 2.11 (95% CI: 1.79, 2.50) in men. The multiple-adjusted RRR for incident CHD was 44% greater in women with diabetes than it was in men with diabetes (95% CI: 27; 63) with no significant heterogeneity between studies (I2=20%). Conclusions: Women with diabetes have more than a 40% greater risk of incident CHD compared with men with diabetes. Sex disparities in pharmacotherapy are unlikely to explain the excess risk in women. Instead, a greater deterioration in cardiovascular risk profile combined with more prolonged exposure to adverse levels of cardiovascular risk factors among pre-diabetic women compared with their male equivalents may be responsible for the excess risk of diabetes-related CHD in women. Future studies are warranted elucidate the mechanisms responsible for the substantial sex-difference in diabetes-related risk of CHD.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Logan Cowan ◽  
Pamela Lutsey ◽  
Jim Pankow ◽  
Kunihiro Matsushita ◽  
Junichi Ishigami ◽  
...  

Introduction: Acute infections are known triggers of coronary heart disease (CHD). It is unclear how the strength of the association varies by infection type. Hypothesis: We hypothesized that all acute infections increase CHD risk but the level of increased risk varies by infection type. Methods: Incident CHD (myocardial infarction and fatal CHD) cases were identified and adjudicated in the ARIC cohort. ARIC participants were linked to Medicare claims data. We used ICD-9 codes to identify 4 infection types based on infection frequency: cellulitis, pneumonia, urinary tract infections (UTI), and bloodstream infections. We used a case-crossover design and conditional logistic regression to compare infections among CHD cases 90 days before the event with two corresponding control periods 1 year and 2 years prior. The Wald test was used to assess differences between infection types. Results: A total of 1,312 CHD cases were identified. Among cases, 43 had cellulitis, 102 had pneumonia, 116 had a UTI, and 28 had a bloodstream infection within 90 days of the CHD event. All infection types were associated with higher CHD risk within 90 days of the infection; (odds ratios and 95% Cis) (cellulitis = 1.41 (0.93, 2.15), pneumonia = 5.60 (3.72, 8.43), UTI = 2.62 (1.92, 3.57), bloodstream infections = 4.77 (2.34, 9.71)) although cellulitis was not statistically significant (Figure). The association between infection and CHD was significantly stronger for pneumonia, UTI, and bloodstream infections compared to cellulitis (p<0.05). Pneumonia and bloodstream infections were stronger CHD triggers compared to UTI but only pneumonia reached statistical significance (p<0.05). Conclusions: Patients with pneumonia or bloodstream infections may be at particularly elevated CHD risk. Clinical trials of CHD preventive therapies during and immediately following infection to reduce the otherwise elevated CHD risk are needed. Healthcare providers should consider CHD risk during and immediately after infection and optimize preventive therapies.


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