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Coronary Artery Disease, Diabetes, And Dementia: What's The Relationship?
Comorbid coronary artery disease (CAD) and diabetes are associated with an increased risk for dementia, according to study findings published in the European Journal of Preventative Cardiology.
Diabetes is associated with increased risk for cardiovascular diseases and those with comorbid CAD are at increased risk for myocardial infarction and cerebrovascular events.
Researchers from Aarhus University in Denmark hypothesized that patients with comorbid diabetes and CAD could also be at increased risk for dementia. The researchers sourced data for this study from nationwide registers in Denmark. Individuals (N=103,859) aged 65 and older who underwent coronary angiography between 2003 and 2021 were evaluated for dementia through 2022 on the basis of diabetes and CAD statuses.
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[T]he risk of dementia associated with diabetes is partly mediated through the presence of atherosclerotic CVD, which underscores the importance of atherosclerotic CVD prevention in diabetic patients to reduce the risk of cognitive decline.
The study cohort comprised patients with:
The events per 1000 person-years for each group were as follows:
Control group:
Diabetes group:
CAD group:
Comorbid diabetes and CAD group:
Compared with control individuals, all-cause dementia was associated with CAD (adjusted hazard ratio [aHR], 1.11; 95% CI, 1.03-1.20) and comorbid diabetes and CAD (aHR, 1.37; 95% CI, 1.24-1.51).
Alzheimer dementia was associated with comorbid diabetes and CAD (aHR, 1.41; 95% CI, 1.23-1.62). Vascular dementia was associated with CAD (aHR, 1.28; 95% CI, 1.10-1.49) and comorbid diabetes and CAD (aHR, 2.03; 95% CI, 1.69-2.45).
Meanwhile, stroke was associated with diabetes (aHR, 1.46; 95% CI, 1.25-1.70), CAD (aHR, 1.27; 95% CI, 1.18-1.37) and comorbid diabetes and CAD (aHR, 1.87; 95% CI, 1.70-2.06).
Among patients with comorbid diabetes and CAD, all-cause dementia (aHR, 1.34; 95% CI, 1.08-1.66) and Alzheimer dementia (aHR, 1.39; 95% CI, 1.01-1.91) were associated with diffuse vessel disease. However, vascular dementia was associated with 1 vessel (aHR, 2.07; 95% CI, 1.41-3.02), 3 vessel (aHR, 1.79; 95% CI, 1.20-2.66), and diffuse vessel (aHR, 2.04; 95% CI, 1.34-3.10) diseases relative to diabetes without CAD.
Diabetes duration, insulin use, and gender were also predictors for all-cause dementia among patients with comorbid diabetes and CAD. Regardless of CAD status, patients with diabetes who had glycated hemoglobin above the 75th percentile were at increased risk for all-cause dementia. Patients with type 1 diabetes were at lower risk for all-cause dementia than those with type 2 diabetes (aHR, 0.73; 95% CI, 0.56-0.96).
The major limitation of this study is that dementia is substantially underdiagnosed, so some cases may have been missed in this study.
"Our results suggest that the risk of dementia associated with diabetes is partly mediated through the presence of atherosclerotic CVD, which underscores the importance of atherosclerotic CVD prevention in diabetic patients to reduce the risk of cognitive decline," the researchers concluded.
Disclosures: Some study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of disclosures.
PAD Effects In Acute Coronary Syndrome Attenuated With Early Medical Management
The effects of peripheral artery disease (PAD) on outcomes of acute coronary syndrome (ACS) may be mitigated with early medical management and ongoing preventative strategies, according to study findings published in The American Journal of Cardiology.
Investigators sought to assess in-hospital outcomes in ACS across varying lower extremity arterial disease severities. In-hospital mortality was the primary outcome. Secondary outcomes included acute kidney injury, cardiac arrest, and rates of cardiogenic shock.
The investigators conducted a retrospective cohort analysis using the 2016 to 2020 Nationwide Readmissions Database (NRD) and ICD-10 codes to identify a national cohort of patients with varying degrees of PAD and query those patients hospitalized for ST-elevation myocardial infarction, non-ST-elevation myocardial infarction, and unstable angina. Briefly, the NRD provides reliable estimates for nearly 60% of all hospitalizations in the US and allows for tracking readmissions across different hospitals within the same calendar year.
Patients (approximately 3,834,181 hospitalizations) were stratified into either PAD, non-PAD, or critical limb ischemia (CLI).
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PAD severity was associated with worse clinical outcomes in patients with ACS, including in hospital mortality and resource utilization."
Among all hospitalizations, 6.4% had PAD, 0.2% had CLI, and the remainder were non-PAD. Patients in the PAD cohort were generally older, more commonly women, with higher median Elixhauser Comorbidity Index compared with non-PAD patients. Patients with PAD were more likely to experience congestive heart failure, end stage renal disease, and liver disease.
Compared with non-PAD, in-hospital PAD mortality was 24% higher (adjusted odds ratio [aOR], 1.24; 95% CI, 1.21-1.28) and CLI mortality was 86% higher (aOR, 1.86; 95% CI, 1.62-2.09).
Compared with non-PAD, CLI was linked to 1.67-fold (95% CI, 1.45-1.86) greater odds of cardiogenic shock, and PAD was linked to 1.23-fold (95% CI, 1.20-1.26) greater odds of cardiogenic shock.
Compared with non-PAD, higher odds of acute kidney injury, cardiac arrest, and mechanical circulatory support usage were linked with PAD and CLI. Additionally, patients with PAD or CLI had greater hospitalization costs, duration of hospital stay, odds of nonhome discharge, and 30-day readmissions.
Study limitations include the retrospective design, inherent coding errors in electronic data, the degree of PAD was assessed using ICD-10 codes instead of direct clinical information, and lack of information on adherence and patient lifestyle.
"PAD severity was associated with worse clinical outcomes in patients with ACS, including in hospital mortality and resource utilization," the investigators concluded. "Insights from our study call for ongoing preventive and early medical management strategies to mitigate the effects of peripheral artery disease on outcomes of ACS."
Man With High Cholesterol Might Need A Higher Dosage Of Meds
FROM NORTH AMERICA SYNDICATE, 300 W 57th STREET, 15th FLOOR, NEW YORK, NY 10019
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TO YOUR GOOD HEALTH #12345_20240723
FOR RELEASE WEEK OF JULY 22, 2024 (COL. 2)
BYLINE: By Keith Roach, M.D.
TITLE: Man with high cholesterol might need a higher dosage of meds
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DEAR DR. ROACH: I am a 69-year-old male who is being treated for high blood pressure and high cholesterol; both are well-controlled. My recent cholesterol level was 150 mg/dL with an LDL of 56 mg/dL and an HDL of 42 mg/dL. I'm on 10 mg of rosuvastatin, and I do intensive workouts with a trainer four days a week and hike two to three days a week. I never get chest pain or unreasonable dyspnea. I have lost 20 pounds in two years. My mother had a cardiac stent put in at 82 and died of aortic stenosis at 86.
Four years ago, my CT calcium score was 920. I had another test done this week, and my score was 1,100. I see a cardiologist annually because of it. My EKG is normal, and my cardiologist appears unconcerned about these results. He told me to take 81 mg of aspirin a day, but advised against a stress test since I'm asymptomatic.
He said that over time, the calcium deposits can "coalesce" and raise the score, but this doesn't mean I have fatty plaque that could rupture and cause an unexpected heart attack. He feels that I probably have stable coronary artery disease that could eventually cause warning symptoms, which is when he would do the testing.
It was my primary care physician who ordered the test. My cardiologist discouraged doing it. His advice makes sense to me, but should I get a second opinion? -- C.S.
ANSWER: I agree with your cardiologist about not getting a stress test. You are already on the appropriate medical treatment for coronary artery disease (blockages in the arteries), so making 100% certain of the diagnosis wouldn't change that. Even if you had an angiogram, in absence of symptoms, there is pretty good evidence that placing a stent would not prevent a heart attack or make you live longer, since you are on effective medical treatment.
There has been much debate about whether a beta blocker would be of benefit in preventing a heart attack in people who have stable coronary artery disease without symptoms. A recent study seemed to show a small benefit in preventing a heart attack, but the jury is still out. Finally, a higher dose of rosuvastatin to get your LDL even lower may also slightly reduce your risk of a heart attack. Studies have shown an increased benefit all the way to an LDL level of 30 mg/dL.
DEAR DR. ROACH: I've lived the majority of my 72 years in great health, which I attribute to daily exercise and good nutrition. So, I was surprised when a mild bronchial infection left me with a severely plugged ear that sounds like someone has slipped a potato chip bag in my ear canal.
I've tried all the Google remedies -- heat, as well as a mixture of water and hydrogen peroxide using a dropper -- but no success. Could this be a wax buildup? -- B.L.
ANSWER: It's possible, but I don't think so. The association with the bronchial infection leads me to suspect the problem isn't in the external ear. It might be in the middle ear because of an inability to equalize pressure due to dysfunction of the Eustachian tube, which probably got congested during your viral respiratory infection. It will get better, but a decongestant can remedy it faster.
Incidentally, I don't recommend hydrogen peroxide in the ear, even if it's diluted. It's too irritating to the ear canal skin. Over-the-counter ear drops are safer, but you should have an exam to see whether your ears are plugged up by wax.
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Dr. Roach regrets that he is unable to answer individual letters, but will incorporate them in the column whenever possible. Readers may email questions to ToYourGoodHealth@med.Cornell.Edu or send mail to 628 Virginia Dr., Orlando, FL 32803.
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